Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
124 Cards in this Set
- Front
- Back
- 3rd side (hint)
|
C = ?
|
UV/P
|
|
|
|
Why is inulin clearance a good estimate of GFR
|
because it is freely filtered and neither secreted nor reabsorbed
|
|
|
|
Why is PAH clearance a good estimate of ERPF
|
Because it is both filtered and actively secreted in the proximal tubule
|
|
|
|
RBF =?
|
RPF/(1-Hct)
|
|
|
|
How does ERPF (as estimated by clearance of PAH) compare to actual RPF?
|
it underestimates it by about 10%
|
|
|
|
How does clearance of creatinine compare to GFR?
|
it is an overestimate because it is moderately secreted by the renal tubules
|
|
|
|
FF =?
|
GFR/RPF
|
|
|
|
Filtered load =?
|
GFR x Px
|
|
|
|
Excretion rate =?
|
V x Ux
|
|
|
|
Reabsorption =?
|
(GFR x Px) - (V x Ux)
|
|
|
|
where is glucose normally reabsorbed?
|
proximal tubules
|
|
|
|
Where are aa's usually reabsorbed?
|
proximal tubules
|
|
|
|
Where in the nephron does PTH exert its affects?
|
proximal tubule at the Na+/PO4 cotransporter
distal convoluted tubule inc. Na+/Ca2+ exchanger |
|
|
|
What are the main exchangers in the brush border cells of the proximal tubule?
|
Na+/H+ exchanger
Na+/glucose cotransporter Na+/K+ ATPase (exchanger) on opposite side |
|
|
|
Where within nephron is ammonium generated?
|
proximal tubule
|
|
|
|
How does AT II exert its effects in the proximal tubule?
|
inc. Na+/H+ exhanger so inc. sodium reabsorption and H+ excretion - contraction alkalosis
|
|
|
|
Where in the nephron is water impermeable?
|
Thick ascending loop of Henle - makes urine less concentrated as it ascends
|
|
|
|
Where in the nephron is impermeable to sodium?
|
Thin descending loop of Henle
|
|
|
|
What are the main exchangers on the luminal side of the thick ascending loop of henle?
|
Na+/K+/2Cl- pump
K+ channel (K+ exits via positive membrane potential) |
|
|
|
What are the main exchangers on the inerstitial side of the thick ascending loop of henle?
|
Na+/K+ exchanger
K+ channel Cl- channel |
|
|
|
Which ions are reabsorbed via paracellular method in PT?
|
Chloride
|
|
|
|
Which ions are reabsorbed via paracellular method in thick ascending loop of henle?
|
Mg
Ca |
|
|
|
Which is the concentrating segment of the nephron (always)
|
thin descending loop of henle - passively reabsorbs water via medullary hypertonicity (impermeable to sodium)
|
|
|
|
Where is the diluting segment of the nephron?
|
distal convoluted tubule
|
|
|
|
What are the main pumps/contransporters on the luminal side of the distal convoluted tubule?
|
NA+/Cl- cotransporter
Ca2+ channel |
|
|
|
What are the main pumps/contransporters on the interstitial side of the distal convoluted tubule?
|
Na+/K+ ATP-ase
Na/Ca exchanger Cl- channel |
|
|
|
What are the main pumps/contransporters on the luminal side of the principal cells of the collecting tubules?
|
Na+ channel (in)
K+ channel (out)( Aquaporin (H20 in) |
|
|
|
What are the main pumps/contransporters on the interstitial side of the principal cells of the collecting tubules?
|
Na+/K+ ATPase
|
|
|
|
What are the main pumps/contransporters on the luminal side of the intercalated cells of the collecting tubules?
|
K+/H+ exchanger
H+ actively pumped out also |
|
|
|
What are the main pumps/contransporters on the interstitial side of the intercalated cells of the collecting tubules?
|
HCO3-/CL- exchanger
(bicarb out Cl in) |
|
|
|
What do the juxtaglomerular cells respond to?
|
dec. BP
|
|
|
|
What do the macula densa cells respond to?
|
dec. Na+ delivery
|
|
|
|
What are the functions of AT II?
|
1) vasoconstriction
2) constricts efferent arteriole (inc. FF even if dec. RBF to preserve GFR) 3) Inc. aldosterone - inc. sodium (and water) reabsoprtion 4) inc. ADH - inc. water reabsorption 5) inc.Na+/H+ exchanger in PT (contraction alkalosis) 6) stimulates thirst in the hypothalamus |
|
|
|
Where are JG cells found?
