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;
74 Cards in this Set
- Front
- Back
Type I RTA
(a) defect (b) effect (c) causes (d) treatment |
(a) Various defects leading to inability to secrete H+ (basol HCO3/CL exchanger, cytoplasmic CA< apical H+ATPase or H+/K+ATPase, basolat K/Cl transp, reduced titratable buffers)
(b) urine pH >5.5; hypokalemia (c) amphoterecin, light chains in multiple myeloma (d) oral admin of HCO3 |
|
Type II RTA
(a) defect (b) effect (c) causes (d) treatment |
(a) Defect in proximal tubule reabsorption of HCO3 (Na/HCO3 transporter or BB CA or generalized defect in PT -Fanconi's or protein overload toxicity))
(b) Urine pH initially >5.5 due to loss of filtered HCO3; when serum HCO3 equal to threshold, the PT tubules reclaim HCO3 causing urine pH to drop; hypokalemia may occur (incr Na+ presentation at DT) (c) carbonic anhydrase inhibitors, primary hyperparathyroidism, proximal tubule nephrotoxic drugs/chemicals (aminoglycosides, heavy metals) (d) thiazides to produce volume depletion which incr renal threshold for HCO3 reclamation |
|
Type IV RTA
(a) defect (b) effect (c) causes |
(a) hypoaldosteronism
(b) causes hyperkalemia, inhibition of ammonia (high K+ leads to decr ammoniagenesis) excretion in proximal tubule leading to urine pH decr and decr buffering capacity (d) destruction of HGA (hyaline arteriosclerosis of afferent arterioles in DM, acute or chronic tubulointerstial inflam) |
|
Possible causes of RBC casts in urine
|
Glomerular inflammation (nephritic syndromes)
Ischemia Malignant HTN Presence of casts indicates renal origin |
|
Possible causes of WBC casts in urine
|
Tubulointerstitial diseases
Acute pyelonephritis Glomerular disorders |
|
Possible causes of granular (muddle brown) casts in urine
|
Acute tubular necrosis
|
|
Possible causes of waxy casts in urine
|
Advanced renal disease/CRF
|
|
Possible causes of hyaline casts in urine
|
Nonspecific
|
|
Acute cytitis: results from macroscopic urinalysis?
|
WBC's no casts
|
|
Bladder cancer: results from macroscopic urinalysis?
|
RBC's no casts
|
|
Define nephritic syndrome
|
Inflammatory process involving glomeruli, leading to hematuria, azotemia, RBC casts in urine, oliguria, hypertension, and proteinuria (3.5g/day)
|
|
Name major nephritic syndromes
|
Acute poststreptococcal glomerulonephritis
Rapidly progressive (crescentic) glomerulonephritis Diffuse proliferative glomerulonephritis (SLE) Berger's disease (IgA glomerular nephropathy) Alport's Syndrome |
|
Define nephrotic syndrome
|
Presents w/massive proteinuria (>3.5d, frothy urine), hyperlipidemia, edema
|
|
Name the major nephrotic syndromes
|
Membranous glomerulonephritis (diffuse membranous GN)
Minimal change disease Amyloidosis Diabetic glomerulonephropathy Focal Segmental glomerulosclerosis Membranoproliferative glomerulonephritis |
|
Alport's Syndrome
(a) etiology (b) clinical presentation (c) EM (d) Treatment |
(a) XLD absence of type IV collagen
(b) nephritis (hematuria; may have RBC casts); hearing loss; eye problems (cataracts, etc) (c) Thickening or attenuation of GBM w/longitudinal splitting (d) ACEI's, renal transplant |
|
Fabry's disease
(a) etiology (b) clinical presentation (c) diagnosis (d) treatment |
(a) XL lysosomal storage dz; deficiency of alpha galactosidase. Accumulates in tissues.
