SURGERY - Complete 2nd Ed

(YEAR 3 & 5 MODULE)
-Student Edition-
Second ed.
Written by:
JP8F.Co (@)
From authors
Salam and hi. This e-book consists of medical notes we made

throughout 5 years of med school. This Year 3 & 5 module consists of
all major postings in medicine. The notes are made for our Final
Profesional Exam. We’ve compiled all the notes we made and turn it
into this e-book. Sleepless nights have we encountered to finish these
notes during our final pro exam.
Pls take into consideration our efforts to come up with the notes.
Do not distribute, print or use this notes freely.
We hope you find them useful.
- JP8F.Co –
Acknowledgement
To our beloved doctors, lecturers, consultants, medical textbooks and

friends. Thank you for your contribution directly and indirectly. 
Second edition: Update on 27 Julai 2016
For orders:
Contact: 016 – 5121732 or [email protected]
RM 80.00 (EM / WM)
Customer’s name here | ©JPBF i
INDEX
34. LIVER ABSCESS 67
TOPICS PAGE 35. VIRAL HEPATITIS 68
1. EXAMINATION SWELLING 1 36. HEPATOCELLULAR
69
2. EXAMIANTION ULCER 2 CARCINOMA
3. ACUTE APPENDICITIS 3 37. CHOLANGIOCARCINOMA 70
4. ACUTE PANCREATITIS 8 38. OBSTRUCTIVE UROPATHY 71
5. ACUTE CHOLECYSTITIS 12 39. URINARY SYSTEM CALCULI 72
6. ABDOMINAL MASS 13 40. URINARY SYSTEM- INFECTION 76
7. GIT OBSTRUCTION 14 41. URINARY SYSTEM TRAUMA 81
8. INTESTINAL OBSTRUCTION 15 42. HEMATURIA 85
9. COLONRECTAL CANCER 17 43. URINARY SYSTEM- NEOPLASM 87
10. DYSPHAGIA 24 44. THYROID DISEASES 97
11. OESOHAGEAL DISEASES 27 45. THYROID MALIGNANCY 99
12. GASTRO OESOPHAGEAL 46. THYROIDITIS 101
29
REFLUX (GERD) 47. BENIGN BREAST DISEASES 103
13. GIT BLEED 31 48. CARCINOMA OF BREAST 105
14. UPPER GI BLEED 34 49. ARTERIAL DISEASE 109
15. VARICEAL BLEEDING- PORTAL 50. TYPES OF ULCERS 111
35
HYPERTENSION 51. VARICOSE VEIN 111
16. PEPTIC ULCER 39 52. BENIGN SKIN DISORDERS 113
17. GASTRIC CARCINOMA 43 53. FAMILIAL ADENOMATOUS
114
18. GASTRIC OUTLET POLYPOSIS (FAP)
46
OBSTRUCTION (GOD) 54. HEAD INJURY 116
19. ACUTE EROSIVE GASTRITIS 46 55. MAXILLOFACIAL TRAUMA 119
20. OESOPHAGITIS 46 56. CHEST TRAUMA 121
21. MALLORY-WEISS SYNDROME 47 57. ABDOMINAL TRAUMA 124
22. LOWER GI BLEED 48 58. BURN 128
23. DIVERTICULAR DISEASES 49 59. PAIN MANAGEMENT 134
24. INTUSSUSCEPTION 51
25. MECKEL’S DIVERTICULUM 51
26. HEMORRHOIDS 53
27. ANGIODYSPLASIA 57
28. INFLAMMATORY BOWEL
58
DISEASES
29. JAUNDICE 61
30. OBSTRUCTIVE JAUNDICE 64
31. GALLSTONES
65
(CHOLELITHIASIS)
32. CHOLEDOCHOLITHIASIS 66
33. ASCENDING CHOLANGITIS 66
Customer’s name here | ©JPBF ii

EXAMINATION OF SWELLING-LUMP Mnemonics: She CutS The Fish PERfectly
3S- Site, Size (+Shape), Skin

Site Describe in exact anatomical term
Used o’clock position and distance from point
• Breast:- from nipple Per rectal:- from anal vulge
Shape + Size Nodular, pear shaped, kidney shaped
Need measurement in various dimensions- used tape (?x?x?)
Skin Underlying skin- smooth, shiny or thick and rough
Present of scars, discharge, ulcer, blood
• 3C- Colour, Consistency, Contour (margin)

Colour Comment on skin- discolouration
Consistency Hard, firm, soft
Contour (margin) Well defined or irregular margin
• S- Surface
Surface Smooth or irregular or globular
• 3T- Temperature, Tenderness, Transillumination (translucence)

Temperature Hot or normal temperature- inflammation (use dorsal of hand)
Tenderness Which part is tender? Area of maximum tenderness?
Transillumination Require bright pinpoint light source and darkened room
(translucence) Place light source on one side of the lump (not at top!)
• Positive:- contain clear fluids (H2O, serum, lymph, plasma, highly refractile fat)
• Negative:- contain opaque fluids (blood) or solid tissues
• 3F- Fixation (or mobility), Fluctuation, Field (Lymph nodes)

Fixation Relation to overlying and deeper structure
(or mobility)  Skin: move when lifting skin up or puckering
 Muscle: reduce mobility (move lump when muscle relax and when contract)
 Bone: unable to move (or very little)
 Vessels or nerve: move side by side across the length, but cannot move up and down
along the length
 Intestine, mesentry or omentum: freely mobile
Fluctuation Fluid filled lump- all surfaces protrude
Solid filled lump- may or may not bulge (if bulge- not in all direction)
Field Examine for palpable lymph node- according to region
• PER- Percussion, Expensile pulsatile, Reducible

Percussion Fluid thrill
Resonance or dull
Expensile Transmitted pulsation- pushed upwards and downwards
pulsatile Expansile pulsation- pushed in same direction (upwards)- aneuryms & vascular tumour
Reducible vs Reducible: disappear after compressing, appear back with cough impulse- hernia or
compression vascular lumps features
Compression: disappear after compressing, appear back after removing pressure- vascular
malformations or fluid collections features
Others: Bruits (auscultate)
Customer’s name here | ©JPBF 1

EXAMINATION OF ULCER
Definition= Break in epithelial lining extending into epidermis & dermis (if only epidermis = erosion)
How to describe ulcer?
INSPECTION (BBEDDS) or can use TIME (Tissue, Inflammation, Moisture, Edge)

Basics- site, size, shape, number
Base- floor of the ulcer
 Colour (red-healing, black-necrotic, yellowish white-slough)
 Granulation tissue, healthy looking
 Exposed structure (bone, joint, tendon, neurovascular bundle)
 Margin (regular, irregular)
Edge Necrotic foot
 Flat, sloping = venous
 Punched out = arterial (pain), neuropathic (no pain)
 Undermined = pressure sores
 Rolled edge = basal cell carcinoma
 Everted edge = squamous cell carcinoma Slough ulcer with
Depth- measure in height regular margin
Discharge/Moisture
 Dry
 Moist
 Hyperexudate
o Serous (clear) 60% of ulcer size
o Blood showed healthy
o Purulent granulation tissue
Surroundings
 SKIN- thin, fragile, hairless = decreased vascular supply
 COLOUR- cyanosis (ischemia), brown (hemosiderosis- subcutaneous bleeding over period of
time),
 CALLUS- thick, rough, yellow skin patches
 SCAR- to assess wound healing
 OEDEMA- localized or extend in one or both direction of wound
 NAIL- brittle, thick, too long, ingrown, fungal infection
 Limb DEFORMITY
Other inspection: gait, pes cavus or planus, shoes wear, muscle wasting
PALPATION
1. Temperature
2. Tenderness
3. Consistency surrounding tissues
4. Palpable lymph node
5. Sensation- pin-prick, 128Hz turning fork, proprioception, monofilament
6. Distal pulse (DPA/PTA)- CRT
*Other palpation: ankle reflexes, sweaty, dry cracked skin (Autonomic neuropathy)

ACUTE APPENDICITIS = is the inflammation of the appendix
Aetiology- Luminal obstruction
i. Fecolith
ii. Neoplasm
iii. Parasite- threadworm (enterobius vermicularis)
iv. Foreign body
Pathogenesis
Obstruction  increased intraluminal pressure 
inflammation  bacterial overgrowth  ischemia 
gangrene/perforation  abscess (mass) or peritonitis
Clinical features
1) Abdominal pain:
 Early – Periumbilical due to appendix obstruction What is length, diameter and position of
(ill defined-visceral pain by sympathetic nerve) appendix?
 Late – RIF due to local inflammation of peritoneum  Length: 8-13cm (average 11cm)
(localized- parietal pain by somatic nerve T5-L2)  Diameter: <5mm (AP direction)
2) Nausea and Vomiting  Position: to posteriomedial surface of caecum
about 2.5cm below ileocaecal junction
3) Low grade fever [40°C- complicated peritonitis/abscess]
(Mc Burney’ point:- grossly at 1/3 from ASIS to
4) Anorexia (LOA) umbilicus)
Physical examination
1) General: septic, fever ± chills/rigor, dehydrated How to identify base of appendix?
2) Abdominal: soft, tender at RIF (at Mc Burney’s point)  Identify teniae coli of caecum & track it down
 Rovsing/obturator/psoas +++  Will converge at base of appendix and merge
 Rebound & guarding +++ (perforated peritonitis) into longitudinal muscle coat of appendix
Investigation
1. FBC- leucocytosis (but not diagnostic) What is the blood supply of appendix?
 Artery: Appendicular A  Post caecal A 
2. To rule out other differential
Iliocaecal A
i. UFEME – UTI and DM
 Vein: Appendicular V  Post caecal V
ii. S.amylase – pancreatitis
iii. LFT When appendix developed?
iv. UPT – ectopic pregnancy  During 5th month of gestation
3. Imaging
i. CXR – to look for air under diaphragm What is function of appendix?
(perforation) or evidence of calculi
ii. AUS – if suspicious to look for fluid (perforation)
Diagnosis: mainly based on clinical
(come to A&E: ill looking, bend forward, hand grip RIF)
Complication
1. Appendicitis mass/abscess
2. Perforation (3 days after onset)
3. Peritonitis

Principle of management
Admit for further management
2. Keep NBM with IV (dextrose)
3. Analgesic
4. Antibiotics (metronidazole + cephalosporin)
 Prophylatic – for non-perforated appendicitis (single dose)
 Therapeutic – for perforated or gangrenous appendicitis (for 3-5 days)
5. Monitor vital signs
6. Appendicectomy
Surgical approach for appendicitis
 Acute or perforated appendicitis  open Appendicectomy
 If unlikely appendicitis but worsening condition  Exploratory laparoscopy
Laparoscopic appendicectomy
Advantages: less pain, shorter recovery, better for obese, allow inspection of peritoneal contents,
lower post-op wound infection rate
How to prepare patient for appendicectomy

1. NBM
2. Set IV line- give IV fluid
3. Call anaesthesia and booked for OT
4. Consult patient
 Explain diagnosis of appendicitis based on clinical features
 Treatment no option- appendicectomy is the definitive treatment
 Risk of surgery (no surgery devoid of risk!)
o Non perforated appendicitis - <0.1% mortality rate
o Perforated appendicitis- ≈5.0% mortality rate
5. Ask about last meal- operate 6-8H after last meal (emergency)
6. Get written informed consent
Possible complication of appendicectomy
1. Anaesthesia complication- Airway and Breathing (aspiration pneumonia, hoarseness of
voice, laryngeal oedema)
2. Surgical complication
Early complication Late complication
i. Wound infection i. Subphrenic and pelvic abscess
ii. Haemorrhage ii. Feacal fistula
iii. Paralytic ileus
iv. Intestinal adhesion
Post –operative Management

1. Check A,B (RR/Spo2- if very ill) & C (PR, BP)- hourly
2. Monitor temperature: fever
3. Nil orally till order
 Why Nil?- for abdominal surgery afraid of paralytic ileus
 Notes for passing flatus and bowel sound before consider orally
*For breast surgery- allow orally when post-nausea and fully conscious (4H)
4. Continue IV fluid and electrolyte
5. Give analgesic (fentanyl/pethidine) - route parental (IM/IV)
6. Give antibiotics (Therapeutic – cefuroxime, 3rd generation Cephalosporin)
7. Wound monitoring

When to discharge patient
1. Improve on general condition
 Look well, take orally, VS stable, no fever
2. Give advices
 Medical leave (MC)- 2 weeks
 No strenuous activity/PJ- 3 months
 Sex or not?- but not so vigorous/let partner do the job
 Can eat anything- no limitation on diet
Complication of acute appendicitis
1. Appendicular abscess
Perforation of appendix but collection of pus enclosed within mass of adhesion
Clinical features: continuous spiking of fever and additional symptoms of abscess (fever +
sweating + rigor + increase local pain)
Examination: oedema + redness of skin
Treatment
i. USG/CT guided percutaneous drainage or open drainage
ii. Discharge
iii. After 6 weeks do interval appendicectomy
2. Perforation of appendix  General peritonitis
Perforation at base of appendix  inflammation of peritoneum
Consequences:
Shift fluid into peritoneal cavity and bowel  severe dehydration & electrolyte imbalance
 untreated lead to sepsis and adult RDS  multiple organs failure  death within days
Who at risk of perforated

1. Elderly:- due to omentum atrophy
2. Children:- due to omentum poorly developed
3. Immunocompromised
Clinical features: rebound and guarding, very high fever (>40°C), pain aggravated by
movement and coughing, generalized board like rigidity, absent bowel sound
Treatments: stabilize patient & operate ASAP

i. Intense IV broad spectrum antibiotics
ii. IV fluid infusion
iii. Gastric aspiration
iv. Removal appendix
v. Thorough peritoneal
toileting

APPENDICULAR MASS
= history suggestive of appendicitis + RIF mass after antibiotic treatment of appendicitis
Pathogenesis
Inflamed appendix  wrapped by omentum (policeman of GIT)  wall of peritoneal cavity of
omentum & adjacent bowel loop formed tender & palpable RIF mass
3 components of appendicular mass
1. Perforated appendix
2. Omentum
3. Surrounding organs (caecum and small bowel)
Examination
 Tender, indistinct RIF mass
 Dull on percussion
 Fixed to RIF (posteriorly)
 + low grade fever
 + tachycardia
Diagnosis- confirm by ultrasound
Treatment – conservative Ochsner-Sherren regime
 Improve in condition within 24-48H, 90% resolve without incident, majority no recurrence
 What is the components of regime
What you need to do
1. Resuscitate
2. Correct electrolyte imbalance
3. Call MO- confirm diagnosis with ultrasound
4. Confirm analgesics, antibiotics
5. Draw circle around the mass- mapping
6. KIV exploratory laparatomy
7. If reduce, discharge and follow up 6 weeks
 If not reduce- appendicectomy once stable
 If reduce- discharge patient from clinic
 CF suggestive that patient is responding to conservative tx

1. Improve in general condition; appetite good
2. VS become normal
3. Reduction in size and resolution of appendicular mass
 Criteria for stopping conservative tx

1. A rising PR
2. ↑ or spreading abdominal pain
3. ↑ size of mass (marked mass on abd wall- raise suspicion of carcinoma or Crohn’s
disease)
4. Development signs/symptoms of peritonitis

Appendicitis ∆∆ (RIF pain differential)
Female Adult
Think of 3 systems
1. GIT
o acute appendicitis
 Perforated peptic ulcer
o Acute cholecystitis
o Diverticulitis
o Acute pancreatitis
o Intestinal obstruction
o Strangulated hernia
2. Urinary
 Right urinary colic
 Recurrent UTI
3. Genito
 Acute right salpingitis
o Vaginal discharge:- foul, scanty discharge (fishy smell)
o Bimanual examination- pain on abdomen when moving the cervix
 Ectopic pregnancy
o Ask LMP, pregnancy features
o Bleeding- hypovolemic shock signs- Pale, BP low, CRT >2s
o Shoulder tip pain, black out hx, Hb low
o Bimanual examination- pain on abdomen when moving the cervix
 Right ovarian torsion/rupture/cyst

 Tubo-ovarian abscess
 PID
Appendicitis mimic by
1. Mesenteric adenitis- enlarged tonsil + palpable neck LN
(appendicitis may often follow viral infection)
2. Right sided basal pneumonia- especially in children
Testicular torsion

PANCREATITIS
=inflammation of exocrine pancreas due to injury to acinar cells
Classification
 Acute/Chronic
 Mild/Moderate/Severe
 Acute interstitial/Acute haemorrhagic
Function of pancreas
1. Food metabolism- digestion &
absorption
2. Secretion of digestive enzymes
into GIT
3. Synthesis and secret insulin &
glycogen to regulate glucose
Aetiology (I GET SMASHED) Symptoms

I- Idiopathic (10%) 1. Acute onset of severe epigastric pain/RHC
 Boring in nature (dull & constant pain) 
G- Gallstones (45%) crescendo pain (become very very painful)
E- Ethanol (alcohol- 35%)  Radiate to back (Right lumbar)- girdle pain
T- Tumours of pancreas, ampulla, choledochocele  +++ by alcohol, eating fatty meals
 Lean patient
S- Scorpion or Snake bites  ---- by lending forward
M- Microbiology  Associated with N+V  shock
Bact:- mycoplasma, campylobacter, TB,  Associated with fever
leptospirosis 2. Pale colour stool and dark coloured urine- OJ
Viral:- mumps, rubella, varicella, hep, EBV, HIV
Parasite:- Ascariasis, Clonorchiasis, Signs
Echinococcosis 1. GE- febrile, tachycardia, dehydrated
A- Autoimmune 2. Transient OJ- jaundice
S- Surgery/Trauma 3. Abdomen distension- in paralytic ileus
Manipulation of sphincter of Oddi (ERCP- 15%) 4. Tender rigid abdomen
H- Hyperlipidemia (TG>11.3mmol/L), 5. Hypoactive bowel sound
Hypercalcaemia 6. Retroperitoneal bleeding (due to
Hypothermia autodigestion)- in severe pancreatitis
E- Emboli or ischemia  Periumbilical discolouration (Cullen’s
D- Drugs or toxins sign)
Steroids, didanosine, thiazide, H2 blocker,  Flank discolouration (Grey Turner sign)
tetracycline
Pathophysio- 3 mechanisms
1. Duodenal reflux (due to damage Splinter of Oddi)
2. Pancreatic juice reflux (due to obstruction- stones)
3. Biliary juice reflux (due to obstruction- stones)

Investigations
1. Serum amylase (Normal= 100-300 iU/L)
 Done within first 24H of clinical features
 ↑4x or >1000 iU/L
 Other causes of hyperamylasemia:- perforated PU, Small IO, parotid gland inflammation or
tumour, RF, Ovarian tumours
2. Serum lipase
 Has longer half life, so more useful than amylase in longer case
 But not done in hospital, we do urine diastase
3. Trans-abdominal US- for confirmation
 To evaluate changes on pancreas- swelling (big size pancrease) or peripancreatic fluid
collection & oedema
 To look for stones in ducts
 Dilatation of CBD (>11cm)
4. Other lab ix- done to do Glasgow score
 FBC- ↑leukocyte to assess severity & prognosis
 RP-
 LFT- to assess cause of pancreatitis- jaundice
 RBS- hyperglycemia due to damage in B cells
 LDH
 BUSE- to determine level of dehydration
5. CXR- Left side pleural effusion
6. AXR (Rarely done in abdominal pain- sebab finding pun rare)
 Sentinel loop- dilated adynamic SI in center
 Ground glass appearance- peritoneal exudates +++
 Colon cut off signs
 Present of gallstones
7. Endoscopic retrograde cholangiopancreatography (ERCP)- tapi may worsen the pancreatitis
8. CT abdomen (the best)

Glasgow scale (IMRIE SCORE)- PANCREAS RANSON CRITERIA
P- P02 <60mmHg Criteria present initially (WALLS)
A- Age >55 years old w- WBC >16000uL
N- Neutrophil >15x109 A- Age >55 years old
C- Ca+ <2.0mmol/L (hypocalcaemia) L- LDH >350 U/L
R- Renal urea >16mmol/L L- LFT- AST >250 u/L
E- Enzyme LDH >600iU/L, AST >100u/L S- Sugar >10mmol/L
A- Albumin <32g/L
S- Sugar >10mmol/L (hyperglycaemia) Criteria developing during 1st 24H (FOr CHUB)
F- Fluid requirement >6L
O- Oxygen (P02) <60mmHg
Score:- 2+ moderate, 3+ severe C- Ca+ <8mg/dL (hypocalcaemia)

H- Haematocrit decreased 10%
U- Urea raised (BUN) >5mg/dL
B- Base deficit >4mmol/L (metabolic acidosis)
Management of pancreatitis
Medical mx
1. Haemodynamic stability- secure ABC
2. Rest bowel – KNBM + IV drip
3. Monitoring vital signs
4. Nasogastric draining for decompression/suction
5. Alleviate pain- analgesics (tramadol)
*Never, and never give analgesics in A&E- only give after diagnosis established & seen by
MO/Specialist
6. Stop progression of damage- suppress pancreatic secretion (Octreotide- somatostatin
analogue)
7. If has potential to develop COMPLICATION : do severe scoring system, to predict whether
mild, moderate (HDU), severe (get into ICU)- then treat complications!
8. No antibiotics given for fever- sebab fever dia due to autoimmune
Surgical mx
Indication
1. Diagnosis uncertain
2. Fail to respond to medical treatment
3. Gallstones developed
4. Complication developed
Approach depend on the causes of pancreatitis

1. Acute gallstone pancreatitis  Cholecystectomy, Spincterotomy (ERCP)
2. Recurrent pancreatitis with sphincter dysfunction  Major papilla sphincterotomy
3. Pancreas divisum (congenital anomaly)  Minor papilla sphinterotomy
Complication of pancreatitis
Local complication Systemic complication
1. Pancreatic pseudocyst 1. Fluid accumulated in pleural space 
2. Infected necrotizing pancreatitis pleural effusion, atelectasis,
3. Hemorrhagic pancreatitis pneumonia, acute RDS
4. Pancreatic abscess 2. Hyperglycaemia
5. Chronic pancreatitis 3. Acute renal failure

What is Pancreatic pseudocyst
 Cyst-like structure encapsulated with fibrous material, not epithelium
 Collection of pancreatic juices outside of the normal boundaries of the ductal system- high
amylase
 Developed 2-3weeks after attack
 Clinical features: Persistent/intermittent abdominal discomfort, vomiting, jaundice
 Classification
o Type 1- normal duct, no fistula between duct and cyst
o Type 2- abnormal duct, no fistula
o Type 3- abnormal duct, with fistula
 Ix: USG/CT/ERCP
 Mx: >50% resolve spontaneously within 3months
o Drainage (percutaneous/endoscope/surgical)
o Surgery if enlarging cyst, to avoid infection, haemorrhage, rupture
Do ERCP with long stenting of pancreatic duct

ACUTE CHOLECYSTITIS = inflammation of GB
 2-3x more common in female
 Incidence increase with age
 Aetiology
Calculous- 90-95% of cases Acalculous- 10% cases
 Related to obstruction of cystic duct by  Related to bile stasis
gallstones  Due to ischemia of GB, spasm of sphinter
 Risk factors: 4F of Oddi, systemic diseases or infection
Symptoms Investigations
1. RUQ pain 1. Trans-abdominal US
 Radiate: Right shoulder/tips of scapula- Boas’  Thickening of GB wall
sign  Acoustic shadow
 Increase with deep breath  +/- GB stones
2. Fever 2. AXR- to rule out other causes
3. Nausea & vomiting 3. Serum amylase- exclude pancreatitis
4. Abdominal distension 4. FBC- WBC raised
5. LOA- anorexia, feeling of fullness 5. LFT- ALP raised
6. CT abdomen and pelvis- gold standard but
only used in uncertain case
Signs
1. Tachycardia Principle of management
2. Jaundice- only present with association of 1. Conservative mx: 90% settle
choledocolithiasis or mirizzi’s syndrome  Keep NBM with IV fluid
3. Abdominal tenderness + rigidity  Antibiotics- cefazolin, gentamicin
4. RHC mass- due to omentum wrapped around  Analgesics- miperidine
inflamed GB 2. Surgery: Cholecystectomy (After 6w
5. Catching of breath during inspiration while conservative treatment- wait for
pressing GB area- Murphy’s sign inflammation to subside)
*GB area:- tranpyloric plane (tips of 9th ICC) + 3. Emergency cholecystectomy- if come back
mid clavicular within 72hours
Complication
1. Empyema (tender mass + rigor + marked pyrexia)
2. Gangrene  perforation  biliary peritonitis
3. Chronic cholecystitis
 Recurrent flatulence, fatty food intolerance
 RUQ pain- worsen by meal, associated with feeling distension and heartburn

