Kidney: Disorders of The

Download as pptx, pdf, or txt
Download as pptx, pdf, or txt
You are on page 1of 52

DISORDERS of the

KIDNEY
CHOLECYSTITIS
CHOLECYSTITIS

§ Inflammation of the gallbladder; usually


caused by the presence of stones
(cholelithiasis) which are composed of
cholesterol, bile pigments and calcium
RISK FACTORS

§ Female
§ Fat
§ Fortys
§ Multiparous State
CLINICAL MANIFESTATIONS

§ URQ Pain, radiating to the back


§ Dyspepsia
§ Nausea
§ Vomiting
§ Fever
§ Elevated WBC
§ Jaundice (25% of cases)
§ Murphy’s Sign
DIAGNOSTIC TESTS

§ Serum Billirubin
§ UTZ
§ Gallbladder series
§ Intravenious Cholangiogram
MEDICAL MANAGEMENT

§ Bedrest
§ Nasogastric Suctioning
§ Narcotics
§ Antispasmodics and Anticholinergics
§ Antibiotic therapy
§ Lithotripsy
SURGICAL MANAGEMENT

§ Cholecystotomy
§ Abdominal Cholecystectomy
§ Laparoscopic Cholecystectomy
§ Choledochotomy
NURSING CONSIDERATIONS

§ Ax for pain
§ Ax for abdominal rebound tenderness that
increases with inspiration
§ Ax stools; clay-colored and steatorrhea
§ Ax Urine for dark color
§ Instruct pt on Low fat diet
§ Observe for signs of bleeding
ACUTE and CHRONIC

GLOMERULONEPHRITIS
ACUTE GLOMERULONEPHRITIS

§ active inflammation in the glomeruli


§ Results in proliferation and inflammation
within the glumerular structure
§ Usually starts w/ an infection.
2 FORMS

§ Infectious
§ Post-infectious
PATHOPHYSIOLOGY

Glomerulus
Antigen membrane Scarring
thickens

Antigen- Leukocytes
Glomerulo
Antibody infiltrate
Product glomerulus nephritis

Deposits Increase in
into the epithilial
Glomerulus cell lining
CLINICAL MANIFESTATIONS

§ Fever § Abd’l/Flank Pain


§ Chills § Headache
§ Weakness § Severe HPN
§ Pallor § Oliguria or even Anuria
§ Anorexia § Ascites
§ N/V § Pleural Effusion
§ Generalized Edema § CHF
(facial and peri-orbital)
DIAGNOSTICS

§ UA (Scanty and smoky or cola-colored)


§ Urine pH is low
§ Serum Crea and BUN is
§ ASO Titer is
MEDICAL MGMT.

§ Plasmapheresis
§ Antibiotic therapy (Penicillin)
§ Diuretics
§ Antihypertensives
§ Corticosteroids
OTHER MGMT.

§ DIET: Increase CHO, Decrease CHON, Na and


fluid intake
§ Bedrest
NURSING RESPONSIBILITIES

§ Ax of Pt’s Hx
§ Recent URI or Skin Infection
§ Hx of Glomerulonephritis
§ Close monitoring of Urine
§ VS monitoring
§ Maintain prescribed Diet
§ Monitor I/O and Daily Wt.
§ Daily measurement of edematous parts
§ Restrict Fluid intake
CHRONIC GLOMERULONEPHRITIS

§ Characterized by inflammation, sclerosis,


scarring and eventually renal failure
§ Usually remains undetected til the
progressive phase which is usually irreversible
§ characterized by irreversible and progressive
glomerular and tubulointerstitial fibrosis,
ultimately leading to a reduction in the
glomerular filtration rate and retention of
uremic toxins.
PATHOPHYSIOLOGY
Sclerosis of Dec.
Unknown glomeruli Kidney
and tubules Size

Fibrous and
scar tissue
Renal Sclerosis of
replace
blood
Dsyfxn non-
vessels
functioning
renal tissue
SIGNS and SYMPTOMS

§ HPN § Metallic taste in mouth


§ Edema § Yellow-gray skin
§ Wt. loss, malaise § Polyuria
§ Mental cloudiness § Nocturia
§ Headache; dizziness § UA = albuminuria,
hematuria
COMPLICATIONS

§ Epistaxis
§ Arteriosclerosis
§ Cardiomegaly
§ Hemmorhage in the kidneys, lungs and retina
MEDICAL MGMT.

§ Dialysis
§ Transplant
§ Anti-inflammatory agents
NURSING RESPONSIBILITIES

§ Control Edema and HPN


§ Dec. Fluid intake
NEPHROTIC SYNDROME
NEPHROTIC SYNDROME

§ Damage in the kidneys resulting to increased


permeability of the glomerular membrane to
plasma CHON resulting in massive CHON loss
in nephrons (20x more than normal)
§ Often caused by any group of diseases that
damages the glomerulus
CAUSES

§ Amyloidosis
§ Congenital Nephrosis
§ Glomerular Sclerosis
§ Glomerulonephritis
§ IgA Nephropathy
§ Pre-eclampsia
CLINICAL MANIFESTATIONS

