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Module 2M: Care of Clients with Alterations in Digestion and Absorption

Hepatic and GI Disorders Inflammatory Diverticular


Biliary Tract Bowel Disease Disease
Disorders (herniation of bowel)
-organs affected:
pancreas,
gallbladder, liver

1. Pancreatitis 1. Gastritis 1. Crohn’s 1. Diverticulum


2. Cholecystitis 2. Peptic Ulcer Disease 2. Diverticulosis
3. Cholelithiasis Disease 2. Ulcerative 3. Diverticulitis
4. Liver 3. Appendicitis Colitis
Cirrhosis
5. Hepatitis

❖ Metabolism
➢ Chemical processes occurring within a living cell or organism necessary for the maintenance of life
➢ digesting food and nutrients
➢ Ways when we do metabolism: breathing, muscles contract, kidneys are filtering waste products
❖ Review of Diagnostic Tests
➢ Serum Laboratory tests:
■ CBC
■ Prothrombin/ Partial Thromboplastin Time
■ Liver Function Tests
■ Serum Amylase, Lipase
● Increase = pancreatic injury
■ Triglycerides
➢ Stool Examination
➢ Abdominal Ultrasonography
■ non invasive using high freq sound waves, useful in large gallbladder, gallstones, ADvantage: not
expensive/low cost, does not need an ionizing radiation, no noticeable side effects ,immediate results)
➢ CT-scan of the abdomen
■ clearer outline of abdo structures, cross sectional images of organs
■ Use for detecting and localizing inflammatory conditions of colon (appendicitis
■ Can eval liver, spleen, kidney and pancreas
■ Done thru with or without IV contrast agents(
● for better enhancement: contrast agents are used so it is needed to
◆ ask if client is allergic to the agent, Iodine, shellfish,
◆ assess the creatinine levels to eval kidney function
● If pt is given sodium bicarbonate - adm one hr before and 6 hrs after iv contrast to give protective
measure to kidneys
➢ MRI of the Abdomen
■ Supplement Ultrasound and Ct, non invasive tech and
■ Useful in eval abdominal soft tissues , blood vessels and fistulas
■ Has a ferum magnetic - metal with iron that can be attracted to magnet =injury like burns
● Nursing reqs before: remove jewelries/metal devices, ask if client has pacemaker, NPO 6-8hrs prior,
remove implants, inform may take 60-90 mins long, explain positioning, what equipment looks like
9lessen anxiety for claustrophobic pt)
➢ Upper GI Series /Upper GI Fluoroscopy
■ Aka: Barium Swallow
■ Radiographic exams/ x ray exam that visualizes the esophagus, stomach and duodenum
➢ Endoscopy / Esophagogastroduodenoscopy - endoscope or scope is onserted via mouth
➢ Endoscopic Retrograde Cholangiopancreatography (ERCP -endoscope plus xray (helpful pancreatitis, common bile
duct stones)
■ NPO 8 hrs prior
■ Local anesthetics via gargle or spray - gag reflux is inactivated or less
➢ Lower GI Series/Lower GI FLuoroscopy
■ Aka Barium Enema
■ Visualizing the colon
➢ Colonoscopy
■ Fiber optic scope inserted via anus

BILIARY TRACT AND HEPATIC DISORDERS


PANCREATITIS

Inflammation of the pancreas, Serious life threatening disorder


Pancreatic enzymes should be activated in the DUODENUM

2 functions: Two Problems:

■ Endocrine- insulin and glucose ■ Autodigestion - premature activation of pancreatic


■ Exocrine - pancreatic enzymes (Acinar cells -yellow enzymes that destroys tissue and pancreatic cells
color, secretes digestive enzymes, respon for ■ Obstruction - causes hypersecretion of pancreatic
releasing of non active form) enzymes
Due to alcohol and gallstones:
 Alcohol = increase secretion pancreatic enzymes and
decrease fluid and bicarbonate levels in pancreatic
duct = thick and viscous pancreatic juices = can form
a plug = cause obstruction = high pressure =
backflow = distention ducts or swelling =
inflammation
 Gallstones=  causes bile reflux to pancreatic duc

Acute pancreatitis Chronic pancreatitis


 Increased amylase/ lipase - leaks to circulation as  nflammatory disorder characterized by progressive
trypsin digests pancreas anatomic and functional destruction of the pancreas.
 not respond to tx. Higher in men  Repeated acute episodes
 Leading cause; alcoholism and gallstones  Usually alcohol induced, gradual, progressive
 Risk factors: overuse of NSAIDS destruction of the pancreatic tissue (70-80% are
 High mortality due: shock, anorexia,hypotension chronic alcoholics)
 Protein plugs and calculi causes obstruction
 Risk factors: Malnutrition (low protein or high fat)
Chronic alcohol consumption
 There is already pancreatic insufficiency
Complications If there are repeated episodes of acute pancreatitis, it can
cause fibrosis of the tissues. The cells in the pancreas are
Swelling of pancreas(head) = JAUNDICE being replaced with fibrous tissues = there is wound
Oversecretion of glucagon = HYPERGLYCEMIA = rf Type scarring which causes pancreatic insufficiency and if and
1 diabetes when there is PI there is a diminished function of the
Trypsin=autodigestion=activates other enzymes= ARDS organ.
Enzymes in bloodstream=rk coagulation defects (DIC)
Pancreatic amylase=low albumin-fvd=hypoxemia=AKD With alcohol, it causes hypersecretion of proteins in
pancreatic secretions so they can result in plugs. With
alcohol induced, protein precipitates the plug and they can
obstruct the ducts in the pancreas. If you have obstruction,
there is inflammation and there is also fibrosis. Fibrosis with
scarring that can cause acinar atrophy or pancreatic
insufficiency. If you have pancreatic insufficiency, there is
loss of exocrine function

Assessment Assessment
PAIN  Recurrent attack of severe abdominal (epigastric) and
 Severe epigastric/LUQ back pain with vomiting
 Radiate to back and shoulder: Boring-feeling  Link with meals(you can experience pain), unrelieved by
something in body and contin food or antacid
 Occurs after heavy meal or alcohol ingestion  Anorexia (have fear if they eat they will feel pain),
 Abdo pain=unrelieved by antacids  Weight loss - fat malabsorption
 Tender from irritation and edema  Constipation, fever, Jaundice, muscle wasting
Vomiting, dec BS,  Edema (it can be in feet, legs, and hands this is due to
Abdo distention and RIGID (sign of peritonitis) protein malabsorption because the pancreas also
provide enzymes that can absorb and digest proteins so
HALLMARK SIGNS (SEVERE PANCREATITIS) it decreases the levels of the circulating albumin so
o TURNER’S SIGN -ecchymosis of flank there is protein malabsorption.
o CULLEN’S SIGN - ecchymosis of periumbilical area  Steatorrhea - fruity foul smelling due to impaired fat
[pancreatic enzymes leaks to tissues=ecchymosis] digestion and the stool looks like igit because it has a
high fat content.
Diag Tests Diag Tests
ELEVATED: To confirm diagnosis but also based on s/s, labs & imaging
 Amylase & lipase w/in 24 hrs  ERCP (endoscopic retrograde
 Bilirubin (acc w/ biliary dysfxn, gallbladder or cholangiopancreatography)
common bile duct inv)  to visualize the pancreas and the common bile duct.
 Glucose (pancreatic cell injury), WBC  Only definitive test
DECREASED:  Used to identify for calcifications of pancreatic
 Calcium (fat necrosis) tissues and biopsies specimens
 HgB, Hcb (in bleeding)  may delineate the presence of pancreatic
Ultrasonography (for gallstones inv or blockage) pseudocyst - a cyst like appearance but not a cyst.
xray of abdo and chest (pleural effusion) A cyst filled with pancreatic fluid.
CT SCAN - reliable diagnosis  MRI, CT Scan, Ultrasound
 Glucose Tolerance Test - eval the pancreatic islet
cell function. If abnormal, this may indicate DM 
 Stool Exam - analysis of fecal fat content, confirmes
steatorrhea
Medical TX Med TX
NPO (let panc rest and reduce enzymes) “Tx is directed towards preventing/managing acute attacks,
TPN relieving pain and discomfort, manage exo/endo insuff of
Pancreatic enzyme replacement pancreas
Biliary drainage Non-opioids &non pharmaco intervs - for pain
NGT Suction (drain the pancreas= dec painful abdo Avoid alcohol
distention Insulin/opral antidiabetic agents (DM)
Intubation & Mec Vent in atelectasis Pancreatic enzyme replacement - Pancrelipase
 Given with meals or snacks- aid in digs and
absorption of proteins and fats
 Take meds before or during meals with water
 No sign of steatorrhea (less fatty content) - sign
that replacement is effective
Pharma TX Surg TX
Pancreaticojejunostomy (Roux-en-Y)
 Ranitidine, Cimetidine (h2 blockers to dec gastric  side to side anastomosis of the pancreatic duct to
secretions) the jejunum allows drainage of pancreatic secretions
 Pantoprazole to the jejunum = provides pain relief
 Opioids (Morphine, Fentanyl) for pain  Occurs within 6 months. Pain returns in a substantial
 Antiemetic agents; Anticholinergic - reduce pancreatic number of patients as the disease progresses.
and gastric secretions Pancreaticoduodenectomy (Whipple resection or procedure)
 removal of the head of the pancreas
 First part of the duodenum, gallbladder and bile duct
is removed.
 For relief of chronic pain
 Usually indicated for pancreatic cancer.
Nursing management Nursing management

 Alteration in comfort/pain:  Reduce pancreatic secretions


 Opioid analgesics as ordered  Low fat diet, avoid alcohol and caffeine, small meals,
 Frequent positioning every 2 hours - prevent  oral antacids (provide list of food that stim gastric and
atelectasis and pulling of respiratory secretions panc secretions = precip pain)
 Anticholinergic drugs - reduce gastric pancreatic  Alleviate fat indigestion
secretions
 NPO - reduces pancreatic secretion
 Complete bed rest - decrease metabolic rate, reduce
the secretions of gastric and pancreatic enzymes
 NGT suction (remove gastric contents)
 Ineff breathing pattern
 Semi-Fowler’s (low pressure on diaphragm)
 Frequent position changes - prevent atelectasis
 Incentive spirometry and deep breathing or coughing
tech - improve resp. Fxn
 ABG analysis, pulse oximetry (to assess oxygenation)
 Analgesics as ordered for pain
 Oxygen inhalation
 FVD
 Asses BP & fluid &electro status
 IVF therapy
 Blood trans
 Antiemetics
 Altered nutri:<body reqs
 NPO -early phase, to rest pancreas
 Weigh daily
 Enteral/tpn if on NPO
 Monitor CBS (due to hyperglycemia
 High CARBs, Low PROTEIN & FATS
 Discourage alcohol, spicy foods, coffee and heavy
meals
ADDITIONAL NOTES
Acute pancreatitis  Chronic pancreatitis - doesn't have a sign for increased amylase/lipase
o increased amylase/lipase o Gradual loss of functional tissue
o Complications: shock, jaundice o Mostly due to alcohol induce = fibrosis/scarring = pancreatic
(bilirubin), hyperglycemia (pancreas insufficiency= diminished function of pancreas
responsible for glucose and insulin), o There are cells that are not functioning anymore
ARDS (due to activation of other o Due to repeated acute pancreatitis due to alcoholism
enzymes, leakage pancreatic enzymes), o Management focus on prevention/ maintenance
AKD,   Enzyme replacement (normal stool = effective replacement)
o Med tx:  Pain meds, avoid alcohol
 NPO to let pancreas  Surgery -depends on type/ functional loss or abnormality of
rest pancreas
 TPN/ Enteral feeding  Pain is very painful, 
 Resume oral diet when  Endoscopic retrograde cholangiopancreatography
amylase are normal limits and (ERCP) - has xray, definitive test 
absence of pain (encourage pt on  Glucose tolerance -eval extent of damage 
what foods are to avoid, low fat  Stool exam - steatorrhea, if normal stool = pancreatic
intake,avoid alcohol) repl is effective
 Biliary drainage thru  Ampulla of vater - pancreatic juices/enzymes are released,
ngt connected to the common bile duct - gallbladder - liver 
 Surgery is case to case   Pancreatic enzymes should be inactive form 
basis  Pain radiates to the back because of compression, worsen by
 Pharma: lying down/supine, 
 H2 blockers to  Best position: leaning forward position
neutralize gastric secretions  Inflammation causes pain
 Opiods for pain  Relieve by antacids, 
 Prevent complications:  Happen due after eating 
 Monitor s/s atelectasis  Leakage of pancreatic enzymes = 2 signs: (severe manifestation)
 Positioning of pt   Turner’s - ecchymosis on the flank  
 Freq position changes -  Cullen’s - discoloration to the umbilical area 
to prevent holding of   Inflammation =perforation = hole = peritonitis = rigid
 Perform coughing techs abdomen
 Diagnostic tests: Increase within 24-72h, glucose
 Increase bilirubin if acc by biliary dysfunction
 Decrease calcium - fatty acids are low since fatty acids tends
to combine with calcium
 CT scan reliable diagnosis
 Ultrasonography to determine what caused the blockage