ABDOMINAL MASS
*how to differentiate and describe organ mass

Shape Location Enlargement Movement
LIVER Triangular Right upper quadrant Cannot get above the Moves with
MASS 7th – 11th rib mass respiration
Lower border palpable
below costal margin
GB MASS Globular Right upper quadrant Cannot get above the Moves with
Below tip of 9th rib mass respiration
Can get around the
mass
SPLEEN Oval Left upper quadrant Enlarges towards Moves with
MASS Beneath 9th – 11th rib umbillicus respiration
Axis of spleen at 10th rib Traube space: Dull Cannot insinuate
hand
Traube space: Dull
KIDNEY Bean Both lumbar area Enlarged towards Does not move
MASS shaped Left higher than right illiac fossa with respiration
Renal angle: 12th rib at Resonance on
the spinous muscle percussion
Ballotable
 Intraperitoneal: moves with respiration
 Retroperitoneal: does not move with respiration
 Abdominal mass will become more prominent when tensing the muscle: raising head or
lifting the leg

GIT OBSTRUCTION
VOMITING COLICKY PAIN ABDOMINAL PERCUSSION- CONSTIPATION Most common causes
DISTENSION AUSCULTATION
OESOPHAGUS  Very early (seconds)  ↓ in passing faeces 1. Ca esophagus
 Undigested foods  Able to pass flatus
 No acid (relative constipation)
 No bile juice
PYLORUS  Within 2hours 1. Congenital- pyloric stenosis
(STOMACH)  Food not yet digested 2. Ca pylorus
 Present of acid 3. Chronic peptic ulcer
 No bile juice
Site of obstruction
1. Above
2. Below- presented with
projectile vomiting bcoz strong
force from stomach due to
high intra-abdominal pressure
SMALL  2-4Hours  2-3x/min  Central  Percussion-  Unable to pass faeces 1. Adhesion due to previous
INTESTINE  Digested food  Every 2-20min (more distal, more resonance (bowel  Unable to pass flatus surgery
 Present of acid & bile juice  Umbilicus greater degree filled with gases) (absolute constipation- 2. Hernia
(higher SBO) distension)  Auscultation- metallic LATE features)
 Brown, foul smell vomitus click (pressure high
(lower SBO) due to gases)
LARGE INTESTINE  Very late (days)  1x/min  Peripheral Gurgling borborygmi  Unable to pass faeces 1. Ca colon (rectum/sigmoid)-
 Faeculent vomitus (thicker,  Once in 30min (generalized marked)  Unable to pass flatus 65% chronic onset
foul smell) (less colicky) (absolute constipation- 2. Pseudo-obstruction- 20%
 Suprapubic EARLY features) 3. Diverticulitis- 10%
4. Volvulus of sigmoid colon-
5%
acute onset
Paralytic ileus  Effortless vomiting Pain not prominent  Distended  Bowel sound absent  Unable to pass faeces Clinically significant if 72H after
(Pt anxious and  Tender (silent abdomen)  Unable to pass flatus operation (eg: laparotomy)
uncomfortable)  No visible (absolute constipation) AXY: gas filled loops of intestine
peristalsis with multiple fluid level

INTESTINAL OBSTRUCTION (Blockage  Obstruction)
= stoppage of cranio-caudal movement of bowel contents due to narrowing or complete blockage of
bowel lumen
 Common surgical emergency, serious in nature, demands early diagnosis and speedy relief
 Small bowel more common & more severe than large bowel
Classification
Dynamic ileus Adynamic ileus
=mechanical ileus =paralytic ileus
 Peristalsis is working against a mechanical obstruction  Paralysis of intestinal musculature
 May be acute or chronic  Characterized by absence of
 Associated with abdominal pain peristalsis and pain
How thing can get block? Common causes
Inside lumen In wall Outside lumen 1. Postoperative
(Intraluminal) (Intramural) (extramural) 2. Peritonitis
 Round worm  Stricture  Adhesion/bands 3. K+ low
(ascariasis)-  Fibrosis  Hernia 4. Pelvic and spinal fracture
children  Cancer/tumor  Volvulus 5. Parturition
 Gallstone  Crohn’s
 Faecal impaction disease (IBD)
 Foreign bodies
Dynamic obstruction- further classification
1. Speed of onset
Acute Chronic Acute on chronic Subacute
Onset rapid Onset insidious Obstruction suddenly Implies incomplete
(within days) (within months) becomes complete obstruction
Symptoms severe Slowly progressive (earlier only 1-2
Usually Small BO Usually Large BO symptoms within
weeks then another
symptoms come
later)
2. Site
SMALL intestine
LARGE intestine
Higher part Lower part
Vomiting occur early Pain is predominant  Distension early and pronounced
and profuse with rapid with central distension  Pain mild
dehydration  Dehydration is late
3. Nature
Simple Strangulated Gangrene/perforated
bowel occluded bowel occluded with damage to 1. Toxic appearance, rapid PR,
without damage to blood supply (cut off) high temperature
blood supply 1. PR ↑, no fever 2. Continuous colicky pain
2. Severe abdominal pain Fixed 3. Rigidity-rebound tenderness
localized tenderness & guarding 4. Bowel sound reduce or absent
3. Bowel sound sluggish 5. Raised TWBC
4. Aetiology (as stated above)- Intraluminal, Intramural, Extramural

Stricture – inflamed
Heal causing fibrosis
Clinical cardinal features of IO

1. Colicky abdominal pain Vary according to
2. Abdominal distension 1. Location (site)
3. Vomiting 2. Age (duration)
4. Absolute constipation 3. Underlying pathology (causes)
4. Intestinal ischemia (complication)
Other manifestations
1. Dehydrations
 Commonly in SBO due to repeated vomiting & fluid sequestration
 Signs: sunken eyes, dry skin, dry lip, poor venous filling, oliguria
 Ix: blood urea & HCT increase giving a secondary polycythaemia
2. Hypokalaemia (not common)
 increase in serum potassium, amylase or lactate dehydrogenase may be associated
with the presence of strangulation
3. Pyrexia
 May indicate:- onset ischemia, perforation, inflammation
 Hypothermia= indicate septicaemic shock
Intra-abdominal surgery- motility usually returns

 Small bowel within 24-48H
 Gastric within 48H
 Colonic within 3-5days

COLONRECTAL CANCER
 Most common GIT malignancy
RIGHT SIDED LESION LEFT SIDED LESION

Asymptomatic until late stage- so poor More common, earlier presentation (better
prognosis prognosis)
May presented with Presented with
1. Signs of anemia 1. Obstructive symptoms
 Due to chronic low grade  Faecal more solid
bleeding - ulcerative type of  Annular type of carcinoma
carcinoma 2. Altered bowel habit (constipation +
2. LOW + LOA diarrhoea)
3. No obstructive symptoms 3. Tenesmus
 Lumen on right sided more wider 4. Blood in stool
 Faeces more watery (liquid) 5. Mucus in stool
4. Palpable mass on RIF
Common sites
Common site Sigmoid Sigmoid-rectal Rectal cancer
1. Ileumcaecum junction cancer cancer junction cancer
Fx: to absorb nutrition (act as  No blood  Blood ++  Blood ++
energy)  Mucus ++  Mucus ++ (at the end of
If loss this fx, pt become very defecation-
weak/lethargy fresh blood)
 Mucus ++
 Tenesmus

History to ask
1. Symptoms as mention above
2. Predisposing factors
i. Long standing diseases- medical condition
 Inflammatory bowel diseases (IBD)
o Ulcerative colitis- Left sided (3 folds risk), pancolitis (15 folds risk)
o Crohn’s diseases- Less risk
ii. Previous surgery
 Gastractomy- altered bile acid metabolism
 Utero-sigmoidostomy
 Cholecystectomy (removal of GB)- increase secondary bile acids  act as
carcinogen
3. Find RISK FACTORS

i. Age- more than 60 years
ii. Ethnic- Chinese community
iii. Genetic factors (20%)- family history
 Familial adenomatous polyposis (FAP)- autosomal dominant syndrome
due to germ line mutation in adenomatous polyposis gene
Precancerous:- 3 subgroups
a) Villous- higher rate of malignancy (25%)
b) Tubular
c) Tubulo-villous (mixed)
Malignancy will depend on

i. Size
ii. Type
iii. Degree of epithelial dysplasia
 Lynch syndrome= hereditary non-polyposis colorectal cancer (HNPCC)
iv. Dietary factors

 High animal fats- HOW?
High excretion of bile salts  promote growth bacteria in colon 
increase degradation of bile salts to carcinogen
 High in carcinogen foods- Types of food?
Steak (well done), Smoke food (BBQ), fast food, process food
 Low in fibers- HOW?
Increase intestinal transit time  increase exposure of colonic mucosa to
potential carcinogens
Ask by serving for each meal
v. Lifestyle
 Alcohol
 Smoking
 Low exercise- obesity
 Radiation exposure
4. Rule out metastasize- 2L3B

Examination
On general examination
 Signs of anaemia
 Signs of IO
 Signs of metastasize
On Abdominal examination
 Area of tenderness
 Palpable mass
 Ascites
 Bowel sound
On per rectal examination (mostly for rectal cancer)

 Any growth
How to describe position?
Relation to anal verge
i. Distance from anal verge
ii. At what clock position- normally at 12o’clock
Other descriptions
i. Neoplasm felt like nodular with indurated bases
ii. Ulcerative and edges raised and irregular
iii. Fixity
iv. Contact bleeding- blood or mucus
Investigations
Immediate ix
1. Abdominal xray
 Faecal matter
 Empty distal rectum
Other investigations
2. Colonoscopy – gold standard
1. Site of lesion
Must know distance from anal valve to to ileucaecal junction = 150cm
(diameter=5cm)
2. Type of lesion- 4types

1. Cauliflower growth
2. Ulcerative growth- left sided IO
3. Tubular growth
4. Annular growth- right sided IO
3. Nature of lesion
1. Active bleeding
2. Partial obstruction
3. Complete obstruction
4. Any associated synchronous lesion
 For biopsy- 4-6 samples from different sites

 Can be diagnostic and therapeutic (polypectomy)

3. Barium enema- double contrast
 If colonoscopy cannot be done
 Not as good as colonoscopy- as only able to see dilatation of colon
 Findings-
o Annular (obstruction)
o Apple core appearance
4. Tumour marker
 Done before surgery and during follow up (post operative)
 2 types of tumour markers can be done
1. Carcino Embryonic Antigen (CEA)
o Not for diagnostic
o Important for progression of disease and risk of recurrence
o Normal value <4μg/ml
o Value expected to reduce after removal of tumour, if raised suspect
 Inadequate removal of tumour
 Distance metastasize
2. Alpha fetal protein
 Normal value <30
For staging purpose

1. Contrast CT abdomen and pelvis
 Helps to detect lesion
 To know extend of tumour
 To know fixation to adjacent structures
2. Ultrasound of abdomen
 Purpose same as CT but for early lesion only
 Cheap and easy
3. Chest x-ray
 Canon ball appearance
Basic blood investigations

1. FBC- Hb for anemia
2. LFT- albumin suggest malnutrition, ↑ transaminase suggest liver involvement
3. BUSE- electrolyte imbalance seen in IO
Other investigations- fix for surgery
Screening investigations
1. Faecal occult blood (FOB)
Detect blood which not visible on gross inspection
Screening in asymptomatic individual above 50 years
Screening for high risk individual (positive family hx of polyps)
FOB done yearly and colonoscopy 5 yearly
False positive results (high incidence) False negative results
 Dietary peroxidase from  Increase concentration of reducing
vegetables/fruits agents- ascorbid acids in citrious
 Hb & myoglobin from red meats fruits and vegetables
 Drug aspirin & NSAIDs- as causing
gastric mucosa erosion

Staging
1. DUKE classification
Stage Description 5 years survival Management
rate
A Confined to bowel wall (mucosa) 90% Resection of
tumour
B Infiltrated bowel wall (from mucosa to serosa) 60% Resection of
C Spread to LN 30% tumour + adjuvant
 Local LN involvement= C1 *C2 worse (radio or chemo)
 Distant LN involvement= C2 prognosis than C1
D Wide spread metastasic involvement Palliative care
2. TNM classification
Management
Preoperative
 Chemotherapy to shrink tumour
 General wellbeing management – electrolyte, anaemia
 Stabilize patient and correct electrolyte
 No solid food (must fast)
 Bowel preparation by enemas and oral stimulants
 To reduce bacterial load (faecal debris)
 Go for fluid diet for 3-4 days
 Give 2 sachets picolax (pico sulphate 1 day before operation)- to purge colon
 Antibiotic prophylaxis
 To reduce wound infection and intra-abdominal sepsis
 Start IV on induction of anaesthesia
o Standard- IV Cefuroxime 750mg + Metronidazole 500mg
o Major penicillin allergy- Ciprofloxacin 200mg + Metronidazole 500mg
Operative
 Right/left Hemicolectomy +/- perineum resection
 Removed one side of colon- 2cm either side of tumour (5cm in all direction if rectum)

 Check for signs of no-viable bowel –need to resected
i. Loss of peristalsis
ii. Loss of sheen
iii. Greenish or black (not purple)
iv. Loss of pulsation in supplying vessels
Complication
1.Perforation risk (1:1500)
2.Heavy bleed risk (1:150)
3.Mortality risk (1:10 000)
4.Sedation risk due to aspiration or RS distress
Postoperative
 Chemotherapy
 Radiotherapy NOT sensitive for adenocarcinoma (cancer colon = adenocarcinoma)
 Thus, give FOLFOX regime chemotherapy
o In combination as it kills cells at different stages
o Given in cyclical
 Monitoring & follow-up
 To look for complication of surgical procedure/adjuvant therapy
 Patient progress well or not
 To check for recurrence, do
i. Faecal occult blood (FOC)
ii. Colonoscopy
iii. Tumour marker (CEA, Alpha fetal protein)
Palliative
Chemo, radio, counselling, physiological mx, pain reliever

Notes**
Stoma
 Permanent  end
 Temporary  loop
o Ileostomy
o Colostomy (common: transverse & sigmoid)
Differences on X- RAY
Large Bowel Small Bowel
• Peripheral • Central
• Haustration- Spaced irregularly and do not • Vulvulae coniventae- Completely pass
cross the whole diameter of bowel and have across the width of the bowel and regularly
indentations placed opposite one another spaced, giving a step ladder effect
Volvulus
Subtype malrotation in which a loop of bowel is twisted about a focal point along mesentry, which
may result in a bowel obstruction
Sigmoid Volvulus Caecal volvulus
 Coffee bean sign: Gas distended sigmoid  Comma shaped

 Dilated loop of bowel presence  Dilated loop of bowel presence
 White line mesentry pointing towards left  White line mesentry pointing towards right
 high risk of perforation and/or bowel ischaemia
 Confirmed at laparotomy

DYSPHAGIA= difficulty in swallowing
Term to know well

 Dysphagia= difficulty in swallowing, not necessarily pain on swallowing
 Odynophagia= pain on swallowing
 Regurgitation= backflow; return of oesophageal contents from above an obstruction in the
oesophagus
 Reflux= passive return of gastroduodenal contents to the mouth
Causes of dysphagia
History to ask History to ask

 Food sticking in throat  What kind of food?
 Difficulty to initiate  Duration of symptoms?
swallowing  Intermittent or progressive?
 Nasal regurgitation  Associated with heartburn?
 Coughing during swallowing
Also complaint of
 Dysarthria
 Nasal speech- associated
with muscle weakness
Commonly followed stroke episode
History not to be missed Other important history

1. Hoarseness of voice  Instrument- OGDS, ETT
2. Shortness of breath  Swallow corrosive agent
3. Difficulty in swallowing  Betel nut chewing

Always remember any tube, think causes by
 Intramural
o Atresia of esophagus
o Benign stricture
 Reflux esophagitis
 Swallowed corrosive agents
 Tuberculosis
 Sclerodermal
 Radiotherapy
o Spasm
 Paterson-kelly syndrome (triad: dysphagia + anaemia + glossitis)
 Achalasia
 Webs & rings
o Neoplasm- cancer esophagus
o Diverticulum
o Neuromuscular disorder
 Bulbar paralysis
 Post-vagotomy
 Intraluminal
o Foreign body
 Extramural
o Thyroid swelling
o Retrosternal goiter
o Pharyngeal diverticulum
o Aneurysm aorta
o Mediastinal growth
o Dysphagia lusoria
Associated symptoms and possible diagnosis

SYMPTOMS DIAGNOSES TO CONSIDER
Difficulty initiating swallowing Oropharyngeal dynsphagia
Food ‘sticks’ after swallowing Esophageal dysphagia
Progressive dysphagia Neuromuscular / carcinoma esophagus
Sudden dysphagia Foreign body, esophagitis
Cough
 Early Neuromuscular
 Late Obstructive
Weight loss
 Elderly Carcinoma
 With regurgitation Achalasia
Progressive symptoms Peptic stricture, scleroderma
Intermittent Rings and webs, diffuse esophageal spasm
Pain with dysphagia Esophagitis
Pain made worse by
 Solid food Stricture / growth
 Solids and liquids Neuromuscular dysphagia
Regurgitation of old food & halitosis Zenker’s Diverticulum
Weakness and dysphagia CVA, muscular dystrophies, myasthenia gravis, multiple
sclerosis
Dysphagia made worse with cold foods Neuromuscular motility disorders

Anatomy and physiology of oesophagus
 40 cm length from incisor of teeth to cardioesophageal junction
 Upper 2/3- striated muscle  squamous cell carcinoma (90% cases)
Lower 1/3- smooth muscle  adenocarcinoma (Barret esophagous)
 3 areas of narrowing
1. At level of cricoid cartilage
2. In the midthorax- compression aortic arch and left main bronchus
3. At level oesophageal hiatus of diaphragm
 Relation to structures
1. Trachea
2. Thyroid gland
3. Carotid artery
4. Aortic arch
5. Main bronchus
6. diaphragm
 Blood supply
1. Cervical segment- inferior thyroid artery branches
2. Thoracic segment- brachial artery & aorta (oesophageal branches)
3. Abdominal segment- inferior phrenic artery & left gastric artery
 Venous drainage
1. Upper 2/3 – drain to azygous vein
2. Lower 1/3 – drain to esophageal tributaries of coronary vein
 Portal vein- connection systemic & portal venous system
 Function
1. To propel food from pharynx to stomach
2. To prevent reflux of gastric content

OESOPHAGEAL DISEASES
CANCER OESOPHAGUS ACHALASIA CARDIA
Clinical features Def: esophageal motility disorder due to
1. Progressive dysphagia loss of ganglion cells in myenteric
(solid  semisolid  liquid) (Auerbach’s) plexus
2. Vomiting
3. LOW + LOA Causes: unknown, may be due to chronic
4. Excessive salivation (water brash) Trypanosoma cruzi infection (chagas’s ds)
Symptoms related to invasion underlying structure Clinical features

 Tracheo oesophageal fistula 1. Dysphagia - intermittent
 Hoarseness of voice- recurrent laryngeal nerve (difficult to swallow liquid/water)
 Horner’s syndrome- sympathetic chain in cervical 2. Pain- often mistaken as reflux
region 3. Feeling food stick at oesophagus
1. Ptosis (drooping of eyelids) 4. Regurgitation- especially at night
2. Miosis (pupil constriction) 5. Vomiting
3. Enophthalmos (impression sunken eyes) 6. LOW
4. Anhidrosis (reduce sweating)
 Hiccups- nerve invasion Examination (not much)
 Pain caused by local spread- spinal pain 1. Epigastric tenderness
2. Signs of aspiration
Symptoms of metastasize
 2L 3B Commonly seen in middle age group
 Hypercalcemia- paraneoplastic syndrome in SCC
Examination (not much)

1. Cachexia patient with muscle wasting
2. Palpable lymph nodes- supraclavicular region
3. Evidence of metastasize
Commonly seen in older age group
2 types of cancer
Squamous cell carcinoma Adenocarcinoma
 More common  Rising trend
 Affect upper 2/3  Affect lower 1/3
Risk factors Risk factors
1. Tobacco 1. Obesity
2. Alcohol 2. GERD
3. Dietary- spicy foods 3. Barrett’s esophagus
4. Betel nut chewing 4. Smoking
5. Predisposing condition
-achalasia
-esophageal diverticula
-webs
-plummer-vinson
syndrome
-HPV infection
Spread- supraclavicular LN subdiaphragmatic +
coeliac LN

Complication
1. Obstruction
2. Bleeding
3. Spread
 Recurrent laryngeal & phrenic nerve paralysis
 Trachea-oesophageal fistula (shown in barium
swallow)
 Empyema,lung abscess, pneumonia
 Pericarditis
 SVC obstruction
Investigations Investigations
1. OGDS + biopsy 1. Esophageal manometry
2. Barium swallow  Raised esophageal
 Irregular luminal filling defect sphincter pressure
 Shouldering effect (dilatation)  Lower esophageal
sphincter (LES) doesn’t
relax completely during
swallowing
2. Barium swallow
 Dilated esophagus
 Can see site of contraction
 Uncoordinated peristaltic
wave- tertiary contraction
 Stricture in distal
esophagus- bird’s beak/rat
For staging/metastasize tail appearance
1. CT chest-abdomen- haematogenous spread 3. Chest x-ray
2. Endoscopic ultrasound (EUS)- local-regional spread  Dilated esophagus shadow
3. Laparoscopy- intra-abdominal, hepatic metastasize  Fluid level (sometime)
4. Bronchoscopy- pulmonary invasion 4. Endoscopy
Management Management
Curable 1. Heller’s cardiomyotomy
 Surgery (esophagectomy)  Making longitudinal
o 3 methods incision of lower
i. Modified Ivor Lewis oesophageal and upper
ii. Mckeown (3 field esophagectomy) gastric muscle wall until
iii. Transhiatal esophagectomy mucosa bulge through
o Contraindication for surgery  Complication:- GERD (add
i. Metastasize N2 (celiac, cervical or partial Nissen
supraclavicular LN) or solid organs fundoplication)
ii. Invasion of adjacent structure (RLN, 2. Hydrostatic balloon dilatation
tracheobronchial tree, aorta,  Involve stretching cardia
pericardium) with balloon to disrupt
iii. Severe associated comorbid muscle
(CVS/RS diseases)  Relieve 80% of cases
 Adjuvant therapy- chemo or radiotherapy  Complication:- perforation
Incurable 3. Endoscopic injection at
 Palliative care (chemo or radiotherapy) gastoesophageal junction with
 Stenting botulinum toxin
 Laser recanalisation

GASTRO-ESOPHAGEAL REFLUX (GERD)
Due to retrograde flow of gastric acid through an incompetent cardiac sphincter into lower oesophagus
May not has oesophageal inflammation
Causes
i. Anatomical (hiatus hernia)
ii. Raised intra-abdominal pressure (pregnancy, fibroid)
iii. Incompetent cardiac sphincter (transient lower esophageal sphincter relaxation; TLOSR)
Clinical features
1. Triad symptoms of
i. Heartburn (retrosternal burning pain- especially after food)
ii. Epigastric pain
iii. Bitter tasting regurgitation
Symptoms worsen when

 Lying flat
 Bending forward
2. Odynophagia with hot drink, citrus drink or alcohol

3. Hypersalivation
4. Angina like chest pain
5. Dysphagia when stricture form
History of taking antacids or PPI

Complication
1. Stricture- worsen dysphagia
2. Reflux esophagitis
3. Barrett’s esophagus
4. Carcinoma esophagus
5. Sliding hiatus hernia

Diagnosis- is assumes rather than proven
Investigation- required when not respond to PPI or dysphagia is present

1. Barium swallow
2. Endoscopy with biopsy
3. Esophageal manometer
 Measure pressure at lower esophageal sphincter
4. Esophageal pH (gold standard)- 24H pH recording
Management
Most cases (mild)- AIM: reducing reflux
1. Advice on
 Weight reduction
 Diet changes (reduce alcohol, coffee, tea, chocolate)
 Avoidance large meal at night
 Modest degree head up tilt of the bed
2. Medication
 Antacids- to dilute acid secretion (take 1H after meal)
 Second line therapy
o H2 receptors antagonist
o Sucralfate (mucosal protective)
o Prokinetic agents (Dopamine antagonist)- Metoclopramide/Cisapride
 If second line FAIL PPI
o Omeprazole 20mg daily
o Heals 96% in 8 weeks
Surgery (rarely need)

Indication
1. FAIL medical treatment
2. Complication occur (Barrett, stricture)
Type of surgery
1. Total (Nissen’s) or partial (Toupet) fundoplication- laparascopic approach
Stricture- dilated the stricture using gastroscope
REFLUX OESOPHAGITIS BARRETT’S OESOPHAGUS

Complication of GERD Also complication of GERD
Oesophageal inflammation (Endoscopic or Metaplastic change in lining mucosa of esophagus (biopsy)
histopathologic evidence)
 Squamous epithelium replaced by metaplastic columnar
 Specialized intestinal metaplasia
 Severe dysplasia
 Lead to malignant changes (pre-malignant state)