|
afferent arteriole
|
|
|
|
Where are macula densa cells found?
|
distal convoluted tubule
|
|
|
|
Which cells of the kidney secrete erythropoietin?
|
endothelial cells of peritubular capillaries
|
|
|
|
Where does the conversion of vitamin D take place within the kidney?
|
proximal tubule cells
|
|
|
|
Which cells of the kidney secrete renin?
|
JG cells (in response to dec. renal arterial pressure and inc. renal sympathetic discharge Beta1 effect)
|
|
|
|
What does aldosterone do?
|
Na+ reabsoprtion
K+ secretion H+ secretion |
|
|
|
What causes potassium to shift into the cell (hypokalemia)?
|
insulin (inc. the Na+/K+ ATPase)
Beta-adrenergic agonists (Na+/K+ATPase) alkalosis (inc. K+/H+ exchanger) hypo-osmolarity |
|
|
|
What causes shift of potassium out of the cell (causing hyperkalemia)?
|
insulin deficiency
Beta blockers acidosis hyperosmolarity digitalis (blocks Na+K+ ATPase) cell lysis |
|
|
|
What does hypochloremia cause?
|
secondary to metabolic alkalosis
hypokalemia hypovolemia inc. aldosterone |
|
|
|
What causes hyperchloremia?
|
secondary to non-anion gap acidosis
|
|
|
|
What does hyperkalemia cause?
|
U waves on ECG
flattened T waves arrhythmias paralysis |
|
|
|
What does hypokalemia cause?
|
peak T waves
wide QRS arrhythmias |
|
|
|
What does hypocalcemia cause?
|
Tetany
neuromuscular irritability |
|
|
|
What does hyeprcalcemia cause?
|
delirium
renal stones abdominal pain |
|
|
|
What does hypomagnesemia cause?
|
neuromuscular irritability
arrhythmias |
|
|
|
What does hypermagnesemia cause?
|
delirum
dec. DTRs cardiopulmonary arrest |
|
|
|
What does hypophosphatemia cause?
|
lbone loss
osteomalacia |
|
|
|
What does hyperphosphatemia cause?
|
renal stones
associated w/ metastatic calcifications |
|
|
|
What are the findings in metabolic acidosis?
|
primary dec. in bicarb ==> dec. pH
compensatory hyperventilation ==> dec. PCO2 |
|
|
|
What are the findings in metabolic alkalosis?
|
primary inc. in bicarb ==> inc. pH
compensatory hypoventilation ==> inc. PCO2 |
|
|
|
What are the findings in respiratory acidosis?
|
primary inc. in PCO2 due to hypovntilation ==> dec. pH
compensatory inc. in bicarb |
|
|
|
What are the findings in respiratory alkalosis?
|
primary dec. in PCO2 due to hyperventilation ==> inc. pH
compensatory dec. in bicarb |
|
|
|
What is the formula for checking compensation for a acid/base shift?
|
for every 1meq/L inc. in bicarb there should be a 0.7mmHg increase in pCO2
|
|
|
|
What causes anion gap metabolic acidosis?
|
MUDPILES:
methanol uremia diabetic ketoacidosis Paraldehyde (or Phenformin) Iron tablets of INH Lactic acidosis Ethylene glycol (oxalic acid) Salicylates |
|
|
|
What causes non-anion gap metabolic acidosis?
|
Diarrhea
renal tubular acidosis hyperchloremia |
|
|
|
What drug toxicity causes respiratory alkalosis?
|
the early response to aspirin overdose
|
|
|
|
What causes metabolic alkalosis?
|
diuretic use
vomiting antacid use hyperaldosteronism |
|
|
|
What is the problem in Type 1 (distal) RTA and what does it cause?
|
defect in collecting tubule's ability to excrete H+
associated with hypokalemia and risk for calcium=contain kidney stones |
|
|
|
What is the problem in Type 2 (proximal) RTA and what does it cause?
|
Defect in proximal tubule bicarb reabsorption.