CHOLECYSTITIS

- Acute inflammation of gallbladder, Problem: bile could not get out (static stage or not moving) of cystic duct due to
obstruction = inflammation = chemical irritant = stasis = bacterial invasion = empyema , pus formation or infection
- Inflamed due to obstruction
- An empyema of gallbladder develops if the gallbladder becomes filled with purulent fluid. There is pus formation because of
infection.
- Bile contents are composed of fat and cholesterol
Pathophysiology

 Blockage in cystic duct by gallbladder stone = impairs flow of bile from gallbladder towards duodenum = increases
pressure of gallbladder wall and mucosa
 Bile can’t be moved = stasis (means it remained there for a long period of time) =chem&bacterial inflammation =
necrosis or perforation
 Obstruction + inflammation+stasis of bile = chemical irritant to gallbladder = mucosa secretes mucus and other
inflam enzymes = increase distention and pressure
 Stasis of bile = good place for bac invasion = peritonitis (pt feels rebounded tenderness)
 Bacterial invasion = emphysema or pus formation due to infection

Calculous Cholecystitis Acalculous cholecystitis


 Due to Gallbladder stone obstruction in biliary  Anatomical abnormality of duct
duct= impairs bile outflow = Bile remains in  Acute gallbladder inflammation in the absence of
gallbladder= inhibits chemical reaction leading to obstruction by gallstones
autolysis and edema
 Occurs after surgical procedures, severe trauma, burns due
 Blocks the cystic ducts  = Inflammation, edema, to anatomic problem or twist or kinking of the cystic duct.
blood vessels in the gallbladder become pressed,
vascular supply is compromised
 can also cause gangrene, perforation, and it can lead
to PERITONITIS

Assessment
CHRONIC PAIN ACUTE PAIN

 VAGUE AND NON-SPECIFIC, Often asymptomatic  SPECIFIC (entire RUQ, may radiate to the back, right
scapula, shoulder), lasts for 12-18HRS
 Results from repeated bouts of acute cholecystitis or  aggravated by movement or DBE
from persistent irritation of the gallbladder wall by  Nausea and vomiting, anorexia,
the stones  Fever with chills (infection)
 BLUMBERG'S SIGN - Rebound tenderness, pain upon
 Bacteria may be present in the bile as well removal of pressure to abdo
 MURPHY'S SIGN - Pain increasing with deep inspiration
(reliable for peritoneal irritation)
Pharma TX Med TX
URSODIOL (ACTIGALL) T- TUBE INSERTION - to maintain patency of duct ad promote
 well tolerated with few side effects bile passage as edema decreases

CHENODIOL (CHENIX) Nursing Management


 has a high incidence of diarrhea at therapeutic doses  Ensure tube is properly connected to a sterile container, keep
 hepatotoxic (requires periodic liver function studies) the tube below the level of the surgical wound (to promote
 reduces cholesterol contents of your gallstone, drain or flow of bile and prevent backflow)
leading to gradual dissolution)  Drainage: Normally after 24 hours after surgery, drain is up
to 500 mL, and gradually decrease to  200 mL, within 2-3
ANTIBIOTICS - If infection is present DAYS 
 Color: from bloodtinge - green - brown
CHOLESTYRAMINE (QUESTRAN) - for itchiness  Place in semi-fowler position: to promote drainage
 For pruritus due to jaundice and bile salts on the  Assess skin bile leakage: it may irritate the skin and you
skin need to change the dressing and apply protection..
 binds with bile salt to promote excretion in the feces  NPO during acute attacks and NGT (low suction) insertion
to relieve nausea and vomiting
ANALGESIC (MORPHINE) - for pain  Low fat intake: cant digest fat, due to prob in bile supply
(esp obese)
Additional Notes:  Replace Fat soluble vitamins (Vitamin A,D,E,K and bile
Chemical irritant salts)
 Spasis = immediate bacterial invasion = pus  W/o oral food & fluids during acute pain
 Vitals q4H
 Weight loss and reduce pain (adms meds)

CHOLELITHIASIS

is the presence of the gallstones


Calculi/ gallstone
Usually form in the gallbladder from the solid constituents of bile: they vary greatly in size, shape and composition
Risk Factors: F4 Female, Fat, Fertile, Forty

Two major composition of Gallstones


Pigment stones Cholesterol Stones
 Unconjugated pigments of bile precipitate to form  Due to an increase cholesterol intake = decreased
stones bile acid synthesis = super saturated = precipitate
 High risk for cirrhosis, hemolysis, infection in biliary  Gallstones are very irritant the gallbladder and it can
tract cause inflammatory changes in the bladder
 Not easily dissolved - Removed surgically  normally constituent of bile, insoluble in water,
soluble in bile
 Can be dissolved w/ meds
 it contains calcium = bind to unconjugated bilirubin
=pigment seen in xrays
Assessment Diagnostic Tests

 Asymptomatic in early stages  Cholescintigraphy


 Abdominal distension, vague pain upper quadrant of  diagnose  ACUTE CHOLELITHIASIS and BLOCKAGE
abdomen OF THE BILE DUCT, to detect gallstones
 Epigastric fullness or mild gastric distress after  With a radioactive via IV
eating large or fatty meal, last for 5 hrs, radiate to  When it reaches to the biliary tract= scan = produce
back, right scapula and shoulder an image of a biliary tract  and gallbladder
 Biliary Colic - severe steady pain in the epigastric  iodide containing contrast agent
region or right upper quadrant of the abdomen  Cholecystography
 Nausea and vomiting  ERCP - visualize biliary structures
 Jaundice (bile duct obstruction)  Percutaneous transhepatic Cholangiography
 Dark colored urine
 Non-surg tx = decompress obstructed extra hep duc
 Feces (grayish.like putty, clay colored) = bile can flow
 Vitamin ADEK deficiency  Injection of dye directly to Biliary Tract for better
outline

Surg TX Med TX

 EXTRACORPOREAL SHOCK WAVE LITHOTRIPSY  Limited to low fat liquids


(ESWL)  High protein, high carbohydrate in skim milk
- Outpatient: several sessions necessary  Avoid: eggs, creams, fried foods, cheese, alcohol
 INTRACORPOREAL LITHOTRIPSY  Ursodeoxycholic acid (UCDA) (Actigall)
- to put laser pulse technology= fragment  Chenodeoxycholic acid (CDCA) (Chenodiol)\
gallstones = cut into smaller pieces  dissolve small cholesterol stones, deolucent
 LAPAROSCOPIC CHOLECYSTECTOMY cholesterol stones; 6-12 month therapy
- New standard for therapy for symptomatic
gallstones Nursing Diagnosis:
- Invasive surgery
- Advantages: complications are not common,  ACUTE PAIN AND DISCOMFORT RELATED TO
death rate is very low, bile duct injuries are TISSUE TRAUMA SUSTAINED DURING SURGERY
rare, recovery is faster, and post operative  IMPAIRED GAS EXCHANGE RELATED TO HIGH
pain is less severe ABDOMINAL SURGICAL INCISION
 IMPAIREFD SKIN INTEGRITY RELATED TO
Post-op Complication JAUNDICE / ALTERED BILIARY DRAINAGE AFTER
SURGICAL INTERVENTION
 Excessive T-tube drainage  IMBALANCED NUTRITION LESS THAN BODY
- T-tube (Drain bile) - drainage 24 hours post- REQUIREMENTS RELATED TO INADEQUATE BILE
operatively (300-500mL bile: lesser) SECRETION
Additional Notes:
Stones are formed due to:
 Increase cholesterol = precipitate  
 pigmented or bilirubin =forms of
unconjugated 
 Pigmented stones are not dissolve by
meds but req surgery 

LIVER CIRRHOSIS

 chronic , progressive liver condition - diffuse fibrotic bands of connective tissue that disrupts liver function

 The last stage of liver disease, irreversible, could lead to liver failure, functional liver tissues gradually destroyed
and is replaced by fibrous scar tissue, blood flow is impaired towards the inferior vena cava w/c results to the
blood to shunt back to the lower organs also called as portal hypertension

 Extensive degeneration and destruction of hepatocytes (fibrotic regeneration)


a. Alcoholic cirrhosis (portal areas)- end result of alcoholic liver disease
b. Postnecrotic cirrhosis (viral)- cause by chronic hep b and c
c. Biliary cirrhosis (obstruction)

Assessment Complications

 Dull, aching pain RUQ LATE SIGNS:  Portal hypertension- the blood is shunted back to the
 Fever, N&V, Diarrhea lower pressure vessels, the affected vessels will be
 Anorexia and malaise  Liver enlargement engorged, this may affect the rectum, stomach,
 Ascites, Edema  Ascites esophagus = one of the manifestation of pt that has
 Jaundice, Hypotension  Infection and liver cirrhosis is esophageal varicose veins
 Muscle wasting, weight loss
peritonitis  Splenomegaly- there's backflow of blood to the splenic
 Edema
 Vit deficiency and
 Continuous mild fever vein, there is decreased platelet, wbc, anemia, 
 Purpura  Ascites- increased pressure in capillaries it pushes fluid
 Spontaneous bruising, to the peritoneal cavity 
epistaxis (because of the lack of vit K)  Hepatic encephalopathy- ammonia is present in the
 Sparse body hair, Gonadal atrophy brain, manifestation of this is asterixis (when the pt
wrist and fingers are observed to flap because of a brief,
rapid relaxation of wrist dorsiflex)

Med TX Diagnostic Tests


Ranitidine- decrease gastric distress ELEVATED:
Vitamin supplements- promote healing  serum globulin-inflammation
Spironolactone for ascites  serum alkaline phosphatase
 AST (aspartate aminotransferase)
Milk thistle (silybum marianum) contains Silymarin- for
 ALT (alanine aminotransferase)
jaundice  GGT (gamma-glutamyl transpeptidase)
Avoid alcohol and provide adequate nutritional intake  prothrombin time

DECREASED:
 albumin
CT scan
MRI
Radioisotope liver scans
Liver biopsy
Surg TX Nursing Management

Liver Transplantation  Monitor v/s, i/o, weight


- Immunosuppression needed  Position appropriately
- Costly without guarantee  Adequate rest periods
-  Small frequent feedings (ascites)
 enteral/TPN for severe anorexia
 Restrict protein to prevent encephalopathy
Nursing Diagnosis:  Restrict sodium
1. Imbalanced nutrition: less than body requirements r/t  Meticulous skin care, avoid adhesive tapes, lotions
anorexia, abdominal distention may be used
2. Altered comfort: chronic pain r/t enlarged liver ascites  Turning schedule- prevent pressure ulcers
3. Fluid volume excess: ascites/edema r/t decreased  Minimize scratching
albumin, portal hypertension  Provide safety (Padded side rails, Prevent bleeding)
4. Disturbed thought process: potential for mental
deterioration r/t increased ammonia levels

Additional Notes:

 Hepatocytes are grad destroyed and replaced


with constrictive bands= scarring = disrupts
blood flow and bile flow = increase pressure
in portal vein (Portal Hypertension) =blood
shunting to lower pressure vessels =
esophageal varices (are like varicose veins in
esophagus= herniation), splenomegaly,
hemorrhoids
 Too much fluid = leaks to abdomen =
ascites 
 Asterixis or liver flap - tremor of hands,
elicited by extending arms and flexion of
wrist 
HEPATITIS
 Viral infection = Inflammation and necrosis of liver cells
 not reversible, could lead to fibrosis and cirrhosis later on
 can be caused by:
a. Viruses: Hepatitis A,B,C,D,E virus
b. Toxic Chemicals( alcohol, drugs)
c. Medications