GASTROINTESTINAL BLEED
UPPER GIB LOWER GIB
Bleeding site: mouth to ligamentum treitz Bleeding site: distal to ligamentum treitz to anus
(4th part of duodenum and jejunum)
May presented as May presented as
1. Haematemesis= vomit coffee brown blood 1. Hematochezia= passing bright red bloody stools
 Have to differentiated with (bleeding per rectum)
Haematemesis Hemoptysis
-From GIT -From RS
-Dark red/brown -Bright red
(coffee brown) (pink & frothy)
-In clump -Foamy/running
-Mixed with food -Mixed with mucus
-Acidic pH -Alkaline pH
-Symptoms GIT -Symptoms RS
**Recent nose bleed- vomiting/swallow blood
2. Melena= passing black tarry stool

 Characteristics
1. Sticky- difficult to flush
2. Foul smell
3. Soft in consistency
(Differentiate with Fe tablet stool-
hard in consistency)
4. Tinge of pinkish area (blood from
melena stool)
 Black colour is caused by the Hb being
altered by digestive acid & intestinal
bacteria
**Both: may also presented as occult blood= bleeding not apparent to patient
Causes include: Causes include:
1. Chronic peptic ulcer 1. Cancer colon
2. Oesophageal varices 2. IBD- chron’s disease/ulcerative colitis
3. Acute erosive gastritis 3. Meckel’s diverticulum
4. Reflux oesophagitis 4. Angiodysplasia
5. Cancer stomach 5. Anal fissure
6. Malloy Weiss Syndrome 6. Diverticular disease
7. Zollinger-Ellison syndrome 7. Hemorroids
8. Polyps- Familial adenomatous polyposis
9. Dysentry

For any bleeding- must know?
1. Confirm it is really bleeding- from where (UGIB, LGIB, RS)
2. Amount of bleeding
o Frequency passing bloody episode
o How much amount blood (~approximately)
o Duration
3. Severity of bleeding
o Chronic loss = anaemic features
o Acute loss Total blood= 6-7L
Minor loss Moderate loss Severe loss
 Loss <10% blood  Loss 10-20% blood  Loss >20% blood
(<500ml) (500-1000ml) (2000ml)
 Vital signs normal  Vital signs postural  Vital signs shock
Except for elderly & -Orthostatic -Resting hypotension
anaemic patient hypotension
-Tachycardia
-Syncope
-Light headedness
-N+V
-Increase thirst
*Hb is not strong indicator for blood loss, patient’s clinical condition is much more important
for assessment of blood loss
4. Causes of bleeding
Initial management for bleeding cases

1. Secure ABC- Resuscitate
 Oxygen
 IV fluid 2 large bore NS- used crystalloid
2. Keep nill by mouth
3. Monitor vital signs
 PR, BP, SpO2 (hourly) Temperature (4 hourly)
 CVP if severe bleeding
 Alarming signs for haemodynamic compromise
i. Tachycardia (>100/min)
ii. Systolic BP (<90mmHg)
iii. Cool extremities
iv. Syncope episode
4. Group and cross match at least 2 units of blood
5. Blood transfusion if needed
 Indications (BP, PR, Hb, symptoms)
i. Systolic BP <110mmHg or Postural hypotension
ii. Pulse >110/min
iii. Hb <8g/dL or Hb <10g/dL in angina or cardiovascular disease patient
6. Fresh frozen plasma & platelet transfusion
 If already transfuse >10units of fresh RBC
7. Emergency scope is indicated if
i. Vomit blood on day of admission, still continue bleed in ward with low BP
ii. After transfuse blood, BP still low
8. Prophylactic antibiotics

UPPER GIB
Etiology
NON-VARICEAL BLEEDING VARICEAL BLEEDING
(80% of cases) (20% of cases)
1. Chronic peptic ulcer 1. Gastroesophageal varices
2. Acute erosive gastritis
3. Reflux oesophagitis
4. Cancer stomach
5. Malloy Weiss Syndrome
6. Zollinger-Ellison syndrome
7. Bleeding disorder (medical)

VARICEAL BLEEDING- PORTAL HYPERTENSION
Portal vein
 Vessel that conducts blood from the GIT and spleen to the liver
 Formed by the union of the splenic and superior mesenteric veins (behind neck of pancreas)
 Has no valve which allows high flow with low pressure
 Branches into
o Left portal vein: supply liver segments II, III, IV
o Right portal vein: Further divided into
 Anterior portal veins: supply liver segments V and VIII
 Posterior portal veins: supply liver segments VI and VII
 Supply 80% of the blood to liver
Blood supply to liver
o Total hepatic blood flow = 1500ml/min (25% of CO)
 Hepatic artery = 20% Each supply 50% O2 to liver
 Portal vein = 80%
Site of portal-caval anastomosis
Portal hypertension
 When portal vein pressure >12mmHg (normal portal vein pressure = 5-10mmHg)
 Causes
o Increase in portal venous resistance
PRE-Hepatic cause HEPATIC cause POST-Hepatic cause
i. Portal vein thrombosis i. Liver cirrhosis- alcohol i. Budd-chiari syndrome
ii. Splenic vein thrombosis ii. Hepatitis ii. Right heart failure
iii. Constrictive pericarditis
o Increase in portal venous flow
i. Secondary to massive splenomegaly
ii. Splenic arteriovenous fistula

OESOPHAGEAL VARICES
Etiology Caused by portal hypertension (>12mmHg)
1. Liver cirrhosis
2. Hepatitis
3. Alcohol
Pathophysiology Increase portal vascular resistance (due to distorted architecture of liver, fibrosis
in portal vein) and increase in portal flow/pressure (as compensatory
mechanism)  obstruction in portal system  formation of collaterals in
systemic circulation  blood flow is shunted into sites of anastomoses 
produce CF accordingly
In oesophageal varices:- wall of veins are easily ruptured when pressure is high.
Another cause, varices located superficially and easily abraded by food particles
and gastric acid. During coughing and straining, rise in intraabdominal pressure
cause rupture of varices.
Clinical features  Hematemesis (fresh blood)
 Melena
 CLD features: Ascites, splenomegaly, spider naevi, flapping tremor
 Anemia features: Fatigue, dizziness, pallor, SOB
Other important history to ask

 History related to CLD/Portal hypertension
i. Alcohol consumption (in details)
ii. History of jaundice or ascites
iii. History of hepatitis
iv. Sharing needle IV drug users, tattoos, promiscuity
v. Family history of CLD
 To exclude other causes of UGIB
i. Usage of NSAIDs and anticoagulant
ii. History of dyspeptic symptoms- belching, epigastric pain
iii. Coagulopathy or bleeding disorders
**in short, cari stigmata of CLD + sign of portal hypertension + anemia features
Investigations 1. LFT- underlying liver diease
2. Coagulation profile- underlying coagulopathy
3. Hepatitis profile
4. FBC
5. Peripheral blood smear- pancytopenia indicated hypersplenism
6. Blood urea and serum electrolytes (BUSE)
7. Oesophageal-Gasto-Duodeno-Scope (OGDS)-
8. Ultrasound of abdomen

Japanese
Classification
Management General
1. Secure airway, breathing and circulation
2. Resuscitation
3. Blood group and cross match (2units)
4. Keep nil by mouth
5. Administer vitamin K (10mg IV)
6. If coagulopathy present, administer fresh frozen plasma (FFP)
7. Short term antibiotic prophylaxis for 7 days
8. Administer IV saline/packed RBC to replace blood loss. Keep Hb ideally
around 8g/dL or HCT of 24%
(Avoid over transfusion- can increase portal pressure and exacerbate
further bleeding)
Definitive
Facilities available:- Endoscopic scleropathy or banding
Facilities not available (Hospital daerah, KK)
1. Drug to stop or reduce bleeding: vasopressin, somatostatin, IV octreotide.
(MOA= vasoconstriction- to temporarily ↓ portal pressure & bleeding)
2. If cannot control by medication, do procedure:

 Sengstaken Blackmore tube (oesophageal balloon tamponade) to achieve
temporary hemostasis, then send to Hospital besar
3. Treal underlying pathology

 Transjugular intrahepatic portosystemic stent shunt (TIPSS) –
temporary management
 Liver transplant – long term management
4. Other Spleen – renal shunt

Sengstaken Blackmore tube (oesophageal balloon tamponade)
 Used when rate of blood loss prohibits endoscopic evaluation to provide temporary
haemostasis
 Procedure:- Inflated gastric balloon with 300 ml of air to a pressure of 40mmHg
 The two remaining channels allow gastric and oesophageal aspiration
 A radiograph is used to confirm the position of the tube
 Balloons should be temporarily deflated after 12H to prevent pressure necrosis of
oesophagus
Transjugular intrahepatic portosystemic stent shunts (TIPSS)

 Main treatment of variceal haemorrhage that has not responded to drug treatment and
endoscopic therapy
 Is an artificial channel within liver that establishes communication between inflow portal
vein and outflow hepatic vein
 This procedure is done by catheterization right hepatic vein via internal jugular vein

PEPTIC ULCER DISEASE (PUD)
= Disruption of mucosal integrity of stomach or duodenum or both  to mucosal defect (ulcer)
Common site of peptic ulcer

1. Junction of antrum
2. Lesser curvature of stomach
3. 1st part of duodenum
4. Oesophageal junction
5. At stoma between stomach and SI
Causes of peptic ulcer
Secara simplenya ulcer happened bila

↓ mucosal resistance by
1. ↑ stimulation/irritant
-↑ HCL stimulate by gastin or vagus
-NSAIDs
-Mucosal irritants: alcohol, tobacco, spicy foods
-Stress: exogenous pressure, trauma or illness
-Helicobacter pylori infection
 Gram negative spiral bacilli
2. ↓ protection
-Compact epithelial cell lining
-Mucus secretion
-Bicarbonate ions

Chronic peptic ulcer
Duodenal ulcer Gastric ulcer
 4x more common  Less common
 Mostly in the 1st part of duodenum  Mostly near lesser curvature (incisura
 Usually due to increase acid secretion- angularis)
Commonly in younger age  Usually due to decrease mucosa resistance-
 Tender at Right hypochondrium Commonly in older age
 Relieved by food (hunger pain)  Tender at epigastrum
 So patient eat more  Gain weight (fat)  Aggravated by food (relieved by vomiting)
 Usually not associated with malignancy  So patient LOA  LOW (thin)
 More commonly associated with malignancy
**Both: relieve by ingestion alkalis/milk
**Vomitus: appear black bcoz HCL act on Hb  hematin (black)
Signs to look for

1. Tenderness of epigastrium
2. Signs of complication
a. Peritonitis signs
b. Succussation splash
c. Anaemia signs
Complication of peptic ulcer
1. Penetration 2. Obstruction
Presented as pain that radiate to back

May involve: (think of underlying structures) Pyloric stenosis:- hour glass appearance on AXR.
Head of pancreas, post. abdominal wall, liver Sign: presented with succession splash
3. Haemorrhage 4. Perforation
Common in anterior wall ulcer

Lead to formation of abscess in lesser sac or
peritonitis
Common in posterior wall ulcer Presented as pain begin in epigastrium
DU erode gastroduodenal artery radiate to RIF (paracolic gutter)
Presented with indigestion, heartburn, or become generalized diffuse pain (peritonitis)
dyspepsia, flatulence Patient also loss of liver dullness. How?- air from
Ix: OGDS findings: visible vessels in ulcer perforated stomach/duodenum escaped to
base, spurting vessels, ulcer with clot in base peritoneal cavity will rise above liver (resonance)-
CXR erect position:- air under right diaphragm
Other ix:- serum amylase (differential pancreatitis)
Peritonitis: first 6H due to acid irritation (clinical peritonitis)  later due to bacteria (bacteria
peritonitis). Presented with board-like rigidity, rebound tenderness, tachycardia, absent bowel
sound

Investigations
1. Endoscopy (OGDS)- view the ulcer and take biopsy
2. Helicobacter pylori test- 5 methods to confirm
i. Culture
ii. C13/C14 Urea breath test
iii. Compylobacter Like Organism (CLO) test= rapid urease test
 Done during OGDS using CLO kits
 Result within 3H
 Change from yellow to pink
iv. Antibody in blood
v. Antibody in stool
3. Erect chest xray (or left lateral decubitus view)- for perforation
4. FBC- to detect anemia and infections
5. Serum creatinine and electrolyte- to identify electrolyte abnormalities (if complicated)
Management
 GOAL: to eradicate H.Pylori and control acid secretion to allow healing of ulcer
Medical therapy
1. Eradication of H.Pylori (do triple therapy)
i. Omeprazole (PPI)
ii. Metronidazole + Amoxicillin (Antibiotics)
Bismuth (↓ inflammation)- xguna dah sekarang
2. Decrease acid secretion
i. Ranitidine (H2 receptor antagonist)
ii. Omeprazole (PPI)
OMAR sakit perut bagi OMAR
Surgical therapy- jarang buat dah sekarang

1. Partial gastrectomy
2. Vagotomy
o Cut vagus nerve to eliminate acid secretion stimulus
o High selective or truncal
Post op complication
1. Bleeding- at the anastomosed site
2. Gastric retention- need to put NG tube
3. Dumping syndrome- with subtotal gastrectomy
o Rapid emptying of food and fluids from stomach into jejunum
o Early- 30 minutes after meal, Late- 90min to 3H after meal
o Symptoms: vertigo, tachycardia, syncope, sweating, pallor, fullness
o How to minimize?
i. Decrease CHO intake, increase fat
ii. Eat slowly, small portion with frequent meals
iii. Avoids fluids during meals
o Complication
 Early:- increase osmotic load  no hypoglycaemia
 Late:- cannot absorb carbohydrate  later on lead to hypoglycaemia
4. Anemia- rapid gastric emptying decrease absorption of iron
5. Malabsorption of fat

“SOVAH & no recent haemorrhage”
Forrest 1a-b, 2a- Management: under endoscopic intervention (OGDS)

1. Thermal
 Heater probe (more commonly used- disadvantage is perforation)
 Argon plasma coagulation (used gas, no contact superficial so more safe)
2. Injection- surround the ulcer
 Sclerosent
 Adrenaline- side effect: transient tachycardia
 Alcohol
3. Mechanical
 Suture, stapler, clip, band ligation
4. Combine any
**If bleeding not stop (fail)- do open surgery
Forrest 2b,2c,3- Management: triple regime

GASTRIC CARCINOMA
History Age >50 years old
Symptoms related to cancer stomach
1. Epigastric discomfort
2. Early satiety (if cancer at pylorus antrum)
3. Bloating
4. Dsphagia
5. Abdominal lump- at epigastrium
6. LOW+LOA
Symptoms related to complication

1. Anemia for chronic blood loss
2. Vomiting in gastric outlet obstruction
Symptoms related to metastasizes

1. Liver- ascites
2. Lung- SOB (malignant pleural effusion)
3. LN enlargement- umbilicus and left supraclavicular area
Risk factors Past medical history
1. Chronic peptic ulcer
2. H.Pylori treatment
3. Pernicious anemia
4. Gastric polyps
Past surgical history

1. Gastric surgery
o Billroth II
o Gastroenterostomy
o Pylorosplasty
Family history of malignancy

Personal/social history
1. Blood group A
2. Nickel, asbestos mining workers
3. Smokers
4. Alcohol
5. Obese
Nutritional history
1. Low fat/protein consumption
2. High nitrate consumption
3. High salted meat or fish
4. High complex carbohydrate
5. Poor drinking water
6. Poor food preparation (smoked, salted)

Examination General examination
o General appearance- check nutritional status (cachexia)
o Sign of jaundice and anemia
o Migratory thrombophlebitis- Trousseau’s sign
o Pedal odema (malnutrition)
Lymph nodes
o Left axillary LN (Irish node)
o Supraclavicular LN (Virchow node or signal node)- Troisier’s sign
Abdominal examination
I o Abdominal distension
o Visible peristalsis
o Sister Mary Joseph node
P o Epigastric mass/right upper abdominal mass
o Hepatomegaly
P o Ascites
A o Normal bowel sound
PR o Evidence of metastasis
In pelvis-rectovesical pouch (Blumer’s shelf)
In ovaries (Krukenberg’s tumour)
Systemic examination
Respiratory
o Presence of pleural effusion – reduced vocal fremitus/vocal resonance,
stony dullness on percussion
Investigation To confirm diagnosis
o OGDS + Biopsy (4-6 quadrant)
 Site of lesion
 Type of lesion
 Nature of lesion
 Associated lesion
o Barium meal (do when bulky proximal tumor that preventing OGDS be done)
To staging the diseases

1. CT scan + Oral, rectal or IV contrast
Advantages Disadvantages
-Detect gastric wall thickening -Can’t detect microscopic
-Enlarged LN peritoneal deposits
-Present other lesion (pelvic -Can’t detect small liver metastasis
deposit, krukenberg tumor, ascites, -LN enlargement cannot
liver metastasis) differentiate between tumor
deposit

2. Endoluminal US
Advantages
-Can identify 5 layers of gastric wall
-90% accuracy for T stage assessment
-Can identify perigastric nodal enlargement up to 80% accuracy
Classification Japanese classification (early stage) Bormann’s classification (advance stage)
Lauren’s classification
TNM classification
o Operable:- T1-T3 + M0+N0
o Non-operable:- others
PHNS classification
 P-Peritoneal dissemination
 H- Hepatic metastasis
 N- Nodal involvement
 S- Serosal surface invasion
Mode of 1. Direct spread
spread 2. Lymphatic spread
3. Blood spread
4. Transperitoneal spread
Complication 1. Obstruction (GOO)
2. Haemorrhage
3. Perforation
4. Fistula formation
5. Varicose vein (compress IVC)
Management 1. Curative surgery- Remove tumor via gastrectomy
2. Palliative surgery- Bypass GOO with gastrojejunostomy
3. Supportive therapy- Relieve pain

GASTRIC OUTLET OBSTRUCTION (GOO)
o As complication of chronic PU and Carcinoma of stomach
o Presented as
o Nausea, vomiting
o Early satiety
o Ball rolling movement
o Weight loss
On examination
o Succession splash
After 2H of drinking H2O or 3H after taking solid food
Shake patient holding near epigastric region- can hear splash without stethoscope
o Result in
i. Hypochrolaemic
ii. Hyponatremia
iii. Hypokalemic
iv. Metabolic acidosis with paradoxical renal acid uria
o Investigations
1. Upper GI endoscopy- to rule out malignancy cause
2. Barium meal- support diagnosis
o Management
Benign case- Gastrojejunostomy ± truncal vagotomy
OTHER CAUSES OF UGIB

ACUTE EROSIVE GASTRITIS OESOPHAGITIS
Also called acute gastric ulcer or acute Occurs when acid pepsin refluxes through
gastritis the lower oesophageal sphincter onto the
**Complications, ix, mx same as chronic PU squamous epithelium lining of the
oesophagus  inflammation of oesophagus
RF or 1. NSAIDs –exacerbate 1. Obesity
Etio 2. STRESS- trauma, shock, burn, sepsis, CNS 2. Fatty food
injury, multisystem failure 3. Caffeinated drinks
4. Alcohol
5. Drugs such as calcium channel blocker,
antihistamine and anticholinergic
CF 1. Haematemesis 1. Heartburn (often at night, worsened by
2. Melena lying flat, initiated by bending, stooping
3. Symptoms like chronic PU or heavy lifting)
2. Bitter taste in the mouth
3. Dysphagia (long term)
IX 1. Barium swallow and barium meal
 Oesophageal ulcer and peptic strictures
2. Endoscopy
 For patients who do not improve on
medical trial, long – standing symptoms
MX PPI: Pantoprazole, Omeprazole
Reflux esophagitis
 Oesophageal mucosal injury that occurs secondary to retrograde flux of gastric contents into the esophagus
 Clinically, this referred to as gastroesophageal reflux disease (GERD)
GERD= chronic symptoms or mucosal damage produced by the abnormal reflux of gastric contents into the oesophagus

MALLORY-WEISS SYNDROME

LOWER GIB
Lower GIT- Start from the distal to Ligament of Treitz
*Ligament of Treitz : ascending part of duodenum (D4) – passes upward on or to the left of aorta and terminate and
duodenojejunal flexure
Etiology
Small intestine Large intestine Rectum Anal-perianal
Children 1. Diverticular disease 1. Polyps 1. Hemorroids
1. Meckel’s 2. Angiodysplasia 2. Rectal cancer 2. Perianal hematoma
diverticulum 3. Polyps 3. Anal fissure
2. Intussucception 4. Colon cancer (fissure in ano)
5. IBD
Adult  Ulcerative colitis
1. Tumor  Crohn’s disease
Blood mixed with stool- ca colon

Blood streak on stool- ca rectum
Blood after defecation- hemorrhoids
Blood & mucus- colitis
Blood alone- diverticular disease
**Massive bleeding in LGIB

1. Diverticular disease
2. Angiodysplasia
3. Meckel’s diverticulum

DIVERTICULAR DISEASES
 An abnormal sac or pouch that develops at a weak point in the intestines
Terms
Diverticulum (Plural= diverticula) An abnormal sac or pouch formed at a weak point in the
body
Diverticular Consists of 3 conditions:- diverticulosis, diverticular bleeding and diverticulitis
Diverticulitis Diverticula with sign of infection or inflammation (Pain)
Diverticulosis Diverticula without sign of infection or inflammation (No pain)
DIVERTICULOSIS DIVERTICULITIS
Herniation of mucosa and submucosa through muscularis Inflammation/infection of diverticula
propria from weaker muscle  Usually happens when
 Formation of numerous tiny pockets, in the lining of outpouchings become blocked
the bowel with waste
 Can range from pea-size to much larger, are formed  Allowing bacteria to build up
by increased pressure on weakened spots of the causing infection
intestinal walls by gas, waste, or liquid
 Can form while straining during a bowel movement,
such as with constipation
Asymptomatic- No pain Persistent lower abdominal pain (LIF)

Or may presented with distension, flatulence, sense of heaviness in lower abdomen
Examination reveal:
 ±fever
 ±malaise
 Palpable, tender, thicken sigmoid
Type
 Congenital- Meckel’s diverticulum
 Acquired- colon (especially sigmoid)
Why sigmoid?- ↓ luminal diameter & ↑ luminal pressure

Causes
1. Raised intraabdominal pressure as in straining or constipation
2. Segmental contraction
Investigations
 FBC- leucocytosis
 Barium enema
o Saw tooth appearance
o To differentiate diverticular disease from ca colon
o To assess extend of disease
 Colonoscopy
o To exclude cancer
Principle of management
DIVERTICULOSIS DIVERTICULITIS
High fibre diet Low residual diet
Bed rest Bed rest
Anti-spasmodic Broad spectrum antibiotics
 Name: Cefuroxime or metronidazole
 Route:
 Duration:
Operation
 For recurrent or complicated case
 Removal of affected segment  end to end anastomosis
Complications
1. Recurrent periodic inflammation and pain
2. Intestinal obstruction
 Sigmoid : due to progressive fibrosis and stenosis
 SI : adherent loop of SI to pericolic abscess
3. Haemorrhage
4. Perforation
 General peritonitis
 Pericolic abscess formation
5. Fistula formation
 Vesicocolic fistula (most common)
i. Presented as pneumaturia or faeces in urine (faecaluria)
**Pneumaturia is the passage of gas mixed with urine

INTUSSUSCEPTION MECKEL’S DIVERTICULUM
 Invagination of proximal intestine into  Situated at antimesentric border of small
adjacent distal bowel, with resultant intestine
obstruction of the lumen (ileocolic  Remnant of vitellointestinal duct
intussusception)  3-5cm long, 60cm from the ileocecal valve,
 When one portion of bowel (intussusceptum)  Contains all 3 coats of the bowel wall and has
telescopes into another (intussuscipiens) it own blood supply
 Contain heterotropic epithelium : gastric,
colonic and pancreatic tissue
 Vulnerable to obstruction and inflammation
 Male baby
 6-12 months of age
Features Features
 Sudden onset of intermittent abdominal  Haemorrhage – painless maroon rectal
pain lasting for few minutes bleeding
 Draws the leg up  Diverticulitis – difficult to differentiate with
 Early stage normal stool, later red currant acute appendicitis
jelly stool  Intussusception – apex is swollen, inflamed,
Palpation heterotropic epithelium at the mouth of
 A curved lump diverticulum
 Sausage shaped in line of colon with its  Chronic ulceration – pain around umbilicus
concavity towards umbilicus related to meal
 If lump harden under examining fingers  Intestinal obstruction – presence of band
synchrounously with screaming between the apex of the diverticulum and
DRE umbilicus
 Blood stained mucous  Perforation
 No fecal odour
After 6 hours, signs of dehydration

After 24 hours, distension and profuse sweating

 Ultrasound – if suspect intussception  Small bowel enema
 X-ray of abdomen – confirmatory, increased gas  Technetium-99m scanning – identify
shadows in small intestine and absence of cecal MD as source or GI bleeding
gas shadow
 Barium enema – if ileocolic intussusception, a
pincer like ending of barium enema/coiled spring
sign
Management Silent MD – if found during abdominal