 3 MAIN Symptoms
 Hypoalbuminemia
 Anasarca
 Hyperlipidemia

 Loss of Appetite
 Fatigue
DIAGNOSTICS

 BUN/Crea.
 UA
NURSING RESPONSIBILITIES

 Reduce Albuminuria and control edema


 Administer cortecosteroids, diuretics and
antibiotics
 Prevent infection
 Restrict Na Intake
 Bedrest
 Prevent prolonged immobility
RENAL TRAUMA
RENAL TRAUMA

 Most renal trauma occurs as a result of blunt


trauma.
 Renal injuries may be generally divided into 3
groups:
Renal laceration
Renal contusion
Renal vascular injury
ETIOLOGY

 Penetrating
 (eg, gunshot wounds, stab wounds)
 Blunt
 (eg, pedestrian struck, motor vehicle crash, sports, fall)
 Iatrogenic
 (eg, endourologic procedures, extracorporeal shock-wave
lithotripsy, renal biopsy, percutaneous renal procedures)
 Intraoperative
(eg, diagnostic peritoneal lavage )
 Other
 (eg, renal transplant rejection, childbirth)
CLASSIFICATION
GRADE INJURY
Renal contusion; non-expanding
1 subcapsular hematoma

2 Laceration < 1 cm in depth sparing


the renal medulla and collecting
system; non-expanding
retroperitoneal hematoma
Laceration > 1 cm sparing the
3 collecting system
Laceration > 1 cm involving the
4 collecting system; renal vessel injury
with hemorrhage
Shattered kidney or avulsed renal
5 vessels
CLINICAL MANIFESTATIONS

 Hematuria
 Lumbar and Abd’l Pain
 Abd’l tenderness
 N/V
 Shock
MANAGEMENT

 Depends on extent/grade of injury.


 Bedrest
 Antibiotics
 Surgery
ACUTE and CHRONIC

RENAL FAILURE
RENAL FAILURE

 Inability of the kidneys to fxn


 State of total or nearly total loss of the
kidneys ability to excrete waste products and
balance body fluids and electrolytes
 TYPES:
 Acute
 Chronic
Acute RENAL FAILURE

 Sudden and almost complete loss of


glomerular and/or tubular function
 Usually follows direct trauma to the kidneys
or overwhelming physiologic stress (burns,
septicemia, blood transfusion reaction,
nephrotoxicity)
 Usually reversible
CAUSES

 Pre-renal (Impaired blood flow)


 Intra-renal (Damage to kidneys)
 Post-renal (Obstructed urine flow)
CLINICAL PHASES
 Period of Oliguria  Recovery Phase
 1-3 weeks  3-12 months
 Urine 400-600 ml/day  Avoid nephrotoxic
 Anuria ( < 100ml/day)
drugs
 Azotemia
 Edema, HPN
 Diuretic Phase
 1 week
 Polyuria (3-5L/day)
 Azotemia
 HPN
 Metabolic Acidosis
 Hypokalemia
CLINICAL MANIFESTATIONS
 Lethargy  Elevated
 Drowsiness  BUN
 Irritability
 Crea
 Anorexia
 Potassium
 Tingling Extremities
 Decreased
 Oliguria
 Restlessness
 Calcium
 N/V  Sodium
 Pallor  pH
 Fector Hepaticus  Anemia
 Anasarca  Albuminuria
 Deep and rapid breathing
MEDICAL MGMT.

 Direct treatment of underlying cause


 CBR
 DIET: Dec. CHON, Fat, Na, K, H2O
 Frequent Monitoring of VS and I/O
 Antibiotic therapy as prescribed
 Dialysis
 Kidney transplant
NURSING RESPONSIBILITIES

 Monitor I/O and VS


 Limit OFI
 Observe for signs of Overhydration
 Monitor for hyperkalemia and hyponatremia
 Provide rest periods
 Protect from injury
 Administer antibiotics
 Encourage proper diet
Chronic RENAL FAILURE

 Kidney is no longer capable of maintaining an


environment consistent with life
 Irreversible
 Results in uremia
ETIOLOGY

 Renal disorder
 Systemic Dse.
 Nephrotoxins
STAGES of CRF

 Decreased Renal Reserve ( 40%-50% Kidney


Fxn)
 Renal Insufficiency ( 20%-40% Kidney Fxn)
 Renal Failure (10%-20% Kidney Fxn)
 ESRD (<10% Kidney Fxn)
CLINICAL MANIFESTATIONS

 Lethargy/Drowsiness  Decreased serum pH


 Headache  HPN
 Nausea  Kussmaul respirations
 Pruritus  Uremic Frost
 Vomiting  Convulsions
 Mental Clouding  Coma
 Anemia  Death
DIAGNOSTICS

 UA
 Blood Exam
 CBC
 Blood Chem.
 Serum Electrolytes
 Renal UTZ
MEDICAL MGMT.

 Fluid and Na restrictions


 Antihypertensive meds.
 Recombinant human erythropoietin
 Dialysis
 DIET: Low CHON, Controlled K
 Kidney Transplant
NURSING RESPONSIBILITIES

 Monitor I/O and VS


 Provide Skin care
 Weigh pt. everyday
 Assess edema
 Provide care for pt undergoing dialysis
THE END

You might also like