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76 Cards in this Set
- Front
- Back
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Renal clearance equation
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UxV/P
Cx < GRF net tubular reabsorption of x Cx > GFR net tubular secretion of X Cx = GFR no net secretion or reabsorption |
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GFR equation
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GFR = Uinulin x V/ P inulin
normal = 100 ml/min |
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Effective renal plasma flow equation
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ERPF = U PAH x V / Ppah
RBF = RPF / 1-hct |
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Filtration fraction equation
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GFR/RPF = Uc x V/ Pc / Upah x V/ Ppah
normal = 20% |
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Filtered load equation
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GFR x plasma concentration
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Afferent arteriole
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Inhibition: constriction = - PG
Active: dilation = +PG |
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Efferent areteriole
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Inhibition: dilation = - ATII
Active: constriction = +ATII |
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Afferent areteriole constriction causes
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Dec RPF, dec GFR, NC in FF
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Efferent arteriole constriction causes
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Dec RPF, inc GFR, inc FF
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Inc plasma protein concentration
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NC RBF, dec GFR, dec FF
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Dec plasma protein concentration
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NC RBF, Inc GFR, Inc FF
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Constriction of ureter
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NC RPF, dec GFR, Dec FF
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Filtered load equation
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GFR x Px
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Excretion rate equation
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V x Ux
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Reabsorption equation
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Filtered - excreted
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Secretion equation
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excreted - filtered
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Plasma osmolarity equation
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2[Na+]plasma + [glucose]/18 + [BUN]/2.8
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Reabsorbs 67% of fluid and electroyltes filtered by glomerulus
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PCT
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Segment responsible for concentrating urine
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PCT
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Site of secretion of organic anions and cations
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PCT
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Always impermeable to water
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Thick ascending loop of Henle
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Permeable to water only when ADH present
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DCT and CT
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Site of Na/2Cl/K co transporter
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Thick ascending limb of loop of henle
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Site of isotonic fluid reabsorption
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PCT
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Site responsible for diluting urine
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Thick ascending limb
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Only site where glucose and amino acids are reabsorbed
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PCT
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Water reabsorption in the Loop of Henle
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Thin ascending limb
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What class of drugs inhibits the Na/2Cl/K symptorter in the thick ascending limb?
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Loop diuretics
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Principle cells of collecting duct
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Function: 1. reabsorb H20 and Na, 2. secrete K+
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Intercalated cells of collecting duct
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Function: 1. Secrete H+ or HCO3, 2. reabsorb K+
Types: Alpha: H+ secreting Beta: HCO3 secreting |
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K+ shifted out of cells --> hyperkalemia
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Low insulin
beta blockers ACIDOSIS digoxin cell lysis (leukemia) |
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K+ shifted into cells --> hypokalemia
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Insulin
beta agonists ALKALOSIS Cell creation/proliferation |
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Normal Ga values
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pH 7.35-7.45
pCO2 35-45 pO2 >90 (45 x 2) HCO3 22 (45/2) |
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Relative concentrations along proximal tubule
TF/P > 1 when: |
solute is reabsorbed less quickly than water
there is net secretion of solute |
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Relative concentrations along proximal tubule
TF/P =1 when: |
Solute and water are reabsorbed at the same rate
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Relative concentrations along proximal tubule
TF/P <1 when: |
Solute is reabsorbed more quickly than water
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Na+ disturbance
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Low: disorientation, stupor, coma
High: neurologic: irritability, delirium, coma |
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Cl- disturbance
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Low: secondary to metabolic alkalosis, hypokalemia, hypovolemia, inc aldosterone
High: secondary to non anion gap acidosis |
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K+ disturbance
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Low: U waves on ECG, flattened T waves, arrhythmias, paralysis
High: peaked T waves, wide QRS, arrythmias |
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Ca2+
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Low: tetany, neuromuscular irritability
High: Delirium, renal stones, abdominal pain, not necessarily calciuria |
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Mg+ disturbance
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Low: neurmuscular irritability, arrythmias
High: Delirium, dec DTRs, cardiopulmonary arrest |
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PO4 disturbance
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Low: Low mineral ion product causes bone loss, osteomalacia
High: high mineral ion product causes renal stones, metastatic calcifications |
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Henderson hasselbach equation
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HCO3/pCO2
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Causes of respiratory acidosis
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Hypoventilation: airway obstruction, acute lung disease, chronic lung disease, opioids, narcotics and sedatives, weakening of respiratory muscles
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Causes of anion gap metabolic acidosis: (Na - Cl + HCO3)
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MUDPILES:
methanol, uremia, DKA, paraldehyde/phenformin, iron tables/INH, Lactic acidosis, ethylene glycol, salicycates |
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Causes of normal anion gap metabolic acidosis (8-12 mEq/L)
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diarrhea, glue sniffing, renal tubular acidosis, hypercholremia
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Causes of respiratory alkalosis
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Hyperventilation (early high altitude exposure), aspirin ingestion (early)
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Causes of metabolic alkalosis with compensation (hypoventilation)
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Diuretic use, vomitting, antacid use, hyperaldosteronism
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Renal tubular acidosis type 1 ("distal")
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Defect in CT's ability to excrete H+. Associated w/ hypokalemia and risk for calcium containing kidney stones
Alkalosis pH>5.3 in urine |
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Renal tubular acidosis type 2 ("proximal")
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Defect in PCT HCO3- reabsorption. Associated w/ hypokalemia and hypophosphatemic rickets
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Renal tubular acidosis type 3 ("hyperkalemic")
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Hypoaldosteronism or lack of CT response to aldosterone. Associated w/ hyperkalemia and inhibition of ammonium excretion in PCT. Leads to dec urine pH due to dec buffering capacity.