1. Nasogastric drainage operation, can be left if : wide mouthed
2. IV fluid resuscitation and wall of diverticulum not thickened
3. Broad spectrum antibiotics
Non-operative 1. Meckel diverticulectomy

 pneumatic or hydrostatic reduction
Operative :
1. Transverse incision to deliver the bowel
2. Gentle retrograde pressure to the telescoped
portion in an attempt at manual reduction
3. Proximal and distal segments should not be pulled
apart because of the risk of injury to the bowel
4. If manual reduction not possible, resection of the
involved segment and primary anastomosis should
be done

HEMORROIDS (pile)
= swelling veins (varicosities) in the lower rectum (anal canal)
o Male more often for longer period
o Women during pregnancy and puerperium

RF 1. Hereditary
2. Aging
(Increase intra-abdominal pressure)
3. Chronic constipation
4. Prolonged straining
5. Rectal carcinoma
6. Obesity
(Increase pressure of blood in pelvic area)
7. Pregnancy
CF Symptoms
1. Bright red rectal bleeding, splatter
2. Bleeding after defecation
3. Painless (unless complicated)
4. Mucus discharge 
5. pruritus ani
6. Prolapse
7. Anemia (rare)
Signs(PR in lithotomy position)

 Inspection (describe accordingly)
1. Anal tags
2. Swelling or lumps
3. Bleeding
4. Scratch marks (pruritis)
5. Prolapse
o Ask patient to strain and look for prolapse mass
If more than an inch- partial prolapsed
If more than 2 inch- complete prolapsed
6. Hemorrhoids
o External- cover with skin
o Internal- cover with mucous membrane
 Palpation
1. Perianal region for lump
2. Digital rectal examination
o Internal hemorrhoids cannot be felt unless thrombosed
o Classical site:- 3, 7, 11 o’clock position
 Systemic examination
Focus on presence of clues of risk factors- raised in intra-abdominal pressure
Differentiate between prolapse piles from perianal haematoma

 Prolapse pile cover by mucosa
 Perianal haematoma cover by skin + irreducible
Cx 1. Profuse haemorrhage
2. Strangulated
3. Thrombosed
4. Gangrene
5. Ulceration
6. Fibrosis (white colour)
7. Suppuration/ infection

Ix Bedsite procedure
Investigation= proctoscopy (diagnostic)
 Just below anorectal ring, internal hemorrhoids will bulge into
lumen of proctoscope when insert- withdraw it slowly
MX Conservative treatment- or treat symptomatically if hemorrhoids are symptom of other
condition
1. Take high fibre diet- banananaaa
2. Advised to heed the call to evacuate bowel
3. Advised not to spend a long time on straining
4. Drink enough water
Medical treatment
1. Daflon- to increase venous tone (if painless- degree1,2,3)
2. Liquid paraffin
3. fibrogel
4. Hydrophyllic colloids- to regulate bowel
5. Docusate sodium- as stool softeners
Internal haemorrhoids- above pectinate line, external haemorrhoids- below pectinate line
Procedures
1. Injection of sclerosants (phenol in oil)
o For 1st degree hemorrhoids
o Irritant solution is inject submucosally around pedicles of three major
hemorrhoids, in the upper canal
o Contraindicate:- acute prolapse thrombosis, severe bleeding & ulceration,
fissure and fistula
o May provoke fibrotic reaction
2. Rubberband ligation- use Barron’s technique

o 2nd hemorrhoids
o Rubber band is placed on redundant mucosa, minimum of 2cm above dentate
line,  cause strangulation of blood supply  hemorrhoids slough off in 5-
7days  leave small ulcer that heals and fix tissue to underlying sphincter (no
anaesthesia)
o Contraindicate:- patient on coumadin or heparin
o Complication:- pain, thrombosis, bleeding, life threatening perianal or pelvic
sepsis, abscess, band slippage, priapism, urinary dysfunction
o May have pressure of feeling of incomplete evacuation
o Can be done in day care- its painless

Surgical procedures
o Candidate for surgery
i. Failure of non-operative treatment for 2 nd degree hemorrhoids
ii. For 3rd and 4th degree hemorrhoids or mixed hemorrhoidal diseases
iii. With large external hemorrhoidal diseases
o Type of surgery
1. Open hemorrhoidectomy (Milligan-Morgan)
2. Closed hemorrhoidectomy
3. Laser hemorrhoidectomy (newest technique)

ANGIODYSPLASIA
= a vascular malformation that is a cause of haemorrhage from the colon (associate with aging >60y)
 malformation consists of dilated tortuous submucosal veins
 commonly happened in ascending colon and caecum (not associated with cutaneous lesion)
= also called angiomas, hemangiomas and arteriovenous malformations
Clinical features
1. Brisk bleeding (rectal)
2. Anemia (if in chronic condition)
3. Associated with aortic stenosis
Investigations
1. Colonoscopy
 may show the characteristic lesion
 lesions are mm in size, appear reddish, raised areas at endoscopy
2. Pill endoscopy
 detect small bowel lesion
3. Selective superior and inferior mesentric angiography
 shows the site and extent of the lesion by a ‘blush’ of contrast provided bleeding is
above 1 mL/min
4. Technetium-99m-labelled red cell scan
 may confirm and localise the source of haemorrhage
Management
o Stabilise the patient
o Localised the bleeding
o Colonoscopy may allow cauterization to be carried out
o The lesions sometimes demonstrated by translumination through the caecum
o If still not clear which segment involved: total abdominal colectomy with ileorectal
anastomosis maybe necessary
Colonoscopy: show many small

vascular malformations
(angiodysplasias) over the entire colon

INFLAMMATORY BOWEL DISEASES
Crohn’s disease Ulcerative colitis (UC)

Chronic relapsing inflammatory disorder of any Diffuse inflammatory disorder of submucosa and
part of GIT (lips to anal canal) mucosa of large bowel
-95% start in rectum and spread proximally
Younger age group Elderly (increasing risk >60 years old)
Disease may skip lesions Disease involve whole colon (continuous lesion)
Severe initial attack
Recurrence more common even after resection Recession of colon and rectum cures patient
Low risk of malignancy High risk of malignancy- poor prognosis
Causes Causes
1. Genetic- 10% in 1st degree relative, 50% 1. Genetic- 10-20% in 1st degree relative
in monozygotic twins 2. Immune disorder
2. Inheritance- NOD2/CARD15 and certain 3. Relapse associated with stress
variants associated with ankylosing
spondylitis Protective cause
3. Immune disorder- defect in suppressor T 1. Smoking
cells
4. Smoking- 3x risk
Clinical features Clinical features
Acute 1. Resemble acute appendicitis 1. Diarrhea
2. Diarrhoea (precede attack) o Severe during acute attacks often
Chronic 1. Hx of mild diarrhoea over causing incontinence
years with pain in RIF o Watery and bloody diarrhea
2. Mass o Mucus discharge only stained blood or
3. Intermittent fever pus
4. LOW 2. Rectal bleeding
5. Secondary anemia 3. Abdominal pain (rare)
o Mild cramping pre-defecation pain with
diarrhea
4. Tenesmus and urgency
Extra- intestinal manifestations
o Joint – arthritis (large joint polyarthropathy type), sacroillitis and ankylosing spondylitis more
common in UC
o Sclerosing cholangitis a/w UC and can progress to cirrhosis and hepatocellular failure
o Skin lesions : erythema nodosum, pyoderma gangrenosum
o Eye problem : uveitis and episcleritis

1. Colonoscopy & OGDS 1. Colonoscopy
o Area of normal and abnormal (inflamed o Extent of inflammation
mucosa + irregular+ ulcerated + o Differentiate between UC & Crohn’s
mucopurulent exudates) o Monitor response to treatment
o Exclude malignancy in stricture area o Malignant changes
2. Barium enema o Biopsy
o Area of delay and dilatation, narrowed 2. Abdominal X-ray
irregular with string sign of Kantor o Can show severity of disease
3. CT scan – fistulae and intra-abdominal o No faeces at diseased part
abscess o Mucosal islands loss
4. FBC – to exclude anemia o Dilated colon
3. Barium enema
o Loss of haustration
o Mucosal changes (granularity)
o Pseudopolyps
o Narrow contracted colon (chronic)
4. Stool specimen- TRO infective colitis
o Campylobacter, shigella, clostridium
difficile
Medical Medical
1. Steroids- 40mg prednisolone 1. Corticosteroids
2. With 5-ASA (if colonic involve) 2. 5-aminosalicylic acid (5-ASA) derivatives
3. Antibiotics (with features of abscess)
4. Immunomodulatory agents- azathioprine Mild Rectal corticosteroid or prednisolone
for 12w or ciclosporin 20-40mg/day for 3-4 weeks
5. Monoclonal antibody- Infliximab Mod Oral prednisolone 40mg/day,
Nutritional support 2times/day steroid enema and 5-ASA
Severe Medical emergency
Surgery- will not cure the disease but to treat -examine for complications
complications -surgical intervention
1. Segmental resection – if stricture
2. Colectomy & ileorectal anastomosis – Indication for surgery
wide spread colonic disease with rectal 1. Severe or fulminating disease
sparing and a normal anus 2. Chronic disease with anemia, frequent
3. Laparoscopic surgery stools, urgency and tenesmus
4. Temporary loop ileostomy 3. Steroid dependent disease – when
5. Protocolectomy remission can’t be maintained
6. Strictureplasty 4. Neoplastic changes – the patients who have
severe dysplasia on review colonoscopy
5. Extra-intestinal manifestations
Complications
6. Severe haemorrhage or stenosis causing
1. Recurrent intestinal obstruction
obstruction (rare)
2. Bleeding
3. Perforation
What type of surgery?
4. Failure of medical therapy
1. Total proctocolectomy + ileostomy
5. Intestinal fistula
2. Restorative proctocolectomy + an ileo-anal
6. Fulminant colitis
pouch (parks)
7. Malignant change
3. Ileostomy + a continent intra-abdominal
8. Perianal disease
pouch (kock’s procedure)

JAUNDICE
What is jaundice?
=Yellowish discolouration skin, sclera, and mucous membrane.
 Detectable clinically when serum bilirubin level increase 2x upper limit
 Normal=5-17 μmol/L (0.3-1.2mg/dL)
*bila albumin level high kita panggil hyperalbuminemia = >50 μmol/L (3mg/dL)
 Where to look for jaundice?
o Skin
o sclera (conjuctive) -first detected sbb higher affinity to bilirubin
o under the tongue
Carotenemia??
= Yellowish discoloration of the skin but not the sclera and mucous membranes, urine color is
normal.
 Due to increase papaya intake, carrot
Other causes
(post-hepatic):
Drug cuz hemolysis of RBC 1. Periampullary Ca
What are the causes of jaundice? -drug utk malaria -persistent J
-pale colour stool
Jaundice + anemia
Other causes (pre):

1. CHF
2. Prosthetic Ht valve (uncommon)
-induced hemolysis due to
Murphy's sign
excessive turbulence 1
Limit bilirubin
conjugation (hemolysis)
2
3
Charcot triad:
1.Pain
Good signs (stigmata CLD): 2.Fever
1. Spider naevi 3.Jaundice
2. Palmar erythema Cholangitis :infection CBD
3. Distended abd vein (caput)
4. Ascites
5. Palpable spleen

Bilirubin metabolism
-urobilin = give colour to urine
-stercobilin = give colour to feaces
Apa itu unconjugated bilirubin?

-H2O insoluble, kena bind dgn
albumin utk transport.
RBC destruction?
-mostly dkt spleen, other site is liver.
-how?
It is hard to differentiate POST hepatic from HEPATIC causes from HT and Examination, so do Ix
1. LFT
Produce by LFT Hepatic POST Hep
Liver cell AST/ALT ↑↑↑ ↑ or N
Bilirury duct mucosa cells ALP ↑ or N ↑↑↑
*PRE hepatic- mesti dtg dgn sign and symptoms of anemia

Other Ix
2. Serum bilirubin (tgok table atas)
3. Urine and stool analysis (tgok table atas)
4. Serum protein and albumin
 Protein and albumin synthesized by the hepatocytes.
 Normal range:
 Total protein = 5 - 8 gm/dl
 Serum albumin = 3 - 5.5 gm/dl
 Often reduced in patient with hepatocellular jaundice cause by liver disease.
 In haemolytic and obstructive jaundice usually normal because liver is not affected
5. Prothombin time
 To measure blood clotting time.
 Reason delayed/increase (PTT)
 Hepatocellular jaundice due to liver disease as liver cannot synthesized clotting
factors
 Absorption of vitamin k in the gut is reduced which involved in the synthesized of
clotting factors in liver
6. FBC
- Anaemia in patient with haemolytic jaundice with no blood loss
- Leucocytosis with neutrophilic = common in bacterial infection and inflammation causes like
cholangitis and alcoholic hepatitis. Uncommon in viral hepatitis
7. US of hepatobilirary system
Look for:
 Dilatation of intrahepatic and extrahepatic ducts
 intrahepatic duct akan dilated
 extrahepatic duct tak akan dilated
 Sign of gallbladder inflammation
 Cause of the obstruction like gallstone and tumors.
 Abnormality of the liver texture.
8. CT scan -kalau suspected cancer
Ix Advantages Disadvantages
ERCP (Endoscopic Retrograde Diagnostic and theraupetic Invasive --> lead to
Cholangiopancreaticography) -can see stone and remove complication
stone
-can put stent
PTC (Percutaneous Transhepatic Diagnostic and theraupetic Invasive --> lead to
Cholangiography) -theraupetic only limited to complication
drainage bile -can poke through the liver
MRCP (Magnetic Resonance Non-invasive Purely for diagnostic purpose
Cholangiopancreaticography) only
Expensive

OBSTRUCTIVE JAUNDICE
Stigmata of jaundice
1. Pruritis
2. Pale coloured stool
3. Tea coloured urine
4. Epigastric pain
Jaundice Pain Fever Due to?

+++ +++ +++ Cholangitis Inflammation of CBD
- +++ +++ Cholecystitis Inflammation of GB
+++ +++ -
Choledocolithiasis Stones in the hepatic or CBD
(RH)
- +++ - Cholelithiasis Stone in the GB
+++ - - Cholangiocarcinoma Cancer in CBD
Progressive J Fluctuating J
Hepatitis Gall Stone (Choledocolithiasis) How to know it is Gall Bladder?
Alcoholic -Most common causes of OJ
1. At tips of Rt 9 costal cartilage
-Painful intermittent J
-Ask about Hx GS 2. Globular in shape
-Pain after fatty meal 3. Move with respiration (sbb below liver)
Periampullary Ca
Complication of obstructive jaundice

a) Infection  ascending cholangitis
b) Steatorrhea (fatty stool)
c) Coagulopathy  fat malabsorption  reduce vitamin K --. Reduce clotting factor
d) Pruritis (increase bile acid)
e) Liver failure + kidney failure (hepatorenal syndrome) look for renal fuction test
LAW and sign need to know

Courvoisier’s law
 Mild jaundice and gallbladder is palpable (feel globular shape) but non tender, the cause is likely
to be malignancy rather than gallstone
- stoneinflammationfibrosis not distensible
- stone obstruction wall thickening not distensible
- 4 exceptions:
Double impaction of stones ( 1 CBD+ 1 in cystic ducts)
Stone converse ( if not palpable does not mean it is due to stone)
Stone in cystic dust ( other thing compress CBD)
Stones in CBD but normal distensible GB
Murphy's sign
 Palpate right subcostal area within the midclavicular line
 Ask patient to breath in deeply
 As liver descends, patient will feel pain due to the inflamed gallbladder = gallbladder tenderness
 Suggesting acute cholecystitis

GALLSTONES (CHOLELITHIASIS)
• Most common biliary pathology.
• Can be divided into 3 types :
 Cholesterol stones
 Pigment stones
 Mixed stones
RF The main factors of gallstones formation are :
 Biliary stasis
 Infection
 Imbalance in the constituents of bile
Complication  Biliary colic

 Acute/chronic cholecystitis
 Empyema of the gallbladder
 Perforation
 Acute pancreatitis
 Acute cholangitis
 Intestinal obstruction
Sequele  Asymptomatic
 Acute & chronic cholecystitis
 Mucoele
 Empyema
 Gangrene
 Carcinoma
Pathophysiology
Stones in the gallbladder might dislodge into the biliary tree and this gives rise
to Biliary Colic
if the obstruction persists, the gallbladder may get inflamed and this gives rise
to acute cholecystitis
In case if the obstruction persists but the gall bladder is not infected,
mucocele will develop
Mucocele can be infected and eventually gives rise to empyema and

perforation of the gall bladder
Rarely, large stones in the gall bladder causes ulceration of the gall bladder
mucosa, this causes the formation of a fistula directly into the duodenum.
Stones may dislodge into the duodenum and lead to Gallstones Ileus
Biliary colic  Stones in the gall bladder causes intermittent obstruction of cystic duct
 Severe right hypochondrium tenderness
 Pain subsides over time or with analgesia and may recur some other time
 No fever ( distinguish it from
 Ac. Cholecystitis)
 Pain aggravates by eating fatty food

CHOLEDOCHOLITHIASIS ASCENDING CHOLANGITIS
Def If stones in the gall bladder migrates and Ascending bacterial infection in biliary
dislodge in the common bile duct tract in association with partial or
o Lead to obstructive jaundice, ascending complete obstruction of bile ducts
cholangitis and acute pancreatitis o Men=women, Age 50-60
o 5% mortality
Etiology Primary Secondary o Gall stones
Usually brown Usually black pigmented o Stricture
pigment stone stone (multiple, differ in o Tumor
(single, smooth, shapes, originated gall o Choledochal/biliary cyst
oval shaped) bladder) o Biliary tract procedure( stent)
Hx &PE  Nausea & vomiting Charcoat triad
 Pintermittent painful abdominal pain o Intermittent fever
 Dark urine o Intermittent right upper quadrant
 Pale stool pain
 Itchy o Intermittent jaundice
Ix  Liver function test o FBC: leucocytosis
o ALP high as the CBD is obstructed o LFT: elevation of serum bilirubin,
o Serum bilirubin high (unconjugated) alkaline phosphatase and
 Transabdominal u/s transaminase
o Stone can be seen in CBD o Blood culture: for antibiotics
o Dilatation of the proximal part of CBD o Transabdominal= find out
 Full blood count and coagulation profile obstruction
 ERCP (T& D)- Done to remove the stones
 Urinalysis= detect urobilinogen
Mx  Definitve tx is ERCP o Broad spectrum antibiotic IV (
 Therapeutic cefuroxime, ampicillin and
o Stenting to drain the bile and pre – metronidazole)
operative bile drainage o Fluid resuscitation and correct
o Endoscopic basket ting & stone electrolyte imbalance
retrieval o Drained bile duct when patient
o Biopsy stabilize
 Choledochotomy= performed when ERCP o Treat underlying cause of
fail or stone is too high obstruction
Pre operation
i. Correct coagulation profile by giving IM
vitamin K or FFP
ii. Keep nill by mouth
iii. Antibiotic= cefutaxime
Post operation
i. Monitor vital sign 24 hour
ii. Keep nil by mouth until gag reflex
Cx o Pancreatitis o Pyogenic liver abcess
o Cholangitis o Acute renal failure
o Duodenal perforation
o Allergic to dye
o Duct stricture
o Bleeding

LIVER ABSCESS
PYOGENIC LIVER ABSCESS AMOEBIC LIVER ABSCESS
def A type of liver abscess that is caused by Spread by faeco-oral route
bacteria
causes o Intra-abdominal sepsis o bad hygiene
o Perforated appendix
o Septicaemia
organism o Streptococcus milleri Liver abscess that is caused by
o E. coli Entamoeba histolytica.
o Klebsiella
o Proteus vulgaris
CF o right upper quadrant pain o Most common presentation is
o on and off pyrexia dysentery
o Patient usually come in with
o Fever with chills and rigor
o Abdominal pain (at the right
hypochondrium)
o Palpable liver
ix o Blood tests—elevated white blood o Diagnosis is made by isolation of the
count and high neutrophil level indicate parasite from the lesion in the liver
infection and confirming its nature by
o Blood cultures and sensitivity—to microscopy.
identify the bacteria and determine the o Ultrasound - very useful for diagnosis
most suitable antibiotic of amoebic liver abscess. The classic
o CT scan—to locate the abscess appearance is a non-homogeneous,
o CT with intravenous contrast—to hypoechoic, round or oval mass with
pinpoint and measure the abscess (very well defined borders.
useful when planning a surgery)
o Abdominal ultrasound—to visualize an
abscess in the right upper quadrant and
aid in diagnosis
tx Antibiotics : Penicillin, Aminoglycosides, o Percutaneous aspiration= small
Metronidazole abscesses although catheter drainage
(standard of care)
o Larger abscesses =catheter drainage
which is also CT- or ultrasound-
guided. Drainage should also be
carried out if there is impending
rupture.
o Treated empirically with
Metronidazole ( 3x a day for 7-10
days)
o Resolution of the abscess can be
monitored using ultrasound

HEPATITIS = inflammation of the liver
HEPATITIS A HEPAITITS B HEPATITIS C

Presented Anorexia Anorexia Loss of appetite
Fatigue Malaise General malaise
General malaise Tenderness on RUQ Weight loss
Tenderness on RUQ Jaundice
Palpable liver
Jaundice
Diagnosis Antibody titre to Hep A Hepatitis B surface antigen HCV antibody enzyme
immunoassay
Prevention Hep A vaccine Hep B vaccine No vaccine yet
Additional notez from dr raja

Hepatitis B
Hepatitis Acute: HCV antibody+ igm anti HCV= acute

C?? Past infection= HCV Igg antibobody
Active= HCV RNA polymerase

HEPATOCELLULAR CARCINOMA (HCC)
Def Primary malignancy of the liver
Epidem o Common primary malignancy of the liver
o High mortality
o Related to hep b
o Men 2-8x> women
o Age>30 years old
Etiology o Liver cirrhosis
o Chronic liver disease( alcoholic liver disease, hep b , c infection, non alcoholic
steatohepatitic disease, drug induced(pcm))
o Metabolic disease= hematochromatosis
CF o Symptoms of chronic liver disease: malaise, weakness, jaundice, ascites, variceal
bleed, encephalopathy)
o Weight loss, loss of appetite , bone pain , chronic cough with hemoptysis as in
advanced cancer
o Hx of portal HTN
PE o Cachexia, ill looking, altered mental status
o Hands , arms= clubbing, palmar erythema, pallor, spider naevi, scratch mark
o Flapping tremor
o Tattoos, bruises
o Ascites, hepatic bruit, hepatomegaly or palpable mass
o Distended abdomen, dilated veins, caput medusa, umbilical hernia
Staging
Ix o Full blood count (anemia, thrombocytopenia)

o Renal profile (hyponatremia, increased creatinine level)
o Liver function test (elevated AST/ALT, raised bilirubin level)
o Child-Pugh classification or MELD score
o Coagulation profile (prolonged PT)
o Hbsag/anti-hbc, anti-HCV (viral hepatitis)
o Alpha fetoprotein level (greater than 400ng/ml)
o Early arterial phase-enhanced spiral CT scan
o Ultrasound of hepatobiliary system
o CT chest
o Bone scan
o Laparoscopy – evidence of intraperitoneal metastasis

Tx 1) Surgical approach to HCC:
o Should remove the cancer with a 1 – 2 cm margin of unaffected liver tissue.
o Minimize volume resected in patients with chronic liver disease – risk of liver failure
o Transplantation - Patients with cirrhosis with single HCC less than 5 cm in diameter or
multiple hccs each less than 3 cm without evidence of metastasis
2) Non-surgical therapy for hepatocellular carcinoma:

Patients with unresectable disease can be offered local ablative treatments, such as
o Transarterial embolisation (TAE)
o Transarterial chemoembolization (TACE)
o Percutaneous ethanol ablation (PEA),
o Radiofrequency ablation (RFA).
CHOLANGIOCARCINOMA= malignant tumours of the biliary tract

Epidemi o Presents with advanced stage, thus limited survival without surgical resection.
o advanced age
Risk fx o Primary sclerosing cholangitis (most common)
o Oriental cholangiohepatitis
o Hepatitis C infection
o Opisthorchis viverrini (Thailand, Laos and western Malaysia)
o Clonorchis sinensis
o Choledochal cysts
o Caroli’s disease
o Thorium dioxide (Thorotrast®)
o Vinyl chloride
o Dioxin
o Asbestos
o Biliary-enteric anastomosis
CF o Early: non specific - abdominal pain, early satiety, anorexia and weight loss.
o In minory of patients - symptoms associated with painless biliary obstruction (puritus
and jaundice)
o By examination: clinical signs of jaundice , cachexia, palpable gall bladder.
Ix o LFT: elevated bilirubin, alkaline phosphatase and -glutamyltransferase).
o Tumour marker CA 19-9 may be elevated.
o Imaging studies: ultrasound, multidetector row computed tomography (MDR-CT) and
MRI/MR.
o ERCP or PTC – biopsy & placement of endobiliary stents for biliary drainage.
Tx o Only 10–15 % are suitable for surgical resection which offers the only hope for long-
term survival.
o Depending on the site of disease, resections may involve excision of a lobe of the liver
and reconstruction of the biliary tree.