Assessment Prevention of Viral Hepatits

 Loss of appetite  Encourage proper sanitation and personal hygiene


 Dyspepsia, abdominal pain Hep b- via blood - Has meds and tx for acute hep b
 Generalized aching Hep a- via food
 Malaise and weakness  Safe practices in food preparation
 Enlarged and tender liver  Vaccination
 Splenomegaly (long term complication, portal  Safe hospital protocols regarding use of needles,
hypertension causing the blood to shunt back to the blood fluids
splenic vein)   Active immunization of hep B
 Jaundice (not all cases) a. For healthcare personnel
b. Hemodialysis patients
 Passive immunization of hep B
a. For those exposed but w/o infection
Med TX Nursing Management
 Maintain adequate nutrition
 Alpha interferon- 5 million units daily or 10 million  Bed rest, activity limitations
units, 3x weekly for 16-24 weeks  Restrict protein intake
 Lamivudine (Epivir)  Antiemetic and antacids as ordered for dyspepsia
 Adefovir (Hepsera)  Fluid therapy for vomiting episodes
GI DISORDERS
GASTRITIS
 Inflammation of the gastric or stomach mucosa from irritation (ass w. gastric irritants)
 acute= hours to days 
 chronic= repeated attacks, recurring episodes, begins w/ inflam and gradually atrophy of gastric tissue due to H. pylori
Physiology:
 Mucosa becomes edematous
 Superficial erosion

Causes Assessment & Diagnostic Tests

 Helicobacter pylori =chronic gastritis  Symptoms: asymptomatic to mild heartburn to severe


 Often caused by dietary indiscretion gastric distress, vomiting and hematemesis.
 Ingestion of irritating foods, aspirin, caffeine, alcohol MILD:
 Overuse of aspirin and NSAIDs  Anorexia
 Excessive alcohol intake  Mild epigastric discomfort relieved by belching or
 Ingestion of strong acid/alkali defecating
 Can be secondary to:   N&V
a. Burns  Melena or hematemesis-gastric bleeding
b. Traumatic injuries
c. Major surgeries DIAGNOSTIC EXAMS:
d. Severe infection  Endoscopy, Stool exam
e. Renal and hepatic failure  Upper GI X-ray
 Histologic exam

Nursing Management Med TX

 Altered comfort: pain ass, provide non-irritating food, IV Therapy, Non-irritating diet, Diluting & Neutralizing acid/alkali,
meds No lavage for corrosive substance, Metrodinazole for h. Pylori,
 Risk for imbalanced nutria: sym management Ranitidine, esomeprazole, sucrafate, NPO, start from liq to solid
 Risk for FVD: I/O monitoring, adequate hydration food, Antacids
PEPTIC ULCER DISEASE
 Excavation that is formed in the mucosal wall of the stomach, pylorus, duodenum and stomach
 More likely in duodenum than stomach, because the duodenum is more sensitive, it cannot withstand the presence
of hydrochloric acid and pepsin unlike the stomach
 Mainly in gastric-duodenal mucosa, this tissue is unable to withstand digestive reaction of gastric acid and pepsin
 More frequently between ages 40-60 years
 Erosion found in the circumscribe of mucosal wall

CAUSES:
A. H. pylori infection = MAIN CAUSE PATHOPHYSIOLOGY:
B. Excessive alcohol intake and smoking 1. Increased gastrin and pepsin
C. Long-term NSAID use 2. Damaged mucosa can't
D. Ingestion of milk, caffeinated beverage(high amount of ingestion) secrete mucus for protection
E. Susceptible to blood type O
STRESS ULCERS ZOLLINGER-ELLISON SYNDROME

1. CUSHING’S ULCER 2. CURLING’S ULCER  Is a peptic ulcer disease caused by a gastrinoma or gastrin-
secreting tumor of the pancreas, stomach or intestines
 head injury/brain  occurs 72 hrs after
trauma extensive burns
 high levels of HCI acid entering the duodenum = diarrhea
 deeper and (antrum, stomach,
penetrating duodenum) and steatorrhea
(esophagus, stomach,
duodenum)
Assessment Med TX

A. Gastric   Combination of metronidazole, omeprazole, bismuth salts


 Pain does not follow a consistent pattern  (pepto-bismol)
 Pain with eating  Ranitidine and omeprazole- for NSAID induced ulcers
 Weight loss
 Ranitidine and cytoprotective agents (sucralfate)

B. Duodenal 
 Decrease pain if patient eats 
 Weight gain
Diagnostic Tests Complications

 Upper GI series (barium swallow)  Hemorrhage- may caused by depolsoration


 Endoscopy (preferred diagnostic, it allows direct  Perforations and penetrations (peritonitis)- board like
visualization)
abdomen,
 Biopsy
 Stool exams- occult blood  client assumes fetal position to decrease the tension,
 abdominal pain felt radiates to the shoulder as well,
hypovolemia might occur
 Pyloric obstruction/stenosis- occurs when the area distal to
the pyloric sphincter becomes scarred
Surgical TX Nursing Management
 Antrectomy (removal of a portion of antrum)
 Altered comfort: acute pain r/t the effect of gastric acid
 Billroth I (gastroduodenostomy)- removal of lower hypersecretion on damaged tissue
portion of antrum; anastomosis of the
duodenum  Altered nutrition less than body requirements r/t dietary
modification
 Billroth II (gastrojejunostomy)- removal of lower  Encourage to stop smoking
portion of antrum; anastomosis of the jejunum  Avoid alcohol and coffee, other caffeinated
beverages, diets rich in milk and cream, extremes in
 Complication: temperature, over consumption of meat extracts
 Encourage 3 regular meals/day (SFF may not be
1. Dumping syndrome- increased stomach emptying( necessary with antacid or H2-antagonist therapy)
because the pylorus is resected and bypassed)  Encourage rest periods
 There is rapid stomach emptying= abdominal  Stress reduction
cramping = occur within 30 mins after eating,
late dumping occur 90 mins to 3 hrs after
Additional Notes:
eating 
Common are gastric and duodenal (most common, can't
withstand hcl)
 Management: (delay stomach emptying)
 Causes: nsaids scan decrease/ disrupt prostaglandin
 Small frequent feedings
and h. Pylori 
 Fluid intake 1 hr before/after meals (not
 Prostaglandin - protect mucosal barrier
within meals)
 s/s
 May assume a lying down/ low Fowler’s
o Pain upon eating (gastric)
position during and after meals
o Duodenal relieved by food but pain is present
 Decrease CHO, fiber; may increase fat
 Antispasmodics may be given 2-3 hrs
o Fluid intake and meals should be 1 hr apart 

APPENDICITIS
 Most common cause of acute surgical abdomen
 Appendix- storage of solid small particles
 Appendix becomes inflamed and edematous as result of either becoming kinked/occluded by a fecalith (hardened mass
of stool) tumor, foreign body; common in males 
 Fecalith (occluded material)=lumen is blocked, intestinal mucosa still continues to secrete the fluid  = cause pressure
build up= blood flow is being restricted=can cause infection=lead to swelling= peritonitis may result, if the swelling
burst= gangrene and hypoxia may occur
 Intestinal mucosa cont to secrete fluid= buildup = inflammation, blood flow is restricted due to blockage = gangrene,
hypoxia = rupture

Pathophysiology Assessment & Diagnostic Tests

 Inflammatory process, high intraluminal pressure,  RLQ pain and usually accompanied by a low grade fever
initiating a progressively severe, generalized or  Anorexia
upper abdominal pain that becomes localized in RLQ  Nausea and vomiting
 Pain on defecation 
of abdomen within a few hours
 Constipation 
 Eventually, the inflamed appendix fills with pus from  Local tenderness on McBurney's point
ileum  Rovsing’s sign- pressure on LLQ and pain is felt in RLQ
 Psoas sign- pain on flexion of the right thigh towards the
body will elicit pain 

DIAGNOSTIC TESTS:
o X-ray
o Ultrasound
o CT scan

Nursing Management Surg Tx


 Altered comfort: abdominal pain r/t tissue trauma
sustained during surgery  Appendectomy 
 Semi-fowler's position 24 hrs after surgery  Exploratory laparotomy (ruptured appendix
 NPO post surgery
 High fiber, high protein diet
INFLAMMATORY BOWEL DISEASES

CROHN’S DISEASE/ REGIONAL ENTERITIS


 AKA Regional enteritis (not all parts of the intestine is affected)
 Subacute and chronic inflammation of the GI tract that expands through all layers (transmural)
 Unknown cause, it may be because of genes and environmental factors
 Remissions and exacerbations
 Common in distal ileum, ascending colon
 Common in smokers
Pathophysiology Diagnostic Tests

 Thickening and edema of mucosa  Proctosigmoidoscopy


 Ulcers begin at inflamed mucosa  Stool exam (occult blood)
 Cobblestone  Upper GI barium study “string sign”
 Granulomas in 50% of patient  Blood test: 
= decreased Hgb, Hct (because of bleeding)
= elevated WBC, ESR (inflammatory process)
Assessment = decreased albumin
 CT scan
 Right lower quadrant abdominal pain  Barium enema
 Diarrhea unrelieved by defecation = cobblestone
 Crampy abdominal pains  Colonoscopy
 Abdominal tenderness and spasm  Sigmoidoscopy 
 Weight loss, malnutrition, anorexia Medications
 Looks thin and emaciated  Biologic agents:
o Natalisumab- crohn’s disease
 Steatorrhea 
ULCERATIVE COLITIS
 Recurrent ulcerative and inflammatory disease
 Affects mucosal and sub-mucosal layers
 Starts in rectum, only in large intestines,

Pathophysiology Diagnostic Tests


 CT scan
 Thickening and edema of mucosa  MRI
 Ulcers begin at inflamed mucosa  Ultrasound
 Cobblestone  Barium enema
 Granulomas in 50% of patient  Sigmoidoscopy 
 Colonoscopy

Assessment Medications
 Diarrhea; 10-20 liquid stools each day  Aminosalicylates (azulfidine)
 Passage of mucus and pus  Corticosteroids (prednisone)
 Left lower quadrant pain   immunodilators:
 Intermittent tenesmus o Azathioprine
 Rectal bleeding; anemia o Mercaptopurine
 Weight loss o Methotrexate 
 Rebound tenderness o Cyclosporine 
 Pain at LLQ  Biologic agents:
o Natalisumab- crohn’s disease
o Infliximab- ulcerative colitis

Nursing management
GOAL: reduce inflammation, suppress inapp immune
response  Altered bowel elimination: Diarrhea r/t inflammatory process
 Bedside commode
 Nutrition and hydration  Chart consistency of stools
 Oral fluids and IVF therapy  Fluid volume deficit r/t diarrhea, nausea
 Low-residue, high protein, high calorie  IVF therapy
 Vitamin and iron supplement  Weigh daily
 Avoid cold foods and milk products( this could  Encourage oral fluid intake
increase intestinal motility)  Dietary restrictions for diarrhea
DIVERTICULAR DISEASE
DIVERTICULOSIS DIVERTICULITIS

 Multiple diverticula but WITHOUT inflammation  Infection, inflammation secondary to obstruction


 Due to low dietary fiber intake  Asymptomatic, common in sigmoid colon
 Divertila Sac = pain, contains food& bacteria
 Asymptomatic
 Complications:
 There is an outpouching of an intestine’s portion
o Perforation, fistula, haemorrhage, obst

Pathophysiology Diagnostic Tests


 Colonoscopy (biopsy can be done)
 Herniation due to increased intraluminal pressure in the  Barium enema (contraindicated in perforations)
bowel lumen which causes the bowel lumen to herniate  CTscan with contrast 
 Low volume in the colon  Blood test: elevated WBC, ESR
 Decreased muscle strength

Assessment Med TX
 Chronic constipation; narrow stools  Clear liquid initially, high fiber& low fat
 Bowel irregular- constipation/diarrhea (to inc stool volume),reduce intraluminal pressure
 Nausea, anorexia  Bulk-forming laxatives as ordered
 Bloating, abdominal distention  Psyllium fiber)
 Pain in LLQ  Stool softeners (docusate)- to decrease intraluminal
Nursing management pressure when you defecate
 Constipation r/t strictures, narrowed colon  Rest the bowel
 Oral fluid intake up to 2L/day  withhold oral intake
 Soft, fiber-rich foods  NGT suctioning
 Veges, cereals (increase bulk in stool)  Meperidine (demerol) for pain as ordered
 Exercise - no morphine (addictive)
 Psyllium and stool softeners as ordered  antispasmodics : oxyphencyclimine (daricon) as ordered
 Oil retention enema  Antibiotics for 7-10 day
 Barium Enema- lower Gi, visualize colon
Module 1M: Concept of Metabolism and Alterations
in Ingestion
Structures and functions of GI system:

Ingestion -intake of food


Appetite center - hypothalamus, stimulated by
hypoglycaemia (empty stomach), low temp and input
from higher brain certers.
Ghrelin - hormone, plays a role in appetite
stimulation
Leptin - appetite suppression
Deglutition (swallowing)- mechanical component of
ingestion, organs involved are mouth, pharynx and
esophagus

