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board review > renal > Flashcards

renal Flashcards

1
Q

what is the effect of dehydration on FF (filtration fraction)

A
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2
Q

decrease circulating BV (diarrhea and vomiting) –> dec renal plasma flow

which will result in the relase of renin –> inc angiotensin II –> efferent glomerular arterioles constriction to maintain the GFR

know that the dec in GFR in hypovolemia is less than the decrease in RPF

so the ratio (FF) GFR/RPF increases

A
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3
Q

Excretion = ?

A

Excretion = (filtration + secretion) - reabsorption

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4
Q

loss of HCO3- in the proximal tubules

diagnosis

A

type 2 RTA

same mechanism as suppressing the carbonic anhydrase enzyme

cant reabsorb bicarb –> acidosis

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5
Q

2 questions on boards

canagliflozin

moa

side effect

A

sodium glucose co-transport inhibitors (SGLT-2 inhibitors)

in the PCT. –> inc renal excretion of glucose

side effect: glucosuria –> UTI, genital mycotic infections

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6
Q

explain how ADH works

know its water soluble (binds to membrane receptors)

vs

aldosterone = lipid soluble (goes into cell)

A

it stimulates V2 receptors (through cAMP) in the late distal tubules and collecting ducts –> facilitates insertion of water channels (Aquaporin) in the renal collecting ducts –> inc free water reabsorption

know that ADH activates V1 receptors (by IP3 mechanism) –> vasoconstriction –> vascular resistance.

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7
Q

a pt with orthostatic hypotension due to blood loss.

what will happen

A

inc ADH

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8
Q

how is lithium nephrotoxic

A

inhibits the renal actions of vasopressin

(blocks aquaporin function!!!!) thus pt will develop diabetes insipidus

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9
Q

on the boards

pt with confusion, stupor, N/V, seizures or coma

pt has hyponatremia.

what paraneoplastic syndrome is causing this

A

SIADH

from small cell carcinoma

“pt has cerebral edema from retaining water. this is causing the symptoms”

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10
Q

hyponatremia

(confusion, stupor, N/V/ seizures or coma)

can be cause by?

A

SIADH

addisons disease

SSRI or diuretics

CHF, nephrotic syndrome, liver cirrhosis ( will have normal NA, however there is more h2o in body diluting it) thus can give loops.

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11
Q

on the boards

elderly pt with dementia and dehydration

(this isthe most common cause of ?)

A

hypernatremia.

excessive losses of water from the Urinary tract, seen in pts with uncontrolled diabets mellitus also.

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12
Q

on the boards

water losses associated with extreme sweating or severe watery diarrhea

can cause

A

hypernatremia

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13
Q

on the boards

pt with ST depression, flattened T waves and U waves on EKG palpitation and Muscle spasm and Weakness.

diagosis

A

hypo kalemia

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14
Q

what are the meds that cause HYPOKALEMIA

know this

A

ampohtericin B

cisplatin

loops

thiazide

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15
Q

pt has disseminated histoplasmosis

and is on amphotericin B

now he has arrythmia, what is the cause

A

hypokalemia and hypomagnesia from amphotericin.

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16
Q

what drugs can cause HYPERKALEMIA

A

ace inhibitors and ARBS

K sparing

Nsaids (ibuprofen)

cyclosporin and tacroimus

Pentamidine (used in HIV)

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17
Q

Q

HIV pt treated for SJS with pentamidine

what electrolyte innbalance do you expect?

A

hyperkalemia

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18
Q

on the boards

HYPERKALEMIA symptoms

A

on the boards

pt with malaise

palpitations

and muscle weakness

EKG = peaked T waves and Widening of the QRS complex

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19
Q

pt is depressed and hasnt gone to his hemodialysis sessions

now he has muscle weakness and palpations

and get an eKG whats the cause?

A

hyperkalemia

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20
Q

Cisplatin

Gentamicin

Amphotericin B

PPi induced

all these cause?

A

hypomagnesemia

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21
Q

hypomagnesemia may cause potassium wasting in the urine –>

A

hypokalemia

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22
Q

magnesium has what effect on PTH

A

stimulus secretion coupling of PTH

thus hypomag will dec PTH secretion –> hypocalcemia

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23
Q

what is the main factor in secondary HTN due to renal artery stenosis

A

renin

thus avoid ACE inhibitors

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24
Q

low na (sensed by macula densa) or low perfusion in the (afferent arterioles)

stimulate the release of renin from the JG cells.

renin will due what?

A

acitvate angiotensin –> aldosterone system –> vasoconstriction, Na, and water retention

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25
Q

pt with BUN =80, Cr = 2.

True volume depletion.

what kind of acute kidney injury?

A

pre renal azotemia

bc BUN: Cr ratio> 20

80/2 = >20

26
Q

68 yo man with hx of CHF - no leg edema and his creatinine is 1.2

seen in a walk in clinic for back pain and started on ibuprofen

two days later he developed leg swelling, sob and his creatinine is 2.8.

what is the most likely cause of his symptoms

A

blocking progstaglandin effect on the afferent arterioles

(prerenal azotemia)

normally prostaglandins normally cause vasodilation of the aff arterioles of the glomeruli

AKI with inc creatinine is seen in prostaglandin dependent pt

e.g. CHF who started on NSAID

27
Q

why will AKI pt on ace inhibitors have increase in creatinine and K

A

angiotensin II keeps the tone of the efferent arteriole.