OBSTRUCTIVE UROPATHY
Mechanical or functional defect  that blocks or decrease in urine flow
Causes of obstructive uropathy

1. Stone
2. Tumour
3. Congenital abnormalities
4. Stricture
Complication of obstructive uropathy

1. Renal impairment
2. Repeated infection
3. Stone formation
4. Complain of colicky pain
5. Dilatation
a. Hydroureter
b. Hydronephrosis
Classification of obstructive uropathy

UPPER urinary tract obstruction LOWER urinary tract obstruction
Consist of kidney, ureter, bladder Consist of neck of bladder and urethra
Lower urinary tract symptoms (LUTS)
Filling or irritative Voiding or obstructive
symptoms symptoms
Increase frequency Poor stream
Increase urgency Hesitancy
Dysuria Terminal dribbling
Nocturia Incomplete voiding
Overflow incontinence

URINARY SYSTEM CALCULI
Aetiology (risk factors)

1. Dietetic
 Deficiency in vitamin A
 Uric acid foods
o Mushroom
o Fish, prawn
o Visceral organs
o Beer/wine (yis)
o Bamboo shoot
2. Inadequate drainage and urinary stasis
3. Hypersecretion stone formation
 Prolonged immobilization: skeletal decalcification  ↑ urinary calcium
 Hyperparathyroidism  hypercalcaemia & hypercalciuria
4. Hyposecretion anti-stone formation
 ↓ urinary citrate during menstruation
 Dehydration: ↓ urinary colloid (absorb solute or mucoprotein, chelate calcium)
5. Renal infection
 Predominant bacteria: staphylococci, proteus, e.coli, klebsilla  produce urease
(urea  ammonium)  create alkaline condition which favour stone formation
 Schistosomiasus infection (rare)
3 main type renal calculus

Oxalate calculus Phosphate calculus Uric acid & urate calculi
(calcium oxalate)
 Hard  Smooth  Oval in shape
 Irregular in shape  Dirty white colour  Hard, smooth
 Sharp projection- tend  Staghorn calculus  Often multiple
to cause bleeding  Contain calcium &  Yellow to reddish
 Surface discoloured by phosphate brown in colour
altered blood (white   Radio-opaque (on xray)  Attractive, multifaceted
dark brown or black) appearance
 Radio-opaque (on xray)  Radiolucent (on xray)
2 other uncommon type of calculus

1. Cystine calculus Xray- radio-opaque (putih), radio-lucent (hitam)
2. Xanthine calculus
Ultrasound- hyper-echoic (putih), hypo-echoic (hitam)
CT scan- dense
MRI

Different location of stone
KIDNEY URETER BLADDER
o 50% present at age of 30-50y o Usually come from kidney o Primary bladder stone: develop in
o Male:female= 4:3 o Single stone sterile urine, often originate from
kidney, rare nowdays due to
improved diet (↑ protein-
carbohydrate ratio)
o Secondary bladder stone: occurs
in present of infection, BOO,
impaired bladder emptying by
foreign body
o Male: female = 8:1
History History History

 Commonly silent even when large  Colicky pain  Asymptomatic & found
 Deep seated aching pain  Referred pain from loin to incidentally
 Localised renal pain at loin or groin/penis/ scrotum/ labium  Frequency (earliest symptom)
hypochondrium or both  Severe exacerbation in  Incomplete bladder emptying
 Worse on movement (climbing background of continuing pain  Strangury: at the end of
stairs)  Haematuria micturition, referred to tip of
 Haematuria  Strangury (painful passage of few penis or labia majora, worsen by
 Rarely last >8H drop of urine)- intramural calculi movement
 Fever- infected septicaemia of ureter (Screaming or pulling of penis
 Impaction: constant dull pain in with hand at end of micturition in
Examination iliac fossa, aggravated by exercise young boy)
 Tenderness on gentle deep and relieve by rest  Haematuria- at the end of
palpation micturition (stone abrading
 Percussion over kidney produce Examination vascular trigone)
sharp pain  Tenderness & rigidity over course  Interruption of urinary stream
of ureter (stone blocking internal meatus)
 Renal pouch ++  Recurrent urinary infection
Investigation
1. Xray KUB
2. US KUB
3. IV Urography
4. Serum calcium- to exclude hyperparathyroidism
5. Serum uric acid
6. Serum oxalate

Management Management Management
Conservative treatment Conservative treatment 1. Litholapaxy- using lithotrite to
Indicated for small calculi <0.5cm- as can Expectant treat for small stone that crush the stone
pass spontaneously unless impacted likely to pass naturally  US lithotripsy- for small stone
1. Analgesics- diclofenac  Laser lithotripsy with holmium
Operative management laser- for larger stone then
Indicated for large calculi or infected Operative management proceed with optical lithotripsy
upper urinary tract Indication are (once small fragment produced)
1. Antibiotics 1. Repeated attack of pain & stone
2. Extracorporeal shock wave not moving
lithotripsy (ESWL) 2. Stone enlarging
3. Percutaneous nephrolithotomy 3. Complete obstruction of kidney
4. Open surgery 4. Urine infected
o Pyelolithotomy 5. Stone too large to pass
o Extended pyelolithotomy 6. Stone obstructing solidary kidney
o Nephrolithotomy or bilateral obstruction
Methods
1. Endoscopic stone removal
o Dormia basket
o Ureteric meatotomy- for
intramural stone (make
endoscopic incision using
diathermy knife)
2. Ureteroscopic stone removal  Evacuation of fragment
 using endoscope that pass i. 200ml fluid introduced into
transurethrally across bladder bladder
into ureter ii. Evacuator filled with solution
 used to remove stone that are fitted into sheath
impacted iii. Bulb compressed &
 stone cannot be caught in permitted to expand,
dormia basket or endoscopic returning solution carries
forceps are fragmented using with it fragments of stone
electrohydraulic, percussive or 2. Percutaneous suprapubic
laser lithotripter litholapaxy
o Push bang- for stone in the 3. Open surgery
middle or upper part of ureter
(flush back into kidney using
ureteric catheter)
o Then J-stent secure
repositioned calculus in
kidney for ESWL
3. Lithotripsy in situ
4. Open surgery- ureterolithotomy
(if large stone)

Prevention for recurrent
 Unless calculi caused by specific biochemical abnormality,
high fluid intake is the best way to discourage recurrent stone formation
1. Excessive intake of following should be taken in moderate:-

 Milk product (calcium stone)
 Strawberry, plums, spinach, asparagus (sodium oxalate)
2. Hyperuricaemia patient should avoid red meat, offal and fish (rich in purine) + treated with
allopurinol
3. Cystinuria patient should restrict eggs, meat and fish (high in sulphur containing protein)
4. Drink plenty of water to keep urine dilute
5. Good urination habit
Complication Complication Complication

1. Hydronephrosis 1. Bladder stone 1. Chronic bladder dysfunction
2. Impaired renal function 2. Ureter colic impacted 2. Recurrent UTI
3. Renal failure 3. Hydrourete

URINARY SYSTEM- INFECTION
KIDNEY
PYELONEPHRITIS = infection of kidney

Aetiology
1. Haematogenous infection
 Primary site: tonsil, carious teeth, cutaneous infection (boil, carbuncle)
 Renal TB: occur by blood borne spread from LN in neck, chest, abdomen
2. Ascending infection
 More common route
 Most likely to occur with vesicoureteric reflux
 Other contributing factors
i. Urinary stasis
ii. Presence of calculi
iii. Anatomical: short urethral in female
iv. Neurogenic bladder
v. Diabetes mellitus
Bacteriology
 Most commonly Escherichia coli and gram negative (proteus spp)
ACUTE PYELONEPHRITIS CHRONIC PYELONEPHRITIS

 More common in women: childhood,  Often associated with vesicoureteric
puberty, after intercourse, during reflux (better name reflux nephropathy)
pregnancy and menopause  May lead to renal damage & death from
 More on right end stage RF
 Frequently bilateral  Woman:man = 3:1
 Extremely dangerous if kidney (2/3 female <40y, 60% male >40y)
obstructed  septicaemia
 Uncommon complication of chronic
urinary retention

1. Prodromal symptoms:- headache, 1. Clinically silent until advanced renal
lassitude, nausea insufficiency occur
2. Sudden onset pain 2. Dull, non specific character lumbar pain
 In flank & hypochondrium (60%)
 May resemble renal colic pain 3. Increase frequency
3. Fever with chills and rigor (≥39°C) 4. Dysuria
4. Vomiting 5. Hypertension (40%)- accelerated
5. Cystitis symptoms: urgency, frequency, malignancy type
scalding dysuria 6. Constitutional symptoms (30%)
 Lassitude
 Malaise
 Anorexia
 Nausea
 Headache
7. Low grade fever
8. Normochromic microcytic anemia

Investigations
1. Urine dipstick
2. Urinalysis- pus cells & bacteria
3. Urine C+S (>100k colonies/ml bacteria)
4. FBC- leukocystosis
5. RP
6. Serum albumin & creatinine
7. Abdominal xray
8. Abdominal US
Treatment Treatment
1. Antibiotics 1. Eradicating predisposing contributing
 Broad spectrum (ciprofloxacin) factors
 Route: parenterally (IV) 2. Treating infection with repeated course
 Time: IV until clinically improved of antibiotics
followed by oral for 2-3days  Unfortunately, once scared-
2. Analgesics vulnerable to blood borne
3. Drink copiously- if not possible set up IV organism & reinfection likely to
drips occur
4. Acidic urine (common coliform infection)  Thus only offer temporary
–alkalinisation of urine with potassium benefit
citrate will help inhibit growth of  Progressive renal damage is
organism and relieving dysuria common
5. Treat underlying abnormality 3. Surgery: if disease confined to 1 kidney
 Nephrectomy or partial
nephrectomy
 May control symptoms of
infection & hypertension
4. Renal replacement: for end stage RF

PYONEPHRITIS = pus in the kidney PERINEPHRIC ABSCESS = suppurative material
(abscess) in perinephric region
 Multilocular sac containing pus or Aetiology
purulent urine
 Usually unilateral
Aetiology
1. Infection
 From infection of
hydronephrosis
 Follow acute pyelonephritis
2. Obstruction
 Renal calculi disease (most
common causes)
Other causes
 Infection of perirenal haematoma
 Perinephric discharge of untreated
pyonephrosis or renal carbuncle
 Extension tuberculous vertebral-
myocobacterial perinephric abscess
1. Classical triad of:- 1. High swinging fever
anemia + fever + swelling in loin 2. Abdominal tenderness
2. Prominent cystitis features 3. Fullness in loin
1. Imaging- calculus & dilatation of pus 1. Plain abdominal X-ray
filled collecting system 2. US & CT = diagnostic
1. Parental antibiotics 1. Parental antibiotics
2. Surgical emergency 2. Aspiration through large percutaneous
 Threatened permanent kidney needle
damage & lethal septicaemia 3. Open drainage (if cannot be aspirated)
 Kidney drainage
i. Percutaneous
nephrostomy
ii. Open nephrostomy:- if
pus too thick
iii. Remove stone if present
iv. Nephrectomy:- kidney
destroyed & function of
other kidney is good
**RENAL CARBUNCLE = abscess in renal parenchyma**

BLADDER
CYSTITIS = infection of bladder

 Lower urinary tract infection (UTI)
 More common in women than men, particularly <50y
 Isolated infection
o single episode lower UTI occur frequently in female, no complication (no ix)
 Recurrent infection
o repeated lower UTI with underlying predisposing factors, bacterial resistance
(required further ix)
Predisposing factors
1. Incomplete emptying of bladder
 Secondary to BOO, bladder diverticulum, neurogenic bladder dysfunction,
decompression of detrusor muscle
2. Obstruction
 Secondary to calculus, FB, neoplasm
3. Incomplete emptying of upper tract- dilatation of ureter associated with pregnancy or
vesicoureteric reflux (commonly in child)
4. Oestrogen deficiency  lower local resistance
5. Colonisation of perineal skin  facilitate adherence to mucosa
6. Diabetes mellitus
7. Immunosuppresion
8. Repeated catheterization
Bacteriology: same as upper UTI

Route of spread
 Commonly ascending infection from urethral
 Organism originate in bowel, contaminate in vulva and reach bladder
 Other route: descending from kidney, haematogenous, lymphatic, spread from adjoining
structure (fallopian tube, vagina, gut)
Clinical features
1. Cystitis features: frequency, urgency, suprapubic discomfort, dysuria, cloudy offensive urine
2. Fever with chill & rigor: suggestive of upper UTI (complicated infection) or septicaemia
3. Tenderness over bladder
Investigations: same as upper UTI
Management: same as upper UTI

PROSTATE
PROSTATITIS = infection of prostate

 Also commonly involved seminal vesicles and posterior urethral
 May spread to epididymides and testes
ACUTE PROSTATITIS CHRONIC PROSTATITIS

Aetiology Aetiology
1. Infection- organism same as other UTI 1. Sequel of inadequate treatment of acute
2. Infection can be secondary to acute prostatitis
urinary infection or from hematogenous
spread
 General CF overshadow local features- 1. Symptoms of posterior urethritis
ill, fever (up to 39°C), shiver, rigor, ache 2. Prostatic and perigenital pain
all over (especially at back) accompanied by intermittent fever
 Dysuria 3. Persistent thread in voided urine
 Perineal heaviness 4. Prostatic massage showing pus cells with
 Rectal irritation or without bacteria in absence of urinary
 Pain on defeacation infection
 Urethral discharge rare 5. DRE: normal or soft, boggy and tender
 DRE:- tender prostate, one lobe swollen prostate
more than other, seminal vesicle maybe
involved
1. Urine test: containing prostatic thread
2. Urethroscopy
Treatment Treatment
1. Prolonged antibiotics that penetrate 1. Antibiotics
prostate: trimethoprim or ciprofloxacin
PROSTATIC ABSCESS
Clinical features
1. Temperature rising steeply with rigors
2. Severe, unremitting perineal and rectal pain with occasional tenesmus
(may confuse with anorectal abscess)
3. DRE: prostate enlarged, hot, extremely tender, fluctuation
4. Retention of urine in men
Treatment
1. Should be drain without delay- perurethral resection (unroofing the whole activity)
Perineal route rarely indicated unless marked periprostatic spread

URINARY SYSTEM TRAUMA
KIDNEY
Clinical features
1. No external bruising
2. Pain and tenderness
3. Haematuria
-severe delay hematuria caused by clot dislodged  clot colic
(3rd day to 3rd week after injury)
4. Abdominal distension due to retroperitoneal hematoma
(24-48H after injury)
Management
Conservative Surgical exploration- nephrectomy
1. Blood group and cross match/save Indication
2. Establish IV line  Signs of progressive blood loss
3. Stay in bed when there is macroscopic  Expanding mass in loin
hematuria and lessen activity for a week Aim
after urine clear  To stop bleeding while conserving as
4. Analgesia: morphine much as renal tissues as possible
5. Antibiotics- to prevent infection of Complication
hematoma  Massive haemorrhage as releasing the
6. Monitoring VS- PR & BP hourly tamponading effect of perirenal
7. Monitoring urine for hematuria- each haematoma
sample of urine
**PREop: make sure other kidney function
Complication
1. Clot retention
Mx: bladder washout using catheter or cystoscope
2. Pararenal pseudohydronephrosis
Due to complete cortical tear & ureteric obstruction caused by scarring
3. Hypertension
Due to renal fibrosis

URETER
 Uncommon result of hyperextension injury of spine
 Rarely made until there is swelling in the loin/iliac fossa + reduction in urine output
 Most commonly get injured during surgery
o Trauma during hysterectomy or other pelvic surgery
o Preoperative catheterization make ureter easier to be identified
o If injury discovered during surgery- need immediate repair
UNILATERAL injuries BILATERAL injury

1. No symptoms- secure ligation of ureter 1. Anuria
may lead to silent atrophy of kidney 2. Ureteric catheter will not pass
2. Loin pain & fever- pyonephrosis
3. Urinary fistula- through abdominal or
vaginal wound
Repaired of injured ureter- when injury discover post-operatively

 Repair need not be delayed if patient is fit
 Variety technique, surgery should be performed by urologist
If there is no loss of length  Spatulation and end-to-end anastomosis
without tension
If there is little loss of length  Mobilise kidney
 Ureteroneocystostomy
o Psoas hitch of bladder
o Boari operation
If there is marked loss of length  Transureteroureterostomy
 Interposition of isolated bowel loop or mobilised
appendix
 Nephrectomy
Boari operation
 Strip of bladder wall is fashioned into a tube to bridge gap between cut ureter and bladder

BLADDER
 Can be intraperitoneal (20%) or extraperitoneal (80%)
INTRAperitoneal (20%) EXTRAperitoneal (80%)
Bladder (intraperitoneal) rupture Extravesical injury
Causes Causes
 Secondary to blow or fall on  Blunt trauma or surgical damage
distended bladder o Herniotomy
o Hysterectomy
Clinical features o Excision of rectum
 Sudden severe pain in hypogastrium
 Syncope
 Once shock subside
o Abdominal distension
o No desire to micturate
 Peritonitis- if urine is non-sterile
 Laparotomy If diagnose during surgery
 Repair and bladder drainage  Bladder repair
 Catheter drainage for 10 days
If undiagnosed- mx same as bladder rupture
 Investigations
o CT scan
o Plain erect abdominal xray- ground glass appearance
o IVU- to confirm leakage
o Retrograde cystography- to confirm diagnosis

URETHRAL- male
BULBAR URETHRAL MEMBRANOUS URETHRAL
History of blow to the perineum- fall astride a Penetrating injuries or pelvis rupture
projecting object Occur near apex of prostate
 Retention of urine  Often associated with bladder rupture
 Perineal hematoma *difficult to distinguish between these 2
 Bleeding from external urinary meatus -pain, bruising, dullness above umbilicus
 Peritonitis
Treatment Treatment
 Analgesic  Suprapubic catheter
 Prophylaxis antibiotics  Exploration and repair of bladder
 Avoid passing urine
 Full bladder drained with percutaneous
suprapubic catheter
Main worry:- urethral catheter convert
partial to complete transection of urethra
If already passed urine & no extravasation
–no need drainage
 Open repair for complete rupture
Complication Complication
 Subcutaneous extravasation of urine  Urethral stricture
 Urethral stricture  Urinary incontinence
 Infection  Impotence
 Extravasation of urine

HEMATURIA
Definition  Blood in the urine

 Defined as the presence of at least 5 red blood cells per hpf of centrifudged urine
History History taking for haematuria
taking First ask all about the haematuria
1 How long have you had blood in your urine?
2 Is the blood mixed with the urine? Is it at the beginning, midstream or end? Is the
urine pink, red, smoky, dark red? Or does the blood come after the urine i.e.
drip out afterwards or is it present on wiping? (Does the patient currently have
her period if female? when was the last period?)
3 Are there any blood clots?
4 Is the blood in the urine constantly there or does it come and go? (Intermittent
porphyria - very rare!) Is it exercise induced for example?
5 Is it associated with any pain? e.g. loin to groin pain, or lower back pain? Is there any
pain whilst passing urine?
6 Ask for other lower urinary tract symptoms (LUTS) other than dysuria: hesitancy,
straining, frequency, dribbling, nocturia
Ask about possible etiologies
1 Infection: Have you had any flu or any other infection recently? Or any fever? Do you
or anyone you know of have TB?
2 Neoplasia: Have you lost any weight or had any loss of appetite? Any fever/night
sweats/chills? Do you smoke? What is your job?
3 Polycystic kidney disease: Do you have any kidney problems? Is there anyone in your
family who has any kidney problems or deafness (Alports)?
4 Calculi: Have you ever passed out any stones?
5 Trauma: Has there been any trauma recently? (may not necessarily be trauma to the
urinary tract - even crush injuries may cause myoglobinuria which is "fake
haematuria")
6 Nephritic/nephrotic: Is there any bubbles in your urine? Do you notice any puffiness
of your face or swelling of your scrotum (males only), or legs?
7 Bleeding diathesis: Do you have any gum bleeding, bleeding from your nose or
bruising anywhere?
Then ask for the complications of the haematuria
1 Anaemia: do you feel tired/short of breath/feel your heart beating very fast/feel dizzy
or giddy especially when getting up? Have you been more pale than usual?
2 Renal failure: Have you felt more tired or ill recently? Do you notice any swelling in
your legs?
How does it affect you?

URINARY SYSTEM- NEOPLASM
KIDNEY
Benign neoplasm
1. Adenoma 2. Angioma 3. Angiomyolipoma
 Pea-like cortical adenomas  Benign vascular  Rare
 Asymptomatic malformation or renal  Often but always associated with
 Discovered during post angiomatous dysplasia tuberous sclerosis
mortem or during  Rare, young adults  High fat content- typical appearance
radiological imaging  CF: profuse haematuria on CT
 Papillary and tubular type  Diagnose by renal  Content malignant elements (one
angiography quarter- may lead to metastasis)
Malignant neoplasm
Children:- Wilms’ tumour (nephroblastoma) Adults
 Usually in first 5 years of life  Renal cell carcinoma (RCC): Grawitz’s
 Typically present with abdominal mass tumour/Hypernephroma/adenocarcinoma
 May cause haematuria, abdominal pain or  Transitional cell tumour of renal pelvis and
fever collecting system
 Metastasis to lung  Squamous cell carcinoma of renal pelvis
 Best treated in paediatric oncology unit  Transitional cell carcinoma of ureter
Adult- malignant tumour

Tumour of renal pelvis and collecting system Tumour of ureter
TRANSITIONAL CELL CARCINOMA SQUAMOUS CELL TRANSITIONAL CELL
(TCC) CARCINOMA (SCC) CARCINOMA
May invade renal parenchyma and  Rare  Rare
have tendency to be multifocal and to  Often associated with  Behave like tumour of
distant spread chronic inflammation & renal pelvis
leukoplakia from stone  Tx: nephroureterectomy
Clinical features  Radiosensitive  Half patient with tumour
1. Haematuria- seek help before  But metastasize early of upper UT will have
mass palpable  Poor prognosis tumour of bladder at
some stage
Investigations  Thus follow up by
1. Cells sampling via brush or cystoscopy with regular
catheter pass up ureter under urography necessary to
radiological control detect recurrent
-Indicate whether tumour well or
poorly differentiate
2. Intravenous urography
-to demonstrate tumour
3. Retrograde pyelography
-if urogram is indistinct
Treatment
1. Conventional surgical treatment-
nephroureterectomy
2. Poorly differentiate will do better
if have short course of
radiotherapy pre-Op

RENAL CELL CARCINOMA (RCC)- tumour of renal
 Also known as Grawitz’s tumour/Hypernephroma/adenocarcinoma
 Common neoplasm of kidney with 75% incidence
 Arise from renal tubular cells
 Twice as common in men than female
Clinical features
1. Haematuria TRIAD: hematuria + loin pain + palpable mass
2. Clot colic
3. Dragging discomfort in loin
4. Palpable mass
5. Rapidly developing varicocele (rare but impressing sign)
 More often in left side because left gonadal vein is obstructed where it joint left
renal vein
6. Atypical presentation
i. No local symptoms in 25% cases
ii. Metastasis symptoms
 Bone: secondary deposits
 Lung: persistent cough or hemoptysis
iii. Persistent fever (37.8-38.9°C) with no evidence of
infection
iv. Constitutional symptoms and anemia
v. Polycythaemia (4%)
 Result of production of erythropoietin by tumour cells
 ESR raised above 1-2mm in idiopathic polycythaemia
 Blood count always return to normal after nephrectomy unless metastasis
vi. Hypercalceamia
vii. Nephrotic syndrome (rare)
*Paraneoplastic syndrome
Spread
1. Local: tumour prone to invade renal vein (local spread)
2. Lungs: invade renal vein  swept into circulation (haematogenous spread) lung
3. Bone: secondary deposit in long bone (distant spread)
4. LN: tumour extending to renal capsule  LN in hilum of kidney  para aortic nodes and
beyond (lymphatic spread)

Investigations
Initial investigations
1. Renal profile- to access remaining function of kidney
2. FBS- to check for polycythemia
3. Serum calcium- hypercalcemia (paraneoplastic syndrome)
4. IV urography- to investigate haematuria
5. Plain Xray of KUB- to look for evidence of mass
 Abnormal calcification in kidney
 Distorted renal outline
 Calyces stretch and distorted
 Check also contralateral kidney (working or not)
Once Xray KUB demonstrated a mass, do

