Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

114 Cards in this Set

  • Front
  • Back
what structures are retroperitoneal
1) duodeonum (not first part), ascending colon, descending colon, rectum. 2) pancreas (not tail) 3) kidneys, adrenals 4) aorta, IVC
metanephric mesoderm gives rise to
renal cortex. except (medullary?) collecting duct
uteric bud gives rise to
(medullary?) CD, calyces, pelvis
describe the path of the ureters
retroperitoneal. behind the uterine artery/ductus deferens
what do you use to measure plasma volume
albumin (radiolabeled)
what do you use to measure ECF
what percent of total weight is TBW
what percent of total weight is ICF
what percent of total weight is ECF
renal clearance of substance x =
equals Ux * V / Px
components of glomerular filtration system?
1) fenestrated endothelium = size barrier. 2) bm = negative charge barrier (heparan sulfate) 3) podocytes
nephrotic syndrome. what part of the glomerular filtration system is lost? what is the result
lose bm (negative charge barrier) => albuminuria/hypoproteinemia => edema + hyperlipidemia
what do you use to measure GFR, why?
inulin or creatinine. because they're not secreted or absorbed so Cx ~ GFR
what do you use to measure RPF, why?
PAH. because it's completed filitered/secreted in 1 pass, so Cx ~RPF
how do you convert RPF to RBF
Hct = 1 - (RPF/RBF)
prostaglandins. what happens to GFR, RPF, and FF
dilate afferent => GFR inc, RPF inc => FF const
NSAIDs. what happens to GFR, RPF, and FF
less afferent dilation = constrict afferent => GFR dec, RPF dec => FF const
AII. what happens to GFR RPF, and FF
constrict efferent => GFR inc, RPF dec => FF inc
ACEi. what happens to GFR, RPF, and FF
dilate efferent => GFR dec, RPF inc => FF dec
constrict ureter: GFR?
GFR down
free water clearance =
Ch2o = V - Cosm. V = urine flow rate. Cosm = clearance of all osms. Volume of plasma filtered that "didn't have any osms in it" (ie. if positive you're extracting free water… diuresing)
at what plasma glucose level does glucosuria begin?
200 mg/dL. proximal tubule absorption is maxed out at 350 mg/dL
what normally happens to blood glucose during filtration?
completely reabsorbed at PT by Na+, glucose co-transporter
amino acid absorption… how does it work?
2° active. competitive inhibition between multiple carrier sstems. saturable
draw out how bicard is absorbed in the PT
how is H+ excreted in the PT and what activates it
Na+/H+ antiporter. AII
where do Mg2+ and Ca2+ get abs… and how!
thick ascending loop. NaK2Cl creates positive lumen => paracellular abs of Ca and Mg. also trans cellular Ca in the early distal convoluted tubule (PTH)
why do loop diuretics dec Ca2+, Mg2+ abs
lumen more negative because NaK2Cl makes it more positive
how does PTH increase Ca2+ abs
increasing Ca abs in the early distal convoluted tubule
what does the principal cell do
Na+ abs, K+ sec
what does the intercalated cell do
H+ excretion
max osmolarity of medulla?
1200 mOsm
what parts of the nephron are permeable to H2O
proximal through thin descending loop. collecting duct is variable
what are the two components of the JGA
JG cells in afferent arteriole. Macula dense in distal convoluted tubule
What does the macula densa sense and how
Cl-. By a NaK2Cl.
describe the endocrine functions of the kidney
1) hypoxia => HIF => epo. 2) PTH => 1 alpha hydroxylase converts 25-OH VitD => 1,25-OH VitD 3) dec bp, inc ß1 => renin 4) prostaglandins keep afferent arteriole dilated
which cells secrete renin
JG cells of afferent arteriole
how can NSAIDs cause acute renal failure?
dec renal prostaglandin synthesis => afferent arterioles constrict
in the kidney, how does ANP work
1) dilate afferent, constrict efferent 2) block ENaC
what exactly does PTH do in the nephron
1) dec PO4 abs in the PT. 2) inc Ca2+ abs in the distal convoluted tubule 3) inc hydoxylation of vitD
specifically, what does aldo do in the collecting duct
1) Principal cells. inc Na abs, K sec: inc Na, K channels, inc NaK ATPase. 2) Intercalated cells: H+ ATPase.
