Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
35 Cards in this Set
- Front
- Back
Renal Function
|
1. Excrete Waste
2. Regulate Water and Sodium Balance 3. Acid-Base Balance 4. Secretion of hormones |
|
Blood Urea Nitrogen (BUN)
|
Amount of nitrogen in the blood that comes from urea.
Urea is normally excreted. |
|
Creatinine
|
Breakdown product of creatine phosphate in muscle.
Excreted by kidneys at a constant rate. |
|
Azotemia
|
Elevation of BUN and Creatinine levels due to DECREASED GFR
|
|
Uremia
|
Urea retained in the blood.
|
|
Measuring Renal Function
|
Plasma BUN, Creatinine, pH, Electrolytes
GFR rate=Creatinine clearance test |
|
Glomerular diseases
(Glomerulonephritis) |
Usually Immune-Mediated
2 Types: 1. Circulating Immune Complex Nephritis 2. Immune Complex Nephritis in situ. |
|
Circulating Immune Complex Nephritis
|
Deposition of circulating antigen-antibody complexes in the glomeruli
|
|
Immune Complex Nephritis in situ
|
Antibodies are directed against components of the glomerulus
|
|
Nephrotic Syndrome
|
MASSIVE PROTEINURIA
Generalized edema (decreased osmotic pressure) Hyperlipidemia and lipiduria In kids, usually associated with minimal change disease. |
|
Lipoid Nephrosis
Minimal Change Disease |
Manifests in young kids
Diffuse loss of foot processes, associated with loss of foot processes and nephrotic syndrome. 90% respond to CORTICOSTEROIDS |
|
Membranous Glomerulonephritis
Membranous Nephropathy |
Characterized by immunoglobulin deposits along the GLOMERULAR BASEMENT MEMBRANE.
85% Idiopathic Glomeruli become SCLEROSED and HYALINZED Don't respond to corticosteroids |
|
Nephritic Syndrome
|
Characterized by:
Hematuria Oliguria Azotemia Hypertension INFLAMMATORY INFILTRATE AND GLOMERULAR CELL PROLIFERATION This leads to CAPILLARY DAMAGE |
|
Poststreptococcal Glomerulonephritis
|
Presents after recovery from Group A beta-hemolytic strep
Usually recovery is complete, but can progress to CRESCENTIC GLOMERULONEPHRITIS |
|
Crescentic Glomerulonephritis
(Rapidly Progressive Glomerulonephritis) |
Presents with glomerular crescents and rapid loss of renal function
Crescents are monocytic infiltrate within Bowman's space 90% NEED A RENAL TRANSPLANT |
|
Crescentic Glomerulonephritis Type I
|
GOODPASTURE SYNDROME
Autoantibodies against Glomerular Basement Membrane (also Alveolar Basement Membrane) |
|
Crescentic Glomerulonephritis Type II
|
Complication of an immune complex nephritis
Infection or Systemic Lupus |
|
Crescentic Glomerulonephritis Type III
|
Pauci (less) Immune
Most have anti-neutrophil cyctoplasmic antibodies (ANCA) May be involved with Wegener's Granulmatosis |
|
IgA Nephropathy
|
Berger Disease
Deposition of IgA into the mesangium MOST COMMON GLOMERULAR DISEASE IN THE WORLD Gross hematuria 1-2 days after URT, GI, or UT infeciton |
|
Chronic Glomerulonephritis
|
End stage of several diseases.
Important cause of renal failure. Kidneys are symmetrically contracted with scarring and hyalinization. Secondary Hypertension, proteinuria, and azotemia Treatment=Transplant or dialysis |
|
Acute Pyelonephritis
|
Kidney Infection
Often associated with a UTI (E. coli is common) Pus and abscess formation in renal pelvis and calyces (pyonephrosis) PYURIA, bacteriuria, dysuria, polyuria |
|
Chronic Pyelonephritis and Reflux Nephropathy
|
UNEVEN scarring of kidneys and papillary blunting.
Usually caused by: 1. Obstructive lesions with recurring pyelonephritis 2.UTI infections with bladder and kidney reflux |
|
Acute Tubular Necrosis (ATN)
|
MOST COMMON CAUSE OF ACUTE RENAL FAILURE
Associated with disturbances in blood flow or toxic tubule injury. Caused by: Trauma, septicemia, poisons, drugs |
|
Progression of ATN
|
Initiating Phase: Slight decline in urine output with a BUN rise for 36 hours
Maintenance phase: Severe drop in urine output that lasts a few days to a few weeks. Recovery Phase: Steady increase in urine volume, but patient is susceptible to infections and electrolyte imbalances. |
|
Drug Induced Interstitial Nephritis
|
Acute Drug-Induced intersitial Nephritis
Analgesic Nephropathy |
|
Acute Drug-Induced Intersitial Nephritis
|
HYPERSENSITIVITY REACTION
Antibiotics, NSAIDS, thiazides, cimetidine. Characterized by: Fever, eosinophilia, rash, renal problems NOT DOSE RELATED Withdrawal of drug usually leads to recovery |
|
Analgesic Nephropathy
|
Chronic interstitial inflammation and papillary necrosis associated with large doses of analgesics.
Acetaminophen (tylenol) and aspirin. Typically occurs in patients with preexisting renal disease. |
|
Diseases Involving Blood Vessels
|
Malignant Hypertension
Autosomal Dominant (adult) Polycystic Kidney Disease Urolithiasis (renal Stones) Hydronephrosis |
|
Malignant Hypertension
|
Diastolic pressure >120 mmHg
Rapid Kidney Failure due to ISCHEMIA 90% of deaths due to uremia |
|
Autosomal Dominant (adult) Polycystic Kidney Disease
|
Multiple expanding cysts in both kidneys which destroy the renal parenchyma
SEVERE FLANK PAIN, intermittent gross hematuria, enlarged kidneys End-stage renal failure at about age 50 |
|
Urolithiasis (Renal Stones)
|
75% made of CALCIUM OXALATE
Hypercalcemia may be due to increased absorbtion or defective renal reabsorption SMALL STONES CAUSE RADIATING PAIN and hematuria |
|
Hydronephrosis
|
Dilation of renal pelvis and calyces with parenchymal atrophy caused by an OBSTRUCTION
|
|
Kidney Tumors
|
Renal Cell Carcinoma
Transitional Cell Carcinoma |
|
Renal Cell Carcinoma
|
80-90% of malignant renal tumors
Increase in smokers, cadmium exposure, and acquired polycystic diseases. Flank pain and hematuria Lung and Bone Metastases my be initial presentation |
|
Transitional Cell Carcinoma
|
Malignant BLADDER tumor
Painless Hematuria Smoking and industrial Solvents 5-year survival is 20% |