1. US KUB- to decide whether it is solid or cystic
2. CT scan with contrast- to look for extend of tumour (check hilar LN and renal vein as well)
3. Transesophageal echocardiogram- if suspected spread of tumour from IVC involving right
atrium
4. LFT: impaired in liver metastasis or paraneoplastic syndrome
5. CXY: lung metastasis(cannonball appearance)
6. Isotope bone: reveal deposits in bone
Treatment
1. Main stay management= surgery –nephrectomy
Approach: loin or transverse or oblique upper abdominal incision
Transabdominal approach more advantage as can widely exposed renal pedicle and IVC
2. Poorly respond to radiotherapy or conversional chemotherapy- cytokine interleukin-2
Prognosis
 Removal of even large neoplasm may cure patient
 Operable case: 70% well after 3y, 60% after 5y
 Worsen prognosis in
i. Macroscopic involvement of renal artery and tributaries
ii. Invasion beyond capsule
iii. Lymphatic involvement

BLADDER TUMOUR
Primary bladder tumour
 95% originate from transitional epithelium
 <5% originate from connective tissue (angioma, myoma, fibroma, sarcoma)
or from extra-adrenal phaechromocytomas
Secondary bladder tumour

 Are common
 Most frequently arise from sigmoid, rectum, prostate, uterus, ovaries
 May also arise from lung
Aetiology (risk factors) Clinical features
1. Cigarette smoking (40%) 1. Painless gross haematuria
2. Occupational exposure to chemical (bladder ca until proven otherwise)
 Aniline dye factories 2. Clot formation & retention  clot colic
 Tyre or cable workers 3. Frequency & discomfort associated
 Shoes manufacture or cleaners with urination
 Hairdressers 4. Constant pain in pelvis- extravesical
 Painters spread
 Textile workers 5. Pain in loin or pyelonephritis –pressure
3. Endogenous carcinogen symptoms causing obstruction &
4. Balkan nephropathy (schistosoma hydronephrosis
haematobium infection  history travel 6. Late manifestation- nerve involvement
to egypt  middle east ) causing pain that referred to
5. Genetics suprapubic, groin, perineum, anus and
6. Drugs: cyclophosphamide (in breast ca) thigh
**carcinoma in situ- severe symptoms of

dysuria, suprapubic pain and frequency
(hence name malignant cystitis)
Investigations
1. FBC- for Hb level
2. BUSE
3. LFT- metastasize
4. Urine culture- examine cytologically for malignant cells
Imaging
1. IVU
 Faint shadow of encrusted neoplasm
 Filling defect (most common finding)
 Irregularity of bladder wall- invasive tumor
 Hydronephrosis
2. US KUB- if kidney non functioning
(benda sama nak tengok dalam IVU)
3. CT/MRI scan- diagnosis & staging
4. Cystourethroscopy
 Mainstay diagnosis- for haematuria patient

Staging
Management Stage 0 and 1 (superficial)

 Transurethral resection of the bladder and follow up cystoscopy
 Intravesicle chemotherapy (Thiotepa, Ethoglucid, Doxorubicin, Mitomycin C)
and
 Immunotherapy (BCG)  concept dia BCG akan produce antibody to fight
against the cancer
Stage 2 and 3 (invasive)

 Radical cystectomy + ilealconduit (to divert the urine)
 Partial cystectomy + radical radiotherapy
 Neoadjuvant radio and chemotherapy to shrink the
tumor before surgery
 Systemic chemotherapy and radiotherapy
Fixed and metastatic tumor

 Systemic chemotherapy

PROSTATE
 Enlargement of prostate due to imbalance of testosterone and oestrogenic steroid
(serum testosterone decreased with age, but oestrogenic steroid doesn’t decreased equally)
 Happened in men age >50y (by age 60, 50% men have histological evidence of BPH)
BENIGN PROSTATIC HYPERPLASIA

Symptoms
1. LUTS (prostatism) symptoms
Voiding Storage
i. Hesitancy (worsen when bladder full) i. Frequency
ii. Poor flow (unimproved by straining) ii. Nocturia
iii. Intermittent stream (stop & start) iii. Urgency
iv. Dribbling (including after micturition) iv. Urge incontinence
v. Sensation of poor bladder emptying v. Nocturnal incontinence (enuresis)
vi. Episodes of near retention
2. BOO symptoms
3. Complications symptoms
Infection- stone formation (due to stagnant urine)
Renal failure accompanied b anemia, dehydration, acidosis, infections
Enlargement of transitional zone: present early with symptoms

PR examination
1. Rubbery firm
2. Smooth
3. Symmetrically enlarged
4. Regular in shape
5. Median sulcus palpable
6. Can be move over
Investigations
1. Urinary analysis by dipstick for blood, glucose & protein
2. Urine culture for infection
3. Serum creatinine
4. BUSE
5. Renal profile
6. Imaging (IVU/US)- no longer done if straightforward symptoms
7. Cystourethroscopy
8. Urinary flow rate & residual volume measurement

Management
Conservative tx
Indication
 Mild symptoms
 Reasonable flow rates (>10ml-1)
 Good bladder emptying (residual urine <100ml)
What to do?
 Wait for 6m- then repeat assessment of symptoms, flow rates & US
 Limit fluid intake in evening
 Reduction in caffeine intake
 Careful use of propantheline to help with irritative symptoms
Medical tx
Indication
 Failed initial tx of watchful waiting
 Wish to avoid surgery for a period- concern about sexual dysfunction
Drug used?
 25% of shrinkage of prostate gland (greatest outcome if prostate >50g)
 Need to be taken for 6months period
 Expensive + subsequently significant portion of men on drugs still need TURP
 2 classes of drugs
α-adrenegic blocker 5α-reductase inhibitor (finasteride) Combination tx with
(prozasin) o To block conversion testosterone antimuscarinic agent
o To relax SM of prostate to DHT (DHT= more active form o Tolterodine
o Work more quickly of androgen) o SE: dry mouth and
o SE: dizziness, orthostatic o Less side effects eyes, constipation
hypotension, ED o SE: libido and decrease
ejaculatory volume
Surgical tx
Indication
 Acute retention in fit men with no other cause of retention (25%)
 Chronic retention & renal impairment (15%)
 Complication of BOO
 Elective prostatectomy for severe symptoms (60%)
 Pre operation: cystoscopy need to be done to exclude: diverticulum, stone, tumor, size of
the prostate (if too large can’t do TURP)
What to do?
Transurethral resection of prostate (TURP) Transurethral incision of prostate (TUIP)
Most common, most proven surgical tx Usually performed in smaller prostate
Performed by inserting scope through penis & Daycare surgery (no admission require)
remove prostate piece by piece Using scope through penis & small incision
made in prostate tissue to enlarge opening of
urethra & bladder outlet

 Complication after prostatectomy
o Risk of re-operating: 15% after 8-10 years
o Retrograde ejaculation (65%)
o Erectile impotence (5%)
o Severe sepsis (6%)
o Severe hematuria requiring transfusion (3%)
o UTI (15-20%)
International Prostate Symptoms Score (to assess severity)

IPSS Scoring system
I
 Increase frequency
 Increase urgency
 Intermittent flow
 Incomplete emptying
P- Poor stream
S- Straining
S- Sleep (nocturia)

PROSTATE CANCER
Pathology:
o Arise from peripheral zone
o Usually adenocarcinoma
o Gleason Scoring – degree of glandular differentiation and relationship to stroma
Risk factors
1. Age >60 years old
2. Family hx of prostate cancer
3. Chronic bacterial proctitis
4. Enlargement of peripheral zone: present late with symptoms
Symptoms
1. Early: asymptomatic
2. LUTS (prostatism) symptoms
3. Pelvic pain & hematuria
4. Metastasize symptoms
o Bone pain, malaise, anemia or pancytopenia
o Renal failure
o Nodal: penile/pedal/ genital edema
PR examination
1. Nodular
2. Hard
3. Asymmetrically enlarged
4. Irregular in shape
5. Median sulcus not palpable
6. Cannot move over prostate (attach to rectal mucosa)
Investigations
1. Transrectal US- to access local stage ± needle core biopsy
PROSTATIC BIOPSY
 Transrectal biopsy using automated gun
 Obtained 10 systematic biopsy core + biopsy of any suspicious areas
 Under LA- to reduce pain
 Antibiotics- to cover for sepsis
2. Serum prostate specific antigen (PSA) > 10nmol

3. Acid phosphatase
4. FBC- anemia due to extensive marrow invasion or RF
5. Metastasize ix
i. LFT- metastasize, raised in ALP
ii. CXRY
iii. Radionucleotide bone scan
iv. RP
Staging- TMN staging

T1 – Clinically inapparent tumor neither palpable nor visible with imaging
T2 – Tumor confined to prostate
T3 – Extend to prostate capsule
T4 – Fixed or invades adjacent structure other than seminal vesicle: bladder neck, external sphincter,
rectum, levator ms, pelvic wall
N1 – Lymph node metastasis
M1 – Distant mets
Management
 Depends on stage of disease, life expectancy & patient’s preference
 PSA, DRE, Biopsy Gleason grades- to predict pathological stage
Localized cancer
1. Radical prostatectomy
2. External beam radiotherapy (ERBT)
 Conform to contours of prostate so limit exposure of adjacent tissues
 Daily for 4-6weeks
 Cx: irritation to bladder, urinary frequency, urgency, urge incontinence, to rectum
(diarrhoea), late radiation proctitis
3. Brachytherapy- place radioactive seeds (I-125 or palladium-103) permanently into prostate
 Deliver intensive, confined radiation dose which fall off rapidly to spare surrounding
structures
 ↓ anaesthesia with TRUS guidance
4. Active monitoring
Advanced cancer
1. Palliative care- General radiotherapy
 For symptomatic metastases- dramatic pain relief for 6m
 IV strontium-89
2. Hormone ablation (1st line therapy)
 Bilateral orchidectomy (total or sabcapsular) is performed to carry androgen ablation
 To eliminate major source of testosterone production
3. Complete androgen blockage
 Abolish testicular secretion by orchidectomy or LHRH (gonadorelin) then inhibit effect of
adrenal androgenic steroids by anti androgen (flutamide)
TREATMENT SUMMARY (NI JE YG PENTING)

1. At any stage  transurethral resection for BOO
2. Stages 1 and 2  active monitoring + prostectomy / radiotherapy
3. Stage 3  radiotherapy + neoadjuvant or adjuvant hormonal therapy
4. Stage 4  Anti androgen therapies (Bilateral orchidectomy) + radiotherapy for painful bony
mets or spinal cord compression OR drug tx with LHRH (gasorelin) agonist or anti androgen
drugs (flutamide, bicalutamide, cyproterone)

THYROID DISEASES
Thyrotoxicosis Myxedema
Intro Diffuse toxic goitre (Grave’ disease) Hashimoto or chronic lymphocytic
Hyperthyroid + diffuse enlarge goitre due to the thyroiditis - an autoimmune disease
action of a circulating immunoglobulin ‘long-acting in which thyroid gland is attacked
thyroid stimulator (LATS) by a variety of cell- and antibody-
 LATS binds to thyroid acinar cells mimicking the mediated immune processes
effects of TSH and producing excess thyroid  Antibodies against thyroid
hormone peroxidase (TPO) (also called
 Often with family history of autoimmune disease TPOAb) and/or thyroglobulin
cause gradual destruction of
 Grave’s disease follicles in the thyroid gland
 Diffuse toxic goitre (commonly)
 Toxic nodular goitre (secondary)
CF  Exophthalamus  Dry skin and hair
 Proptosis (lid lag for confirmation)  Periorbital puffiness
 Lid retraction  Hoarse voice
 Opthalmoplegia  Bradykinesis, slow movements
 Tremor  Delayed relaxation phase of ankle
 Proximal myopathy jerks
 Palpitations/ Atrial fibrillation  Signs of heart failure
Ix  Most cases are diagnosed clinically  Thyroid function test to elicit
 Thyroid Function Test hypothyroidism
 Radioisotope scan is required to diagnose an toxic  Fine Needle Aspiration cytology
nodule (hot, cold scan)
 Long acting thyroid antibody test
 All the baselines investigations
Mx 1. Antithyroid drugs 1. Thyroxine replacement therapy
 Block the synthesis of thyroid hormone 2. Steroid therapy for the goitre
Eg: Carbimazole, Propylthiouracil, Propranolol that increases in size despite
thyroxine treatment
2. Radioactive iodine (I-131) 3. Thyroidectomy may be
 Destroy thyroid tissue necessary if the goitre is large
 Indications: primary thyrotoxicosis >45 years old, and causes discomfort.
toxic nodule >45 years old, relapse, or
contraindication for both medical/surgical
 Advantages- No surgery and no prolonged drug
therapy
 Disadvantages- Radiation exposure. Patient will
eventually go into hypothyroid
*Contraindicated in pregnancy
3. Surgery
 Total thyroidectomy or subtotal thyroidectomy
 Advantages- Goitre is removed, cure rate is high
 Disadvantages- Risk of permanent
hypoparathyroidism and nerve injury
*Supplement with lifelong thyroxine

Drug used in thyrotoxicosis
Carbimazole Propylthiouracil Beta-adrenergic blocking drugs
 Inhibit iodination and  Inhibit peripheral conversion (propranolol)
coupling T4-T3  40mg in 3 divided doses
 Can restore serum hormone  Lower risk of placental  Rapidly control the
levels to normal over 4-8 transfer so boleh pakai distressing and dangerous
weeks. dalam pregnancy effects of thyrotoxicosis
 Lower maintenance dose  Substitution when patient  May be used initially in
ids? Prescribed for 1 and developed side effects with extremely toxic patients
half year then stop Carbimazole until anti-thyroid drugs take
 Sometimes block and effect
replace regime may be  Or if a patient urgently
given. Block thyroid needs to be stabilized
hormone production before thyroidectomy
altogether with a standard
replacement dose of
thyroxine
 Side effects : rashes,
nausea, headache,
arthralgia, reversible
neutropenia (WBC
monitoring every 3 months-
agranulocytosis)
Preparation for thyroidectomy surgery
 Preparation aims to make the patient biochemically euthyroid at operation
 Carbimazole 30–40 mg per day is the drug of choice for preparation
 When euthyroid (after 8–12 weeks), the dose may be reduced to 5 mg 8-hourly
 The last dose of Carbimazole may be given on the evening before surgery
 Iodine may be given with Carbimazole for 10 days before operation
 Iodide produces a transient remission and may reduce vascularity, improving safety
 Direct laryngoscopy to view vocal cords (documentation)
 Lugol’s iodine for 5 drops a day for 10 days prior surgery (reduce vascularity of the gland)

THYROID MALIGNANCY
Dunhill’s classification
BENIGN MALIGNANT
Primary Secondary
1. Follicular epithelium differentiated 1. Metastatic
i. Follicular carcinoma (20%) 2. Local infiltration
ii. Papillary carcinoma (60%)
Follicular 2. Follicular epithelium undifferentiated
adenoma i. Anaplastic carcinoma (10%)
3. Parafollicular cells
i. Medullary carcinoma (5%)
4. Lymphoid cells
i. Malignant lymphoma (5%)
MALIGNANT LYMPHOMA
• Response to radiotherapy is dramatic and radical surgery is unnecessary
• Diagnosis may be made via FNAC
• Prognosis is good if no cervical lymph nodes involvements
• Most lymphomas occur against a background of lymphocytic thyroiditis
• Combined modality therapy that includes CHOP regimen consists of : cyclophosphamides,
doxorubicin, vincristine and prednisone- Radiation therapy
PAPILLARY FOLICULAR ANAPLASTIC MEDULLARY
 Irradiation of the thyroid under 5 years of age. (cases of childhood thyroid cancer)
CF  Sex ratio is 3:1 (female: male)
 Thyroid swelling
 Anaplastic growth is usually hard, irregular and infiltrating
 Enlarged cervical lymph nodes
 Recurrent laryngeal nerve paralysis (hoarseness of voice)
 Firm, irregular nodules suggestive of benign or differentiated origin
 Pain referred to the ear, is frequent in infiltrative growths
Dx  Sometimes obvious on clinical examination (especially anaplastic carcinoma)
 Failure to take up radioidine is a common characteristic of cancer. Hence, a CT with iodine
contrast media should be avoided.
 Thyroid function test – Usually euthyroid, thyroglobulin level should be low (monitor
efficacy if the thyroidectomy)
 Fine Needle Aspiration
 Imaging with MRI
 Age: 30-40 &  Age: 40-50  Age: 60-80  Age: 50-60
children  Macroscopically  Elderly women  Tumour of the
 Young female encapsulated but  Extremely lethal parafollicular cells
 Predisposing microscopically tumour (C cells) derived
factors: there is invasion  Some present from neural crest
irradiation, of the capsule with tracheal  High level of
hashimoto,  Hurtle cell obstruction and calcitonin and
thyroiditis, tumour – variant require urgent carcinoembryonic
thyroglosal cyst of follicular ca. tracheal antigen are
 Histologically: Poor prognosis. decompression produced (valuable
psammomma Mortality rate is tumour marker)
body and twice of papillary  Associated with

characteristic pale carcinoma MEN II, family hx
empty nucleus multiple endocrine
(Orphan Annie’s Good prognosis neoplasia
Eye) Bone pain
At endemic area *May occur in
combination with
60% adrenal
Good prognosis pheochromocytoma
&
hyperparathyroidism
*Not TSH dependent

and not take up
radioactive iodine
Spread to the lymph Spread usually Spread by lymphatics Lymph nodes
node is common hematogenous, and and hematogenous involvement and
seldom seen in blood borne
Blood borne lymphnodes metastases are
metastasis is rare common
unless the tumour is
extrathyroidal *Progression of this
type of tumour is very
*Extrathyroidal = primary slow and even though
tumour has infiltrated there is no cure,
through the capsule of
thyroid gland patient will survive
longer
Tx Total thyroidectomy **FNAC cannot  Complete resection  Manage by total
with modified radical differentiate can be done if the thyroidectomy and
dissection for nodes + between follicular growth is confined resection of the
life long thyroxine adenoma/ca so to the thyroid central and bilateral
must do total  Even then, the lymph nodes
thyroidectomy -> survival rate rarely  Genetic screening
HPE exceed 6 months for RET mutations in
 Thyroxine is  Trachea families
prescribed decompression and  Prophylactic surgery
postoperatively to tissue histology by is recommended for
suppress TSH isthmusectomy infants with genetic
stimulation on  Radio/chemo- traits
thyroid gland palliative  Calcitonin as
 Chemotherapy tumour marker
>0.08mg/ml
**In all cases, before
the surgery,
pheochromocytoma
must be excluded by
measurement of
urinary
catecholamine
levels
*If any metastasize do post-operative radioiodine ablation

THYROIDITIS
Acute Suppurative
Caused by bacterial infection (usual organisms responsible include staph aureus ,
streptococcus hemolyticus, and pneumococcus)
Subacute Thyroiditis (De Quervain)
Caused by viral infection (eg:mumps, measles, infectious mononucleosis)
Chronic Lymphocytic Thyroiditis (Hashimotos Thyroiditis)
Autoimmune in nature
Hashimoto Riedal’s De Quervain

 Most common type  Rare  Follows viral cause
 Autoimmune in nature  Thyroid tissues are  Hyperthyroid >
 Associated with raised titres of replaced by fibrous euthyroid >
thyroid antibodies tissues which infiltrates hypothyroid
 Presents as a goitre, which may be into muscles and  During hyperthyroid
diffused or nodular with a adjacent structures stage, radioiodine
characteristic ‘bosselated’ feel  Goitre may be unilateral uptake is low
 Enlargement of thyroid is due to or bilateral, and is very (differentiate from
lymphocytic infiltration and hard and fixed graves)
fibrosis rather than tissue  It is one manifestation
hypertrophy of a systemic disease
that can affect many
organ systems called
IgG4-related disease
(multi-organ disease)
RF  Family history of thyroid disease  Common in middle age  Common in middle age
 Female to male ratio 7:1 women women
 Excessive iodine intake
 Radiation exposure (treatment of
cancer)
CF  Asymptomatic  Painless hard anterior  Pain in the neck
 Sudden onset of pain around the neck mass (woody non  Fever
neck tender thyroid  Malaise
 Goitre that is lobulated and either enlargement mimics ca)  Firm & irregular
diffused or localised to one lobe  Pressure symptoms enlargement of one or
 Initially, may present with both thyroid lobes
symptoms of hyperthyroidism
 Eventually presents with
symptoms of hypothyroidism
Dx  Thyroid function test abnormality  FNAC is not adequate  Raised inflammatory
 Raised serum levels of one or  Must do open thyroid markers but absent
more thyroid antibodies: anti- biposy thyroid antibodies
thyroid peroxidase antibodies  Serum T4 is normal or
(TPOAb)/ anti-thyroglobulin slightly raised
antibodies (anti-Tg)  If in doubt, FNAC,
 Fine needle aspiration cytology radioactive iodine
 If still in doubt, proceed with a uptake and rapid
diagnostic lobectomy symptomatic response
to prednisone is done
to confirm the diagnosis

Mx  Full replacement dosage of  High dose steroid with Self-limiting; therefore,
thyroxine tamoxifen and thyroxine the goals of treatment
 Steroid therapy should be replacement are to relieve
considered if goitre increases in  Wedge resection of discomfort and to
size despite hormone therapy isthmus to release control the abnormal
 Thyroidectomy if goitre is large pressure symptoms thyroid function
and causes discomfort -Give prednisone 10-20
 Long term surveillance due to risk mg daily for 7 days and
of late thyroid failure gradually reduce the
dose over the next
month.
-If thyroid failure is
prominent, treatment
with thyroxine may be
required

BENIGN BREAST DISEASES **ACC favourite cases- breast diseases (please make sure you know this topic well)
Aetiologies
1. ANDI (Aberrations of normal development 2. Duct ectasia / periductal mastitis
and involution) 3. Pregnancy related
- Disturbances in the breast physiology - Galactocele
- Lumpy breasts, tenderness or a smooth lump - Puerperal abscess
 Cyclical nodularity 4. Congenital disorders
 Cysts - Inverted nipple
 Fibroadenoma - Supernumary breasts /
nipple
FIBROADENOMA
 Age : 15-25 year
 Arise from hyperplasia of a single lobule GIANT FIBROADENOMA
 Surrounded by condensed connective tissue capsule Occasionally during puberty
Features :
 >5 cm in diameter
2-3 cm in size
Very mobile  Rapidly growing
Non-tender  Must excised
Firm, smooth, rubbery
Consist of
 Fibrous component (fibrosis)
 Abnormal multiplication of ducts and acini (adenoma)
FIBROADENOSIS
• Also called fibrocystic breast disease
• Age : 30-50 year
• Due to nonintegrated involution of stroma and epithelium
• Exaggeration of fibrotic element (fibrosis), epithelial element
undergoes hyperplasia (adenosis)
Features:
Single or multiple cyst + cyclical breast pain + nipple discharge
(clear to green)
Related to menses: pain before, disappear after
Treatment:
 Usually does not require treatment
 Do biopsy, common site mcm cancer, at upper outer quadrant
PHYLLODES TUMOUR
• Also known as serocystic disease of Brodie or cystosarcoma phyllodes
• Age: >40 years olds
Features:
Mobile tumour
Large, sometimes massive
Unevenly bosselated surface
Sudden, rapid growth
Ulceration of overlying skin (pressure necrosis)
Treatment
 Enucleation (young women) or wide local excision
 Mastectomy – massive, recurrent and malignant type

TRAUMATIC FAT NECROSIS
• Trauma (6 months ago) rupture of fat cells  inflammatory  calcified
Features:
Lump is painless
Hard, irregular, tethered skin
Nipple retraction
Mimic a carcinoma
DUCT ECTASIA/ PERIDUCTAL MASTITIS

• Dilatation of breast ducts with periductal inflammation
• Common in smokers and >50 years
Features:
Thick cheesy nipple discharge (Any colour)
Subareolar mass (Poorly defined)
Nipple retraction (Scarring)
Mimic a carcinoma
Treatment:
 Mass or nipple retraction – exclude carcinoma by histology
 Antibiotic : Co-amoxiclav or flucloxacilin + metronidazole
 Surgery : Excision of all major ducts (Hadfield’s operation)
BREAST ABSCESS (STAPH AUREUS INFECTION)

Aetiologies:
 Lactation
 Diabetes Mellitus
 Immunocompromised patient
Features:
Malaise and fever, night sweat
Varies from ache -> continuous throbbing pain. Progressively severe.
Examination:
o Pus discharge
o Tender lymphadenopathy
Treatment :
 Stop feeding on affected breast
 Antibiotics (Flucloxacillin or Co-amoxiclav)
 Incisional & drainage if not subside >48 hours
Prevention: good hygiene
PAGET’S DISEASE
• Involve nipples
• Malignant condition that has an appearance of
eczema
• Uncommon disease accounting
for 1-4.3% of all breast cancers