(b) Proteinuria/hematuria purples papules (trunk, lower genitalia) heart problems (LVH, arrythmias, premature CAD) Corneal opacities (c) incr levels of ceramide and digalactosidase in urine (d) recomb alpha galactosidase |
|
Minimal change disease
(a) Etiology/epidemiology (b) secondary diseases (c) clinical presentation (d) LM (e) EM (f) treatment |
(a) unknown; usually following an upper resp tract infx
Mainly in young children (b) Hodgkin's; hypersensitivity (c) Nephrotic presentatoin (edema, wt gain, selective proteinuria, hyperlipidemia) (d) normal glomeruli (e) fusion of podocyte foot processes (f) predinisone Cyclophosph or chlorambucil if resistant to steroids |
|
Focal Segmental Glomerulosclerosis
(a) associations (b) clinical presentation (c) LM (d) IF (e) EM (f) treatment/outcome |
(a) heroine use, morbid obesity, HIV, HTN, mainly adults
(b) Nephrotic syndrome w/microscopic hematuria (c) sclerosis w/in capillary tufts (focal, segmental) w/hyalniosis (d) IgM and C3 in sclerotic regions (e) Fusion of epithelial foot processes (f) prednisone; most progress to ESRD in 5-10yr |
|
Membranous glomerulonephritis
(a) epidemiology (b) secondary diseases (c) clinical presentation (d) LM (e) EM (F) complications (g) treatment |
(a) adults; immune complex dz of unknown etioloty
(b) SLE, malignancy, infection (Hep B, syphilis, drugs (c) nephrotic syndrome w/azotemia (d) LM: diffuse capillary wall and BM thickening (e) subepithelial deposits (spike and dome w/methenamine stain) (f) renal vein thrombosis (g) cyclophos, ACEI, transplant (little response to steroids) |
|
Acute Poststreptococcal Glomerulonephritis
(a) epidemiology/etiology (b) clinical presenation (c) gross (d) LM (e) EM (f) outcomes |
(a) children due to GAS infx
(b) nephritis syndrome 1-2 wks post infx; periorbital edema (c) inflammation of all glom and both kidneys; punctate surface hemorrhages (d) LM shows hypercellulra glom w/prol of mes/epi (normal BM) (e) subepithelial humps ("lumpy bumpy") (f) resolves spontaneously |
|
Rapidly Progressive Glomerulonephritis
(a) epidemiology (b) etiology (c) clinical presentation (d) LM (e) outcomes |
(a) adolescents and young adults (type II); >40 usually type III
(b) Type I: antiGBM ab (goodpasture's) Type II: Immune c omplex (SLE, IgA, HSP, Wegener's) (c) rapidly progressive nephritic syndrome (d) crescents b/w Bowman's space and glomerulus (fibrin and prolif of parietal cells in bowman's space) (e) dialysis and/or transplant; rapid course to renal failure |
|
Membranoproliferative glomerulonephritis Type I
(a) epidemiology (b) secondary diseases (c) clinical presentation (d) LM (e) EM (f) course and therapy |
(a) adults (involves both classic and alternative pathway)
(b) hep C, hepB, lupus (c) more often presents w/nephrotic pattern (d) splitting of BM, expansion of mesangial matrix "tram track" (e) subendothelial electron dense depositis (f) corticosteroids and antiplatelet drugs, usually progresses slowly to CRF |
|
Membranoproliferative glomerulonephritis Type II
(a) epidemiology (b) secondary diseases (c) clinical presentation (d) LM (e) EM (f) course and therapy |
(a) younger adults (only involves alternative complement pathway)
(b) HepC,B, HIV, SLE (c) nephritic or macroscopic hematuria or chronic renal failure (d) "tram track" appearance due to splitting of BM and expansion of mesangial matrix (e) dense deposits within BM (f) corticosteroids/antiplatelet drugs; usually slowly progress to CRF |
|
IgA nephropathy aka Buerger's
(a) epidemiology (b) secondary diseases (c) clinical presentation (d) LM (e) EM (f) labs (g) course and therapy |