Associated with hypokalemia and hypophosphatemic rickets |
|
|
|
What is the problem in Type 4 RTA and what does it cause?
|
Hypoaldosteronism or lack of collecting tubule response to aldosterone
Associated with hyperkalemia inhibition of ammonium excretion in PT ==> dec. urin pH due to dec. buffering capacity |
|
|
|
When do you get RBC casts?
|
glomerulonephritis
ischemia malignant HTN (NOT cancer or kidney stones) |
|
|
|
When do you get WBC casts?
|
tubulointerstitial inflammation
acute pylonephritis transplant rejection (NOT acute cystitis) |
|
|
|
When do you get granular casts?
|
acute tubular necrosis
|
|
|
|
What are the sx of nephritic syndrome?
|
hematuria
RBC casts in urine azotemia oliguria hypertension proteinuria (<3.5g/day) |
|
|
|
Acute poststreptococcal histopath:
|
LM - "lumpy-bumpy"
EM - subepithelial IC "humps" IF - granular pattern |
|
|
|
RPGN glomerulonephritis is associated with which disease?
|
Goodpasture syndrome
Wegener's granulomatosis Microscopic polyangitis |
|
|
|
RPGN glomerulonephritis histopath:
|
LM and IF:
crecent-moon shape consisting of fibrin and plasma proteins (C3b) with PMN's and macros |
|
|
|
Diffuse proliferative glomerulonephritis is due to:
|
SLE or MPGN
|
|
|
|
Diffuse proliferative glomerulonephritis histopath:
|
LM - "wire looping" of capillaries
EM - subendothelial ICs IF - granular |
|
|
|
Berger's disease (IgA glomerulopathy) histopath:
|
LM and IF: ICs deposit in mesangium
|
|
|
|
Alport's syndrome nephritic syndrome
|
mutation in type IV collagen ==> split basement membrane
|
also nerve disorders, ocular disorder, deafness
X-linked dominant |
|
|
Presentation of nephrotic syndrome
|
proteinuria >3.5g/day
hyperlipidemia fatty casts edema |
associated with thromboembolism and inc. risk of infection (loss of Ig)
|
|
|
What causes membranous glomerulonephritis (aka diffuse membranous glomerulopathy)?
|
SLE
drugs infections solid tumors |
most common cause of adult nephrotic syndrome
|
|
|
Membranous glomerulonephritis (aka diffuse membranous glomerulopathy) histopath:
|
LM - diffuse capillary and GBM thickening
EM - "spike and dome" appearance with subepithelial deposits IF - granular |
this is SLE's nephrotic version
|
|
|
Minimal change disease histopath:
|
LM - normal glomeruli
EM - foot process effacement |
selective loss of albumin, not globulins due to GBM polyanion loss
|
|
|
Diabetic glomerulonephropathy histopath:
|
nonenzyamtic glycosylation of GBM ==> inc. permeability, thickening
NEG of efferent arterioles ==> inc. GFR ==> mesangial expansion LM - mesangial expansion, GBM thickening nodular glomerulosclerosis (Kimmelstiel-Wilson lesion) |
|
|
|
Focal segmental glomerulosclerosis histopath:
|
LM - segmental sclerosis and hyalinosis
|
most common glomerular disease in HIV patients
|
|
|
Membranoproliferative glomerulonephritis histopath:
|
LM - subendothelial ICs
IF - granular EM - type I = tram-track appearance due to GBM splitting causes by mesangial ingrowth TypeII - "dense deposits" |
can also present as nephritic syndrome
|
|
|
What is Membranoproliferative glomerulonephritis associated with?
|
Type I - HCV/HBV
Type II - C3 nephritic factor |
|
|
|
Which are the nephrotic syndromes?
|
Membranous/Diffuse membranous
Minimal change Focal segmental Membranoproliferative Amyloidosis Diabetic |
|
|
|
Which are the nephritic syndromes?
|
Acute poststrep
Rapidly progressive (crescentic) Diffuse proliferative Berger's Alport's |
|
|
|
What makes calcium oxalate stones worse?
|
Vitamin C
|
|
|
|
What makes ammonium magnesium phosphate stones worse?
|
urease positive bugs (PSK)
stag-horn calculi alkaline urine |
|
|
|
Who gets uric acid stones?
|
hyperuricemia conditions like gout and inc. cell turnover like leukemia
|
|
|
|
What makes cystine stones worse?
|
acidic urine
treat by alkalinizing the urine |
|
|
|
What condition is associated with renal cell carcinoma?
|
VHL - gene deletion on chromosome 3p
|
|
|
|
What is the WAGR complex?
|
Wilm's tumor
Aniridia Genitourninary malformation mental-motor Retardation |
|
|
|
What is the genetic abnormality in wilms' tumor?
|
deletion of tumor suppressor gene WT1 on chromosome 11(p)
|
|
|
|
What is associated with transitional cell carcinoma?
