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132 Cards in this Set

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what conditions do you see RBC casts?
nephritic syndomres (glomuerulonephritis), ischemia, malignant hypertension
What conditions do you see WBC casts?
acute pyeonephritis, tubulointerstitial inflammation, transplant rejection
What conditions do you see granular (muddy brown) casts?
ATN - acute tubular necrosis
What conditions do you see waxy casts?
advanced renal disease - chronic renal failure
What condition do you see hyaline casts?
nonspecific
What does seeing casts mean?
That the cause of hematuria/pyuria is of renal orgin
do you see casts in bladder cancer or kidney stones?
NO - could see RBCs but no casts
If you have acute cystitis what can you see in the urine?
WBCs but no casts
What causes nephrotic syndrome? What do you see in those with nephrotic syndrome?
loss of charge barrier - fused basement membrane
see proteinuria (>3.5 g/day; frothy urine), hyperlipidemia (increased lipoprotein synthesis because of low proteins and the liver is trying to make more), hypoalbuminema, edema, fatty casts. Increased risk of infection and thromboembolism
What are the things that cause primary nephrotic syndrome?
FMMMM
Focal segmental glomerulosclerosis, Minimal change disease, Membranous glomerulonephritis, Membranoproliferative golmerulonephritis, mesangial proliferation
What are the things that cause secondary nephrotic syndrome?
SAD
SLE
Amyloidosis
Diabetic nephropathy
Minimal change disease
Type of primary nephrotic syndrome - commonly seen in young children - on LM everything looks normal on; on EM loss of podocyte foot processes - loose albumin not Ig's - may be triggered by infection or immune stimulus - responds to corticosteroids
What do you give to treat minimal change disease?
corticosteroids
Focal segmental glomerulosclerosis
type of primary nephrotic syndrome
LM - segmental sclerosis and hyalinosis
similar to minimal change disease but seen in adults
most common glomerular disease in HIV patients - more severe in these patients too
What is the most common glomerular disease in HIV patients?
Focal segmental glomerulosclerosis
What is the damage seen in focal segmental glomerulosclerosis?
involves parts of some of the glomeruli
Membranous glomerulonephritis
LM - diffuse capillary and GBV thickening; EM - spike (basement membrane material) and dome (immune complex deposition) appearance with sub epithelial deposits; IF - granular
SLE's nephrotic presentation
What is SLE's nephrotic presentation?
membranous glomerulonephritis (diffuse membranous glomerulopathy)
What is the most common cause of adult nephrotic syndrome?
membranous glomerulonephritis (diffuse membranous glomerulopathy)
What causes membranous glomerulonephritis?
drugs infections, SLE, and solid tumors - most common cause of adult nephrotic syndrome
Membranoproliferative glomerulonephritis
Subendothelial ICs with granular IF.
Type I EM: "tram-track" appearance due to GBM splitting caused by mesangial ingrowth - associated with C3 nephritic factor
type II EM: "dense deposits" - associated with HBV>HCV

*usually progresses slowly to CRF
What is the nephrotic syndrome that present as nephritic syndrome?
Membranoproliferative glomerulonephritis
What happens in diabetic glomerulonephropathy?
Nonenzymatic glycosylation (NEG) of GBM - increase premeability, thickening. NEG of efferent arterioles - increased GFR - mesangial expansion. LM - mesangial expansion, GBM thickenign, nodular glomerulosclerosis (kimmelstiel-Wilson nodules)
Kimmelstiel-Wilson nodules
seen in diabetic glomerulonephropathy - GBM thickening, nodular glomerulosclerosis
renal disease of amyloidosis
LM - congo red stain, apple-green birefrigence (under polarized light)
associated with multiple myeloma, chronic conditions, TB, and RA.
What is amyloidosis associated with?
multiple myeloma, chronic disease, RB, and RA
Nephritic syndrome - symptoms and causes
Inflammatory process - hematuria and RBC casts in the urine. Associated with azotemia, hypertension. oliguira, and proteinuria (<3.5 g/day)
Types of nephritic syndrome
PAST HAM
Poststreptococcal
IgA nephropathy (Berger's disease)
SLE
TTP/HUS

