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Step 1- System embryology, A and P > renal > Flashcards

renal Flashcards

1
Q

horseshoe kidney associated with

A

Turner’s syndrome

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2
Q

horseshoe kidneys get fixed low by

A

inferior mesenteric atrery

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3
Q

normal GFR

A

100 ml/min

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4
Q

nephrotic syndrome results in

A

albuminuria, hypoproteinemia, generalized edema, hyperlipidemia

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5
Q

normal filtration fraction

A

20%

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6
Q

location of juxtaglomular cells

A

efferent aterioles

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7
Q

effect of NSAIDS on aterioles

A

contrict (Prostoglandins dilate) afferent arteriole, increases RPF, GPR and FF stayes consistent (nsAid - Afferent)

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8
Q

Filtration fraction calulation

A

GFR/RPF

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9
Q

GFR estimated with

A

creatine clearance

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10
Q

RPF estimated with

A

PAH clearance

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11
Q

ACE inhibitors effect on arterioles

A

contstrict (Angiotensin II dilates) efferent arteriole, so RPF down, GFR up, so FF increases acE - Efferent)

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12
Q

plasma glucose level above which glocsuria begins

A

160mg/dL

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13
Q

plasma glucose level that saturates all glucose transporters

A

350 mg/dL

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14
Q

hartnup’s disease

A

deficnecy of neutral amino acid transporter (tryptophan), results in pellagra

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15
Q

reabsorbs all glucose and amino acids and most bicarb, Na, Cl, phophate and water

A

early PCT

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16
Q

PTH effect on early PCT

A

excretion of phosphate

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17
Q

Angiotension II effect on early PCT

A

increased Na, water, and bicarb absorption

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18
Q

part of nephron impermeable to sodium

A

thin decending loop

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19
Q

actively absorbes Na, K, Cl-

A

thick ascending loop

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20
Q

actively reabsorbs Na, Cla dnmakes urine hypotonic

21
Q

part if nephron impermeable to water

A

thick ascending loop

22
Q

PTH effect on DCT

A

Ca reabsorption

23
Q

aldosterone effect on kidney

A

insertion of Na channel on luminal side of collecting duct and reasorbs Na

24
Q

ADH effect on kidney

A

inserts aquaporin channels on luminal side to reasorb Na and water

25
Q

carbonic anhydrase inhibotors work at

26
Q

thiazide diuretics work at

27
Q

loop diuraetcs work at

A

thick ascending loop

28
Q

K sparing (amiloride/traimterene) diuretics work at

A

collecting tibule

29
Q

histology of JxG apparatus

A

modifed smooth muscle cells of afferent artierole

30
Q

ANS receptor at JXG

31
Q

MOA of B blockers on BP at kidney

A

inhibit B1 recpetors at JGA, causing lower renin release

32
Q

release Epo

A

intersistial cells in the peritubular cappilary bed in response to hypoxia

33
Q

convert 25-OH vit D to active form

34
Q

can cause hyperkalemia

A 
digitalis,hyperOsmality
insulin deficency
lysis of cells
acidosis
Beta antagonist
35
Q

can cause hypokalemia

A

hypo-osmolality
high insulin (insulin shifts potassium INTO cells, out of serum)
alkalosis
Beta agonist

36
Q

low pH, low Pco2, low bicarb signs of

A

metabolic acidocis

37
Q

high pH, high PCO2, high bicarb signs of

A

metabolic alkalosis

38
Q

low pH, high PCO2, high bicarb sighs of

A

respiratory acidosis

39
Q

high pH, low PCO2, low bicarb signs of

A

respiratory alkalosis

40
Q

compensatory response to met acid

A

hyperventalation

41
Q

compensatory response to met alk

A

hypoventalation

42
Q

compensatory response to resp acid

A

increase of renal reabsorption of bicarb (delayed)

43
Q

compensatory response to resp alk

A

decrease of renal reabsorption of bicarb (delayed)

44
Q

can cause metabolic acidosis with an increased anion gap

A 
methanol
uremua
diabetic ketoacidosis
propalyne glycol
iron tabs
INH
Lactic acidosis
ethylene glycol
salicytes
45
Q

can cause resp acidosis

A 
airway obstruction
Acute lung disease
chronic lung dx
opiods
weakening of resp muscles
46
Q

can casue metabolc acidosis with NORMAL anion gap

A 
hyperalimentation
addisons
renal tubula acidosis
diarrhea
acetaxolamids
spirolactone
saline infusion
47
Q

can casue resp alk

A

hyperventalation (early high alt exposure)

early salicyte poisoning

48
Q

can cause metabolic alk with compensation (hypoventalation)

A

loop diuretics
vomiting
antacid sue
hyperaldosterism

Step 1- System embryology, A and P (10 decks)

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