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132 Cards in this Set
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- Back
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what conditions do you see RBC casts?
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nephritic syndomres (glomuerulonephritis), ischemia, malignant hypertension
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What conditions do you see WBC casts?
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acute pyeonephritis, tubulointerstitial inflammation, transplant rejection
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What conditions do you see granular (muddy brown) casts?
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ATN - acute tubular necrosis
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What conditions do you see waxy casts?
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advanced renal disease - chronic renal failure
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What condition do you see hyaline casts?
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nonspecific
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What does seeing casts mean?
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That the cause of hematuria/pyuria is of renal orgin
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do you see casts in bladder cancer or kidney stones?
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NO - could see RBCs but no casts
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If you have acute cystitis what can you see in the urine?
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WBCs but no casts
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What causes nephrotic syndrome? What do you see in those with nephrotic syndrome?
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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 |
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What are the things that cause primary nephrotic syndrome?
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FMMMM
Focal segmental glomerulosclerosis, Minimal change disease, Membranous glomerulonephritis, Membranoproliferative golmerulonephritis, mesangial proliferation |
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What are the things that cause secondary nephrotic syndrome?
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SAD
SLE Amyloidosis Diabetic nephropathy |
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Minimal change disease
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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
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What do you give to treat minimal change disease?
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corticosteroids
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Focal segmental glomerulosclerosis
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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 |
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What is the most common glomerular disease in HIV patients?
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Focal segmental glomerulosclerosis
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What is the damage seen in focal segmental glomerulosclerosis?
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involves parts of some of the glomeruli
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Membranous glomerulonephritis
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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 |
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What is SLE's nephrotic presentation?
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membranous glomerulonephritis (diffuse membranous glomerulopathy)
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What is the most common cause of adult nephrotic syndrome?
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membranous glomerulonephritis (diffuse membranous glomerulopathy)
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What causes membranous glomerulonephritis?
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drugs infections, SLE, and solid tumors - most common cause of adult nephrotic syndrome
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Membranoproliferative glomerulonephritis
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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 |
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What is the nephrotic syndrome that present as nephritic syndrome?
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Membranoproliferative glomerulonephritis
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What happens in diabetic glomerulonephropathy?
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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)
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Kimmelstiel-Wilson nodules
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seen in diabetic glomerulonephropathy - GBM thickening, nodular glomerulosclerosis
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renal disease of amyloidosis
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LM - congo red stain, apple-green birefrigence (under polarized light)
associated with multiple myeloma, chronic conditions, TB, and RA. |
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What is amyloidosis associated with?
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multiple myeloma, chronic disease, RB, and RA
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Nephritic syndrome - symptoms and causes
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Inflammatory process - hematuria and RBC casts in the urine. Associated with azotemia, hypertension. oliguira, and proteinuria (<3.5 g/day)
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Types of nephritic syndrome
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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 |
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acute poststreptococcal glomerulonephritis
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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 |
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How do you treat the condition commonly seen in kids that presents with peripheral and periorbital edema?
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resolves spontaneously
acute poststreptococcal glomerulonephritis from immune complex deposition |
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Rapidly progressive (crescentic) glomerulonephritis (RPGN)
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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 |
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c-ANCA
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wegners can cause crescentric glomerulonephritis
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p-ANCA
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microscopic polyarteritis - can cause crescentric glomerulonephritis
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what is the most common cause of death in patients with SLE?
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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 |
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wire looping of capillaries in kidney
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diffuse proliferative glomerulonephritis
from SLE - most common cause of death |
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IgA nephropathy
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(Berger's disease) type of nephritic syndrome - deposition of IgA in mesangium
* usually presents/flares with URI or acute gastroenteritis |
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What nephritic syndrome presents/flares with an URI or acute gastroenteritis?
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IgA nephropathy - Berger's disease
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Alport's syndrome
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nephritic syndrome - mutation in type IV collagen - split basement membrane
KEEN! Ears (deafness), Eyes, Kidneys and nerve disorders |
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Kidney stones complications and how to treat?
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Complications: hydronephrosis and pyelonephritis
Treatment: encourage fluid intake |
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What are the 4 types of kidney stones?
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1) calcium
2) ammonium magnesium phosphate 3) Uric acid 4) Cystine |
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Calcium kidney stones
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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 |
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What is the most common type of kidney stone?