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RBC casts from
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glomerulonephritis, ischemia or malignant hypertension
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WBC casts from
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tubulointerstitial inflammation, acute pyelonephritis, transplant rejection
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Granular (muddy brown) casts from
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ATN
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Waxy casts from
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advanced renal disease/CRF, urine stasis
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Hyaline casts
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nonspecific
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Nephritis syndrome
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an inflammatory process
When it involves the glomeruli, it leads to hematuria and RBC casts in urine. Associated w/ azotemia, oligouria, hypertension and proteinuria (<3.5 g/day) |
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Acute poststreptococcal glomerulonephritis
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LM: glomeruli enlarged and hypercellular, neutrophils, LUMPY BUMPY appearance
EM: subepithelial immune complex humps IF: granular Other: Most frequently seen in kids. Peripheral and periorbital edema. Resolves spontaneously. |
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Rapidly progressive (crescentic) glomerulonephritis (RPGN)
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LM and IF: cresecent moon shaped. Crescents consist of fibrin and plasma proteins with glomerular function parietal cells, monocytes and macrophages
Other: poor px. Rapidly deteriorating renal function (days to weeks) See other cards for subtypes |
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Goodpasture's syndrome (type of RPGN)
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Anti glomerular GBM ab's --> linear GBM deposits of IgG and C3 on immunoflourescence.
Anti GBM cross reaction with pulmonary alveolar GBM --> hemoptysis Type II hypersensitivity Reacts with alpha 3 chain of collagen type IV |
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Wegner's granulomatosis (type of RPGN)
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C ANCA +
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Microscopic polyangitis (type of RPGN)
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P ANCA +
no Ig or complement deposition on BM |
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Diffuse proliferative glomerulonephritis (due to SLE or MPGN)
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LM: wire looping of capillaries
EM: subendothelial DNA anti DNA IC's IF: granular Other: most common cause of death in SLE. SLE and MPGN can present as nephrotic syndrome. Remember WIRE LUPUS |
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Berger's disease (IgA glomerulonephropathy)
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Inc synthesis of IgA
LM and IF: IC's deposit in mesagnium Other: often presents/flares with URI or acute gastroenteritis |
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Alport's syndrome
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Mutation in type IV collagen --> split basement membrane
Other: nerve disorders, ocular disorders, deafness. X linked dominant. Can't see, can't pee, can't hear |
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Nephrotic syndrome
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presents with massive proteinuria (>3/5 g/day, frothy urine), hyperlipidemia, fatty casts, edema.
Associated w/ thromboembolism and inc risk of infection (loss of Ig's) |
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Membranous glomerulonephritis (diffuse membranous glomerulopathy)
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LM: diffuse capillary and GBM thickening
EM: spike and dome appearance w/ subepithelial deposits IF: granular. SLE's nephrotic presesntation Other; caused by drugs, infections, SLE, solid tumors. Most common cause of adult nephrotic syndrome. |
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Minimal change disease (lipoid nephrosis)
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LM: normal glomeruli
EM: foot process effacement Selective loss of albumin not globulins due to dec sialiac acid a poly anion in BM Other: associate w/ chronic conditions (MM, TB, RA) |
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Amyloidosis
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LM: congo red stain, apple green birefringence
Lambda light chain immunoflourescence |
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Diabetic glomerulonephropathy
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Nonenzymatic glycosylation (NEG) of GBM --> inc expansion
NEG of efferent arterioles --> INc GFR --> mesangial expansion LM: mesangial expansion, GBM thickening, nodular glomerulosclerosis (Kimmelsteil Wilson Lesion) |
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Focal segmental glomerulosclerosis
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LM: segmental sclerosis and hyalinosis
Other: Most common glomerular disease with HIV patients |
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Membrano proliferative glomerulonephritis
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Subendothelial ICs with granular IF
Type I EM: tram track apperance due to GBM splitting caused by mesangial ingrowth Type II EM: dense deposits Other: can also present as nephritic syndrome Type I: is associated w/ HBV, HCV, SLE, Subacute bacterial endocarditis, mixed cryoglobulinemia Type II: associated with C3 nephritic factor |
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Acute renal failure labs
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Inc BUN and creatinine with abrupt decline in renal function over several days
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Prerenal azotemia
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due to DEC RBF --> dec GFR
Na/H20 and urea retained by kidney in an attempt to conserve volume so BUN/Creatinine ratio Inc >500 osmolality <10 urine Na <1% Fena >20 Serum BUN/Cr |
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Intrinsic renal
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generally due to ATN or ischemia/toxins, less commonly due to acute glomerulonephritis
patchy necrosis leads to debris obstructing tubule and fluid backflow across necrotic tubule --> dec GFR Urine has epithelial/granular casts. BUN reabsorbtion is impaired --> dec BUN/creatinine ratio <350 urine osmolality >20 Urine Na >2% Fena <15 serum BUN/Cr |
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Postrenal
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due to outflow obstruction. Develops only with BILATERAL obstruction
<350 urine osmolality >40 Urine Na >4% Fena >15 serum BUN/Cr |