(a) most common primary GN in world; in adults and young adults; M>F
(b) May be a part of henoch schloenlein purpura or manifest after infx (c) hematuria w/in 1-2 days of URI (d) Focal proliferative w/mesangial expansion (e) mesangial IgA deposits (f) incr IgA and normal complement |
|
5 types of SLE involving kidneys (general presentations)
|
Type I: mild mesangial proliferation (asymptomatic or low grade proteinuria)
Type II: Mesangial nephritis (low grade hematuria and/or proteinuria) Type III: focal proliferative nephritis (nephritic urinary sediment, proteinuria) Type IV: Diffuse proliferative : Mot severe. Nephritic and nephritic Type V: membranous nephropathy (nephrotic syndrome) |
|
Histology of the 5 types of SLE nephropathies
|
Type I: normal
Type II: mesangiall FS glom involv; incr mesangial matrix Type III: Less than half glomeruli involved Type IV: All glom involv; mesangial prolif -LM: wire loop abnormality (omm complex thicken BM) -EM/IF: subendothelial imm complex deposition Type V: similar to membranous glomerulonephritis (Subepithelial) |
|
Treatment of SLE nephropathies
|
Type I to II: no treatment
Type III to V: aggressive immunosuppression w/corticosteroids, cyclophos, azathioprine, chlorambucil |
|
Diabetic nephropathy
(a) epidemiology (b) clinical presentation (c) LM (d) labs (e) treatment |
(a) ESRD more prevalent in TIIDM but more change of getting in TIDM
~20yrs after onset of DM; M>F, AA, NA>whites (b) nephrotic syndrome and retinopathy invariably present (c) microalbuminemia (early) and proteinuria (late) (d) Thick GBM (NE glycosylation); mesangial damage; Kimmelstiel Wilson "wire loop" nodules (e) strict control of DM and HTN; no effective treatment once proteinuria; progress to ESRD |
|
Goodpasture's
(a) etiology (b) presentation (c) histology (d) treatment |
(a) anti GBM antibodies
(b) pulmonary hemorrhage; nephritic presentation and rapidly progressive GN (c) antiGBM Abs (linear Ig staining of BM) (d) plasma exchange and coeticosteroids |
|
4 major types of kidney stones
|
Calcium (oxalate, phosphate or both)
Ammonium magnesium phosphate (struvite) Uric acid Cystine |
|
Calcium based kidney stones
(a) cause (b) appearance (c) notes |
75% of all renal stones; calcium oxalate, phosphate, or both
(a) conditions that cause hypercalcemia (cancer, incr pTH, incr vitD, milk alkali syndrome) can lead to hypercalcuria and stones (b) radiopaque (c) oxalate crystals can result from ethylene glycol (antifreeze) or vitC abuse |
|
Struvite stones
(a) composition (b) cause (c) appearance |
(a) ammonium magnesium phosphate
(b) infection w/ urease positive bugs (Proteus, staph, klebs) which make urine more alkaline causing precipitation of magnesium ammonium phosphate salts (c) can form staghorn calculi; radiopaque or radiolucent |
|
Uric acid stones
(a) associations (b) appearance |
(a) strong association w/gout and often seen as a result of diseases with increases cell turnover (leukemia and myeloproliferative disorders)
(b) radiolucent |
|
Cystine stones
(a) causes (b) appearance |
(a) most often due to secondary cysteinuria
(b) hexagonal shaped stones; rarely form staghorn calculi; faintly radioopaque; treat w/alkalinization of urine |
|
Cortical adenoma
(a) description (b) gross (c) micro |
(a) benign tumor of the kidney; common finding at biopsy
(b) yellow, encapsulated cortical nodules (c) may be identical to renal cell carcinoma, distinguished by size |
|
Angiomyolipomas
(a) composition (b) disease association |
(a) hamartomas; composed of fat, smooth muscle, and blood vessels