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Calcium stones - make of calcium oxylate or calcium phosphate
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What do calcium kidney stones look like?
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radiopaque. oxalate crystals can result from ethylene glycol (antifreeze) or vitamin C abuse
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Abuse of what can cause calcium kidney stones?
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ethylene glycol (antifreeze) or vitamin C
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Struvite kidney stones (ammonium magnesium phosphate) NHPO4)
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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
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What do struvite stones look like?
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radiopaque or radiolucent
worsened by alkaluira |
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what stone is worsened by alkaluria?
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Struvite`
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Uric acid kidney stone
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strong association with hyperuricemia (eg. gout). often seen in diseases with increased cell turn over (leukemia, myeloproliferative disorders)
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What does a uric acid kidney stone look like?
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radiolucent
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Cystine kidney stone
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often secondary to cystinuria. Hexagonal shape. rarely, may form cystine stagohrn claculi
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What do cystine kidney stones look like? What do you treat them with?
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faintly radiopaque. treat with alkalinzation of the urine
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What is the most common renal malignancy?
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Renal cell carcinoma
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Renal cell carcinoma
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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 |
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How does renal cell carcinoma present clinically?
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hematuria, palpable mass, secondary polycythemia, flank pain, fever, and weight loss
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What paraneoplastic syndromes is renal cell carcinoma associated with/
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ectopic EPO, ACTH, PTH related peptide, and prolactin
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renal cell carcinoma most commonly affects who?
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men ages 50-70
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increased incidence of renal cell carcinoma if what?
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smoke or obese
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renal cell carcinoma is associated with what genetic condition?
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von hippel-lindau gene deletion in chromosome 3
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What tumor originates from polyclonal clear cells?
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renal cell carcinoma
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what is the most common renal malignancy of childhood (ages 2-4)?
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Whilms' tumor (nephroblatoma)
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Whilms' tumor (nephroblastoma)
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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
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WAGR complex is associated with what?
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Whilms' tumor (nephroblastoma)
Whilms' tumor, aniridia, GU malformation, mental-motor retardation |
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what happens in WAGR complex?
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deletion of tumor suppressor gene WT1 on chromosome 11
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What tumor contains embyronic glomerular structures?
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whilms' tumor - most common tumor of children (age 2-4)
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Transitional cell carcinoma
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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
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What is the most common tumor of the urinary tract system?
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transitional cell carcinoma
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Painless hematuria is sign of what?
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bladder cancer
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What things are associated with transitional cell carcinoma?
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Pee SAC
Phenacetin, Smoking, Analine dyes, Cyclophosphamide |
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actue pyelonephritis
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affects cortex with relative sparing of glomeruli/vessels. White cell casts in urine are classic. presents with fever, CVA tenderness, nausea and vomiting
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chronic pyelonephritis
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coarse, asymmetric cortiocmedullary scarring, blunted calyx. Tubules can contain eosinophilc casts (thyroidization of kidney)
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thyroxidization of the follicles
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occurs in chronic pyelonephritis - becuase of eosinophilic casts in the tubules - looks like follicles of the thyroid
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drug induced intersitital nephritis
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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 |
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pyuria, azotemia, fever, rash, hematuria, CVA tenderness 2 weeks after starting a drug
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drug-induced interstitial nephritis
drugs that can cause it are: diuretics, NSAIDs, penicillin derivatives, sulfonamides, rifampin *act as haptens, inducing hypersensitivity |
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diffuse cortical necrosis
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acute generalized infarction of cortices of both kidneys. Likely due to vasospasm and DIC. Associated with obstetric catastrophics (abrupito placentae) and septic shock
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generalized infarction of both cortices of kidneys
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diffuse cortical necrosis - likely due to DIC and vasospasm. Associated with obstetric catastrophies (abrupito placentae) and septic shock
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Acute tubular necrosis
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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
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most common cause of acute renal failure in hospital? What do you do?
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acute tubular necrosis - self reversible - get them through it via dialysis
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What is associated with renal ischemia (shock, sepsis), crush injury (myoglblinuria), and toxins?
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acute tubular necrosis
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In acute tubular necrosis when does death usually occur?
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during the initial oliguric phase
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What happens to the cells during ATN?
