Flashcards
UWorld Renal
Cards in this deck (78)
- 1#Schistosomiasis-haematobium: North + sub-Saharan Africa + middle east - urinary terminal hematuria + dysuria; hydronephrosis, pyelo, + SCC of bladder
-mansoni: above + south America and caribbean - #intestinal diarrhea + ab pain, intestinal ulceration and IDA, hepatosplenomegaly, periportal pipestem fibrosis and portal HTN
-japonicum: Asia; same as mansoni
-not in US bc don't have freshwater snails that incubate inf larvae
#-mature in liver and adults stay in blood vessels and release eggs that penetrate and get excreted in location of preference, eggs then inf snails
#-TH2 granuloma rxn, eosinophils, and macrophages --> fibrosis - 2#Fabry's disease-X linked lipid storage disorder --> alpha galactosidase A deficiency needed to break down globotriaosylceramide (sphingolipid)
-Gb3 accumulates in vasc smooth muscle, glomerulus/distal tubule cells, cardiac myocytes and dorsal root /autonomic ganglia
-early (teens): neuropathic pain/burning, hypohidrosis, distal loss of hot/cold sensation, angiokeratomas (dark red non blanching macules in clusters on butt, groin, umbilicus), telangiectasias
-late (adulthood): TIA, stroke, LVH, and proteinuria/polyuria (renal failure) - 3Rapidly progressive glomerulonephritis-macrophages and T cells pass into Bowman's space --> leakage of fibrin
-damage to glomerulus and BM
-fibrin deposits and parietal cells proliferate (macrophages mediate) --> fibrosis
-severe renal injury w/in weeks/months and irrev loss of fxn - 4Type I RPGN-goodpasture's syndrome
-C3 and IgG deposited in glomerular BM
-immunostain: linear deposition of immune complexes - 5Filtration fraction-fraction of plasma flowing through glomerulus that is filtered into the Bowman space (usu 20%)
-FF = GFR/RPF
-GFR est by clearance of creatinine or inulin (amount excreted = amount filtered bc no reabsorption or secretion)
-RPF est by clearance of PAH (mostly tubular secretion --> amount excreted > amount filtered) but is still filtered - 6Clearance calculation= ([urine conc of x] x [urine flow rate]) / plasma concentration of x
- 7Catheter inf risk-duration of catheterization most sig factor for UTI
-reduce risk by avoiding unnecessary cath, sterilization techniques, and removing ASAP
-antibiotic coating, bladder irrigation, and routine replacement not helpful
-prophyllactic antibiotics reduce risk but increases MDR - 8Focal segmental glomerulosclerosis-risks: AA, obesity, heroin, steroids, hepatitis, HIV
-slerosis of some portions of the glomeruli - 9Horsehoe kidney-incr risk of uretopelvic jxn obstruction, recurrent inf, urolithiasis, Wilms tumor in children, and RCC in adults
-central isthmus gets caught in IMA - 10RBFRBF = RPF/ (1 - hematocrit)
1 - hematocrit represents volume occupied by plasma (excluding RBCs) - 11#Henoch Schonlein purpura-most common systemic vasculitis in kids
-IgA ICs deposit in walls of small vessels and renal mesangium --> mesangial proliferation and crescent formation
#-activate complement in alternative/lecithin pathways
#-leads to organ dysfunction and palpable purpura (usu on LEs); also lower GI bleeding, bowel wall edema, and intussusception; self limited migratory arthralgias and arthritis
#-condition is self-limited and clears when ICs clear --> just supportive therapy - 12Fetal hydronephrosis-usu not clinically sig, due to high compliance of fetal renal pelvis (fetal kidney is susceptible to dilation)
-most common pathological cause of unilateral hydronephrosis is narrowing of proximal ureter at the ureteropelvic jxn (last segment to canalize)
-babies will have palpable abdominal mass from the dilated enlarged kidney
-obstruction from persistent membrane at posterior urethral valves most common cause of bilateral hydronephrosis (defect of Wolfian duct and only occurs in males)
-nonobstructive cause: incomplete closure of intravesicular portion of ureter during bladder contraction --> vesicoureteral reflux - 13Acyclovir nephrotoxicity-5-10% of pts getting IV
-toxicity can lead to crystallization and renal tubular damage --> acute rise in serum creatinine
-prevent with aggressive hydration and slowing the rate of IV infusion - 14Acute ureteral obstruction and FF-GFR decreased when obstruction causes pressure in Bowman's capsule to rise