Henoch-Schonlein purpura
Alport's syndrome
Membranoproliferative glomerulonephritis
RPGN (rapidly progressing glomerulonephtritis)
Anti-GBM: Goodpasture's
Immune Complex: Henoch-Schonlein purpra, Hypersensitivity vasculitis, Cryoglobulinemia, SLE
Pauci-immune: Wegner's, Churg Strauss, Microscopic polyarteritis, PAN
acute poststreptococcal glomerulonephritis
nephritic syndrome
LM - glomeruli enlarged and hypercellular, PMNs, lumpy-bumpy appearance
EM - subepithelial immune complex humps
IF - granular
*commonly in children post streptococcal infection - peripheral and periorbital edema. Resolves spontaneously
How do you treat the condition commonly seen in kids that presents with peripheral and periorbital edema?
resolves spontaneously
acute poststreptococcal glomerulonephritis
from immune complex deposition
Rapidly progressive (crescentic) glomerulonephritis (RPGN)
LM and IF - crescent-moon shape. crescent consists of fibrin and plasma proteins with glomerular parietal cells, monocytes, and macrophages. Several disease processes can cause this pattern:
1) goodpastures - type II hypersensitivity; antibodies to GBM; male dominant disease - hematuria/hemoptysis (lung involvement)
2) Wegner's granulomatosis; c-ANCA
3) Microscopic polyarteritis; p-ANCA
c-ANCA
wegners can cause crescentric glomerulonephritis
p-ANCA
microscopic polyarteritis - can cause crescentric glomerulonephritis
what is the most common cause of death in patients with SLE?
diffuse proliferative glomerulonephritis (due to SLE or MPGN)

see subendothelial DNA-anti-DNA immune complexes - wire looping of capillaries

granular IF

SLE can also present as nephrotic syndrome
wire looping of capillaries in kidney
diffuse proliferative glomerulonephritis
from SLE - most common cause of death
IgA nephropathy
(Berger's disease) type of nephritic syndrome - deposition of IgA in mesangium
* usually presents/flares with URI or acute gastroenteritis
What nephritic syndrome presents/flares with an URI or acute gastroenteritis?
IgA nephropathy - Berger's disease
Alport's syndrome
nephritic syndrome - mutation in type IV collagen - split basement membrane
KEEN! Ears (deafness), Eyes, Kidneys and nerve disorders
Kidney stones complications and how to treat?
Complications: hydronephrosis and pyelonephritis
Treatment: encourage fluid intake
What are the 4 types of kidney stones?
1) calcium
2) ammonium magnesium phosphate
3) Uric acid
4) Cystine
Calcium kidney stones
most common kidney stone (75-85%). made of calcium oxylate or calcium phosphate or both
increased risk in conditions that cause increased calcium: PTH, vitamin D, cancer, milk-alkali syndrome) - lead to hypercalciuria and stones - tend to recur
What is the most common type of kidney stone?
Calcium stones - make of calcium oxylate or calcium phosphate
What do calcium kidney stones look like?
radiopaque. oxalate crystals can result from ethylene glycol (antifreeze) or vitamin C abuse
Abuse of what can cause calcium kidney stones?
ethylene glycol (antifreeze) or vitamin C
Struvite kidney stones (ammonium magnesium phosphate) NHPO4)
second most common type of kidney stone. caused by infection with urease positive bug: staphylococcus, Proteus, Klebsiella - can form staghorn calculi that can be a nidus for UTIs
What do struvite stones look like?
radiopaque or radiolucent
worsened by alkaluira
what stone is worsened by alkaluria?
Struvite`
Uric acid kidney stone