Mouth - consists of
lips (for speech)
oral cavity
formed by soft and hard palate,
contains the teeth : used in mastication/chewing
tongue : solid muscle mass, assist in chewing and
moving food, important in speech
three pairs of salivary glands parotid, submaxillary
and sublingual : produce saliva
Four layers (inner to outer): mucosa, submucosa,
muscle, serosa Pharynx -divided into
Main function- to supply nutrients to body cells nasopharynx, laryngeal
thru process : ingestion, digestion, absorption, oropharynx
elimination provides route for food from mouth to esophagus
Epiglottis: covers larynx during swallowing
Tonsils and adenoids: assist in preventing infection
Energy
o capacity to perform activities Patho/Disease process of alteration in ingestion
 Human energy - muscle contractions ♥ Cleft lip
and heat production  Caused by failure of the nasal and
 Heat=calories=energy maxillary processes to fuse between the
 Metabolic Rate 5th and 8th week of gestation
o Amount of energy expended in a given unit of  Cleft lip POST OP CARE:
time o Choking, Logan bar, Evaluate
o 3 components: bmr airway, Feed slowly, Teaching,
 Basal Metabolic Rate Lamb’s nipple, Incidence high in
o Amount of energy used in a unit time by males, Prevent crust formation
and aspiration
fasting, resting subject to maintain vital
functions
♥ Cleft palate
o 60-75%
 Caused by failure of the palatine plates
o Increase in activities, thermal effect of food
to fuse between the 7th and 12th week
 Aka BEE -basal en expenditure
of gestation
 Nutrient
o substance that provides nourishment essential
 Diagnostic exams:
for growth and the maintenance of life.  Visual inspection and palpation after birth
 Metabolism - processes of biochemical reactions  Ultrasound or sonogram while in the uterus
occurring in the cells necessary to maintain life  Surgical Management:
 CHEOLIOPLASTY (left lip repair) - reqs more
Basic activities and process of the GI tract than 1 procedure
 Closure of the lip-performed app 3
 Ingestion - entry of food into the digestive months of age or 12 pounds
tract through the mouth  Closure of the palate-performed app 1
 Propulsion- movement of food through the year or within 6-18 months
GI tract  Nursing Actions
 Digestion -breakdown of food mechanically  Suction secretions gently
into smaller bits and chemically by  Place infant on side to prevent pressure and
enzymes tearing of suture line after CL surgery
 Absorption - nutrients and water are  Feed infant using commercial cleft lip nipple
absorbed in the intestines *Brecht or Haberman Feeder)
 Defecation - removal of undigested  Method: Enlarge, Stimulate, Swallow and Rest
materials from the body as waste (ESSR)
 Secretion -
 Instruct mother how to pump or manually
express breast milk to maintain supply at this
time
 Bubble th infant well after feeding ♥ Kwashiorkor
 Offer small sips of fluid (clear water) or place  Maladaptive response to starvation
membranes as crust formation  Protein PEMS
 Keep suture line as clean as possible after ♥ Marasmus
feeding
 Adaptive response to starvation
♥ Malnutrition  Protein PMS
 Causes:
 Indicators for undernutrition:
o Inadquate food intake (main problem)
o Stunting
o Poor standard living
o Wasting
o Inadeq knowledge of optimal nutri intake
o Underweight
o Inadeq absorption
♥ Esophageal fistula/ Treacheoesophageal Fistula/
 Nutrition on the 1st 1000 days of a Child
TEF
 In 2015, global community adopted the
 Abnormal passage between windpipe and esophagus
17LGobal Goals for Sustainabel Dev to improve
 Congenital anomaly (6-8 weeks)
people’s lvies by 2030
 Goal 2: Zero Hunger - pledges to end hunger,  Life-threatening
 S/S:
achieve good security, improve nutri and
o Copious, fine, frothy bubles of mucus in mouth and
promote sustainable agriculture and si the
sometimes in nose
priority of World Food Programme. o Rattling respirations
 Malnutrition in the Phils o Episodes of coughing, choking, cyanosis (3C)
 Metro manila (CNN Phils, May 2, 20170 - acc
 Med/Sug tx:
to Save the Children Foundation 1 in 3
o Gastrostomy feeding /TPN
children below 5 yo in the Philippines is
o Closing of fistula and gastrostomy tube
malnourished
insertion (to minimize GERD)
 Food And nutrition Research Institute: 26% of
o Anastomosis
children up to 2 yo suffer from chronic
malnutri, the highest number in 10 years  Complicaiton:
 Many children, including those in poor o Aspiration Pneumonia
communities, may have access to food, but  Objectives of care:
they’re not eating right, because parents lack o Airway will remain patent
basic knowledge on proper nutri o Hydration maintained
o Family teaching
 Obs for esophageal stricture-dysphagia,
increased drooling, coughing, choking
 Gastrostomy, care and feeding

 Malignant TEFS
 Individualized and started promptly
 Palliative care
o Relief of obstruction
o Diversion fo contamination from Respi
Tract
 Procedures
o Endoprosthesis (covered self-expandable
metal stent/SEMS)
o Esophageal exclusion or bypass, resection
or direct closure

 Total Parenteral Nutrition (TPN)


o Supplies all daily nutri reqs
o Given before & after tx to severely
undernourished pts who cant ingest large
volumes of oral feedings and are prep for
surgery, radiation or chemotherapy
More active=more metabolic rate= high need for calories

Carbs metabolism begins when glyconlysis to pyruvic to krebs- be


oxidized
Pyruvic to acetyl reqs vit D
1 glucose = 31 molecules to ATP
Energy from atp thru hydrolysis =chemical rxt with water for
biological work
Liver and kidney cells can produce glucose from amino acids,
Liver and muscle cells store glucose in for mof glycogen others
from blood
Lactic acid- energy demands > oxygen supply
Proten catabolism - co2, o2, atp , water, urea, ammonia
Fat or lipid metabolism - cmiricons
Mitochondira of cell, 2 c are removed =atp, co2, h2o
 athletic
 hard body and defined mucles
 rectangular shaped body, strong
 gains muscles easily
 gains fat more easily than ectomorphs

 soft round body


 gains muscle and fat very easily
 small “delicate: frame and bone structure
 gen short and “Stocky”
 classic “hardgainer”
 round physique
 flat chest small shoudlers, lean muscle mass
 Finds it ghard to lose fat
 finds it hard to gain weight
 slow metabolism
 fast metabolism
ALL MED THERAPIES ARE UNSUCCESSFUL WITHOUT PROPER
NUTRITION AS A RESULT OF GOOD METABOLISM
Module 3M: Care of Clients with Alterations in GI 15. The largest intestinal nematodes that affect humans
Elimination and can result to intestinal obstruction -ASCARIS
1. Acute diarrhea is most often associated with infection LUMBRICOIDES
and may return sporadically - FALSE 16. Peritonitis is caused by leakage of contents from
2. No passage of stool within 24-48H after birth is a abdo organs into abdominal cavity -TRUE
sign of what condition - HIRSCHSPRUNG DISEASE 17. In irreducible hernia, the contents of the hernial sac
3. One function of large intestine is the reabsorption of can be placed beck into the abdominal cavity by gently
water and electrolytes -TRUE pressure. -FALSE
4. Amyloidoisis is a condition that causes functional 18. During an intestinal obstruction, dehydration occurs
obstruction -TRUE more slowly in the large intestine than in the small
5. The inflammation of the serous membrane lining the intestine -TRUE
abdominal cavity and covering the viscera 19. Acquired umbilical hernia are most commonly seen in
-PERITONITIS people who are obese - TRUE
6. From proximal to distal, give three sections of the 20. Stool characteristic that involves the large bowel
small intestine -DUODENUM, JEJUNUM, ILEUM -Semi-solid
7. Bacteria is a major component of the contents of large 21. The following are signs that peritonitis is subsiding
intestine -TRUE except: BP is 130/100
8. Semisolid stools are associated more often with 22. The other name of congenital aganglionic megacolon
disorders of the large bowel - TRUE - HIRSCHSPRUNG DISEASE
9. A type of hemorrhoid that is associated with severe 23. Significant fluid and potassium loss while having
pain from the inflammation and edema caused by diarrhea can lead to metabolic alkalosis -FALSE
thrombosis - EXTERNAL HEMORRHOID 24. The blood supply to the herniated segment of the
10. A degree of hemorrhoid in which it prolapses outside bowel is cut off by pressure of the hernial ring
the anal canal during defecation but reduces -STRANGULATED HERNIA
spontaneously -SECOND DEGREE 25. The following are health prevent tips for constipation,
11. Adhesions are the most common cause of small except -DEFECATE DAILY
bowel obstruction -TRUE 26. Volvulus is a problem that can occur after birth in
12. It involves the alternating waves of contraction and which the intestines become twisted and causes
relaxation of the muscles in the organ wall and propels intestinal blockage. Malrotation is a birth defect that
the contents of the small intestine to the colon - malformation of the intestinal tract that occurs while
INTESTINAL PERISTALSIS the fetus is still on the uterus- ONLY SECOND STATE
13. Hypertension is a complication of constipation- TRUE IS CORRECT
14. A ribbon like stool is a clinical manifestation of 27. It is a painless procedure for hemorrhoids that is not
intussusception -FALSE widely used because discharge is foul- smelling and
wound healing is prolonged- CRYOSURGICAL 41. This is where most common large bowel obstruction
HEMORRHOIDECTOMY occur -SIGMOID
28. Identify the degree of hemorrhoidal prolapse: 42. Hernioplasty is the reinforcement of the weakened
irreducible and at risk for strangulation -FOURTH outside muscles with a mesh patch -TRUE
DEGREE 43. The color of the stool after barium enema -WHITE
29. Internal hemorrhoids are not usually painful until it 44. To patients who urgently needs relief from
bleeds or prolapse when it become enlarge -TRUE obstruction in the large bowel, cecostomy may be
30. There is a functional anal sphincter in a high level performed - TRUE
defect imperforate anus -FALSE 45. In small bowel obstruction ,fecal vomiting occurs
31. Ventral hernias result from inadeqaute healing of the when there is - ILEUM OBSTRUCTION
surgical incision -TRUE 46. The stool characteristic that involves the large bowel
32. This is the treatment of choice for intussusception -SEMI-SOLID
-NON SURGICAL HYDROSTATIC REDUCTION 47. The stool characteristics that involves the small bowel
33. It is often associated with bacterial toxins and -WATER STOOL
neoplasms -SECRETORY DIARRHEA 48. Decompression of the bowel through a NGT is
34. Most bowel obstructions occur in the small intestine necessary for patients with small bowel obstruction
-TRUE -TRUE
35. Enemas are not recommended for treating 49. It is often associated with bacterial toxins and
constipation unless rectal evacuation is a problem neoplasms -SECRETORY DIARRHEA
-TRUE 50. High consumption of fiber results to constipation
36. A pad that is held in place over the hernia with a belt -FALSE
to help the abdominal contents from protruding into 51. Medication of choice for diarrhea -LOPERAMIDE
the hernial sac -TRUSS 52. With the progression of peritonitis, the client may
37. Decompression of the bowel through a nasogastric experience low blood pressure -TRUE
tube is necessary for some patients with small bowel 53. The megacolon should return first on the normal size
obstruction -TRUE before conducting the second complete surgery
38. Bland diet of semisolid food is recommended to -FALSE
clients with diarrhea -TRUE 54. This manifestation may indicate obstruction and
39. To patients who urgently needs relief from strangulation of hernia -ABSENT BOWEL SOUNDS
obstruction in the large bowel, may be performed 55. The most common site of intussusception
-TRUE -ILEOCECAL VALVE
40. A normal response in an anorectal manometry is the 56. The peristaltic movement of the large bowel
contraction of the internal sphincter then followed by occurring five to six times daily that are triggered by
the contraction of the external sphincter - FALSE distention of the stomach -GASTROCOLIC REFLEX
57. There is a functional and sphincter in a high level  An abnormal hardening of the stools that makes
detect imperforate anus -FALSE their passage difficult and sometimes painful-
58. A pad that is held in place over the hernia with a belt CONSTIPATION
to help the abdominal contents from protruding into
the hernial sac -TRUSS  Frequent passage of loose stools -DIARRHEA
59. This type of hernia mostly occurs in men because it
follows the tract that develops when the testes  It is when the muscles of the intestines do not
descend into the scrotum before birth -INDIRECT allow food to pass thru resulting in a blocked
INGUINAL HERNIA intestine - PARALYTIC ILEUS
60. Bland diet of semisolid flood in recommended to
clients with diarrhea -TRUE  Exist when blockage prevents the normal flow of
61. The first-line tehrapy used in constipation with rectal intestinal tract -INTESTINAL OBSTRUCTION
evaluation problems -GLYCERIN  Wavelike and colicky cramping pain -SMALL
62. The following are signs that peritonitis in subsiding BOWEL OBSTRUCTION
except: BLOOD PRESSURE OF 130//100 mmhg  Constipating as the only symptom - SIGMOID
 A weakness in the abdominal muscle well thru COLON OBSTRUCTION
which a segment of the bowel or other abdominal  Ribbon foul like smelling stool - HIRSCHSPRUNG
structure protrudes - HERNIA DISEASE
 Diffuse pain- constant and localized in the area
 The rectum ends above the puborectalis muscle -PERITONITIS
-IMPERFORATE ANUS  Currant jelly stool - INTUSSUSCEPTION
 Tingling throat - ASCARIS BOLUS
 Presence of dilated portions of veins in the anal
canal - HEMORRHOIDS