CARCINOMA OF BREAST
RF 1. Late childbirth (1st child during age >30 years)
2. Family history: BRCA1,BRCA2,P53, HER2
‘Estrogen 3. Long interval between menopause and menarche
related’ 4. Nulliparity /absent breast feeding
5. Age: risk increases with age (40-60y/o)
6. Obesity
7. Diet: high fat, high soy bean ingestion
8. Smoking
9. Exposure to radiotherapy
10. Atypical hyperplasia in previous breast biopsy
11. Oral contraceptive pills /hormonal replacement therapy
12. Female sex
CF Symptoms suggesting malignancy Signs suggesting malignancy
• Mass underneath the arm/breast  Skin dimpling
• General malaise, LOA and LOW  Visible lump
• Nodules in the skin  Peau d’orange
• Metastasize features (2B, 2L)  Surface erythema
o Mental changes and fit  Surface ulceration
o Backache, bone pain,  Recent nipple ulceration
pathological fracture  Recent nipple inversion
o Dyspnoea or pleuritic pain  Bloodstained nipple discharge
o Jaundice  ‘Eczema’ around nipple (paget’s)
Histology suggesting malignancy
1. Abnromal cellular differentiation
2. Tubule infiltration
3. Nuclear pleomorphidm
4. Mitotic count/ figure (twin cell)
Type INVASIVE
1. Ductal- common 3. Special types
• Solitary firm mass with poorly • Tubular
defined margin • Cribriform
2. Lobular • Mucinous
• Multifocal bilateral • Medullary
• Multicentric 4. Mastitis carcinomatosa
• Very aggressive
• Only in pregnancy & lactating mom
NON-INVASIVE
1. Ductal Carcinoma In Situ (DCIS) 2. Lobular Carcinoma In Situ (LCIS)
Common types • Multicentric and bilateral
• Comedo
• Intermediate
• Non comedo solid

Stage Stage I: T1-T2/N0 Confine
Stage 2: T1-T2/ N1 Surgery
Stage 3: T3-T4/M0 Spread
Stage 4: T3-T4/M1 Palliative
Spread METASTASIS:
1. Site: GIT, urinary, CSF, biliary system
2. Mode of spread:
1. Lymphatic 2. Hematogenous 3. Transcoelemic/ trans peritoneal (krukenberg)
3. Method of spread:
1. Embolization 2. Permeation: spread like tree root, stop at right atrium dt fast
circulation in heart
4. Treatment: palliative. Chemotherapy tru CVL is better to prevent
thrombophlebitis
KRUKENBERG TUMOUR:
1. Cancer from distance (usually from stomach and breast) spread to ovary
2. Usually by transperitoneal spread
3. Rupture luteal cyst will expose raw area for implantation
Ix TRIPLE ASSESSMENT: CLINICAL EXAMINATION + IMAGING + BIOPSY
IMAGING
1. Mammography (>40 y/o)
All women >40 yearly
If suspicious biopsy/come again 6 months later
2. Ultrasonography (USG) (<40 y/o)
BIOPSY
 Fine needle aspiration cytology (FNAC): when cannot see the mass
 Tru-cut biopsy/core needle: take small tissue
 Excisional biopsy: mass already seen clearly
*Know different types of biopsy and when they are use
Other investigations
1. MRI: to look for evidence of metastasize
2. Test for HER2 : well respond to monoclonal AB
3. ER/PR receptor: if negative not improve with chemo, only monoclonal AB can help

Investigations done during operation
o Sentinel LN biopsy in early breast cancer: to see nearest LN involvement
o Methelene blue dye: for anterior LN, frozen section = excise LN
o Sinus histocytosis: to detect normal active LN, not to excise them
Tx Surgery
Breast conservative surgery Mastectomy + axillary clearance
Remove cancer completely in as small Total removal of breast together with
volume of tissue as possible lymph node
o Lumpectomy
o Wide local excision + radiotherapy: Indication for mastectomy
modified radical level 1,2,3 • Large tumour
• Central tumour beneath/involving
Contraindication for local excision nipple
• >4 cm tumour • Multifocal disease
• Improper tumour: breast ratio • Local recurrent
• Patient wish to remove all • Patient preference
• Skin/ collagen vascular diseases that
maybe complicated by radiotherapy
• Not compliant to radiotherapy
Systemic therapy
Chemotherapy
• Aim: destroy micrometasis and any circulating tumor cell
• Offered to high risk category and moderate risk
• Can be given by IV or tablets
• Should be start 4-6 weeks after surgery
• CMF, FAC, FEC : cyclophosphamide, methotrexate, 5-flourouracil,- given every
month for 6months
• Cisplatin, fluoracil
Hormonal therapy
- Tamoxifen: anti estrogen (block effect estrogen). Dosage is 20 mg OD for 5 years.
- ER +ve, ER unknown status
- Aromatase inhibitor: block conversion androgen to estrogen (anastrozole)
- Ovarian ablation: destroy the ability of ovaries produce estrogen
Biological therapy
- Monoclonal antibody therapy – Tratuzumab. Respond well in HER2
- Drugs: Herceptin and Avastatin
Radiotherapy
• Indicated in
- Post breast conserving surgery : stage I, II,DCIS
- Chest wall therapy mastectomy
• Should be given as soon as possible after surgery
• Given 5days a week for 6-7 weeks
Breast reconstruction
1. Tissue expansion
2. Silicon breast implant
3. Myocutaneous transposition flap

Screening for breast cancer
 Breast self-examination (BSE)
 Begin at age 20
 Performed monthly
 On the days immediately following the menstrual cycle
 Clinical or physician breast examination (CBE)
 Begin at age 20
 Performed annually for women at average risk for breast cancer
 Screening mammography
 Begins at age 40, 30% decrease in death from breast cancer
 Performed annually
MASTITIS CARCINOMATOSIS
 Only in lactating mother and pregnant women
 Very invasive
 Tx: aggresive
1. Mastectomy
2. Bilateral oopherectomy
3. Radio and chemotherapy
4. HER2 +ve: monoclonal AB
DEALING WITH BREAST CANCER PATIENT- OSCE

General principles:
1) Greeting
2) Introduce
3) HT, PE
4) Verbal consent
5) Reassurance
6) Thanks patient
Physical examination:
1. Confirm privacy- screen bedside
2. Be with a chaperone
3. Honesty is the best policy: be sincere if u don’t know/ don’t do
4. Adequate exposure
5. Inspection:
 Describe the skin: puckering, peau d’orange, redness, dimpling, tether, ulcer
 Describe the nipple: deviation, retraction, discharge, crack, eczematous lesion
 Ulceration signs: edge raised and everted, irregular margin, bleed to touch, dirty looking
with blood/ slough, fixed based
6. Palpation: circular/split/wedge pattern
 Describe the lump: site, size, shape, surface, number, margin, consistency, distance from
nipple
“There is a single lump, round, about 2 cm sized, hard in consistency at between 10 to 11
o’clock, in upper outer quadrant, 2 cm away from the nipple”
 Palpate LN: anterior groove, central, posterior, apical, lateral
 + infraclavicular, supraclavicular, deep transverse cervical LN

ARTERIAL DISEASE
ACUTE LIMB ISCHEMIA CHRONIC LIMB ISCHEMIA
Intro • Occur within < 14 days when an arterial • Occur > 14 days, develop more slowly than
occlusion suddenly reduce the blood flow acute
to the arm or leg • Pain precipitated by exercise & relieve by rest
• Producing a wet gangrene • Producing dry gangrene
Aetio Embolism & thrombus Atherosclerosis
RF  Causes of embolus:  DM & HPT
 Rheumatic heart disease  Hyperlipidemia
 Atrial fibrillation  Smoking
 Acute MI  Family history
 Polycythemia Vera  Obesity & sedentary lifestyle
CF 6P 4 Stages (Fontaine Classification)
I. Asymptomatic
II. Intermittent claudication (Non-Critical)
III. Rest pain
IV. Ulcer @ Gangrene @ Both (Critical)
Ix
Invasive: Angiography –Gold standard, especially in case medium to large vessel for
planning of bypass or stenting
Other investigation:
 Full Blood Count, Blood & Urine Glucose, Fasting Lipid Profile, Renal Profile
 ECG : may show Coronary Ischemia, Left Ventricular Hypertrophy Or Rhythm
Abnormalities
Tx 1) Anti coagulant (IV Heparin) 7) Amputation
2) Thrombolytic (Streptokinase) 8) Advice: exercise , stop smoking, reduce
3) Embolectomy weight
4) Arterial reconstruction (eg: femoral- 9) Other:
tibia or femoral-popliteal bypass)  Pain relieve
5) Balloon angioplasty  Vasodilatation
6) Reconstruction arterial surgery (bypass)  Lumbar sympathectomy

Pain from limb ischemic Pain from DVT
 More Severe  Less severe
 Pallor  Red
 Cold  Warm
 No swelling  Swelling / Edema
 Pulseless (periphery)  Peripheral pulse present
Intermittent Claudication Rest Pain

 Pain at the calf  Pain at foot or toe
 Brought on by walking  Worse at night which
 Relieved when stopped wakes patient from sleep
 Relieved by hanging foot
out of bed or sleeping in chair
Claudication distancefrom walk no pain to pain- how far?
Claudication time time patient rest- how long?
GOOD TO KNOW
Raynaud’s Phenomenon
 Intermittent spasm of the small arteries/ arterioles of the hands and feet
 Precipitate by cold exposure
 White – blue – red
 Aetiology
-Connective tissue disease
-Blockage of main artery – atherosclerosis, emboli
 Treatment
 Conservative
 Keep warm!
 Vasodilator drugs
 Smoking cessation
 Surgery
 Amputation
 Sympathectomy
Thromboangiitis Obliterans (Buerger’s Disease)

• Progressive non-atheroslerotic segmented inflammatory
disease that most often affected small & medium sized
vessels
• Affect primary feet and hands
• Strong correlation with smoking
Classic history: “young male (20-40 years old) who is heavy
smoker”
• Confirmed by angiogram
• Management: lifestyle changes (no smoking)

TYPES OF ULCERS
ARTERIAL ULCER NEUROPATHIC ULCER VENOUS ULCER
Also called ischemic ulcers Also called diabetic ulcer Origin: venous
Origin: main arteries Origin: neutrophic Causes: venous disease (stasis)
Causes: PAD, Burger’s, acute Causes: neuropathy
occlusion Characteristics
Characteristics  Slopping ulcer
Characteristics 6P  Callus presence  Associated with varicose
 Punch out ulcer  Well-demarcated vein
 Pain- severe  Painless  Inverted Champaign leg
 Parasthesia  Punch out appearance  Hyperpigmentation
 Pulselessness  Loss of sensation (glove &  Pain- mild
 Pale socks), reflexes & vibration
 Perishingly cold Appearance: irregular, pink
Appearance: often deep, base
Appearance: irregular, pale infected ulcer
base
Site: malleolar
Site: tips of toe & heel
At pressure site: toe & heel
VARICOSE VEIN
Def Dilated, tortuous & elongated superficial veins in the lower limbs
Due to damage & incompetent of the venous valves
Woman more common than man
Causes Primary: idiopathic
Secondary
Venous return obstruction
o Pregnancy
o Pelvic tumour (ovary, uterus, cervix, rectum)
o Ascites
o Abdominal lymphadenopathy
o Iliac vein thrombosis
Valve destruction: DVT
High pressure flow: arteriovenous fistula
CF • Aching leg after standing- relieve by elevation • Venous eczema
• Poor cosmetic appearance • Ankle oedema
• Leg ulcer • Recurrent superficial thrombophlebitis
Tx 1. Bandage
2. Sclerotherapy: inject inside vein, causing inflammation & damage to endothelial 
resulting disappearance of vein after a period of time (8-12weeks)
3. Operation: either ligation of incompetent perforator site or removal of varicosities
Post treatment:- encourage walking and mobilization

BENIGN SKIN DISORDERS
LIPOMA SEBACEOUS (EPIDERMOID) CYST DERMOID CYST GANGLION CYST
 Collection of mature fat cells enclosed in thin  Cyst formation due to obstruction of draining duct of Congenital  Cystic swelling related to synovial lined cavity
fibrous capsules sebaceous gland (mostly open in hair follicle)  Cystic teratoma derived from ectoderm & mesoderm either joint or tendon sheath
 Developed in line of embryonic fusion
Acquired
 Trauma that bring ectoderm to subjacent tissues
 Occupation like tailor
Description Description Description Description
Site Felt just beneath skin Site Anywhere except palm and sole Site In line of embryonic fusion or Site Commonly around wrist, on
(anywhere with fat- except (common: scalp, neck, axilla, midline of body dorsum of hand & ankle
brain) groin, scrotum) Shape+size Round in shape Shape+size Single,
Shape+size Discoid or hemispherical Shape+size Single/multiple (5mm-2cm) 1-4cm in diameter Hemispherical in shape
Skin Normal Skin Normal unless infected (redden Skin Appear blue, no sign of 1-4cm in diameter
Consistency Soft, rubbery + tender + ↑°C) inflammation Skin Normal
Contour (margin) Well defined margin Surface Smooth Surface Smooth Surface Smooth or multiloculated
Temperature Consistency Soft/firm Consistency Soft/firm cyst Consistency Large: soft
Tenderness No pain Contour (margin) Well-defined margin Contour (margin) Distinct margin Small: firm
Transillumination Pseudotransillumination Temperature Temperature Contour (margin) Clearly defined margin
Fluctuation Pseudofluctuant Tenderness No- unless infected Tenderness No pain Temperature
Fixation If from intramuscular- Transillumination Negative Transillumination Negative (due to pultaceous Tenderness No pain
disappear on contraction Fluctuation Negative material) Transillumination Weakly positive
muscle Fixation Fixed to skin Fluctuation Positive Fluctuation Positive if large
If fixed to muscle- not Associated features Present of punctum (diagnostic Fixation Not fixed to underlying skin or Fixation Not fixed to skin
mobile criteria) where foul-smelling structures Not mobile either (fixed to
Otherwise- freely mobile cheesy exudates (sebum) Others Not compressible tendon)
Special sign Slippage sign positive squeezed out/sebaceous horn Not reducible Others Compressible but not
Special sign Indentition sign positive reducible
Ix: do FNAC to differentiate from liposarcoma Management Ix: CT/xray depending on site of origin to rule out Management: Wait & see policy
Management  Removal of entire cyst wall + punctum to prevent intracavitary extension (skull/vertebral)  No great clinical significant
 Usually watch & wait with reassurance after FNAC recurrent Management  Spontaneous regression is common
confirmation  Intralesional steroid 5mg/5ml to control small inflamed  Surgical excision  Aspiration with or without steroid injection into
 Excision followed by HPE symptomatic lesion cyst, followed by weeks of immobilization
 Liposuction  I&D + antibiotics (cover S.Aureus) if infected
 If rupture or infected (after I&D), excision deferred until
inflammation subside to prevent wound dehiscence
Complication Complication Complication Complication
1. Malignant change 1. Rupture of cyst  sinus formation  calcification 1. Infection (include meningitis) if lesion connect to 1. Bursae
2. Neurolipomatosis (lipoma contain nerve tissues- 2. Cock’s peculiar tumour (sebaceous cyst rupture & chronic brain 2. Cystic protrusion from synovial cavity of arthritic
very painful) infection surrounding mass  painful, boggy, fungating & 2. May adhere to periosteum or erode underlying skull joint
3. Dercum’s disease (adiposis dolorosa- tender discharging mass) 3. Damage to nasal bone if nasal dermoids 3. Benign giant cell tumour of flexor tendon sheath
lipomatous swelling that effect trunk) 3. Sebaceous horn (slow discharge wide punctum harden as 4. Kienbock disease (AVN of lunate)
soon as it come out which is inspissated sebaceous
material)

FAMILIAL ADENOMATOUS POLYPOSIS (FAP)
 Autosomal dominant (strong family history)
 High degree of penetrance
 Early onset of 100-1000 adenomatous polyps- age of 10-15 years old
 Risk of malignancy by age of 35-40 years old
o High risk area: duodenum and periampullary cancer
Clinical  Initially asymptomatic
features  Blood from rectum
 Diarrhoea + mucus discharge
 Tenesmus
Investigations i. Endoscopy- also check involvement in small intestine
ii. Screen all family members
Management  Total colectomy (total resection)
-reason: universal progression to cancer
4 syndromes with germline

mutation in ADENOMATOUS
POLYPOSIS COLI (APC) gene
Gardener’s Syndrome Turcot Syndrome Attenuated Adenomatous

Polyposis Coli (AAPC)
1. Colonic polyposis typical of FAP 1. Colonic polyposis typical 1. Fewer colonic polyps
2. Osteoma (skull & mandible) of FAP compared to classical FAP
3. Dental abnormalities 2. CNS tumours (average no of polyps: 30-35)
4. Soft tissues tumour (medulloblastoma)

BENIGN NEOPLASM- ADENOMA
 Colonic polyps
o Growth from glandular or epithelial cells
o Are slow growing overgrowths of colonic mucosa
o Carry small risk of malignancy (1%)
Risk factors 1. Low fibre diet
2. High red meat
3. High fat diet
4. Strong family history
Clinical i. Asymptomatic (mostly)
features o Incidental: on screening
ii. Symptomatic
o Rectal bleeding- chronic bleeding
o Iron deficiency anemia
o Diarrhoea
o Constipation
iii. Large villous adenoma
o Severe diarrhoea with massive fluid and electrolyte loss (commonly
potassium- hypokalaemia)
Histology 1. Tubular polyps (90%) 2. Villous polyps 3. Tubular-villous
classification polyps
 Pedunculated &  Multifronded & sessile  Multifronded &
spherical  Presented with sessile
 Symptomless or  Excessive mucous
 Prolapsed through discharge from anus
anus  Hypokalaemia
 Intussucception  PR palpable
 Intestinal obstruction
Investigations  Colonoscopy
 Barium enema
 Stool occult blood
Management  Polypectomy- colonoscopic removal
 Regular lifelong surveillance

HEAD INJURY
• Trauma to the head with or without trauma to the brain
• Types
Closed head injury Open head injury
A hard blow to the head Hit with an object that broke the skull and entered the brain
from striking an object, but • Going through the windshield during MVA
the object did not break • Gunshot to the head
the skull Skull fracture can cause
 Bleeding between the meninges of the brain
 Increasing pressure within the brain
 Altering brain function
o Elevated intracranial pressure cause compression
of the brain and neurological damage
o Therefore, primary and secondary survey are
important for every patient
Classification of Head Injury
Primary Secondary
• Injury sustained by brain at the • Injury sustained by brain after
time of impact the impact
• Can be divided to • Damage & death of brain cells
i. Focal:- epidural & subdural that initially survived during
hematoma, brain contusion traumatic event
ii. Diffuse:- brain concussion, • Often preventable
diffuse axonal injury
Primary: Focal brain injury

Epidural/Extradural haematoma Subdural haematoma Brain contusion
• Associated with skull fracture: • Accumulates in space between • Bruises of the neural
accumulates in space between dura & arachnoid parenchyma and they
bone & dura meter • Impaired conscious level from represent extravasation
• Lucid interval time of injury, further of erythrocytes around
(LOC  regain, ok  LOC) deterioration as haematoma small lacerated vessels in
• Rapid deterioration (after expands the neural parenchyma
minutes or hours):-
contralateral hemiparesis,
reduced conscious level,
ipsilateral pupillary dilatation

Primary: diffuse brain injury
Brain concussion Diffuse axonal injury
 Insult to the brain that caused it to stop  Injury to the axon (structural) secondary to
functioning momentarily but no structural shearing effect following acceleration –
damage deceleration rotational injury and loss
 Neurotransmitter, synapse suddenly SHOCK function
 Transient alteration of conscious  Associated with prolonged comatose state
 No radiological abnormality  Common location : grey-white matter
 Radiological : normal > cerebral edema >
Cannot remember event  then OK multiple contusion
Principle of management for head trauma

Advanced Trauma Life Support (ALTS) philosophy
 Primary survey with simultaneous resuscitation : identify and treat what killing the patient
 Secondary survey: proceed to identify all other injuries
 Definitive care : Develop a definitive management plan
1. INITIAL MANAGEMENT
o Patient’s neck should be immobilized until cervical spine injury has excluded
o ABCDE
2. RESUSCITATION
o Resuscitate patient with fluid & electrolytes
o Any bleeding on the scalp should be compressed & covered by dressing
Monitor :
o Airway
o Verbal response
o Response to pain
o Consciousness
3. EARLY NEURO-ASSESSMENT
o Assess for the conscious level by using Glasgow Coma Scale
o Cranial nerves examinations if possible
o Assessment of pupillary size & reaction
o Search for CSF leaks from nose, mouth & ears
o Examine scalp for laceration and fractures
o Assessment of maxillofacial skeleton
o Monitor neurological symptoms
o Vomiting
o Severe & persistent headache
o Altered behavior (confusion) or seizure

4. INVESTIGATIONS
• Imaging (CT scan of brain)
• Other baseline investigations (FBC, coagulation profile, GXM)
DISCHARGE criteria
i. GCS 15/15 with no focal deficits
ii. Normal CT brain
iii. Not under influence of drugs or alcohol
iv. Accompanied by a responsible adult
Give verbal and written head injury advice to seek medical attention if:
• Persistent/worsening headache despite analgesia
• Persistent vomiting
• Drowsiness
• Visual disturbance
• Limb weakness and numbness

MAXILLOFACIAL TRAUMA
Causes of fracture
 Road traffic accidents
 Intentional violence
 Sport activities
Facial skeleton and associated fracture

UPPER third MIDDLE third- Above mouth LOWER third- Mandible
Above eyebrows Le Fort Criteria i. Mandibular #
i. Frontal sinuses # Lefort I : maxilla only moves
ii. Supra orbital ridges # Lefort II : maxilla & base of nose move
Lefort III : whole face moves
i. Zygomatic complex #
ii. Nasoethmoidal complex #
iii. Orbital #
Nasomaxillary Pyramidal
Fracture classification
1. MAJOR - Le fort I, II, III or mandibular
2. MINOR - Nasal, sinus wall, zygomatic, orbital floor, antral wall, alveolar ridge
General management for maxillofacial trauma

 Airway control / immobilize cervical spine
 Oxygen for all patients
 May need to keep patient sitting or prone
 Stabilize C-spine early
 Large bore (Yankauer) suction available
 Bleeding control- Can be major threat to life
 Use universal precautions
 Direct pressure dressings initially. Contraindicated: blind vessel clamping
 Complete the primary survey
 Secondary survey- Consider NG or OG tube placement
 Plain radiographs if fractures suspected
 CT if suspect complex fractures
NASAL BONE #
CF: Epistaxis, obstructed nares
Mx: local anesthesia
 Nasal septal hematoma: incise & drain, anterior pack, antibiotics, follow-up at 24 hours
 Follow-up timing for recheck or reduction:
◦ Children: 3 to 5 days
◦ Adults: 7 days

ZYGOMATIC #
 Tripod (tri-malar) fracture + Depression of malar eminence
+ Fractures at temporal, frontal, and maxillary suture lines  punch
CF: Unilateral epistaxis
 Subcutaneous emphysema
 Altered relative pupil position
 Periorbital ecchymosis
 Subconjunctival hemorrhage
 Infraorbital hypoesthesia
ORBITAL
1. Supraorbital Fractures
 Frontal sinus fracture
 Often associated with intracranial injury
 Often show depressed glabellar area
 If posterior wall fracture, then dura is torn
 Ethmoid fracture
 Blow to bridge of nose
 Often associated with cribiform plate fracture, CSF leak
 Medial canthus ligament injury needs transnasal wiring repair to prevent telecanthus
2. Orbital Fractures
 “Blow out” fracture of floor (tennis ball hit)
 Rule out globe injury
 Diplopia: double vision
 Enophthalmos: sunken eyeball
 Impaired EOM’s
 Infraorbital hypo-esthesia
 Maxillary sinus opacification
 Treatment
 extraocular muscle dysfunction can be due to edema and will correct without
surgery
 Persistent or high grade muscle entrapment requires surgical repair of orbital floor
(bone grafts, Teflon, plating, etc.)
MANDIBLE FRACTURES
 Airway obstruction from loss of attachment at base of tongue
 Condylar fractures associated with ear canal lacerations & high cervical fractures
 High infection potential if any violation of oral mucosa
Signs and symptoms

 Malocclusion
 Decreased jaw range of motion
 Trismus
 Chin numbness
 Ecchymosis in floor of mouth
 Palpable step deformity
Treatment
 Prompt fixation: intermaxillary fixation (arch bars), +/- body wiring or plating