(b) particularly common in patients with tuberous sclerosis |
|
Renal cell carcinoma
(a) epidemiology (b) risk factors/associations (c) symptoms (d) gross (e) micro (f) prognosis |
(a) 90% of all renal cancers; 50-70YO no sex prediliction
(b) incr incidence with smoking and obesity Associated w/paraneoplastic syndromes(ectopic EPO, ACTH, PTHrP, prolactin) Von Hippel Lindau and gene deletion on Ch3 (c) "classic" triad: hematuria, palpable mass, costovertebral pain; also secondary polycythemia, flank pain, fever, wt loss (d) usually upper pole; solitary w/necrosis and hemorrhage; often invades renal vein and extends into vena cava and heart (e) high incidence of mets on presentation |
|
Wilm's tumor
(a) epidemiology (b) cause (c) symptoms (d) gross (e) micro (f) prognosis |
(a) most common renal malignancy of early childhood
(b) deletion of tmor suppressor gene WT1 on C11 (c) huge, palpable flank mass, hemihypertrophy; nausea, hematuria, intestinal obstruction (d) Large, demarcated mass; usually unilateral but may be bilateral if familial (e) embryonic glomerular and tubular structures surrounded by spindle cells (f) 90% survival when treated with Sx/Rx/Cx |
|
WAGR complex
|
Wilm's tumor
Aniridia Genitourinary malformation Mental motor retardation |
|
Transitional cell carcinoma
(a) epidemiology (b) symptoms (c) associations |
(a) MCC tumor of urinary tract system
(b) painless hematuria (c) phenacetin, smoking, aniline dyes, and cyclophosphamide |
|
Pyelonephritis (acute)
(a) risk factors (b) epidemiology (c) symptoms (d) urine (e) gross (f) micro |
(a) urinary obstruction, vesicoureteral reflux, pregnancy, intrumentation, diabetes mellitus
(b) F<40 most common; over 40, men due to BPH (c) fever, CVA tenderness, WBC casts (dysuria, frequency, urgency_ (d) WBCs and WBC casts (casts are pathognomonic) (e) yellow microabscesses in cortex w/relative sparing of glomeruli (f) suppurative and tubular necrosis |
|
Chronic pyelonephritis
(a) cause (b) symptoms (c) gross (d) microscopic |
(a) reflux nephropathy most common
(b) present with renal failure or HTN (c) irregular scarring , coarse, asymmetric at corticomedullary jct and blunted calyx (d) chronic inflammation w/eosinophilic casts (thyroidization) |
|
Diffuse cortical necrosis
(a) describe (b) cause (c) associations |
(a) acute generalized infarction of cortices of both kidneys
(b) likely due to combo of vasospasm and DIC (c) associated w/obstetric catastrophes and septic shock |
|
Drug induced interstitial nephritis
(a) describe (b) symptoms (c) cause |
(a) acute interstitial renal inflammation
(b) fever, rash, eosinophilia, hematuria 2 wks after drug admin (c) penicillins derivatives, NSAIDs, diuretics act as haptens |
|
Acute Tubular Necrosis
(a) 3 stages (b) associations (c) outcomes |
(a) inciting event, maintenance (low urine), recovery
(b) renal ischemia (shock, sepsis), crush injury, toxins (c) 2-3 wk recovery, death most often occurring in renal phase; treat w/dialysis; MCC of ARF |
|
Renal papillary necrosis
(a) define (b) major associations |
(a) sloughing of renal papillae leading to gross hematuria and proteinuria
(b) DM, acute pyelonephritis, chronic phenacetin use, sickle cell anemia |
|
Gouty nephropathy
(a) describe (b) diagnosis |
(a) urate crystals in tubules inducing tophus formation and chronic inflammatory rxn
(b) birefringent needle shaped crystals |
|
Acute urate nephropathy
(a) describe (b) cause |
(a) precipitation of crystals in collecting ducts causing obstruction
(b) lymphoma and leukemia, esp after chemo |
|