 One part of the intestine slips into another part


that is located below or above it -
INTUSSUSCEPTION

 The bowel twists and turns on itself and occluded


the blood supply - VOLVULUS

 Also called the Hirschprung disease -MEGACOLON


Module 3M: Care of Clients with Alterations in GI Elimination
INTESTINAL OBSTRUCTION
 Exists when blockage prevents the normal flow of intestinal contents through the intestinal tract

Two types Degree of obstruction:

 Mechanical Obstruction  Partial


 intraluminal obstruction or a mural  Complete
obstruction from pressure on the intestinal
wall occurs, more like a physical
obstruction Degree of severity depends on:
 examples
o Intussusception, polypoid tumors and  Region of the bowel affected
neoplasms, stenosis, strictures,  Lumen occluded
adhesions, hernias and abscesses  Vascular supply to the bowel wall is disturbed

 Functional obstruction
 the intestinal musculature cannot propel the Two Classifications:
contents along the bowel, more on
problems on the muscles in the  Small Bowel Obstruction
intestines  Large Bowel Obstruction
blockage is temporary and  the result of
manipulation of the bowel during surgery
 examples
o amyloidosis, muscular dystrophy,
endocrine disorders [diabetes] or
neurologic disorders[ Parkinson’s
disease])

SMALL BOWEL OBSTRUCTION


 Most bowel obstruction occurs in the small intestine
 Adhesions most common cause of small bowel obstructions, followed by hernias and neoplasms

Approach focuses on:


 Confirming the diagnosis
 Identifying the etiology
 Determining the likelihood of strangulation

Pathophysiology:
Due to intestinal obstruction, there is accumulation of intestinal contents, fluid and gas on the upper
part of the intestinal obstruction =abdominal distention and retention of fluid that reduces absorption
of fluids and stimulates more gastric secretions = increasing distention = increases pressure in within
intestinal lumen =decrease in venous and arteriolar capillary pressure= edema, congestion, necrosis
and eventual rupture or perforation of the intestinal wall, with resultant peritonitis.
S/S Nursing Management

 Initial symptom: For nonsurgical patient


 Crampy pain that is wavelike and colicky -  Maintain the function of the NGT
 Assess and measure NGT output
due to persistent peristalsis above and below
 Assess for F/E imbalance
the blockage  Monitor nutri status
 May pass blood and mucus but no fecal  Assess improvement: return of bowel sounds,
matter and no flatus decrease abdo distention, subjective
improvement in abdominal pain and tenderness,
 Complete obstruction passage of flatus or stool
 PRIORITY: maintain f/e balance - the presence
 The peristaltic waves initially becomes
of NGT+NPO status= risk for fluid imbalance
extremely vigorous and eventually assumes a  Report the discrepancies in: I/O, worsening pain
reverse direction (instead peristalsis going or abdo distention, Increased NGT output
down, it goes up or towards mouth)  Prepare for surgery if the patient’s condition
does not improve

 Ileum obstruction
 fecal vomiting
Medical Management
o characteristic of vomitus: client will vomit
first the stomach contents, then the bile-  Decompression of bowel through a NGT
stained contents of the duodenum and the  Mandatory monitoring of bowel ischemia
jejunum, and finally, w/ each paroxysm of  Administration of IV fluids before surgery 
pain, the darker, fecal-like contents of the
ileum)
Surgical Management

 Evident signs of dehydration  Depends on the cause of obstruction


 intense thirst, drowsiness, generalized malaise,  Laparoscopy - for diagnosis and can be converted
aching and a parched tongue and mucous to open laparotomy if needed
membranes

 Distended of abdo = reflux vomiting


 Vomiting = loss of hydrogen ions and potassium
from stomach =  metabolic alkalosis

 Sodium and water  due to dehydration=


dehydration and acidosis = hypovolemic or septic
shock
LARGE BOWEL OBSTRUCTION
 Most large bowel obstruction occurs in the sigmoid colon 
 Common causes: carcinoma, diverticulitis, IBD, nematodes
 Dehydration occurs more slowly in large intestine because the colon has the ability to absorb water and even
if there is obstruction, the colon keeps on absorbing the fluid =slow/gradual dehydration

Pathophysiology:
 dramatic because if the blood supply to the colon is not disturbed = not have a lot of complications 
 if there is a cut off of blood supply, intestinal strangulation, necrosis  = life-threatening
 Adenocarcinoid tumors account for majority of large bowel obstructions

S/S Nursing Management

 monitor the patient for symptoms indicating that


 Sigmoid and rectal obstruction - constipation as the
the intestinal obstruction is worsening
only symptom 
 provide emotional support and comfort
 administers IV fluids and electrolytes as prescribed
 Altered stool shape - gradually increasing in size as
 Prep for surgery, if the patient’s condition does not
it passes the obstruction
respond to nonsurgical treatment
 Preoperative education
 Stool blood loss - Iron def anemia = weakness,
 After surgery, routine postoperative nursing care is
anorexia, weight loss
provided, including abdominal wound care
 Markedly distended abdomen
 Visible outline of the loops of the large bowel
 Crampy lower abdominal pain
 Fecal vomiting
 Symptoms of shock may occur

Diagnostic Tests Medical Management


 Abdominal X-ray and CT findings - distended colon  Restoration of intravascular volume
and pinpoint the site of obstruction  Correction of electrolyte abno
 NGT aspiration and decompression
 Flexible sigmoidoscopy - used to confirm the  Colonoscopy  - untwist and decompress the
diagnosis bowel

 Barium studies are contraindicated


Surgical Management

 Cecostomy- surgical opening is made into the


cecum, may be performed in patients who are poor
surgical risks and urgently need relief from the
obstruction.

 Total/Partial Colectomy - surgical removal of any


part of the bowel to remove obstructing lesions 
 Colostomy - outlet where feces can go out,
either temporary or permanent

 Ileoanal anastomosis - may be performed if


removal of the entire large bowel is necessary
o If there is a removal = the lining of the
rectum is removed and lower end of small
intestine, ilem is attached to the opening of
the anus 
o A S-pouch or j-pouch
HERNIA
 Under the mechanical obstruction
  Weakness in the abdominal muscle wall through which a segment of the bowel or other abdominal structure
protrudes

Pathophysiology
Congenital or acquired muscle weakness, Increased intra-abdo pressure, 
Obesity, pregnancy, lifting of heavy objects, abdominal distention, coughing, ascites = weakens
collagen - widens the spaces at the inguinal ligament = defects in the muscle wall = presence of
lump or protrusion in the area (s/s)

FIVE TYPES
Indirect Inguinal hernia Direct inguinal hernia Femoral Hernia

 A sac formed from the  Passes through a weak point in  Protrudes through the
peritoneum that contains a the abdominal wall femoral ring 
portion of the intestine or  Occurs more in older adults  A plug of fat in the femoral
omentum canal enlarges and pulls
 Pushes downward at an peritoneum and urinary
angle into the inguinal canal bladder into the sac 
 Common in males because  Common in obese or
the follow the tract that pregnant woman
develops when the testis
descends into the scrotum Umbilical hernia Incisional/Ventral hernia
before birth 
 In males = becomes large  Congenital - appear in  Occurs at the site of a prev
and descends in the scrotum infancy  surgical incision due to
 Acquired - result from inadeq healing of incision
increasing abdo pressure, caused by post op wound
common in people who are infection, inadeq nutrition
obese and obese
CLASSIFICATIONS
Reducible hernia Strangulated hernia Irreducible hernia/
incarcerated
 Contents of the hernial  Blood supply to the
sac can be placed back into the herniated segment of the bowel is  Cannot be reduced or
abdominal cavity by gentle cut off by pressure from the hernia placed back into the
pressure ring = ischemia & obstruction of abdominal cavity, 
 During assessment - lump bowel = necrosis and possibly  Reqs immediate cervical
or protrusion disappear when bowel perforation evaluation 
client is lying flat  Never forcibly reduced
o Ask the client to because it can cause strangulated
strain or perform valsalva intestine to rupture, never force a
maneuver - bulging of hernia
hernia   S/s:
o Ask client to cough o Abdo distention
o Auscultate bowel o Absence of bowel
sounds - absence indicates sounds
obstruction and strangulation o Nausea, vomiting
,pain, fever, tachycardia
Assessment
 Perform an abdominal assessment
 Client is lying down  For male client suspects a hernia in the groin
 Client is standing
 Have the client stand
 For inguinal hernia  Use index finger on the right hand on the
 Health care provider gently examines the client’s right side and left hand on the left side 
ring and its contents by inserting a finger in  Examiner invaginates the loose scrotal skin with
the ring and noting any changes when the the index finger, following the spermatic cord
client coughs upward to the external inguinal cord 
 Ask client to cough - palpate hernia
 Never forcibly reduced because it can cause
strangulated intestine to rupture, never force a
hernia
Nonsurgical Management Nursing Management
Truss
 A pad made with firm material  Thorough Physical Exam
 Held in place over the hernia with a belt to help  Pre op - NPO (most important pre op
keep the abdominal contents from protruding into preparation)
the hernial sac.
 Post op:
 For patients who are not a surgical candidate.
Often given to older male clients and has multiple o difficulty in voiding (immediate postop prob)
health problems.  Encourage male clients to stand to allow a more
 Most likely given to clients with inguinal hernia.  natural position for gravity to facilitate voiding
 Applied only after the physician has reduced the and bladder emptying.
hernia, if it is none incarcerated.  Let the client hear a dashing sound of water that
 applies the truss upon patient awakens. stimulates voiding.
 As a nurse, teach the client to assess the skin
 Let the client have a fluid intake of at least 1,500-
under the truss daily and protect it with a light
layer of powder to check if there are any sores 2,500mL to prevent dehydration, maintain urinary
function, minimize constipation and to allow the
Surgical Management client to void.
o Avoid coughing  (Place a pillow on the abdomen of
Herniorrhaphy the pt and then that’s when you let the pt cough)
o Teach the client to rest for several days
 Surgery of choice, open the client and perform
herniorrhaphy, o Remind the client to observe the small incisions for
 The end result should have a mesh.  redness, induration, heat, drainage and increased
 Minimally Invasive Inguinal Hernia Repair pain and report their occurrence to the surgeon.
(MIIHR) through a laparoscope (The surgeon Especially if you are just having MIIHR there will be
makes several small incisions, identifies the just a small incision so always check if there are any
defect, and covers the weakened area with a
signs of inflammation with those incisions.
mesh patch on the inside of the abdominal wall.
o Encourage deep breathing
Hernioplasty o Assist in placing scrotal support and ice bags and
 The surgeon reinforced the weakened outside elevate to the scrotum to prevent swelling
muscle with a mesh patch. o Instruct the client to keep the wound dry and clean
with antibacterial soap and water.
INTUSSUSCEPTION
 One part of the intestine slips into another part located below or above - “telescoping of the intestine” 
 more common in infants (3rd month - 3 yo, peak: 5th-9th month) & adults (common in male, w/ cystic
fibrosis)
 Most common site: ileocecal valve (inv ileum and the cecum) - cause is Unknown.