strong association with hyperuricemia (eg. gout). often seen in diseases with increased cell turn over (leukemia, myeloproliferative disorders)
What does a uric acid kidney stone look like?
radiolucent
Cystine kidney stone
often secondary to cystinuria. Hexagonal shape. rarely, may form cystine stagohrn claculi
What do cystine kidney stones look like? What do you treat them with?
faintly radiopaque. treat with alkalinzation of the urine
What is the most common renal malignancy?
Renal cell carcinoma
Renal cell carcinoma
most common renal malignancy - invades IVC and can travel up it and metastasize hemotogenously; lung and bone
most common in men 50-70
increased incidence with smoking and obesity. associated with von hippel-lindau and gene deletion in chromsome 3, originates in renal tubule cells - polygonal clear cells
How does renal cell carcinoma present clinically?
hematuria, palpable mass, secondary polycythemia, flank pain, fever, and weight loss
What paraneoplastic syndromes is renal cell carcinoma associated with/
ectopic EPO, ACTH, PTH related peptide, and prolactin
renal cell carcinoma most commonly affects who?
men ages 50-70
increased incidence of renal cell carcinoma if what?
smoke or obese
renal cell carcinoma is associated with what genetic condition?
von hippel-lindau gene deletion in chromosome 3
What tumor originates from polyclonal clear cells?
renal cell carcinoma
what is the most common renal malignancy of childhood (ages 2-4)?
Whilms' tumor (nephroblatoma)
Whilms' tumor (nephroblastoma)
most common renal malignancy in children. presents with huge palpable flank mass and/or hematuria. may be associated with hemihypertorophy syndromes. Contains embryonic glomerular structures. Deletion of tumor suppressor gene WT1 on chromosome 11. Can be part of WAGR complex: whilms' tumor, aniridia (absent iris), GU malformation, mental-motor retardation
WAGR complex is associated with what?
Whilms' tumor (nephroblastoma)
Whilms' tumor, aniridia, GU malformation, mental-motor retardation
what happens in WAGR complex?
deletion of tumor suppressor gene WT1 on chromosome 11
What tumor contains embyronic glomerular structures?
whilms' tumor - most common tumor of children (age 2-4)
Transitional cell carcinoma
most common tumor of urinary tract system (can occur in the renal calyces, renal pelvis, urters, and bladder). Painless hematuria is suggestive of bladder cancer. Associated problems in your Pee SAC: Phenacetin, Smoking, Aniline dyes, Cyclophosphamide
What is the most common tumor of the urinary tract system?
transitional cell carcinoma
Painless hematuria is sign of what?
bladder cancer
What things are associated with transitional cell carcinoma?
Pee SAC
Phenacetin, Smoking, Analine dyes, Cyclophosphamide
actue pyelonephritis
affects cortex with relative sparing of glomeruli/vessels. White cell casts in urine are classic. presents with fever, CVA tenderness, nausea and vomiting
chronic pyelonephritis
coarse, asymmetric cortiocmedullary scarring, blunted calyx. Tubules can contain eosinophilc casts (thyroidization of kidney)
thyroxidization of the follicles
occurs in chronic pyelonephritis - becuase of eosinophilic casts in the tubules - looks like follicles of the thyroid
drug induced intersitital nephritis
actue intersitial renal inflammation. pyuria (usually eosinophils) and azotemia occurring 1-2 weeks after administration. Associated with fever, rash, hematuria and CVA tenderness