CHEST TRAUMA
Types
Blunt Trauma Penetrating Trauma
 Usually high velocity injury Low Energy
 Subdivision Mechanisms  Arrows, knives, handguns
o Blast  Injury caused by direct contact and
o Crush (Compression) cavitation
o Deceleration High Energy
 Age Factors  Military, hunting rifles & high powered
 Pediatric Thorax: More cartilage = hand guns
Absorbs forces  Extensive injury due to high pressure
 Geriatric Thorax: Calcification & cavitation
osteoporosis = More fractures Shotgun
 Injury severity based upon the distance
between the victim and shotgun &
caliber of shot
CARDIAC TEMPONADE
Definition: Restriction to cardiac filling caused by blood or other fluid within the pericardium
Clinical features
 Restriction to cardiac filling caused by blood or other fluid within the pericardium
 “Beck’s Triad”
o Hypotension
o Neck vein distension (JVP raised)
o Distant heart tones
 Kussmaul’s sign- Decrease or absence of JVD during inspiration
 Pulsus Paradoxus
o Drop in SBP >10 during inspiration
o Due to increase in CO2 during inspiration
Progression
Intra-pericardial pressure exceeds filling pressure of right heartImpairs venous return and cardiac
fillingleading to hypotension, narrow pulse pressure, PEA
Management
 Ensure adequate oxygenation (100% oxygen via non-rebreather mask at 15L/min)
 Establish 2 large bore IV lines
 IV fluid bolus 500 ml stat – maintain MAP at >90mmHg
 Pericardiocentesis is the definitive treatment

OPEN PNEUMOTHORAX TENSION PNEUMOTHORAX MASSIVE HEMOTHORAX
DEF  Occurs when lung tissue is disrupted and air leaks into the Progressive build-up of air within the pleural space due to a lung Defined as blood loss of >1500ml inside the
pleural space laceration which allows air to escape into the pleural space but not to chest (upon insertion)
 Normal breathing pattern is affected as the usual negative intra return
thoracic pressure is abolished by the open chest wound
CF  Reduce chest movement and breath sound  Haemodynamic instability  Pallor, flat neck veins, shock.
 Resonant on percussion  Severe respiratory distress  Chest pain and dyspnea
 Can be confirmed by CXR  Neck vein distension  Tachypnea and hypovolumia
 Tracheal deviation  Reduced air entry
 Unilateral absence of breath sound  Dull upon percussion of the affected
 Precussion hyperresonnance side
PROGRESSION Air accumulates in pleural space Lung collapses Alveoli collapse
(atelectasis) Reduced oxygen and carbon dioxide exchange
Ventilation/Perfusion Mismatch  Increased ventilation but no alveolar
perfusion Reduced respiratory efficiency results in HYPOXIA
MX  100% oxygen should be delivered via a facemask.  Needle thoracostomy  Replacement of blood
 intubation = oxygenation / ventilation is inadequate. A 14-16G intravenous cannula is inserted into the second rib space in  Tube thoracostomy on the affected
 Definitive management = an occlusive dressing over the wound the mid-clavicular line. side (do not drain more than >1L at a
and immediately place an intercostal chest drain.  Chest tube (definitive) time to prevent acute heamodynamic
 Cover the wound with any sterile/clean non-porous dressing instability)
taped only on 3 sides leaving one side free to act as a flutter  Emergency thoracotomy if:
valve o Intial blood drained is >1.5L
o Ongoing drainage of >500ml/hr for
the first hour, 300ml/hr for the 2 cons
hours or 200ml/hr for the 3 cons hour
o Persistent blood transfusion required
o Continued hemodynamically
instability

FLAIL CHEST PULMONARY CONTUSION MYOCARDIAL CONTUSION AORTIC RUPTURE TRAUMATIC DIAPHRAGMATIC RUPTURE TRACHEOBRONCHI
AL INJURIES
DEF Occur when >2 (segmental) Injury to lung parenchyma, leading Bruising of cardiac wall  Traumatic Aneurysm or Aortic
contiguous ribs have been to oedema and blood collecting in Rupture
fractured in >2 places alveolar spaces and loss of normal  Aorta most commonly injured
lung structure & function in severe blunt or penetrating
(Ribs terapung) trauma
 85-95% mortality
CF  Paradoxical chest wall  Associated with rib #, blunt  Tachycardia and/or irregular rhythm  Blind or penetrating injury to  Persistent or progressive respiratory  Hemoptysis,
movements injury to chest wall.  Retrosternal pain similar to MI the chest distress subcutaneous
 Respiratory distress  Signs are non specific  Associated injuries  Massive hemothorax  Bowel sound in the chest emphysema over
 External evidence of chest  Rib/Sternal fractures  Rapid & deterioration of vitals the neck and
trauma  Chest pain unrelieved by oxygen  Pulse deficit between right chest
 Pain on respiratory effort  May be relieved with rest and left upper or lower  Tension
 Palpable crepitus  THIS IS TRAUMA-RELATED PAIN extremities pneumothorax
 Persistent
Progressive Problems pneumothorax
 Hematoma despite
 Hemoperitoneum treatment
 Myocardial necrosis
 Dysrhythmias
 CHF & or Cardiogenic shock
MX  Adequate oxygen  Management of pulmonary  Triage patient to critical care area  Assess using ATLS protocol  Laparotomy  Supplemental o2
supplementation contusion is supportive.  Secure ABC and give o2 if needed  High resolution ct scan of  Ventilatory
 Analgesic to ease respiration  Supplemental oxygen  Do ECG- abnormal ,need continuous thorax support
(analgesic, analgesic, analgesic)-  Ventilatory support if necessary cardiac monitoring  GXM 6 units of whole blood:  >1 chest tube
can died because stop breathing  Judicious fluid therapy call cardiothoracic and general insertion
due to pain  Analgesia and antibiotic surgery  Early
 Intubation and mechanical cardiothoracic
ventilation is rarely indicated consultation ,
for chest wall injury alone Bronchoscopic
(usually for hypoxia due to examination/thor
underlying pulmonary acic computed
contusions) tomography
 Rib fracture fixation
NOTES Pathophysio Chest x ray Chest x-ray
Blunt lung injury develops over the  Widened mediastinum  Vague and indistinct diaphragmatic
course of 24 hourspoor gas  Left sided pleural effusion shadow
exchange, increased pulmonary  Blunting of left aortic knuckle  Herniation of abdominal organs into
vascular resistance and decreased  Depressed left bronchus chest cavity
lung complianceAcute  Pleural cap  Displacement of ng tube into chest cavity,
Respiratory Distress Syndrome left side more commonly affected
(ARDS)
Figure 1. Acute aortic dissection presenting with the following radiographic signs:
rightward deviation of the trachea (red arrow); left apical pleural capping (blue arrow);
aortic “double-calcium” sign (between white arrows); depression of the left bronchus
(purple arrow); pleural effusion (green arrow); widened mediastinum and loss of the
aorto-pulmonary window (not labeled).

ABDOMINAL TRAUMA
Types
1. BLUNT: 2. PENETRATING:
- MVA acceleration/ deceleration injuries - Stab
- Direct blow to the - Gunshot injury
abdomen
- Iatrogenic injury
Signs to recognise
Cullen’s Sign: Grey-Turner’s Sign:
- Bluish discoloration around umbilicus - Bluish discoloration of the flanks.
- Hemoperitoneum - Retroperitoneal Hematoma
- Severe pancreatitis - Hemorrhagic pancreatitis
Kehr’s sign: Balance’s Sign

- Referred pain, left shoulder - Dullness on percussion of the left upper
- Irritation of the diaphragm quadrant(ruptured spleen)
- (Splenic injury, free air,intra-abdominal
bleeding)
SPLENIC INJURY
 Most common intra-abdominal organ to injured (40-55%)
 Commonly associated with blunt trauma
 20% due to left lower rib fractures
 20% unintentionally during other abdominal operations
 Clinically apparent either early or delayed
 Delayed injury is usually due to rupture of subcapsular haematoma
 In some patients spontaneous rupture can occur following trivial trauma
Grading

Management
Conservative management
1. Hemodynamic stability
2. Negative on abdominal examination
3. Absence of contrast extravasation in CT
4. Absence of other indication of Laprotomy
5. Grade 1 to 3 (Subcapsular Hematoma ,Laceration <3 cm)
Success rate of conservative m(x) is >80%
Monitoring
1. Serial abdomen examinations & Haematocrit are essential
2. If conservative management successful, patients should remain on:
- Bed rest for 72 hours
- Limited physical activity for 6 weeks
- No contact sports for 6 months
Surgical management
1. Approximately 30% of patients fail conservative management
2. Splenectomy surgery needed if clinically hypovolaemic if they have a falling haematocrit
3. Usually occurs within the first 72 hours of injury.
Type of operation
1. Capsular tears - Compression & topical haemostatic agent
2. Deep Laceration - Horizontal mattress suture or Splenorrhaphy
3. Major Laceration not involving hilum – (Partial Splenectomy)
4. Hillar injury –Total Splenectomy
Overwhelming Post Splenectomy Infection (OPSI)

 Infection due to encapsulated bacteria
 50% due to strep.Pneumoniae Main benefit of
 Other organisms include: retaining the spleen is
 Haemophilus influenzae the prevention of
 Neisseria meningitidis
Overwhelming
 Occurs post splenectomy in 4% patients without prophylaxis
Postsplenectomy
 Mortality of OPSI is approximately 50%
 Greatest risk in first 2 years post op Infection (OPSI)
Prevention:
Antibiotic prophylaxis
 Penicillin or amoxycillin
 children up to 16 years
Immunisation
 Pneumococcal and Haemophilus
 Perform 2 weeks prior to
planned operation
 Immediately post op for
emergency cases
 Repeat every 5 – 10 years

LIVER INJURY
 Liver is the largest organ in abdomen
 2nd most common organ injured (35-45%)
 Driving and fighting responsible for 50% of deaths due to liver injury
 Usually venous bleeding
 85% of all patients with blunt hepatic trauma are stable
 Mortality of liver injury is 10%
 CT is the mainstay of diagnosis in stable patient
Non Operative management Operative management
 Haemodynamically Stable  Packing- 34% survival with packing only
 No other intra-abdominal injury require • Pack removed after 48 hours
surgery • Haemostatic agents can be used
 < 2 units of blood transfusion required  Suturing: -Simple suture or deep mattress suture
 Hemoperitoneum <500 ml on CT  Laceration
 Grade I-III subcapsular & intr- • Mesh hepatorrhaphy
perenchymal hematoma) • Omental flap to cover the laceration
• Debridement
 Lobar Resection
 Liver Transplantation
 Ligate or repair damaged blood vessels & bile duct
RENAL INJURY
Types Grade
MINOR injuries MAJOR injuries o Grade I-Contusion / Subcapsular haematoma
o Subcapsular o Lacerated kidney o Grade II-Perirenal haematoma or Cortical
haematoma o Polar avulsion laceratoion < 1cm
o Cortical tear o Pedicular injuries o Grade III-Parenchymal laceration > 1cm
o Corticocalyceal tear o Grade IV-Parenchymal laceration through
corticomedullary junction / collecting system
o Grade V-Multiple Lacerations / Shattered
kidney
Clinical features Investigations
 Haematuria (Immediate/ Delayed)  Ultrasound:
 Loin Pain and Mass - Perirenal haematoma
 Intraperitonial Injuries - Free fluid in peritoneum
 Internal Hemorrhage  KUB X-ray/ Urgent IVU
 CT scan
 Renal Angiography
- Diagnostic: Renal Pedicle Injury
- Therapeutic: Transarterial embolization
Management
Conservative management Operative management
o Minor Injuries o Major Injuries
o Haemodinamicaly stable patients o Haemodinamically unstable patients
 Bed Rest  Suturing
 Resuscitation  Partial Nephrectomy
 Continuous Assessment  Total Nephrectomy
 Pulse/BP/Temp
 Urine colour
 Size of haematoma

URETERIC INJURIES BLADDER INJURIES URETHRAL INJURIES
Intro o Surgical trauma during o Commonest of the
pelvic surgery is the most Urinary Tract Injuries
common cause.
o Unilateral or bilateral Mechanism of injury
o Commonest at lower o Anterior Urethra- more
most 5cm of the pelvic common
ureter • Blunt Injury
• Fall Astride
• Penetrating Injuries
o Posterior Urethra
• Crush Injuries to
pelvis MVA
CF Unilateral injuries • Pain/ tenderness over Rupture of Bulbous Urethra
3 possibilities: suprapubic area (Posterior Urethral Injuries)
• No symptoms – may lead • Haematuria • Perineal bruising &
to silent atrophy • Dysuria haematoma
• Loin pain & fever – • C/F of Pelvic fracture • Bleeding from urethral
infection of obstructed • Peritonism and free fluid meatus
system • Retention of urine
• Urinary fistula – develops
through abdominal/ Rupture of Membranous
vaginal Urethra
• Wound Associated with Pelvic #
(10%)
Bilateral injuries • Urinary retention
• Anuria • Blood at urethral meatus
• Ureteric catheter cannot • High riding prostate on PR
pass through examination
• Urgent nephrostomy
Ix • Ultrasound • Plain X-ray • Trial Catheterization
• Intravenous Pyelogram • IVU • Ascending Urethrogram
• Retrograde Ureterogram • Ascending cystogram • Urethroscopy – Rigid/
• Cystoscopy/ • CT Scan Flexible
Chromocystoscopy
Mx Conservative Treatment Conservative Treatment Emergency Treatment
 Ureteric Stenting • Bladder Drainage - Urinary Diversion –
 End to End Anastamosis Suprapubic Cystostomy
 Ureteric reinplantation Operative Treatment - Urgent Exploration
o Psoas Hitch • Laparotomy - Rest and Antibiotics
o Boari Flap • Suture
 Trans Uretero- • Drain Bladder/ Peritoneum Delayed Treatment
Ureterostomy - For Strictures
 Ileal Loop interposition - Urethral Dilation
- Optical Urethrotomy
- Urethroplasty -
Anastamotic/ Patch
Urethrotomy: cut open segment

Urethroplasty: replace skin w
buccal mucosa

BURN (burn baby burnnnn )
Definition Burn is defined as a wound caused by exogenous agent leading to coagulative
necrosis of the tissue
Causes Thermal Burns
 Dry heat: contact burn, flame burn
 Moist heat: Scald burn
 Smoke and inhalational injury Function of the skin:
Chemical Burns: acid and alkali 1. Water and electrolyte balance!
Electrical Burns: High and low voltage electricity 2. Infection barrier
Cold Burns: frostbite 3. Excretion (sweat)
Radiation 4. Temperature
5. Sensation
Pathophysiology
6. Respiration secretion
Burn can cause damage in different ways but mainly it affected skin! 7. Vitamin D production
8. Cosmetic appearance
How does burn injure the skin?
 Human skin is injured by heat in two ways
o An immediate direct cellular injury occurs first
o Delayed injury inflicted as a result of progressive dermal ischemia
 Pathologically, thermal injury to the skin results in 3 distinct zones of trauma
Central inner zone / zone of coagulation or necrosis: irreversible tissue necrosis. It forms the inner
layer of the visible burn eschar
Zone of stasis: Ischemia which may be

reversible depending on management. It
contains viable tissue that may die over the
next 48 hours post burn if tissue oxygenation
and adequate nutrition are not maintaned
Zone of hyperemia: Reversible erythema. This

area contains inflammatory mediators
(prostaglandin, histamine and kinins) which
contribute to the formation of tissue edema.
Tissues in this zone normally recover within 7-
10 days unless subjected to infection
What else burn can cause?

 Injury to the airway and lungs (inhalational smoke)
 Metabolic poisoning (carbon monoxide and hydrogen cyanide)
 Inflammatory and circulatory changes
 Immune system
 Changes to the intestine:
o Damage and ischemia to the gut mucosa and prevent absorption of food.
o Can also cause translocation of gut bacteria, which can be important source of infection
in large burns
o Swelling and stasis peritoneal edema and can cause abdominal compartment syndrome
 which splints the diaphragm and increases the airway pressure needed for
respiration
 Danger to the peripheral circulation:
o Full thickness burn can coagulate collagen fibers and normal elasticity is lost
o Circumferential full thickness can act as torniquet and cause limb ischemia

What is important in assessing burn wound?
1. The size of the wound
2. The depth of the wound (classification)
Important things to determine in burn injury

1. Percentage of surface area involved
2. Depth of burns
3. Presence of inhalational injury
Classification
Superficial partial- thickness burn (2nd degree burn)

Deep partial – thickness burn (2nd degree burn)
Full – thickness burn (2nd degree)

2nd degree Superficial partial – thickness Deep partial – thickness Full thickness
burn (not beyond papillary (deeper part to reticular (whole dermis)
dermis) dermis)
Color Pink and moist Red to white Normal skin to
charred black
Blanching Yes No No
Edema Mild Moderate No
Pain Yes Yes No
Sensation Normal Reduced (unable to Lost
distinguish sharp from blunt)
Scaring No > 3 weeks + hypertrophic Hard leathery feel
scarring
Treatment Non surgical Non surgical Surgical (excision
and grafting
Size of the wound

Total Body Surface Area
 using patient’s own hand which represents 1% of the area
Lund and Browder chart

Principles of 1. ABCDE: make sure patient is stable, if need o2, give!
management 2. Fluid resuscitation: important (as explained below)
3. Treating the wound
4. Analgesia: simple oral analgesia, PCM, NSAIDS (large burns need
continuous infusions and analgesia)
5. Energy balance and nutrition (start feeding within 6 hours of gut injury.
Burn > 15% TBSA needed nasogastric feeding)
6. Monitoring and control of infection
7. Nursing care
8. Physiotherapy
9. Psychological
10. Surgery if needed
Fluid Principle: Maintain intravascular volume following a burn to provide sufficient
resuscitation circulation to essential organs and peripheral tissues
*Pastikan kita Indication for fluid resuscitation:

dok kira  Children > 10%
bahagian burn  Adults > 15% : shock
tapi bukan  > 60 died
erythema Must add salt to prevent hyponatremia
Monitor urine output
What formula Parkland Formula
to use?  calculates the fluid needed to be replaced in the 1st 24 hours
TBSA x weight (kg) x 4 = volume (ml)
• First 8 hours = half of volume
• Subsequent 16 hours = another half of the volume
In children? Holiday – Segar formula
100ml/kg for 1st 24 hours = first 10 kg
50ml/kg = next 10 kg
20ml/kg for 24 hours = subsequent kg(s)
What fluid to Crystalloid: Ringer’s lactate / Hartmann’s solution
give?  As effective as colloid for maintaining intravascular vol
 Less expensive
 Another important reason: in burn, even though large protein molecules can
leak out from the capillaries, we still have the non burnt capillaries to retain
protein normally
Hypertonic saline: Human Albumin Solution (HAS)
 Produces hyperosmolarity and hypernatremia
 Reduces the shift of intracellular water to extracellular space
 Less tissue edema
Colloid
 Plasma proteins are responsible for inward oncotic pressure that counteracts
the outward hydrostatic pressure
 Without protein, plasma volume will not be maintained resulting in edema
 Protein should be given after first 12 hours of burn because massive fluid
shifts cause proteins to leak out of cells.
 Colloid formula (Muir and Barclay formula): 0.5 x % body surface area x weight
= one portion
 Periods: 4/4/4, 6/6 and 12 hours respectively
 One portion in each period

Monitoring? 1. Urine output:
• Should be around 0.5 – 1.0 ml/kg/hour (if low?  increase the infusion
rate by 50%)
• If patient shows signs of hypoperfusion: restlessness, tachycardia, cold
peripheries and high HCT  give bolus 10ml/kg/weight
• If urine output > 2ml/kg/hour  decrease the rate of infusion
2. Acid base balance
3. Haematocrit
4. More invasive central line if patient has cardiac dysfunction
Treating the Surgery: Escharotomy (In circumferential full thickness burn to the limbs)
wound
Epidermal: Supportive therapy with topical antimicrobial + oral analgesia

Superficial dermal burn: Adequate analgesia + topical antibiotic cream + dressing
Deep dermal: if extensive may need skin excision and grafted within 5-10 days
(delayed skin grafting)
Full thickness: excision and grafting
INHALATIONAL Yang penting kena tau!
INJURY When the airway is burned, it will creates symptoms by swelling and if not
managed proactively, can completely occlude the upper airway  usually late
symptoms (4-24 hours)
What does it cause?  laryngeal edema (change in voice, stridor, anxiety and
respiratory difficulty  so nak buat apa? Intubate
 ni laryngeal edema (ploop ploop)

What are the  Suspect airway or inhalational injury
criteria to  Require fluid resuscitation
admit to burn  Require surgery
unit?  Burn with any significant (hand, face, feet, perineum)
 Psychiatry or social background
 Suspicion of non accidental injury
 Extreme age
 Chemical burn (acid and alkali)
 Electrical burn

SAMPLE BURN QUESTION
A 40 years old woman was caught in a house fire. She could not escape due to thick smoke. Her
husband who just returned home rushed in to bring his wife out of the burning house. He was
successful in bringing his wife out before she sustained external injuries, but the man’s clothes
caught fire and this 60kg man sustained 20% total body surface area burns.
They were both brought to the emergency department of the hospital. The lady was able to talk
but look frightened.
1. What is your immediate management for her?

Admit overnight for observation
2. What is the reason?

To observe for respiratory injury for signs and symptoms which might appear later
3. List 4 steps in a logical manner the management of this man

 Quick assessment (ABC)
 Take out the clothes to cool down the patient (to reduce the trap heat)
 Give analgesic
 Set up IV line (Fluid resuscitation)
On further questioning, after the emergency management, you noted that the man got burned at
about 12pm and arrived at the hospital at 2pm. You decided he need fluid resuscitation.
Calculate his fluid requirement and infusion schedule for his first day.
4. State the formula

Parkland Formula: Total body surface area x body wt. (kg) x 4 = volume (ml) over 24Hr
5. Show your calculation using the formula

20 x 60 x 4 = 4800 ml
6. Write a prescription of fluid requirement for this man, stating what type of fluid
From 2pm-8pm, give Ringer’s Lactate /Hartman’s solution, half of this volume is given in
the first 8 hours and second half is given in the subsequent 16 hours
7. What can you monitor in bed to know his fluid requirement is enough?
Hourly urine output

PAIN MANAGEMENT
What is pain?
“Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue
damage, or described in terms of such damage”- International Association for the Study of Pain
(IASP)
Non-pharmacological methods
• Positioning/Posture
• Education/Anticipatory Guidance
• Touch- Gentle pressure or massage
• Heat/cold treatment
• Relaxation/Distraction/Music/Pet Therapy
• Meditation/Guided imagery
• Aromatherapy
• Acupuncture/Acupressure
• TENS (nerve stimulator)
Pharmacological methods

SURGERY - Complete 2nd Ed

Uploaded by

Copyright:

Available Formats

SURGERY - Complete 2nd Ed

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

SURGERY - Complete 2nd Ed

Uploaded by

Copyright:

Available Formats

What are the main topics covered in the document?

What are the main topics covered in the document?

What are some methods discussed for managing pain?

What are some methods discussed for managing pain?

(YEAR 3 & 5 MODULE)

Salam and hi. This e-book consists of medical notes we made

To our beloved doctors, lecturers, consultants, medical textbooks and

Second edition: Update on 27 Julai 2016

Customer’s name here | ©JPBF ii

3S- Site, Size (+Shape), Skin

• 3C- Colour, Consistency, Contour (margin)

• 3T- Temperature, Tenderness, Transillumination (translucence)

• 3F- Fixation (or mobility), Fluctuation, Field (Lymph nodes)

• PER- Percussion, Expensile pulsatile, Reducible

Others: Bruits (auscultate)

Customer’s name here | ©JPBF 1

INSPECTION (BBEDDS) or can use TIME (Tissue, Inflammation, Moisture, Edge)

Customer’s name here | ©JPBF 2

Customer’s name here | ©JPBF 3

How to prepare patient for appendicectomy

Post –operative Management

Customer’s name here | ©JPBF 4

Who at risk of perforated

Treatments: stabilize patient & operate ASAP

Customer’s name here | ©JPBF 5

 CF suggestive that patient is responding to conservative tx

 Criteria for stopping conservative tx

Customer’s name here | ©JPBF 6

 Right ovarian torsion/rupture/cyst

Customer’s name here | ©JPBF 7

Aetiology (I GET SMASHED) Symptoms

Customer’s name here | ©JPBF 8

Customer’s name here | ©JPBF 9

Score:- 2+ moderate, 3+ severe C- Ca+ <8mg/dL (hypocalcaemia)

Approach depend on the causes of pancreatitis

Customer’s name here | ©JPBF 10

Customer’s name here | ©JPBF 11

Customer’s name here | ©JPBF 12

*how to differentiate and describe organ mass

Customer’s name here | ©JPBF 13

Customer’s name here | ©JPBF 14

4. Aetiology (as stated above)- Intraluminal, Intramural, Extramural

Customer’s name here | ©JPBF 15

Heal causing fibrosis

Clinical cardinal features of IO

Intra-abdominal surgery- motility usually returns

Customer’s name here | ©JPBF 16

RIGHT SIDED LESION LEFT SIDED LESION

Customer’s name here | ©JPBF 17

3. Find RISK FACTORS

Malignancy will depend on

 Lynch syndrome= hereditary non-polyposis colorectal cancer (HNPCC)

iv. Dietary factors

4. Rule out metastasize- 2L3B

Customer’s name here | ©JPBF 18

On per rectal examination (mostly for rectal cancer)

2. Type of lesion- 4types

4. Any associated synchronous lesion

 For biopsy- 4-6 samples from different sites