S/S Nursing Management


 Sudden onset of crampy abdominal pain,
inconsolable crying and drawing up of the  Ask the parents description of the child’s physical
knees to the chest - infants and behavioral symptoms.
 Progressing obstruction: bilious vomiting and  For the child with signs of electrolyte imbalances,
lethargy increases hemorrhage or peritonitis, additional medical
preparations such as replacement fluids,
Classical triad: antibiotics and NG suctioning may be indicated.
 Pain or abdominal pain  After hydrostatic reduction, observe for passage of
 Palpable sausage - shaped abdominal barium or water soluble contrast materials with
mass due to the telescoping part of the stool. Usually, if there is a barium solution, the
intestine stool will be whitish for 1-2 days.
 Currant jelly like stools because of the  Inform the parents that the child should be
venous engorgement admitted to the hospital for 12-24 hours for
observation after the hydrostatic reduction.
Diagnostic Findings:
Abdominal Radiograph - to detect intraperitoneal Medical Management
air from a bowel perforation
Barium Enema
Rectal Exam = Reveals mucus, blood and low
 treatment of choice
intussusception
 Water soluble contrast or administration of air
pressure.
Surgical Management
 Probe into anus - barium will flow =air pressure =
 if barium enema is not effective
push back to original position
 Manually reducing the invagination and  Nonsurgical hydrostatic reduction
resecting any non viable intestine.
VOLVULUS
 “Volvere - to roll”  Bowel twists and turns on itself and occludes the blood supply
 already a problem that occurs after birth as a result of the intestinal malrotation ( malrotation then volvulus)
 Malrotation - caused by abnormal rotation of the intestine around the mesenteric artery during embryonic
development, occurs when the intestine does not make the turns as it should, more s/s in boys by the 1 st month
 Intestinal malrotation - birth defect involving a malformation of the intestinal tract that occurs while a fetus
is forming in its mother’s uterus.
 intestine becomes twisted =intestinal blockage =prevent digestion + dehydration + can cut off the blood supply
= damaged intestines.

TYPES Clinical Manifestations Nonsurgical Management

Sigmoid Volvulus - most  Mesentery is twisted = blood flow Sigmoidoscopy (the probe is only
common and common during is cut off = infarction inserted to the sigmoid part of the
pregnancy (fetus can cause  Intermittent vomiting colon)
displacement and twisting of the  Recurrent abdominal pain  Treatment for sigmoid volvulus
colon), abdo adhesions  Abdominal distention  Untwist and decompress the
 Middle aged and elderly - most  Lower GI bleeding/bloody stool colon to relieve pressure
common symptom: chronic Colonoscopy (probe is inserted in
constipation Diagnostic Findings the colon)
 May be used to resolve cecal
Cecal Volvulus (affects the  Upper GI series - definitive volvulus
cecum) procedure for infants. It is what
 Young adults (most we also call the barium swallow Surgical Management
common) in which the client is asked to
 Abdominal mesentery didn’t take in the barium solution so Untwisting of the colon
develop normally that we will have a clear view  Attaching the intestine up
of the affected area.  against the abdominal wall to
Midgut Volvulus   Abdominal X-ray - shows a coffee prevent it from twisting
 Twisting of the small intestine, bean image Bowel resection - infarction
dueto abno dev of fetus  Barium enema - shows a bird's (removing the part of the colon
 Common in babies and small beak shape. which has the infarction due to the
children
volvulus)
ASCARIS BOLUS
 there is a ball of ascaris worms into the intestine = obstruction
 Ascaris lumbricoides is the largest of the intestinal nematodes affecting humans, measuring 15-35
cm in length in adulthood.
Pathophysiology:
“Fertilized eggs passed in feces = Infective larva develops within egg in soil = man ingests eggs in
food or soil = Intestine = Venous system = Lungs = Trachea = Esophagus = Adult worms in
intestine (live for 6-24 months = cause partial or complete bowel obstruction)”
“egg ingestion to new egg passage takes 9 weeks + 3 weeks needed for egg moting before capable of
infecting new host. Eggs are not shed in stool until roughly 40 days after the de of the pulmonary symp”
S/S Diagnostic Findings Surgical Management

 Asymptomatic at first   CBC= eosinophilia (due to parasites)  Milking of worms to the


large bowel-used to
Two categories:  Sputum Analysis = larvae Charcot- manage bowel
 Early phase (larva migration) Leyden crystals (collections of obstruction
 4-16 days after ingestion crystalloid composed of eosinophilic
 Respiratory symptoms may proteins, early pahse) Nursing Management
be non productive cough,
dyspnea, wheezing and  Stool exam = after 40 days= positive  Isolation, use STANDARD
fever PRECAUTION
 C- Leyden crystals  Chest x-ray = reveal patchy infiltrates  Proper disposal of stool
of eosinophilic pneumonia and soiled linens
 Late phase (mecha effects)  Monitor: vital signs, intake
 6-8 weeks after egg  abdominal radiography=signs of bowel and output, appearance of
ingestion obstruction = air-fluid levels or the stool
 GI symptoms “cigar bundle” appearance of a worm  Health teachings: proper
 Passage of worms (adult) bolus hand washing, bathing,
 Epigastric pain, N/V changing underwear and
 Pharyngeal globus  CT scan=linear/cylindrical filling bed linens and also proper
“tingling throat” (frequent defects in the presence of contrast in food preparation.
groups or masses,whirled appearance
throat clearing)

PERITONITIS
 Inflammation of the peritoneum (the serous membrane lining of the abdominal cavity and covering the
viscera)
 CAUSES: Bacteria Inf (common: e coli, klebsiella, proteus pseudomonas and streptococcus), Injury/
Trauma, Inflam from organ that extends to the cavity, Abdo surgical procedures/ peritoneal dialysis

S/S Pathophysiology
 Diffuse pain-constant-localized-more intense over
the site of pathologic process (site of the maximal  Leakage of contents from abdominal organs
peritoneal irritation) into the abdominal cavity( there is
 Abdomen- extremely tender and distended and inflammation,infection, ischemia, trauma, and
muscles become rigid tumor perforation) 
 Rebound tenderness and paralytic ileus  Bacterial proliferation occurs
 Diminished perception of pain (if peritonitis occur of  Edema of the tissues results, and exudation of
people receiving corticosteroids and analgesics) fluid develops in a short time
 Anorexia, nausea and vomiting  Fluid in the peritoneal cavity= turbid w/ high
 Peristalsis is diminished amounts of protein, WBC, cellular debris and
 Inc Temp & PR blood (the immediate response of the
 Hypotensive- progression of peritonitis intestinal tract is hypermotility, ff by paralytic
ileus with an accumulation of air and fluid in
Diagnostic Findings the bowel)

 CBC- = elevated WBC Surgical Management


 Serum electrolyte studies = altered K, Na, Ch
 Abdominal x-ray = air and fluid levels as well as Obj: Removing the infected material and correcting
distended bowel loops the cause 
 Abdominal ultrasound = abscess formation Excision (appendix)
 MRI- used for diagnosis and culture and sensitivity Resection with or without anastomosis (intestine)
studies of the aspirated fluid = infection and Repair (perforation)
identify the causative organisms. Drainage (abscess)- with extensive sepsis a fecal
diversion may need to be created, need to use CT
Medical Management scan
Common compli of surg:
 Fluid, colloid and electrolyte management- to Wound evisceration and abscess
prevent hypovolemia (hypovolemia occurs when formation
there is a massive amount of fluid and electrolyte
move from the intestinal abdomen into the Nursing Management
peritoneal cavity and depletes fluid into the vascular
space) Intensive care
 Analgesics - for pain  BP is monitored by arterial line if shock is
present
 Antiemetics - nausea and vomiting
 CVP or pulmonary artery wedge pressure and
 Intestinal intubation and suction - to relieve urine output are monitored frequently assist in
abdominal distention calculating fluid replacement
 Oxygen therapy by nasal cannula or mask  Ongoing assessment of pain, GI function and
 Intubation and ventilation (since peritonitis could fluid and electrolyte balance is important 
lead into septic shock)  Administer analgesic medications and
 Antibiotic therapy-broad spectrum positioning the patient comfortably to decrease
pain (patient is placed to the side with knees
o early treatment for peritonitis: large doses
flexed to decrease the tension of the
of antibiotic which is admins intravenously until abdominal organs)
there is a specific organism causing the infection  Administer and closely monitor IV fluids
and then we can give appropriate antibiotic to  Nasogastric intubation may be necessary
that client   Increase fluid and food intake gradually and
reduce parental fluids as prescribed 
Signs that indicates peritonitis is subsiding
POST-OP
 Decrease in temperature and pulse rate  Monitor and record the character of the
 Softening of the abdomen drainage
 Return of peristaltic sounds  Assist in moving and turning the patient to
 Passing of flatus and bowel movements prevent drains from being dislodged
 Patient and family discharge teaching for the
drains
PARALYTIC ILEUS
 intestinal blockage W/O actual physical obstruction
 caused by a malfunction in the nerves and muscles in the intestine that impairs digestive movement
 More on the functional obstruction

Causes Diagnostic Findings


 Abdominal X-ray = signs of trapped gas &
 Physiologic, neurologic or chemical imbalance obstruction
associated with decreased peristalsis from trauma  CT scan with contrast = signs of trapped gas and
or the effect of a toxin on autonomic intestinal the area of obstruction
control  Abdominal ultrasound
 Handling of the intestines during abdominal  More commonly used to identify an ileus
surgery or trauma  in children 
 Thoracic diseases MI, rib fracture and pneumonia  Barium enema
 Electrolyte imbalance - hypokalemia 
 Peritonitis- leakage of colonic contents = severe Medical management
irritation and triggers an inflammatory response  Nasogastric suctioning
 Intestinal ischemia- vascular insufficiency to the  Administration of intravenous fluid and correction of
bowel due to arterial/venous thrombosis or electrolyte imbalance
embolus decrease blood flow to the mesenteric  Treatment of underlying cause
blood vessels surrounding the intestines
(severe=bowel infarction) Nursing management
 Pain management
S/S  Monitor intake and output
 Abdominal cramping, Appetite loss  Measure abdominal girth (to check for distention or
 Feeling of fullness, Constipation
bloating)
 Inability to pass gas, Stomach swelling 
 Vomiting stool like content, Nausea  NG decompression monitoring
CONGENITAL AGANGLIONIC MEGACOLON / HIRSCHSPRUNG DISEASE
 congenital anomaly due to mechanical obstruction from inadequate motility of part of the intestine
 absence of ganglion cells in the myenteric plexus of Aurbach and submucosal plexus of Meissner
 bowel obs from anus and progresses upwards = bowel obstruction = colon enlargement
 part of the large intestine is unable to remove waste materials properly, which can lead to intestinal
blockage in the newborn
 ganglion signals the walls to relax = external sphincter contracts normally but the internal sphincter fails
to relax
 Common in males; autosomal dominant genetic mutations, associated w/ down syndrome

S/S Diagnostic Findings:


Newborn:
 Barium enema-demonstrates the transition between
 Abdominal distension, Vomiting, Constipation
the dilated proximal colon (megacolon) and the
 Failure to pass meconium within the first 48
aganglionic distal segment 
hours of life
 Rectal biopsy- Confirmatory test 
 Signs of acute intestinal obstruction
o surgically to obtain full thickness biopsy
specimen 
Older infants/ Children:
o Suction biopsy for histologic evidence of
 Abdominal distension relieved by rectal
absence of ganglion cells 
stimulation or enema
 Anorectal manometry
 Chronic constipation, Vomiting
o a catheter with a balloon attached is inserted
 History of delayed meconium passage
into the rectum 
 Ribbon like foul smelling stools (due to
o records the reflex pressure response of the
contracted part of the colon)
internal anal sphincter to the sanction of the
balloon 
Medical Management:
o Normal response- relaxation of the internal
 Stabilized fluid and electrolyte  sphincter followed by a contraction of the
 Administration of enemas frequently to external sphincter 
extract the stool that is obstructed 
Surgical Management Nursing Management:

Goal of Surgical Management  Perform a thorough history and physical exam 


 removal of the aganglionic portion of the  Check for frequency of bowel movements
bowel to relieve obstruction characteristics of stool (ribbon-like and foul smelling)
 Restore normal motility  and onset of constipation 
 Preserve the function of the external anal  teach the parents on how to correctly perform enema
sphincter and how it is prepared 
  Preoperative Care
 symptomatic treatment with enemas (low fiber,
Two stages:
high calorie, and high protein)
 severe (total parenteral nutrition)
1. Temporary ostomy
o Vital signs monitoring and bp for signs of
o created proximal to the aganglionic
segment to relieve obstruction and shock 
 -monitor fluid and electrolyte replacement, plasma
allow the normally innervated dilated
bowel to return to normal size  or other blood derivatives 
 -observed symptoms of bowel perforation 
 -measure abdominal girth to determine
2. Swenson, Duhamel, Boley, Soave procedure
o Soave Endorectal pull through progressive distention of the abdomen 
 -provide education and emotional support and
procedure is often performed and
having ostomies
consists of pulling the end of the
Postoperative Care
normal bowel through the muscular
 monitor I/O 7 IV fluids  (NGT to losses and stool
sleeve of the rectum from which the
from ostomy)
aganglionic mucosa has been removed
 diaper should be pinned below the dressing (foley
o Second complete corrective surgery 
catheter)
o Performed if the infant already weights
 perform abdominal assessment; monitor return of
9 kgs bowel sounds and
 passage of stool -perform ostomy care with the
parents guardian 
 explain to the parents of the function of
equipment attached to the infant (ostomy)
IMPERFORATE ANUS
 Congenital defect in which the opening to the anus is missing or blocked

