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Renal/Endocrine/Repro > Renal Basic Facts Check > Flashcards

Renal Basic Facts Check Flashcards

1
Q

What expresses AT1R

A

efferent arteriole

JG cells

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2
Q

UV/P=

A

Clearance

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3
Q

Solute filtered/unit time

A

filtered load

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4
Q

What monitors GFR as tubular flow?

A

macula densa

TGF mechanism

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5
Q

What 3 things are used for hormonal compensation for hypotension?

A

aldosterone
AVP
Angiotensin II

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6
Q

What receptor is used for compensation for HTN?

A

AT2-R

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7
Q

What are pharmacologic targets for HTN?

A

AT1-R
Renin
Aldosterone
ENaC

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8
Q

What are the renal mineralocorticoid targets?

A

ENaC
ROMK
NHE3

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9
Q

What’s responsible for proximal tubule Na+ transport?

A

“Reabsorption”
SGLT
NHE3
Angiotensin II

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10
Q

What’s responsible for distal nephron Na+ transport?

A 
"Reabsorption"
ENaC
NKCC
NHE3
Aldosterone
NCC
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11
Q

What is responsible for renal glucose handling?

A

“Reabsorption”
GLUT
SGLT

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12
Q

What is a Ca2+ sparing drug?

A

HCTZ

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13
Q

What is a K+ wasting drug?

A

HCTZ

Furosemide

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14
Q

What targets NKCC?

A

Furosemide

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15
Q

Name a mineralocorticoid antagoinist.

A

sprinolactone

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16
Q

What is responsible for renal excretion of H+?

A

NHE3
Aldosterone
NH4+

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17
Q

What condition is characterized by:

metabolic acidosis: aldosterone resistance?

A

Type 4 RTA

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18
Q

What condition is characterized by:

high plasma aldosterone with hyperkalemia?

A

pseudohypoaldosteronism

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19
Q

What condition is characterized by:

metabolic acidosis: glucosuria w/ euglycemia?

A

Type 2 RTA

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20
Q

What condition is characterized by:

euvolemic, hypovolemia, hypervolemic?

A

hyponatrimia

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21
Q

What condition is characterized by:

metabolic acidosis: defect in NH3 and carbonic anhydrase?

A

Type 2 RTA

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22
Q

What is the (potential) pathogenesis of salt-sensitive hypertension?

A

ouabain

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23
Q

What conditions can be neurogenic or nephrogenic?

A

DI and SIADH

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24
Q

What condition is characterized by:

elevated serum PTH with hypocalcemia?

A

secondary hyperparathyroidism

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25
Q

What is synthesized in response to PTH?

A

calcitriol

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26
Q

If unchecked, what would cause hyperphosphatemia?

A

calcitriol or secondary hyperparathyroidism

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27
Q

If unchecked, what would cause hypoglycemia?

A

insulin

28
Q

What is secreted in response to hyperglycemia?

A

insulin

29
Q

What is a marker to monitor DM2?

A

hyperglycemia; Hb1Ac

30
Q

What is used for glycemic control?

A

insulin

31
Q

What are signs of DM2?

A 
glomerular hyperfiltration
microalbuminuria
glomerulosclerosis
hyperglycemia
insulin resistance
32
Q

What condition is characterized by:

hyponatremia w/ elevated urine specific gravity?

A

SIADH

33
Q

What condition is characterized by:

polydipsia with polyuria?

A

DI and DM1

34
Q

What condition is characterized by:

V2R loss of function?

A

SIADH

DI

35
Q

What mediates distal H2O reabsorption?

A

AVP

36
Q

What condition is characterized by:

dyslipidemia, hypoalbuminemia and proteinuria?

A

nephrotic syndrome

37
Q

What condition is characterized by:

doubling of plasma creatinine?

A

acute kidney failure

38
Q

Does aldosterone increase reabsorption/excretion of:
Na+?
K+?
NH4+?

A

Na+: reabsorption
K+: excretion
NH4+: excretion

39
Q

What is the effect of K+ regarding volemic state? (the aldosterone paradox)

A
  • In hypovolemia with eukalemia, AII and aldosteone work together to facilitate Na+ secretion w/o overt hypokalemia
  • in hyperkalemia (w/o hypovolemia), there is a blunted response in terms of Na+ reabsorption and a profound response in K+, so you can get K+ secretion without hypervolemia (due to a change in gene expression to upregulate ROMK (K+ excretion) coupling with aldosterone)
40
Q

What condition classically presents with glucose urea with euglycemia?

A

Type 2 (proximal ) RTA

41
Q

What are classic symptoms of Type 4 RTA?

A

(aldosterone deficiency/resistance)
metabolic acidosis, hyperkalemic, normal AG, BP MAY be a little off, Urinary AG > 0 (decreased NH4+ excretion means less Cl- (low NH4Cl), therefore less urinary anion: POSITIVE AG

42
Q

What are characteristics of primary hyperaldosteronism?

A

increased pH (bc high H+ secretion due to aldosterone’s effect on NHE3 in PT and TAL) –> HYPOKALEMIC METABOLIC ALKALOSIS

43
Q

What are the characteristics associated with hypoaldosteronism?