|
phenacetin
smoking aniline dyes cyclophosphamide |
|
|
|
What causes "thyroidization of the kidney"?
|
chronic pyelonephritis
|
|
|
|
What is renal papillary necrosis associated with?
|
diabetes mellitus
acute pyelonephritis chronic phenacetin use sickle cell anemia |
|
|
|
How does renal papillary necrosis present?
|
gross hematuria
proteinuria May be triggered by a recent infection of immune stimulus |
|
|
|
What happens to the BUN/Cr ratio in pre-renal azotemia?
|
increases (>20)
|
|
|
|
what happens to the BUN/Cr ration in acute tubular necrosis?
|
decreases (<15)
|
|
|
|
What happens to the BUN/Cr ratio in post-renal AKI?
|
increases (>15)
|
|
|
|
What happens to fractional excretion of sodium in prerenal azotemia vs. acute tubular necrosis?
|
pre-renal it decreases (<1%)
ATN it increases (>2%) |
|
|
|
What are the consequences of uremia?
|
nausea and anorexia
pericarditis asterixis encephalopathy platelet dysfunction |
|
|
|
What happens to your metabolic panel in chronic kidney failure?
|
hyperkalemia
metabolic acidosis |
|
|
|
What is ADPKD associated with?
|
polycystic liver disease
berry aneurysms mitral valve prolaps |
|
|
|
What is the presentation of ARPKD?
|
in utero - Potter's
congenital - hepatic fibrosis later - HTN, portal HTN progressive renal insufficiency |
|
|
|
Acetazolamide clinical use
|
glaucoma
urinary alkalinization metabolic alkalosis altitude sickness |
|
|
|
Acetazolamide toxicity
|
hyperchloremic metabolic acidosis
neuropathy NH3 toxicity sulfa allergy |
|
|
|
Furosemide MOA
|
loop diuretic. inhibits cotransport system (Na+/K+/Cl-) of thick ascending limb of loop of Henle ==> decrease osmolarity of the medulla ==> less concentrating of urine
*loose Ca2+ |
|
|
|
Furosemide toxicity
|
ototoxicity
hypokalemia dehydration allergy nephritis gout |
|
|
|
Ethacrynic acid clinical use
|
diuresis for patients with sulfa allergy
safe in patients with hyperuremia/gout |
|
|
|
Hydrochlorothiazide MOA
|
inhibits NaCl reabsorption in early distal tubule, reducing diluting capcity of the nephron
dec. Ca2+ secretion |
|
|
|
HCTZ clinical use
|
HTN
CHF idiopathic hypercalciuria nephrogenic diabetes insipidus |
|
|
|
HCTZ toxicity
|
hypokalemia
metabolic alkalosis hyponatremia hyperglycemia hyperlipidemia hyperuricemia hypercalcemia |
|
|
|
Spironolactone MOA
|
competitive aldosterone receptor antagonist in the cortical collecting tubule so decrease Na+ reabsoprtion and dec. K+/H+ secretion
|
|
|
|
Spironolactone clinical use
|
hyperaldosteronism
hypokalemia CHF |
|
|
|
Spironolactone toxicity
|
hyperkalemia
gynecomastia |
|
|
|
Which diuretics can cause hypokalemia?
|
All but K+-sparing (spironolactone)
|
|
|
|
Which diuretics can cause acidemia?
|
Acetazolamide
Spironolactone |
|
|
|
Which diuretics cause alkalemia?
|
loops (furosemide)
thiazides (HCTZ) |
"contraction alkalosis"
|
|
|
Which diuretics cause hypercalcemia?
|
thiazides
|
|
|
|
Which diuretics cause hypocalcemia?
|
loops
|
|
|
|
ACE inhibitors MOA
|
inhibit angiotensin converting enzyme in the lungs so less angiotensin II and more bradykinin (less inhibition)
|
|
|
|
ACE toxicity/side effects
|
hyperkalemia
proteinuria angioedema taste changes rash (increased renin) *avoid with bilateral renal stenosis |
|
|
|
Which glomerulonephropathy has subepithelial deposits?
|
acute glomerulonephritis
membranous glomerulonephritis (SLE's nephrotic presentation) |
|
|
|
Which glomerulonephropathy has subendothelial deposits?
|
Membranoproliferative
Diffuse proliferative (SLE nephritis) |
|
|
|
Which glomerulonephropathy has mesangial deposits?
|
IgA glomerulopathy
|
|