Nursing Management S/S Types

 Monitor for signs and  No passage of stool within 24 to 48  Low level defect
symptoms of infection hours after birth  o Rectum descends through
 presence of an anal membrane  puborectalis muscle 
 
 missing or misplaced opening to the
 side lying with legs flexed o functional anal sphincters 
anus 
or prone   external fistula to the perineum or o no connection with the
GUT urinary tract 
 teach SO on how to take
temperature via axillary  High level defect
route  Surgical TX
o Rectum ends above
 Anoplasty + daily manual dilations
(Low level defect) puborectalis muscle it is
 Toilet training  ineffective 
 closing any small tube like o non-functional anal
 Karaya gum powder (onto openings (fistulas) creating an sphincters
the ostomies) anal opening and putting the
 Easy to use rectal pouch into the anal Tests
 absorbs moisture opening 
for better  Abdominal x-ray overview of the
 Temporary Colostomy anatomical location 
adhesion   closure: 6months - 1yr  abdominal ultrasound 
 Soothes and helps
 rectal thermometer is insert
to heal sore skin
and 
 alcohol free 
HEMORRHOIDS
 Presence of dilated portions of veins in the anal canal, common in men
 unnaturally swollen or distended veins in the anorectal region
 There is a shearing in the mucosa during defecation results in the he sliding of the structure in the wall
of the anal canal including the hemorrhoidal and vascular tissues
 The increased pressure on the hemorrhoidal tissue actually due to pregnancy Initiate hemorrhoids or
aggravate existing hemorrhoids

Degree of Prolapse Classification Causes


 Increased abdominal pressure
 First degree - does not prolapse and protrude into o Pregnancy, Constipation with straining,
the anal canal  obesity,HF, prolonged sitting or standing and
 Second degree - prolapses out of the anal canal strenuous exercise and weight lifting 
during defecation or straining but reduces  Decreased fluid intake
spontaneously  o Development of hard stools and
 Third degree - protrudes through the anus during subsequent constipation 
o straining while evacuating stool 
straining or evacuation but needs to be manually
return to position 
S/S
 Fourth degree - Irreducible and is at risk for Classic symptoms:
strangulation Bright red bleeding, prolapse, anal pruritus , pain 

Types Diagnostic Findings


Internal Hemorrhoids
 Located above the internal sphincter  INTERNAL
 Not usually painful and till it bleeds or prolapse  Digital rectal exam 
when they become enlarged   Anoscopy
External Hemorrhoids  sigmoidoscopy 
 Appears outside the external sphincter 
 severe pain from inflammation  EXTERNAL
 Edema caused by thrombosis (clotting of blood  Digital rectal exam and 
within the hemorrhoid)  visual inspection
Medical Management Non Surgical Treatment
 Infrared photocoagulation - probe contact area
 Apply cold packs to the anorectal region for few above hemorrhoid exposes the tissue to a quick
minutes at the beginning of the onset of pain and burst of infrared light = painlessly coagulates veins
tepid sitz baths 2-4 times per day to relieve as they enter the hemorrhoid = shrink and recede
discomfort   Bipolar diathermy- using the cautery to excise the
 witch hazel soaks- pain reliever  hemorrhoids
 topical anesthetics   Laser therapy- affix mucosa to underlying muscle 
o Ex. lidocaine (Xylocaine)-severe pain  Sclerotherapy
o Dibucaine (Nupercainal) ointment- mild to o Small bleeding hemorrhoids 
moderate pain and itching o injecting of sclerosing agent (5% phenol in
 Hydrocortisone for itching and inflammation  saline) into the base of a hemorrhoid to
 cleansing the anal area with moistened cleaning cause blood vessel thrombosis
tissues, dabbing rather than wiping   
 Diet- high fiber and fluids to promote regular Surgical Management
bowel movements without straining   Rubber band ligation -a rubber band is slipped in
 stool softeners -docusate sodium (Colace)- use the hemorrhoid = causes necrosis and sloughs off
temporarily the hemorrhoid
 Cryosurgical hemorrhoidectomy-freezing the
Nursing Management hemorrhoid = cause necrosis 
 ND YAG Laser- is useful in excising hemorrhoids
 Avoid irritating laxatives, spicy foods, nuts, coffee, particularly external hemorrhoid tags, this
and alcohol  treatment is quick and relatively painless
 Avoid sitting for long periods of time  o Hemorrhage abscess  is rare postoperative
 Oral analgesics for pain and thrombosed complication of ND Yag Laser
hemorrhoids    Stapled hemorrhoidopexy- newer procedure
 Prevention of constipation  o Uses surgical staples to treat prolapsing
 Fiber in the diet (Whole grains, nuts, raw F/V)
hemorrhoids and is associated with less
 drink plenty of water 
postoperative pain and fewer complications 
 remind to avoid straining at stool 
 Hemorrhoidectomy - resection/ removal of the
 exercise in moderation 
hemorrhoids
 Maintain a healthy weight
DIARRHEA
 An increased frequency of bowel movements more than three times a day
 there is an increased amount of stool which is 200 grams or more per day 
 there is an outward consistency of stool or an increase in liquidity
 the contents of major diarrhea move so rapidly through the intestine = inadequate time for the GI
secretions to be absorbed
 diarrhea is not a disease, but it is actually a symptom
 Watery stool - Small Bowel / Semi-solid - Large Bowel (colon can still absorb =semi-solid)

Classifications Five types


Chronic
 persists more than two to three weeks and may 1. Secretory
return sporadically - ass w/ bacterial toxins and neoplasms
- due: increased prod & secretion of the water
Acute  and electrolytes by intestinal mucosa
 most often ass w/ infection and usually self- 2. Osmotic
limiting, last up to 7 to 14 days only - water is pulled into the intestines by the
Nursing Resp: osmotic pressure = slowing the reabsorption
 encourage bed rest (caused by a lactase def, pancreatic dys)
 increased intake of fluids and food (low in bulk 3. Malabsorptive
until the acute attack subsides) - mechanical + biochemical actions=inhibit
 bland diet of semi-solid and solid foods absorption of the nutri= low serum albumin
 avoid caffeine carbohydrate drinks and very hot levels = intestinal mucosa swelling and liquid
and very cold foods (stimulates intestinal stool
motility) 4. Infectious
 restrict milk products, fat whole grain products, - Due to infectious agents invading the
fresh fruits and vegetables for several days intestinal mucosa (clostridium difficile is the
 Administer meds, IV (rapid rehydration) most common identified agent)
 monitor serum electrolyte levels  5. Exudative
 encourage to do perianal skin care - Due: tissue destruction by radiation or
 Check on discrete decrease turgor especially in chemotherapy
older clients and reduce subcutaneous fat layers - caused by a large usage of laxative
S/S Medical management

 abdominal cramps distension  control the symptoms


 borborygmus (rumbling noises due togas)  prevent complications until the definitive cause is
 anorexia , thirst discovered we need to control infection 
 painful spasmodic contractions of the anus  Medication: Antibiotics and anti-inflammatory
 tenesmus (ineffective or painful straining with a agents, anti-derical agents (loperamide, imodium
strong urge of defecation) which is very common) 
 severity of diarrhea (relate to F/E imbalances)  need to know first the cause because client might
end up having clostridium difficile infection
Diagnostic findings
Nursing management
 stool examinations for infectious or parasitic
organisms or bacterial toxins  assess and monitor the characteristics and pattern
 blood fat electrolytes and white blood cells   complete health history (meds, food, med/surg
 endoscopy or barium enema to assist in identifying history)
the cause of diarrhea so these are used if the  report any recent acute illness or recent travel to
cause of that diarrhea is not obvious another geographic area
 assess the abdomen of the client so we need to
Complications auscultate first and then palpate
 for any tenderness - inspect mucous membranes
 cardiac dysrhythmias (due to significant fluid loss to check the hydration status
in electrolyte esp potassium)  obtain stool exam to test what are the possible
 loss of the bicarbonate with diarrhea=metabolic cause it might be bacterial or viral causative
acidosis agents 
 check on the urinary output of the client again  assess for skin exfoliation
 skin care issues because with chronic diarrhea
related to irritant dermatitis
CONSTIPATION
 abnormal infrequency or irregularity of the defecation 
 an abnormal hardening of the stools that makes their passage difficult and sometimes painful
 there is a decrease in stool volume and there is a retention of stool in rectum for a prolonged period
that often with a sense of incomplete evacuation after defecation
 S/S: persistent sensation of abdomen abdominal fullness
 constipation is not a disease but its a symptom

Causes S/S
 Meds: Anticholinergic, Antidepressants anti-  fewer than three bowel movements per week
hypertensives, diuretics and opioids (side effects)  abdominal distension 
 erectile or anal disorders (hemorrhoids & fissures)  pain & pressure on the lower abdo & rectum 
 obstructions (vowel tumors)   decreased appetite, headache, fatigue 
 metabolic and neurologic, neuromuscular conditions  indigestion
(sprong disease, parkinson's parkinson's disease,  sensation of incomplete evacuation and straining
endocrine disorders: hypothyroidism, at stool and elimination of small volume lumpy
pheochromocytoma, lead poisoning and connective hard and dry stools that req manual removal
tissue disorders such as SLE)
 weakness immobility debility fatigue and inability to Complications
increase intra-abdominal pressure to facilitate the
passage of stools (emphysema, spinal cord injury)  Hypertension - due to straining
 not taking time to defecate or ignoring the urge to  Fecal impaction - feces cant expelled= manual
defecate = rectal mucous membrane and the removal
musculature becomes insensitive to the presence of
 Hemorrhoids - passage of perianal vascular
the fecal masses = reqs stronger stimulus
congestion causing by straining
consequently required to produce the necessary
 Anal fissures - hard stool = tears anal lining
peristaltic rush for defecation and
 Mega pollen
 aging = decrease in muscle tone
- common in infants & adults
 dietary habits (low consumption of fiber or water)
- a dilated anatomic colon caused by fecal
 lack of regular exercise and stress
mass that obstructs the passage of the
colon contents
Management Nursing management

 sit onto the toilet with legs supported and to utilize  Inform how to defecate properly
the gastrocolic reflex  emphasize importance of responding to the urge to
 following a meal and warm milk, gastrocolic defecate 
reflex it is the peristaltic movement of the large  describe how to establish a bowel routine
bowel occurring 5-6 times daily that are triggered  Best time to defecate is after meal
by this tension of the stomach  provide dietary information: suggest eating high
 not recommended: 90 degree angle in sitting into residue high fiber foods such as fruits and
the toilet, you need to have a 35 degree angle, vegetables, adding bran daily must be introduced
(can really push right) gradually and increase fluid intake unless
 routine exercise to strengthen abdominal muscles. contraindicated to the client
 Biofeedback helps to relax the sphincter  explain how to exercise, increased ambulation and
mechanism to expel stool. abdominal muscle toning = increase muscle
 25 to 30 grams of fiber per day strength and help propel colon contents
 Laxatives: bulk forming agents (fiber laxatives  describe abdominal toning exercises to contract
saline and osmotic agents, lubricants and the abdominal mass muscles like 4 times daily and
stimulants and fecal softeners) leg the chest lip lifts 10 to 20 times each day to
prevent constipation 
long-term laxative   normal position in defecating is semi-squatting
 bulk forming + osmotic
= maximizes the use of the abdominal muscles
 laxative (not overuse= rebound effect)
and force of gravity 
Enemas and rectal suppositories   Educate patients to avoid overuse of stimulant
 not recommended for treating constipation laxatives because it will result constipation.
unless there is rectal evacuation.

Glycerin suppository
 first line therapy ff by sakodal suppositories and
mini-enemas.
Module 4M: Disturbances in Glucose Metabolism

Carbohydrate metabolism - summary of all processes.