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loss of cell polarity, epithelial cell detachment, necrosis, granular (muddy brown) casts. 3 stages
1) inciting event - maintenace (low urine) - recovery (2-3 weeks) |
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renal papillary necrosis
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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 |
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what happens to BUN and creatinine in a normal nephron
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BUN is reabsorbed for countercurrent multiplication, but creatinine is not
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Acute renal failure (acute kindey injury) causes
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1) prerenal azotemia
2) intrinisc renal 3) postrenal |
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Acute renal failure
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abrupt decline in renal function with increase in creatinine and BUn over a period of several days
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Prerenal azotemia
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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
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intrinsic renal: acute renal failure
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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
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postrenal acute renal failure
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outflow obstruction (stones, BPH, neoplasia, congenital anomalies). develops only with bilateral obstruction
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What acute renal injury if urine osmolality > 500, urine Na < 10, FeNa < 1%, and serum BUN/Cr > 20
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prerenal cause
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what acute renal injury if urine osmolality <350, urine Na>20, FeNa>2%, serum BUN/Cr<15
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renal cause
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What acute renal injury if urine osmalality <350, urine Na+>40, FeNa>4%, Serum BUN/Cr>15?
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postrenal cause
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If you have renal failure what can't you do? What are the 2 types?
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create urine and excrete nitrogenous wastes
2 types: 1) acute (ATN) 2) chronic (hypertension and diabetes) |
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What are the consequences of renal failure?
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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 |
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What is wrong in fanconi's syndrome?
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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)
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What can expired tetracycline cause?
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fanconi's syndrome
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What drugs can cause fanconi's syndrome?
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cisplatin, expired tetracycline
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What do you see in someone with fanconi's syndrome?
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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 |
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mannitol
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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 |
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When is mannitol contraindicated?
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anuria and CHF
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Acetazolamide
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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 |
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Ferosemide
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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 |
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the diuretic used in edema?
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Ferosemide - loop diuretic - works on ascending loop of henle - inhibits Na+/K+/2Cl- channel
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Ethacrynic acid
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same as ferosemide - but given to those with sulfa allergy - loop diuretic
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If someone needs a loop diuretic for edema and they have a sulfa allergy what can you use?
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Ethacrynic acid
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Hydrochlorothiazide
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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 |
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What do you use to treat nephrogenic diabetes insipidus?
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Hydrochlorothiazide
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K+ sparing diuretics
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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) |
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What does diuretics do to urine NaCl?
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all of them increase it - and water follows - serum NaCl may decrease as a result
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What does diuretics do to urine K+?
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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+
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What does CA inhibitors and K+ sparing diuretics do to the blood pH?
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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 |
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What do loop diuretics and thiazides do to blood pH?
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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 |
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What do loop diuretics do to Ca+?
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Loops Loose Calcium - abolish lumen positive potential in thick ascending limb of henle - decreased paracellular Ca+ resorption - hypocalcemia, increased urinary Ca+
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What do thiazide diuretics do to Ca+?
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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
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ACE inhibitors
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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 |
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What can you give a person if they have a cough from an ACE inhibitor?
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angiotensin II receptor blocker (ARB) - does not cause cough!
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ADPKD
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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 |
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ARPKD
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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
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dialysis cysts
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cortical and medullary cysts resulting from long standing dialysis
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simple cysts
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benign, incidental finding. cortex only
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Medullary cystic disease
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megullary cysts sometimes leads to fibrosis and progressive renal insufficiency with urinay concentrating defects. Ultrasound shows small kidneys - poor prognosis
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small kidneys on ultrasound
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medullary cystic disease - poor prognosis
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low serum Na+
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disorientation, stupor and coma
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high serum Na+
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neurologic; irritabiltity, delirum, coma
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low serum Cl-
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secondary to metabolic alkalosis, hypokalemia, hypovoluemia, increased aldosterone
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high serum Cl-
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secondary to non-anion gap acidosis
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low serum K+
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torsades, U waves on ECG, flattened T waves, arrhythmais, paralysis
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high serum K+
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peaked T waves, wide QRS, arrhythmias
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Low serum Ca2+
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tetany, neuromuscular irritability
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high serum Ca2+
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delirium, renal stones, abdominal pain, not necessarily calciruia
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low serum Mg2+
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neuromuscular irritability, arrythmias
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high serum Mg2+
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delirium, decreased deep tendon reflexes, cardiopulmonary arrest
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low serum PO4-
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low-mineral ion product causes bone loss, osteomalacia
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high serum PO4-
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high-mineral ion product causes renal stones, metastatic calcifications
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