-GFR decreases more than the compensatory increase in RPF --> FF also decreases - 15#Urea-filtered than reabsorbed passively (20-50%)
-no Tm/transporters - 16#Pelvic sgx risk-ureter close to pelvic vessels (iliac) where pelvic nodes are resected --> can be damaged in hysterectomy w/ pelvic LAD
-accidental ureter ligation causes obstruction w/ hydronephrosis and flank pain (ballotable mass)
#-urine output and cre normal bc other kidney compensates - 17#Vesicoureteral reflux#-complication of prostatectomy or bladder sgx or congenital right angle of the valve
-can lead to pyelonephritis and hydroureteronephrosis --> renal scarring/atrophy of upper and lower poles #(compound papillae in these regions are always open and are more vulnerable) - 18#Post strep GN-subepithelial humps on EM
-granular depositions w/in mesangium and glomerular capillary walls on IgG/C3 immuno (alternative complement pathway)
-neutrophils/monocytes infiltrate mesangium --> hypercellular appearance
-worst prognosis is older age --> less likely to resolve
#-due to antigens i.e. strep pyogenic exotoxin B
#-gross kidney swelling and surface punctate hemorrhages - 19Acid buffers in urine1) HPO4-: titratable acid that combines w/ H+ to form H2PO4-
2) NH3: generated by proximal tubular cells via metab of glutamine --> NH4+ (more impt bc kidneys can greatly incr NH3 in chronic acidosis)
-allows kidney to excrete acid w/o changing pH too much - 20Urine dilution and concentration throughout the nephron-DCT relatively impermeable to water and reabs of solutes continue to occur --> urine is most dilute in dehydrated states
-in dehydrated states, the collecting ducts contain most conc urine - 21Membraneous Nephropathy-nephrotic
-85% idiopathic
-other causes: diabetes, solid tumors, SLE, drugs (gold, penicillamine, NSAIDs), infs (hepatitis, malaria, syphilis)
-diffuse thickening of capillary wall w/o incr in cellularity
-spikes on EM
-immuno: IgG and C3 - 22Multicystic kidney dysplasia-nonhereditary renal malformation
-multiple cysts of varying size in kidney
-absence of normal pelvocaliceal system
-assoc w/ ureteral or ureteropelvic atresia
-affected kidney is nonfunctional but can be compensated by normal kidney
-abdominal US of fetus or newborn is diagnostic - 23Minimal change disease-nephrotic
-most common cause in kids
-usu occurs after resp inf, immunization, insect bite --> T cell dysfunction --> glomerular permeability factor (cytokine) --> damages podocytes and decreases negative charge of lining --> selective loss of albumin
-negative heparin sulfate usu repels anions
-no changes on LM, EM --> foot process effacement and fusion
-no immune complexes or IgG - 24Pyelonephritis-usu unlikely unless predisposition i.e. vesicoureteral reflux
- 25Renal papillary necrosis-obstruction of small renal vessels --> ischemia
-grey/yellow necrosis distal renal pyramids
-sloughed papillae visible as tissue flecks
-dark, bloody urine and colicky flank pain
CAUSES:
-sickle cell disease or trait: otherwise healthy pt w/ acute onset gross hematuria
-analgesic nephropathy: NSAIDs decr prostaglandins which vasoconstrict and decr renal blood flow
-diabetes, pyelo, and obstruction - 26Fanconi syndrome-polyuria, acidosis, and hypophosphatemia
- 27Kimmelstiel Wilson Nodules-diabetic nephropathy
-hyaline acellular deposits made of plasma proteins
-glomerular BM thickening, increased mesangial matrix deposition
-over time the nodules compress the capillaries --> decr fxn
-urine sediment usu normal i.e. neg for hematuria and casts, pos for proteinuria
-nodules are eosinophilic and PAS+ - 28Work up of metabolic alkalosis-check pts volume status and urine chloride
-can lose HCl from vomiting or nasogastric suction --> hypovolemia and low urine Cl- [saline responsive]
-thiazides and loop diuretics make you lose NaCl at first but then aldosterone kicks in --> high Cl- in urine then low [saline responsive]
-mineralocorticoid excess i.e. Conn syndrome or Cushing --> K and H loss and high urine Cl- bc of pressure natriuresis (HTN) [salt unresponsive bc aldosterone is autonomous] - 29Urachus-remnant of the allantois that connected the yolk sac to the urogenital sinus