Pancreas
 Plays a big role in digestion. 
 It is located inside our abdomen just behind our stomach. It is about the size of our hand. 
 During digestion, our pancreas makes pancreatic juices called enzymes. These enzymes break down sugars, fats, and
starches. It also helps our digestive system by making hormones - these are chemical messengers that travel to our
blood. 
 Pancreatic hormones help regulate our blood sugar levels and appetite. It stimulates stomach acid and tells the
stomach when to empty. It has two fxns: exocrine and endocrine. Exo= ducts, endo=blood.
 The bulk of the pancreas is composed of exocrine cells that produce enzymes to help with the digestion of food. These
exocrine cells/ acinar cells release their enzymes into a series of progressively larger tubes called ducts that eventually
join together to form the main pancreatic duct. The main pancreatic duct runs the length of the pancreas and drains the
fluid produced by the exocrine cells into the duodenum.
 The second fxnal component of the pancreas is the endocrine pancreas. It is composed of small islands of cells,
called the islets of langerhans. They don’t release their secretions into the pancreatic ducts, instead they release
hormones such as insulin and glucagon into the bloodstream and help control blood sugar levels.
 The pancreatic islets are small islands of cells that produce hormones that regulate blood glucose levels. Hormones
produced in the pancreatic islets are secreted directly into the blood flow by five different types of cells. The endocrine
cells subsets: alpha, beta and delta cells. Other two types of cells in the pancreas (more on exocrine fxns): Gamma and
epsilon cells
 Gamma cells produce pancreatic polypeptides and make up 3 to 5% of the total islet cells. Pancreatic polypeptide
regulates both the endocrine and exocrine pancreatic functions or secretions. 
 Epsilon cells that produce ghrelin and make up less than 1% of total islets cells is a protein that stimulates hunger.
ALPHA CELLS
 Produces glucagon and makes up 15-20% of total islet cells. It is a hormone that raises blood sugar levels by stimulating
the liver to convert glycogen into glucose. 
  It is the first endocrine cell inside the islet of langerhans. 
 Secretes glucagon to increase blood glucose levels.
 It undergoes:
Glycogenolysis - glycogen to glucose
Gluconeogenesis - a non carb is turned into glucose
Lipolysis - fat breakdown & ketone formation.
Types of Pancreatic Cells:
 ALPHA CELLS 
 BETA CELLS 
o Only cells in the body w/ natural capacity to make insulin = last and only hope for regulating blood glucose levels
on its own
o secretes insulin and amylin 
o Make up 65%-80% of the total islet cells 
o Insulin lowers blood glucose levels by stimulating cells to intake glucose = enhances membranes transport of
glucose, responsible for a disease and important for treatment
 Main task: help turn food into energy. After food is eaten, carbs are broken down  in the sugar glucose,
then enters blood stream for distribution
 Key that opens the cell to glucose 
 Insulin is a hormone and a protein (manufactured in the body using information in the genes
o Amylin slows gastric emptying, prevents spikes of blood glucose levels 
o Exemptions: This is because these cells don't use GLUT4 for importing glucose, but rather, another transporter
that is not insulin-dependent.

 brain - Blood brain barrier stops insulin from entering in the brain
 Liver -
 intestinal mucosa - 
o Glycogenesis = glucose= glycogen - stored energy

 Primary digested is carbs, second is fats and third is proteins


 Somatostatin - balances production of insulin and glucagon
 Glucose is liberated from dietary carbs (starch or sucrose) from hydrolysis in the small intestine =absorbed in the blood 
 Elevated of concentrations of glucose in the blood stimulates release of insulin = acts on the cells for the uptake and
utilization and storage of glucose 
 Effects of insulin in glucose vary, depending on the target tissue
o Important effect: Facilitates entry of glucose into muscle, adipose and several tissues
 There are some tissues that don't require insulin for uptake of glucose (examples: brain, liver and intestinal
mucosa) because theses cells don't use GLUT4  for importing glucose, rather another transporter not insulin
dependent 
 Role of insulin (key) : NO INSULIN = NO GLUCOSE = NO ENERGY (indirectly proportional (one incr =
one dec vice versa)
o The process must drive with other metabolic & endocrine  processes in the body to attain optimum function 
 Hyperinsulinism = increase uptake of glucose = hypoglycemia
 Hypoinsulinemia = hyperglycemia
 If entire pancreas is damaged= transplant 
 Insulin facilitates entry of glucose into muscle, adipose and several other tissues. The only mechanism
by which cells can take up glucose is by facilitated diffusion through a family of hexose transporter. in many
tissues - muscle being a prime example - the major transporter used for uptake of glucose (called GLUT4) is made
available in the plasma membrane through the action of insulin.

When insulin concentrations are low, GLUT4 glucose transporters are present in cytoplasmic vesicles, where they are
useless for transporting glucose. Binding of insulin to receptors on such cells leads rapidly to fusion of those vesicles with
the plasma membrane and insertion of the glucose transporters, thereby giving the cell an ability to efficiently take up
glucose. When blood levels of insulin decrease and insulin receptors are no longer occupied, the glucose transporters are
recycled back into the cytoplasm.

NORMAL PHYSIOLOGY OF INSULIN AND ITS EFFECTS ON TYPE 1&2 DIABETES

- Prolonged depolarization of insulin 


Fasting Plasma Oral Glucose Tolerance Glycosylated Hgb
Glucose (FPG) g/dl Test (OGTT) mg/dl (HbA1C) %

Normal <100 <140 <5.7

Prediabete 100-125 140-199 5.7-6.4


s

Diabetes 126 or higher 200 or higher 6.5 or higher

Target= Customized/Individual
eAG/A1C
 Average of glucose levels 24H/day
 A1C-extending to within 2-3 months
 Helps us manage diabetes by confirming self test results by the physician, judging whether a treatment plan is working,
showing how a healthy choice can help in diabetes control

A1C (if higher=diabetes) eAG

% mg/dl mmol/L

6 126 7.0

6.5 140 7.8

7 154 8.6

7.5 169 9.4

8 183 10.1

8.5 197 10.9

9 212 11.8

9.5 226 12.6

10 240 13.4

Carbohydrate Metabolism
 Sum of the anabolic and catabolic processes of the body involved in the synthesis and breakdown of CHO (principally:
glucose, fructose, and galactose)

 Symptoms of CHO deficiency: fatigue, depression, electrolyte imbalance and body protein breakdown

20:59
Types of CHO
 Simple (Monosaccharides)
 is any of the basic compounds that serves as a building block of carbohydrates.
 The term sugar can refer to both monosaccharides and disaccharides.
 Monosaccharides are the simple sugar, since they are the most fundamental type of sugar or glucose.
 This means that they cannot be broken down any further into simpler sugar by hydrolysis.
 Nevertheless monosaccharides can combine with each other to form more complex types.
 Glycosidic bonds also called glycosidic linkages are the covalent bonds that join the monosaccharides.

Examples: 
1. Glucose: blood sugar, Major fuel of the body.
2. Fructose:  from fruit sugar
3. Galactose: from milk sugar

 These are all readily absorbed by the small intestines, and because of their  structure they are also the hexoses.
 monosaccharides perform vital biological roles. Just like other carbohydrates are an important source of nutrition.
 They are consumed and metabolized to derive metabolic energy and ATP that fuels various biological activities. 

Simple Disaccharides
 are composed of two monosaccharides joined together by the glycosidic bond or glycosidic linkage.

Maltose:
 Glucose + Glucose
 sweetener, a nutrient in infant feeding in bacteriological culture media, 
 Also used in pastries it makes bread dough rise when CO2 is produced and released during the conversion of starch into maltose by
reacting the starch with enzymes. 

Sucrose: 
 Glucose + Fructose combined in condensation reaction. 
 Digested or broken down into its monosaccharide units through hydrolysis, with the help of enzyme sucrose.
 sucrose is extracted from plants (sugar cane/ sugar beets) and processed to a refine to be marketed as a common cable sugar. 
 used as a sweetening agent in food and beverages.

Lactose
 Glucose + Galactose
 is produced naturally and is present in milk of mammals including humans.
 It is collected from Bovine to be used in preparing infant formulas. 
 a cow's milk has a particular about 4.7% of lactose.
 people who are lactose intolerant cannot digest or breakdown lactose, this becomes food for gas producing flora, this could lead to
GI disturbance and flatulence.
 Lactose can be converted into lactic acid.
 microorganisms such as lactobacilli  can convert lactose to lactic acid which is used in the food industry. 
 An example is the production of dairy products like yogurt and cheese.

The second category under the types of carbohydrates is COMPLEX CARBOHYDRATES.

Disaccharides:
 made up of 2 monosaccharides

Oligosaccharides:
 made up of more than 2 monosaccharides
 has shorter chains than polysaccharides.

Polysaccharides:
 are a type of macromolecule composed of monosaccharides units.
 multi saccharides: cellulose, starch and glycogen

 Simple sugars are transported to the cells of other tissues, specially to the liver and bloodstream.
 The glucose in the blood may be utilized by the body to produce ATP, otherwise it is transported in the liver together
with the galactose and fructose which are largely converted into glucose for storage as glycogen.

Glycogen:
 Storage form of energy in the body, made up of glucose units in the liver, muscle cells and fat cells for later use.

 The remaining carbohydrates not absorb by the small intestine, enter the large intestine, the got flora in the colon
metabolizes them anaerobically, example: fermentation as such this leads to production of gases.
 Like hydrogen, CO2 and methane and fatty acids such as acetate and mucirate that immediately metabolize the body.
The gases in the turner excreted via breathing them out erruptation or burping or flatulence.

 To conclude, carbohydrate metabolism is one of the fundamental or basic biochemical processes in our body, it enables
us to perform our daily activities as it constantly supplies our living cells with energy.  

Glucose metabolism
Glycolysis = glucose (enters cytoplasm) = 2 pyruvate = 2 atps and electrons
Rbc (don’t have mitochondria) - pyruvate changes to lactate (anaerobic process)
Cells with mitochondria + oxygen, pyruvate will transfor in to acetyl Co-a, enter krebs or citric
cycle = electrons and 2 atp = Oxygen will enter oxydative phosphorylation (30-34 atp will be
produced)
Increase # of atps = acetyl co-a will not enter krebs cycle, convert to fatty acids
Type 1 = autoimmune, destroy insulin cells = body doesn’t produce insulin during intake of
carbs = glucose cant get in cells = body compensate thru kidneys = increase urination = thirsty
, urine contains glucose (med for bacterial = thrush or genital itching), blood contains glucose=
wounds heals slowly, blurred vision, lethargic, fatigue. Body destroy fats = weight loss, glucose
builds up in the front of the eye =liq in the lens to become cloudy= blurred vision,

Type 2 (90% of cases) common in over 40 in white, 25 in asian, either body isnt prod insulin
enough or insulin isnt working properly =overweight. Glucose cant get in the cells because filled
with fats = body prod insulin and glucose, cells needs energy and release sotred insulin = cant
cope anymore and wears out, s/s : come slowly and asymptomatic , lvie for 10 yrs before thery
realize they have it . needs exercise and food, progressive condition=needs meds

 Cbs sliding scale - capillary blood sugar - guide for injecting insulin, found in the doctor order’s sheet
 NPH (neutral protamine hagedorn (cloudy
 Humulin R (clear)
 Clear to cloudy to prevent mixing of insulin
 Insulin injection log - sheet for writing the amount , site, blood sugar level, date and time
 Medical management goal: restore or manage glucose levels at the normal level
 Nursing maangement goal: empowerment
 Normal blood glucose level for a nondiabetic based on ADA, 2021: 60-100mg/dL

● Diabetes Mellitus
● Diabetic Ketoacidosis
● Hyperglycemic Hyperosmolar nonketotic Syndrome =hypoglycemia
● Hypoinsulinism
● Hypoglycemia
Adrenergic =epi increases=shakiness, nervousness, hunger, diaphoresis, pallor
Neuroglycopenic= confusion,headache, mental illness, inabiltiy to concentrate, slurred speech
and vision, lethary, severe drowsiness,

Type 1: juvenile
Type 2: adult onset

Lipid profile or panel - fats is related form glucose uptake (risk for atherosclerosis)
Type 1: juvenile, abrupt or sudden onset, little or no insulin, mostly thin, prone to ketosism 3 p
+fatigue + weight loss

Type 2: adult onset, lead to HHNS (hyperglycemic, hyperosmolar non ketotic syndrome)

Maintstay therapy for DM: diet,exercise, insulin for type 1


Type 2: diet exercise, oral hypoglycemics
Cornerstone or important or basic
Suldo -stimulate beta cells to function and decrease glucose prod in the liver (-nase)
Biguanides - increase sensitivity of tissues and fats (metformin)
Alpha glucosidase inhibitors - inhibits or delay dig of complex carbs (ends with ose
Thiazolidinediones - increase insulin action at receptor sites (glut 4) (example avandia)
Meglitinides - stimulate insulin secretion by closing the potassium channels in the beta cells (ex.
Prandin)
Incretin - newest form, met hormone stmulate decreasing blood glucose levels, stimulate
insulin secretion with glycogen (sitagliptin, linagliptin

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