A

lowered aldosterone so less H+ secretion –> lowered pH –> HYPERKALEMIC METABOLIC ACIDOSIS

44
Q

What is insulin’s bioactivity at low concentrations?

A

Cellular K+ uptake (caution: treating someone with low K+ with insulin can lead to hypokalemia)

45
Q

What is the reason and effects for DM1?

A

lack Beta cells so can’t make insulin or recognize glucose, therefore: hyperglycemic with insulin resistance (due to signaling or receptor probs)
-3 Ps (polydipsia, polyuria, polyphagia

46
Q

How can metabolic acidosis lead to hyperaldosteronism?

A

when cells swap EC H+ for intracellular K+, they can get to a state of hyperkalemia, which induces release of aldosterone

47
Q

Describe Type 2 DM

A

syndrome of metabolic obesity (adroid pattern)

  • hyperinsulinemia (make a whole bunch of insulin)
  • insulin resistance

Tx:

  • metformin (biguanides: block GI Glu absorption, block gluconeogenesis, stimulate glucose intake)
  • sulfonylureas: stimulate insulin production
  • DPP-4: inhibit glucagon secretion and stim insulin prod
  • SGLT2 inhibitor blocks glucose reabsorption
48
Q

How do the kidneys interact with insulin?

A

They break it down

In case of renal failure –> hyperinsulinemia –>hypoglycemia

49
Q

Tx for pts in diabetic kidney failure w/ electrolyte imbalence

A

DON’T GIVE ARB (mineralocorticoid receptor agonist or ACEI)

instead target aldosterone receptor (sprinolactone)

50
Q

What is the effect of calcitriol on PTH? on Kidney? on Small intestine?

A

PTH: negative feedback
Kidney: stimulates Ca2+ reabsorption
Small intestine: Ca2+ absorption

51
Q

What is the effect of PTH in kidneys?

A

stimulates Ca2+ reabsorption, PO4 elimination (blocks PO4 reabsorption), stimulates synthesis of calcitriol (bioactive Vit D)

52
Q

What is the effect of calcitriol in small intestine?

A

stimulate Ca2+ reabsorption form diet

53
Q

What is the effect of PTH on bone?

A

Reabsorption:
breaking apart Ca2+ and PO4 from salts to put back into circulation

NB: excess PO4 would promote the ppt of Ca2+. This effect is counteracted by renal effects of PTH

54
Q

Where does Vit D synthesis occur?

A

proximal tubule epithelium

55
Q

What is the effect of CYP27B1? What affects it?

A

CYP271B metabolizes 25-OH vit D (inactive) into 25-(OH)2D: Calcitriol (active

PTH stimulates it’s activity
Ca2+, hyperphosphatemia, and calcitriol downmodulate its activity

56
Q

What are the mineral effects on urine after a surge of PTH?

A

hyperphosphateurea and hypocalcmiurea

57
Q

What is the effect of amilorides?

A

block Na+ reabsorption in the CT

58
Q

What are the effects of chronic kidney disease on calcium?

A
  • inability to produce sufficient calcitriol (lose Ca2+ reabsorption in kidney and absorption in GI) –>
  • hypocalcemia stimulates the release of PTH (SECONDARY HYPERPARATHROIDISM) –> stimulates PO4 and Ca2+ reabsorption in bone (can cause hyperphosphatemia, which has (-)fb on PTH production)

NB: Ca2+ increase does not stay in plasma because kidneys get the FL but can’t reabsorb it –> elevated Ca2+ excretion and metastatic calcifications

59
Q

What are the signs and symptoms of hypoparathyroidism?

A

Loss of resistance to PTH
Labs: hypocalcemia, hyperphosphatemia, hypocaliurea
Symptoms: impaired neuromuscular function

Tx: give PTH, Vit D, and Ca2+

60
Q

What is the countercurrent multiplier and exchange?

A

maintenance of medullary interstitial osmotic gradient

61
Q

What is the significance of a decreased PRA:PAC ratio?

A

Primary hyperaldosteronism

62
Q

What is the significance of a increased PRA:PAC ratio?

A

Secondary hyperaldosteronism

63
Q

What are the functions of insulin? (what does it simulate? prevent?)

A

Promotes: STORAGE OF GLU IN SKEL MUSCLE, storage of fat, and storage of glucose in liver

Prevents: (general) lipoloysis and (liver:) glucogenolysis, gluconeogenesis

64
Q

What is the effect of carbonic anhydrase IV?

A

(located within the apical membrane of the tubule epithelium)

CAIV maintains a favorable gradient for proton secretion
- catalyzes the dissociation of HCO3- into CO2 and OH-

65
Q

CAII

A

catalyzes the formation of HCO3- from OH- and CO2-

66
Q

What are the common states of K+ and Cl- in a pt with metabolic alkalosis?

A

hypokalemia; hypochloremia; HYPERGLYCEMIA (esp with hyperosmolality; if hyperglycemic with glucosuria, they will have polyurea)

Renal/Endocrine/Repro (10 decks)

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