-can be patent leading to straw colored urine discharge from the umbilicus
-can form a sinus or a cyst - 30Leukocyte adhesion def-decr expression of neutrophil call adhesion proteins (beta2 integrins)
-neutrophils fail to adhere to vessels and cannot move to inf
-delayed separation of umbilical cord > 1 month, and omphalitis (infection of the umbilical stump) - 31Embryonic kidney-comes from intermediate mesoderm
-ureteric bud from the caudal mesonephric duct forms collecting tubules --> ureters
-metanephric blastema forms everything up to the DCT - 32Serum Cre vs GFR-balance b/t cre syn in muscle and excretion via GFR (relatively constant and dependent mostly on GFR)
-nonlinear relationship: when GFR is normal, changes result in little change in cre
-when GFR is abnormal, small changes result in large changes in cre --> more sensitive - 33Uric acid-can be released along w/ phophorus, and K due to tumor lysis syndrome
-uric acid precipitates in low pH (lowest at DCT and collecting duct)
-prevent w/ urine alkalinization and hydration + allopurinol - 34Constriction of the efferent arteriole-increases GFR and decreases the RPF --> increases the FF
-as resistance increases though, a decr RPF causes more time for filtration --> high oncotic pressures overwhelm the hydrostatic pressure --> GFR falls at very high efferent arteriole resistances - 35Blood supply to ureters-proximal = branches of renal artery
-distal = branches of superior vesical artery
-in between: gonadal, common and internal iliac, aorta, and uterine arteries - 36Calcineurin inhibitor toxicity-i.e. cyclosporine and tacrolimus
-dose dependent renal vasoconstriction and tubular cell damage --> acute renal failure
-cyclosporine metab via liver and guy cytochrome p450 CYP3A (inhibited by grapefruit juice) - 37Aging kidney-renal function will decline but since muscle mass also declines --> cre can be normal
-always caution w/ dosing in elderly - 38Digoxin pharmacokineticsInfluencing factors:
-intestinal absorption (gut bacteria can degrade)
-excreted primarily unchanged by kidney (not cleared by liver)
-less than 1/3 is protein bound
-muscle mass primary source where digoxin is stored - 39Cholesterol emboli-blue toe, livedo reticularis following invasive vascular procedure
-cholesterol from large arteries lodge into small arteries --> ischemia
-AKI common after esp in elderly but no frank pain or hematuria bc cholesterol are small and needle shaped - 40Cystinuria-suspect in case of recurrent stones in young patient
-AR disorder of sodium indep dibasic a.a. transporter (cystine, ornithine, lysine, and arginine) [others are pretty soluble and do not form stones]
-hexagonal shaped crystals in urine or sodium cyanide nitroprusside test (add cyanide to urine to convert cystine to cysteine --> nitroprusside reacts to -SH and color changes to red/purple)
-tx: hydration and urine alkalinization - 41Orthostatic proteinuria Transient proteinuriaORTHOSTATIC
-usu adolescents
-higher protein excretion in upright position < 1 g/day (normal supine)
-renal function is normal
TRANSIENT
-change in blood flow through glomerulus due to exercise, fever, stress, or cold exposure
-common in young adults w/ normal renal fxn
-disappears in repeat testing - 42Idiopathic membraneous nephropathy-PLA2R antibodies that are mainly IgG4 --> immune deposition in glomerulus (not in secondary membraneous nephropathy)
-is a transmembrane R found on podocytes
-secondary causes: class V lupus nephritis - 43Mixed cryoglobulinemia-assoc w/ HepC
-IgM deposition in glomerulus --> BM thickening and cellular proliferation - 44Calcium oxalate tx-thiazides prevent excretion of Ca --> less Ca in urine to form stones
-although acetazolamide alkalinizes urine, it causes a metabolic acidosis which releases Ca from bone (potassium citrate is better) - 45IgA nephropathy-most common GN
-usu older children/YA w/in 5-7 days for URI
-painless hematuria lasts for several days, subsides and recurs with another URI
-mesangial hypercellularity and mesangial IgA deposits - 46JG hyperplasia-JG cells = modified smooth muscle cells w/ renin containing zymogen granules located in the wall of afferent arteriole