drugs: diuretics, NSAIDs, penicilin derivatives, sulfonamides, rifampin act as haptens, inducing hypersensitivity
pyuria, azotemia, fever, rash, hematuria, CVA tenderness 2 weeks after starting a drug
drug-induced interstitial nephritis
drugs that can cause it are: diuretics, NSAIDs, penicillin derivatives, sulfonamides, rifampin

*act as haptens, inducing hypersensitivity
diffuse cortical necrosis
acute generalized infarction of cortices of both kidneys. Likely due to vasospasm and DIC. Associated with obstetric catastrophics (abrupito placentae) and septic shock
generalized infarction of both cortices of kidneys
diffuse cortical necrosis - likely due to DIC and vasospasm. Associated with obstetric catastrophies (abrupito placentae) and septic shock
Acute tubular necrosis
most common cause of acute renal failure in hospital. self-reversible, but fatal if left untreated (provide supportive dialysis). Associated with renal ischemia (shock, sepsis), crush injuries (myoglobinuria), toxins. Death most often occurs during initial oliguric phase
most common cause of acute renal failure in hospital? What do you do?
acute tubular necrosis - self reversible - get them through it via dialysis
What is associated with renal ischemia (shock, sepsis), crush injury (myoglblinuria), and toxins?
acute tubular necrosis
In acute tubular necrosis when does death usually occur?
during the initial oliguric phase
What happens to the cells during ATN?
loss of cell polarity, epithelial cell detachment, necrosis, granular (muddy brown) casts. 3 stages
1) inciting event - maintenace (low urine) - recovery (2-3 weeks)
renal papillary necrosis
sloughing of renal papillae - gross hematuria, proteinuria. May be triggered by a recent infection or immune stimulus
associated with:
1)DM 2) acute pyelonephritis 3) chronic phenacetin use (acetaminophen is a phenacetin derivative) 4) sickle cell anemia
what happens to BUN and creatinine in a normal nephron
BUN is reabsorbed for countercurrent multiplication, but creatinine is not
Acute renal failure (acute kindey injury) causes
1) prerenal azotemia
2) intrinisc renal
3) postrenal
Acute renal failure
abrupt decline in renal function with increase in creatinine and BUn over a period of several days
Prerenal azotemia
acute renal failure from decrased RBF (hypotension) - decreased GFR. Na+/H20 and urea reabsorbed by kidneys so BUN/creatinine ratio increase (usually greater than 15) in attempt to conserve volume
intrinsic renal: acute renal failure
usually due to ATN or ischemia/toxins; less commonly due to actue glomerulonephritis (RPGN). Patchy necrosis leads to debris obstructing tubule and fluid blackflow across necrotic tubule - decreased GFR. urine has epithelial cases. BUN resorption is impaired - decreases BUN/creatinine ratio
postrenal acute renal failure
outflow obstruction (stones, BPH, neoplasia, congenital anomalies). develops only with bilateral obstruction
What acute renal injury if urine osmolality > 500, urine Na < 10, FeNa < 1%, and serum BUN/Cr > 20
prerenal cause
what acute renal injury if urine osmolality <350, urine Na>20, FeNa>2%, serum BUN/Cr<15
renal cause
What acute renal injury if urine osmalality <350, urine Na+>40, FeNa>4%, Serum BUN/Cr>15?
postrenal cause
If you have renal failure what can't you do? What are the 2 types?
create urine and excrete nitrogenous wastes
2 types:
1) acute (ATN)
2) chronic (hypertension and diabetes)
What are the consequences of renal failure?
1) Na+/H20 retention (CHF, pulmonary edema, hypertension)
2) Hyperkalemia
3) Metabolic acidosis
4) Uremia (clinical syndrome marked by increased BUN and creatinine): nausea, pericarditis, asterixis, encephalopathy, platelet dysfunction
5)anemia (can't make EPO)
6) renal osteodystrophy (can't make active form of vitamin D)
7) dyslipidemia (especially increase in triglycerides)
8) growth retardation and developmental delay in children
What is wrong in fanconi's syndrome?
problem with proximal tubules - cannot transport amino acids, glucose, phosphate, uric acid, protein, and electrolytes. Can be congenital or acquired. causes include wilson's disease, glycogen storage diseases, and drugs (cisplatin, expired tetracycline)
What can expired tetracycline cause?
fanconi's syndrome
What drugs can cause fanconi's syndrome?
cisplatin, expired tetracycline
What do you see in someone with fanconi's syndrome?
defect with: early Na+ resorption, decrease phosphate reabsorption, decrease HCO3- reabsorption

complications: ricketts, metabolic acidosis (loose HCO3- type 2 RTA)
increase distal Na+ reabsorption - hypokalemia
mannitol
osmotic diuretic that acts in the proximal tubules - increases the osmolality of the tubular fluid - producing increased renal flow
used for: increased intracranial pressure, drug overdose, shock
toxicity: plumonary edema, dehydration
don't use in anuria and CHF
When is mannitol contraindicated?
anuria and CHF
Acetazolamide
inhibits carbonic anhydrase - causes HCO3- diuresis and reduced stores of HCO3- also inhibits formation of aqueous humor
uses: glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness
toxicity: hyperchloremic metabolic acidosis, neuropathy, NH3 toxicity, sulfa allergy
*acetazolamide causes acidosis
Ferosemide
loop diuretic - works on ascending loop of henle on the Na+/K+/2Cl- channel (inhibits it) - abolishes hypertonicity of the medulla - so urine cannot be concentrated - Loops Loose Calcium!
uses: edematous states (CHF, cirrhosis, nephrotic syndrome, pul edema), HTN, hypercalcemia
toxicity: OH DANG
ototoxicity, hypokalemia, dehydration, allergy (sulfa), Nephritis (interstitial), gout
the diuretic used in edema?
Ferosemide - loop diuretic - works on ascending loop of henle - inhibits Na+/K+/2Cl- channel
Ethacrynic acid
same as ferosemide - but given to those with sulfa allergy - loop diuretic
If someone needs a loop diuretic for edema and they have a sulfa allergy what can you use?
Ethacrynic acid
Hydrochlorothiazide
Works on distal convoluted tubules - inhibits Na+/Cl- reabsorption - reducing the diluting capacity of the nephron - decreased Ca2+ excretion
uses: HTN, CHF, idiopathic hypercalciuria, nephrogenic diabetes insipidus
toxicity: Hypokalemic metabolic alkalosis, hyponatremia, hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia (hyperGLUC). sulfa allergy
What do you use to treat nephrogenic diabetes insipidus?
Hydrochlorothiazide
K+ sparing diuretics
K+ STAEys
Spironolactone, Triamterene, Amiloride, explerenone