Hendersen-Hasselbach equation
pH = pKa + log( [HCO3-] / 0.03 • PCO2)
weak respiratory muscles would cause what sort of acid base disturbance
respiratory acidosis
Anion gap =, what's NL
Na - Cl - HCO3. 8-12
pH cut off for acidosis/alkalosis
normal PCO2 level
causes of anionic gap metabolic acidosis
MUDPILES: Methanol, Uremia, Diabetic ketoacidosis, Paraldehyde + Phenformin (~metformin), INH + Iron tablets, Lactic acidosis, Ethylene glycol, Salicylates (aspirin may first causes respiratory alkalosis)
causes of respiratory acidosis
hypoventilation (lung diseases, weak respiratory muscles, sedation eg opioids)
causes of non anion gap metabolic acidosis
diarrhea, hyperchloremia, RTA, glue sniffing
causes of metabolic alkalosis
vomitting, diuretics (loop, thiazide), antacids, hyperaldosteronism (K out of cells for H?)
causes of respiratory alkalosis
hyperventilation, e.g. aspirin (early effect… then metabolic acidosis)
draw the acid/base compensation matrix
potter's syndrome: cause? findings? death from?
bilateral renal agenesis => oligohydramnios => deformed face/limbs + pulmonary hypoplasia (death). Cause = malformation of uteric bud
Horseshoe kidney. where?
interior poles fused. during ascent, trapped under IMA. can p/w with urinary tract obstruction
RBCs (not casts) in the urine, what should you be worried about?
bladder cancer
WBCs (not casts). what could be the cause
acute cystitis
RBC casts a/w
nephritic syndromes (glomerular inflammation), ischemia, malignant htn
WBC casts a/w
pyelonephritis, tubulointerstia/glomerular dz
Granular casts a/w
chronic renal failure
Adult polycystic kidney disease. inheritence? gene? a/w? not a/w?
AD. PKD1. a/w BERRY ANEURYSM, liver cysts, polycythemia. p/w htn, hematuria, palpable mass. prognosis: renal failure
infantile polycystic kidney disease. inheritence? prognosis?
cysts at birth. quick death
what's the effect of long term dialysis on kidneys?
acquired cystic disease. multiple, with scarring. => RCC
name the four common types of nephrolithiasis
**calcium (phosphate or oxalate or both), *ammonium magnesium phosphate (struvite), uric acid, cystine
calcium stones, causes?
cancer, PTH, Vit D, mlik alkali, ethylene glycol
ammonium magnesium phosphate, causes?
infection w/ urease + bug: proteus, staph, klebsiella
uric acid stones. cause?
hyperuricemia (e.g. gout). often w/ leukemia, myeloproliferative
cystine stones. cause? what do they look like? test?
cystinuria (failure to absorb basic aa). yellow-brown hexagonal. + nitroprusside cyanide test.
which kidney stones are radiopaque
the two common ones: Calcium and ammonium magnesium phosphate. (cystine if it's complexed with Ca)
RCC. who gets it? risk?
men 50-70, smoking, obesity
RCC. a/w what gene? chromosome?
VHL, 3
RCC. histo?
polygonal clear cells
RCC. presentation? spread?
hematuria, mass, polycythemia, pain. invade IVC => hematogenous spread.
RCC. paraneoplastic syndrome (4)?
EPO, ACTH, PTHrp, Prolactin.
Wilm's tumor. who? p/w?
kids. mass, hemihypertrophy
Wilm's tumor. Genes? Ch? A/w?
WT1: WAGR (Wilm's tumor, aniridia, genitourinary malformations, motor/mental Retardation), Denys-Drash syndrome (interesex, nephropathy, WT). WT2: Beckwith-Wiederman syndrome (macroglossia, m ret)
Transitional cell cancer p/w
painless hematuria
transitional cell cancer. caused by
Pee-SAC: Phenacetin, Smoking, Analine dytes, Cyclophosphamide
Thyroidization of the kidney
chronic pyelonephritis: tubules w/ esoinophilic casts
diffuce cortical necrosis. what is it, what causes it, a/w
obstetric complications (abruptio placentae) or septic shock => DIC + vasospasm => acute generalized infaction of both renal cortices
what's the most common cause of acute renal failure?