-long standing renal hypoperfusion i.e. renal stenosis leads to incr renin production and JG hyperplasia - 47Stones after colectomy-decreased absorption of bicarb from gut --> chronic metabolic acidosis and increased acid excretion from the kidney and increased bicarb reabs from kidney --> acidic urine (exacerbates certains stones i.e. uric acid)
- 48Urea and vasopressin-cortical collecting ducts are impermeable to urea but vasopressin activates urea transporters in the medullary collecting duct (passive) --> increases medullary osmotic gradient which maximally concentrates the urine
-normally: passively reabs in PCT and medullary collecting duct; also secreted by thin regions of the loop of Henle - 49Calcium handling-majority is passivley reabs in the PCT and ascending loop of Henle
-reabs from DCT stimulated by PTH - 50Foscarnet-used to treat gancyclovir resistant CMV
-can chelate calcium causing hypocalcemia
-also induces the wasting of Magnesium which can also decrease calcium
-changes in these --> seizures - 51Amphotericin B toxicity-nephrotoxic (decr GFR and direct tubular damage)
-can decrease EPO --> anemia
-increased membrane permeability of distal tubule --> hypokalemia and hypomagnesemia (weakness and arrhythmias) - 52Complications of chronic kidney disease-renal osteodystrophy/low calcium due to low vit D --> osteopenia or osteomalacia
-accumulation of uremic toxins decr peripheral conversion of T4 --> T3 (hypothyroidism)
-build up of uremia toxins --> fatigue, weakness, and itching - 53Renal vein thrombosis-flank pain, hematuria, and left testicular varicocele in setting of nephrotic syndrome bc loss of anticoagulant factors i.e. antithrombin III
-also incr LDH bc of ischemia - 54Citrate and stones-high urine citrate binds to calcium preventing crystallization and facilitating excretion
-low citrate can occur in metabolic acidosis i.e. distal renal tubular acidosis and chronic diarrhea bc of incr citrate reabsorption - 55Thiazide diuretics and calcium-causes hypercalcemia
-inhibition of the NaCl symporter reduces the Na inside DCT cells --> incr activity of basolateral Na/Ca exchanger (Na goes out, Ca goes in)
-volume depletion can also increase Ca reabs in the PCT - 56Analgesic nephropathy-modest elevation in cre, mild proteinuria, polyuria/nocturia (microscopic hematuria and sterile pyuria may be present)
-NSAIds conc in medulla and papillae --> uncouple oxidative p'ation --> deplete glutathione --> lipid peroxidation/damage --> chronic interstitial nephritis (fibrosis, tubular atrophy, papillary necrosis)
-calcium may deposit in areas of inflammation - 57Ischemic tubular necrosis-usu acutely after prolonged hypoTN (post sepsis, sgx)
- 58Stones and urine and serum levels-usu just an increase in urine conc and not necessarily increase in conc in blood
-i.e. calcium stones usu not due to hypercalcemia bc of regulation via PTH and vitD
-same with uric acid - 59ACEIs and acute renal failure-normally can expect serum cre to increase by 30%
-can cause acute renal failure in pts with renal artery stenosis, decompensated HF, CKD, and volume depletion - 60Drug induced kidney injury1) drug induced glomerular disease: usu immune mediated and not direct tox; heroin and pamidronate (FSGS) + gold (membraneous)
2) drug induced tubular necrosis: toxic or ischemic (aminoglycosides, radiocontrast, cisplatin, amphotericin B, and foscarnet)
3) drug induced tubular obstruction: tubular precipitation w/ sulfonamides, MTX, IV acyclovir, and triamterine
4) Interstitial nephritis: methicillin, cephalosporins, acetazolamide, allopurinol, sulfonamides, and NSAIDs; lithium and cyclosporine (CIN) - 61Ethylene glycol poisoning-acute tubular necrosis (PT cell ballooning and vacuolar degeneration)
-rapid absorption from GI --> metab to glycolic acid and oxalic acid (calcium oxalate crystals in tubular lumen)
-symptoms of alcohol intoxication, acute renal failure 24-72hrs after, high anion gap metabolic acidosis
-UA: tubular casts and oxalate crystals
-glomeruli are normal - 62Multiple Myeloma kidney injury-cast nephropathy: free light chains precipitate with Tam Horsefall proteins and form obstructive, glassy, intensely eosinophilic casts