Spirnoolactone is a competitive aldosterone receptor antagonists in the cortical collecting tubule
Triameterene and amiloride act at the same part of the tubule by blocking Na+ channels in the CCT
uses: hyperaldosteronism, K+ depletion, CHF
toxicities: hyperkalemia (can lead to arrhythmias), endocrine effects with aldosterone antagonists (spironolactone causes gynecomastia, antiandrogen effects)
What does diuretics do to urine NaCl?
all of them increase it - and water follows - serum NaCl may decrease as a result
What does diuretics do to urine K+?
All of them except K+ sparing (spirnolactone, triamterene, amiloride, eplerenone) increase urine K+ (because by inhibiting Na+ reabsorption more Na+ is delivered to distal convoluted tubule which stimulates aldosterone - and Na+ reabsorbed and K+
What does CA inhibitors and K+ sparing diuretics do to the blood pH?
decrease it - causing acidemia -
CA inhibitors - inhibit reabsorption of HCO3-
K+ sparing - aldosterone blockade prevents K+ secretion and H+ secretion. also hyperkalemia leads to K+ entering cells and H+ exiting cells
What do loop diuretics and thiazides do to blood pH?
increase it (alkalosis)
1) volume contraction - loose water - so low blood volume - AT II - increased Na/H exchange in proximal tubules - more H+ into urine - which gets reabsorbed and HCO3- diffuses into the blood
2) K+ loss leads to K+ exiting cellls (H+/K+ exchanger) in exchange for H+ entering cells
3) in low K+ states, H+ (rather than K+) is exchanged for Na+ in the collecting duct leading to alkalosis and paradoxical aciduria
What do loop diuretics do to Ca+?
Loops Loose Calcium - abolish lumen positive potential in thick ascending limb of henle - decreased paracellular Ca+ resorption - hypocalcemia, increased urinary Ca+
What do thiazide diuretics do to Ca+?
volume depletion - upregulation of Na+ reabsorption - enhanced paracellular Ca2+ in proximal tubul and loop of henle. thiazides block luminal Na+/Cl- cotransport in distal convoluted tubule - increase Na+ gradient - increase interstitial Na+/Ca2+ exchange - hypercalcemia
ACE inhibitors
Captopril, enalapril, lisinopril

Inhibit ACE (in lung) so no production of AT II and preventing inactivation of bradykinin a potent vasodilator - increase renin b/c of loss of feedback
uses: HTN, CHF, diabetic renal disease
toxicity: CAPTOPRIL
Cough, angioedema, proteinuria, taste changes, hypotension, pregancy problems (fetal renal damage), rash, increased renin, lower AT II - ALSO hyperkalemia
avoid with bilateral renal artery stenosis - because ACE inhibitors significantly decrease GFR by preventing constriction of efferent arterioles
What can you give a person if they have a cough from an ACE inhibitor?
angiotensin II receptor blocker (ARB) - does not cause cough!
ADPKD
multiple, large, bilateral cysts that ultimately destory the parenchyma. Enlarged kidneys. presents with flank pain, hematuria, HTN, urinary infection, progressive renal failure.
AD mutation in APKD1 and APKD2
death from complications of chronic kidney disease or HTN (due to increased renin production). Associated with polycystic liver disease, berry aneurysms, mitral valve prolapse
ARPKD
infantile presentation in parenchma - AR. associated with congential hepatic fibrosis. significant renal failure in utero can lead to potters; concern beyond neonatal peroid are HTN, portal HTN, and progressive renal insufficiency
dialysis cysts
cortical and medullary cysts resulting from long standing dialysis
simple cysts
benign, incidental finding. cortex only
Medullary cystic disease
megullary cysts sometimes leads to fibrosis and progressive renal insufficiency with urinay concentrating defects. Ultrasound shows small kidneys - poor prognosis
small kidneys on ultrasound
medullary cystic disease - poor prognosis
low serum Na+
disorientation, stupor and coma
high serum Na+
neurologic; irritabiltity, delirum, coma
low serum Cl-
secondary to metabolic alkalosis, hypokalemia, hypovoluemia, increased aldosterone
high serum Cl-
secondary to non-anion gap acidosis
low serum K+
torsades, U waves on ECG, flattened T waves, arrhythmais, paralysis
high serum K+
peaked T waves, wide QRS, arrhythmias
Low serum Ca2+
tetany, neuromuscular irritability
high serum Ca2+
delirium, renal stones, abdominal pain, not necessarily calciruia
low serum Mg2+
neuromuscular irritability, arrythmias
high serum Mg2+
delirium, decreased deep tendon reflexes, cardiopulmonary arrest
low serum PO4-
low-mineral ion product causes bone loss, osteomalacia
high serum PO4-
high-mineral ion product causes renal stones, metastatic calcifications