ACE inhibitor will dilate the efferent decreasing glomerular pressure thus less creatinine is filtered out

28
Q

tumor lysis syndrome

can cause POST renal AKI

how

A

metabolites of nucleic acid turnover –> increase during cell destruction –> inc URIC ACID –> renal and ureteric stones.

  • uric acid precipitates in the ACIDIC medium in the DCT and collecting ducts.

prevention hydration and alkalinization of urine,

29
Q

interstitial edema and infiltration with mononuclear cells (lymphoctes and macrophages)

and

eosinophils in urine

A

seen in interstitial nephritis

30
Q

on boards

pt started on antibiotics (B-lactam) or allopurinol, or cimetidine

classic triad

fever

rash

eosinophilia and eosinophil in urine

A
31
Q

what are the two important drugs (on boards) that cause

post renal azotemia

A

acyclovir

indinavir

32
Q

what are the two important drugs (on boards) that cause

post renal azotemia

A

acyclovir

indinavir

33
Q

hexagonal kidney stone

A

cystine

34
Q

for the boards

the only stone that is radiolucent on xray

A

uric acid

(even though first aid say cystine stones)

35
Q

referred pain to the groin and the scrotum may be seen in male pts with ureteric colic

A

renal calculi (kidney stone)

36
Q

causes of metabolic alkalosis

A

vomiting and nasogastric suction –> HCL loss

  • dec serum chloride –> dec urinary chloride

thiazides and loops diuretics –> renal Na loss (followed by Cl-)

  • inc HCO3- reabsorption to maintain electric neutrality
  • volume contraction induced by diurectic –> inc aldosterone -> inc H loss

primary hyperaldosteronism

37
Q

normal anion Gap metabolic acidosis

RENAL TUBULAR ACIDOSIS

DIARRHEA

REMEMBER that the pt will be dehydrated and that will stimulate?

A

release of ADH

38
Q

in renal tubular acidosis

why are they all

normal anion gap metabolic acidosis

A

bc hypercholermic

39
Q

boards

which diuretic induced normal anoion agap acidosis

A

acetazolamide

40
Q

what kidney tumor metasizes to lung where you see

CANNONBALL lesions

A

renal clear cell carcinoma

41
Q

wilms tumor arises from embryonal renal cells of?

A

metanephros

42
Q

bleeding time is prolonged in pts with uremia (Chronic kidney disease) why?

A

due to platelet dysfunction not thrombocytopenia

43
Q

what is the most common cause of CKD in the US or they could ask what is the most common cause of hemodialysis in the US

A

type 2 DM

followed by persistent HTN

44
Q

in minimal change disease

you get (albumin) proteinuria why?

A

loss of the negative charges on the basement membrane

albumin is negative charged so it normally doesnt cross.

the negatively charaged glycosaminoglycans

(such as heparan sulfate)

45
Q

dehydration

your

RPF ___

GFR ___

FF___

A

RPF DEC DEC

GFR dec

FF inc

46
Q

membranous nephropathy

A

good question!!!

what is the most common nephropathy associated with

renal vein thrombosis???

47
Q

membranoproliferative GN

A

hepatitis C virus infection

48
Q

minimal change disease (lipoid nephrosis) is associated with lymphoma

membranous nephropathy is associated with?

A

solid tumors

49
Q

EM: spike and dome

A

membranous nephropathy

50
Q

in minimal change disease

how does hodgkins lymphoma effect the glomerulus

A

the lymphokines from the T lymphocytes cause fusion of the podocytes

51
Q

Boards (presentations)

  1. african american male, drug abuser, could be homeless

obese, NOT diabetic

2. heavy proteinuria in an obese caucasian individual

3.chronic vesico-ureteric reflux

EM: no immune complex deposition - effacement of foot processes

A

FSGN

(focal segmental sclerosis)

52
Q

on boards

tx of minimal change disease

A. prednisone

B. prednisone and cyclophosphamide

A

prednisone

53
Q

Q on boards

what is the most common SECONDARY cause of nephrotic syndrome in adults

A

diabetic nephropathy

54
Q

trick question

diabetic pt,

his blood pressure in your clinic is always 110/70. however, on UA he has microalbuminurea.

what is your next best step in tx?

A

start ACEI or Arbs even if normotensive

55
Q

diabetic nephropathy can induce what type of RTA?

A

type 4 RTA with hyperkalemia

56
Q

pathogenesis

know that glomerular hyperfiltration is caused by dec ristance in both the afferent and efferent arterioles (aff> eff)

-diffuse BM thickening and mesangial cell overproduction -> microalbuminuria (the earliest clinical sign)

persistentHYPERGLYCEMIA is an important factor in pathogenesis of microalbuminuria

A

diabetic nephropathy

57
Q

what is the earlier clinical sign of diabetic nephropathy

A

microalbuminuria

58
Q

Q

HIV associated nephropathy

what is the pathology

A

collapsing focal glomerulosclerosis with tubular microcyst formation

A focal segmental variant

59
Q

Question!!!!

treament of HIV -associated nephropathy

A

ACE -inhibitor

60
Q

glomerular pathology in eclampsia

A

Endothelial dysfunction

glomerular endotheliosis

(diffuse endothelial swelling + fibrinogen deposition on the endothelial side of the capillaries) –> proteinuria (endothelial proliferation)

this is the cause of the proteinuria in eclampsia pt

61
Q

pt with elampsia

develops confusion, has cerebral edema

what is the cause of this

A

not HTN

but do to damage

endothelial cells in the cerebral vessels.

62
Q
A

board review (20 decks)

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