-AL amyloidosis: deposition of light chain fragments in glomerular mesangium and capillary loops - 63Ischemic acute tubular necrosis-during oliguric phase (24-36hrs) --> hyperkalemia, metabolic acidosis, decr sodium and calcium, incr phosphate and magnesium; urine --> muddy brown casts, low urine osmolarity, high urine Na and fraction of sodium excretion
-tubular epithelial cells can regenerate --> recovery phase (1-2 weeks) --> vigorous diuresis, decr K, Mg, phosphate, and calcium; can become dehydrated (GFR fixed before absorption capability of the tubular cells)
-straight portion of PCT and TALH most susceptible bc in medulla and has high O2 demand - 64Kidney position in respect to ribs-12th rib false rib the overlies the parietal pleura medially and the L kidney laterally (fracture can lacerate the kidney)
-L ribs 9-11 overlie the spleen - 65Membranoproliferative GN-assoc w/ HepC inf
-hypercellular glomeruli, thickening and splitting of GBM bc of subendothelial IC deposition - 66Waxy casts-shiny tubular stuctures that form in dilated nephron tubules that hypertrophy in response to reduced renal mass
-due to chronic kidney failure - 67Acute hemolytic transfusion rxn-fever, chills, hypoTN, dyspnea, chest/back pain, hgb-nuria (red or brown urine)
-usu mins to hrs w/in blood transfusion and usu due to ABO incompatibility
-usu IgM --> complement --> shock and complement mediated cell lysis - 68CKD and metabolic bone disease-decr kidney fxn --> incr phosphate levels --> decr in calcium and increased prod of FGF-23 --> decreases PCT phosphate reabs and decr calcitriol production
-leads to elevated PTH --> osteitis fibrosa - 69Risk factors for stones-incr protein intake --> acid load --> buffered w/ bone salts --> hypercalciuria (also increases citrate reabs causing hypocitruria)
-incr sodium intake --> less reabs in PCT --> less calcium reabs --> hypercalciuria
-pyridoxine useful for hyperoxaluria bc decreases endogenous production - 70Net renal excretion rate=(GFR x plasma conc of X) - tubular reabsorption of X
- 71Psoas abscess-muscle: transverse processes/lateral vertebrae T12-L5 --> deep to inguinal ligament to insert onto lesser trochanter of the femur [hip flexor]
-risk factors: diabetes, IV drug use, HIV, immunosuppression
-signs: fever, flank or back pain, inguinal mass, difficulty walking
-psoas sign = pain when extending the hip - 72Fibromyalgia-abnormal central processing of pain stimuli
-exercise can exacerbate but incremental aerobic exercise can help
-TCAs and SNRIs considered when severe or refractory
-most common in women 20-55
-psych component - 73Polymyalgia rheumatica-inflammatory disorder in >50
-subacute pain/stiffness in shoulders, hips (not really soft tissue like fibromyalgia)
-weight loss, fever, and malaise - 74Polyarteritis nodosa-segmental, transmural inflammation of arterial wall with fibrinoid necrosis affecting small to medium arteries (not lung)
-hepB in 30% of cases showing surface Ag/Ab complexes
-internal elastic lamina disruption - 75Microscopic polyangiitis-also leukocytoclastic or hypersensitivty
-most common vasculitis assoc w/ antibiotic use
-affects only small vessels and is ANCA+ - 76COX-2-not constitutively active
-activated by inflammation (induced by IL-1 and TNF-alpha) --> syn of pro-inflammatory prostaglandins
-selective COX-2 inhibitors decrease inflamm but preserves protection of the GI (protected by COX-1) - 77Acute gout-first line are NSAIDs, 2nd line = colchicine; 3rd line = glucocorticoids (if pt has renal failure or is elderly)
-negative birefringent crystals - 78Rheumatoid arthritis-swan neck, ulnar deviation deformations
-rheumatoid nodules: firm, nontender subcutaneous nodules that occur at pressure points i.e. elbows or forearms
-autoreactivity to type II collagen and citullinated vimentin --> act CD4+ cells
-T cells tell B cells to make rheumatoid factor (IgM specific for Fc portion of IgG) and anti citrullinated Abs --> form immune complexes that act complement and cause chronic inflamm
Information
- Description
- Flashcards on UWorld Renal, created by Amanda Le on 19/12/2016.
- Created by
- Amanda Le
- Views
- 0
- Rating