Exstrophy of bladder
(a) describe (b) associations |
(a) absence of anterior musculature of bladder and abdominal wall; failure of mesoderm to grow over anterior bladder
(b) incr incidence of adenocarcinoma; site of severe chronic infx |
|
MCC of bladder obstruction in men
|
BPH or carcinoma
|
|
MCC of bladder obstruction in women
|
Cystocele of bladder
|
|
Acute renal failure (3 types)
|
Abrupt decline in renal fct w/increased Cr and BUN over a period of several days
|
|
Prerenal ARF
(a) cause (b) expected urine osm (c) expected urine Na (d) expected FeNa (e) expected BUN/Cr ratio |
(a) decreased RBF (like hypotension) causes decr GFR, incr sodium and water retention of kidney; BUN/Cr increase in the attempt to conserve volume
(b) >500 (c) <10 (d) <1% (e) >20 |
|
Renal ARF
(a) cause (b) expected urine osm (c) expected urine Na (d) expected FeNa (e) expected BUN/Cr ratio |
(a) usually due to tubular necrosis/ischemia/toxins; debris is obstructing tubule causing backflow and decr GFR; urine has epithelial/granular casts; BUN absorption impaired
(b) <500 (c) >20% (d) >2% (e) <15 |
|
Postrenal ARF
(a) cause (b) expected urine osm (c) expected urine Na (d) expected FeNa (e) expected BUN/Cr ratio |
(a) outflow obstruction (stones, BPH, neoplasia) but only if bilateral
(b) <350 (c) >40 (d) >4% (e) >15% |
|
Fanconi's syndrome
(a) describe (b) cause (c) complications (cause) |
(a) decr proximal tubule transport of AA, glucose, phosphate, uric acid, protein, and electrolytes
(b) congenital or acquired (Wilson's disease, glycogen storage disease, drugs like cisplatin, expired tetracycline) (c) Rickets (decr phosphate reabsorption) Metabolic acidosis (decr bicarb reabsorption) Increased distal Na reabsorption leading to hypokalemia (decr early Na reabsorption) |
|
ADPKD
(a) description (b) cause (c) presentation (d) outcomes (e) associations |
(a) multiple, large, bilateral cysts; enlarged kidneys
(b) flank pain, hematuria, HTN, urinary infx, progressive renal failure (c) flank pain, hematuria, hypertension, urinary infx, progressive renal failure (d) AD mutation in APKD2 (e) death from uremia or HTN due to incr renin (f) polycystic liver disease, berry aneurysm (HTN), mitral valve prolapse |
|
ARPKD
(a) clinical presentation (b) associations |
(a) infantile presentation in parenchyma
(b) hepatic cysts and fibrosis |
|
Dialysis cysts description
|
Cortical and medullary cysts resulting from long standing dialysis
|
|
Simple cysts description
|
Benign incidental finding; cortex only
|
|
Medullary cystic disease description
|
Medullary cysts; US shows small kidney; poor prognosis
|
|
Medullary sponge disease
|
collecting duct cysts; good prognosis
|
|
Low Na+ symptoms
|
Disorientation, stupor, coma
|
|
High Na+ symptoms
|
Neurologic; irritablity, delirium, coma
|
|
Low Cl- symptoms
|
Secondary to metabolic alkalosis, hypokalemia, hypovolemia, incr aldoesterone
|
|
High Cl- symptoms
|
Secondary to non anion gap acidosis
|
|
Low K+ symptoms
|
U waves on ECG, flattened T waves, arrhythmias, paralysis
|
|
High K+ symptoms
|
Peaked T waves, wide QRS, arrythmias
|
|
Low Ca2+ symptoms
|
Tetany, neuromuscular irritability
|
|
High Ca2+ symptoms
|
Delirium, renal stones, abdominal pain, not necessarily calciuria
|
|
Low Mg2+ symptoms
|
Neuromuscular irritability, arrythmias
|
|
High Mg2+ symptoms
|
Delirium, decreased DTR's, cardiopulmonary arrest
|
|
Low phosphate symptoms
|
Low mineral ion product causes bone loss and osteomalacia
|
|
High phosphate symptoms
|
High mineral ion product causes renal stones and metastatic calcifications
|