acute tubular necrosis
what causes acute tubular necrosis
renal ischemia, crush injury (myoglobinuria), toxins
how does acute tubular nerosis progress
oliguric phase (1 wk) => death or diuretic phase (2 wk) => recovery
Acute interstitial nephritis caused by?
hypersensitivy to drugs (penecillin, NSAIDs, sulfa). a/w ARF, eosinophilia, rash
renal papillary necrosis is a/w
DM, acute pyelonephritis, chronic phenacetin use. if pathy => sickle cell
Acute renal failure: blood levels? 3 types? what causes them?
BUN, and Cr inc over days. Prerenal (dec RBF), Renal (glomerular dz => RBCs, acute tubuluar necrosis => epi/granular casts, inflammation => WBC), Postrenal (outflow tract obstruction, must be bilateral)
Prerenal azotemia: Uosm, Una, FEna, BUN/Cr
dec flow to kidney => inc blood volume => abs. Uosm >500. Una < 10 (abs with water), FEna <1, BUN/cr (BUN is abs, Cr is not)
Renal azotemia: Uosm, Una, FEna, BUN/cr
can't concentrate. Uosm <350. UNa > 20 (can't abs, follow water), FEna > 2%, BUN/Cr < 15
Postrenal azotemia: Uosm, Una, Fena, BUN/cr
trying to get rid of fluid b/c "backs up". Uosm < 350. Una > 40 (get rid of w/ water) FEna > 4%, BUN/Cr > 15 (automatically gets abs?)
what causes chronic kidney failure?
diabetes, hypertension… chronic pyelonephritis?
consequences of chronic kidney failure
1) uremia => encephalopathy 2) dec EPO => anemia 3) dec D => renal osteodystrophy 4) inc renin => hypoK (arrhythmias), hyperNa, volume overload (CHF) 5) dec H+ sec, dec HCO3 abs => met acid 6) chronic pyelonephritis
low/high Na
low: stupor/coma. high: delirium/coma
low/high Cl. when?
low: met alk. high: met acid (non ion gap)
low/high K
low: U, flat T, arrhythmias. high: peaked T, arrhthmia
low/high Ca2+
low: tetany. high: stones, delirium
low/high Mg2+
low: arrythmia. high: dec DTRs, delirium
low/high PO4-2
low: bone loss (ion product). high: metastatic calcification (ion product).
minimal ∆ dz vs. membranous GN. c&c
both nephrotic. minimal: kids, steroids, NL LM, fused foot on EM. membranous: adults, eh steroids, LM thick bm/cap, IF: granular IgG C3, EM "spike & dome", fused feet
nephrotic syndrome findings
lose charge barrier => albuminuria, hypalbuminemia, hyperlipidemia => edema (peripheral + periorbital)
name the nephrotic syndromes
minimal change dz, membranous GN, focal segmental glomerulosclerosis, diabetic nephropathy, SLE nephropathy
name the nephritic syndromes
acute poststrepococcal glomerulonephritis, RPGN (inc GP), membranoproliferative GN, IgA nephropathy, Alport's syndrome
LM, IF in focal segmental glomerulosclerosis
LM: capillary sclerosis + hyalinosis, IF: IgM C3
membranous GN vs. FSGS on IM
membranous is IgG+C3, FSGS = IgM+C3
Kimmelstiel Wilson
diabetic nephropathy
SLE nephropathy
membranous on LM, subendothelial on IF
acute poststrep GN on LM
hypercellular enlarged glomeruli w/ PMNs
subepithelial deposits
aucte postrep GN, membranousGN
RPGN what's in the crescents?
cells and fibrin in Bowman's space
GP on renal histo?
crescentic. IF: antiGBM linear pattern
IgA nephropathy histo
(Berger's dz): IF, EM: mesangial depsoites of IgA
Alport's syndrome on EM
splitting of BM
membranoproliferative GN on EM
subendothelial humps, tram-track (split BM)
subendothelial deposits
membranoproliferative GN (also tram track)
which glomerular pathologies are associated with IC
SLE, post-strep, membranous
orthostatic proteinuria. who?
tall, thin adolescents