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Renal > 05.15 - HTN (Gosmanova) - PP, No reading > Flashcards

05.15 - HTN (Gosmanova) - PP, No reading Flashcards

1
Q

Increase NaCl delivery to MD increases ___ production

A

Adenosine

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1
Q

Wet HTN

A

Essential with Low Renin

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1
Q

Mechanism of Volume Expansion in Glucocorticoid Excess (Cushing’s)

A

Cortisol excess activates ENaC (same as aldosterone)

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1
Q

Gordon Syndrome is characterized by

A

Salt-sensitive HTN, HyperK, Metabolic Acidosis

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2
Q

Individuals from INTERSALT had higher ___ compared to rural populations

A

Average systolic and Diastolic BP

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3
Q

Tx for Genetic PseudoHypoAldosteronism

A

Triamterene Amiloride

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4
Q

Which activate and which inhibit Renin: B1 rec, Adenosin2 rec, Prostaglandin rec

A

B1 and PG activate, Adenosin2 inhibits

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4
Q

Activating WNK-1 and Inactivating WNK-4 both cause

A

Increased activity of NaCl channel and incr Na reabsoprtion (Gordon’s)

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5
Q

Gene mutation leading to Aldosterone Synthetase responsive to ACTH

A

Glucocorticoid Remediable Aldosteronism

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6
Q

Ouabain acts on

A

Na/K ATPase

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6
Q

Infusion of Saline in normal kidney patient vs anephric

A

Small changes of BP in normal; rapid rise in anephric

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6
Q

Dry HTN

A

Essential with High Renin

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7
Q

Pressure-Natriuresis: ___ is mediator

A

Changes in interstitial medullary pressure

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7
Q

% of HTN and Normotensive individuals with salt sensitivity

A

50 and 26

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7
Q

Gordon Syndrome is due to

A

Constitutive activation of Thiazide-Sensitive NaCl channels in DCT

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9
Q

Inability of kidneys to appropriately excrete Na load

A

Guyton’s theory

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11
Q

Increase in CO in Essential HTN

A

does not persist

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12
Q

Effect of Ouabain on SVR and Venous Tone

A

Increases SVR and Venous Tone

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12
Q

Brenner’s Hypothesis

A

Reduction in Nephron Mass

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12
Q

Decrased NaCl delivery to MD increases ___ production

A

NO and PG

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12
Q

All forms of Secondary HTN are characterized by

A

Salt-sensitive HTN

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13
Q

Ignores role of ANS: Fails to explain incr BP in pre-HTN, where CO incr is mainly driven by SNS activaiton

A

Cons of Guyton’s Theory

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14
Q

Mechanisms of Salt’s role in HTN

A

Dec Na excretion, Incr SNS activity, Incr activity of Na-H exchanger, Incr Ca in vascular SM cells

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15
Q

Laragh’s Hypothesis

A

Some nephron’s are ischemic and produce high renin, while others are not but will have impaired natriuresis from AT2 - Total PRA is diluted/normal

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15
Q

Tx for Liddle’s

A

Triamterene or Amiloride

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16
Q

Does salt-sensitivity change with age

A

Yes, increases

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17
Q

Renin and Aldosterone in Secondary HTN

A

Low Renin and Aldosterone, except Aldosterone Excess obv

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18
Q

Liddle’s disease is due to

A

Activating ENaC mutation

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19
Q

Psuedohypoaldosteronism Type 2 is aka

A

Gordon Syndrome

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20
Q

Cause of Liddle’s Syndrome

A

Constitutive activation of ENaC in DT due to mutaiton in subunit

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22
Q

Decr Na excretion leading to Incr CO is corrected by autoregulation at expense of

A

Incr SVR and BP

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23
Q

Causes of PseudoHypoAldosteronism (non-Liddle’s)

A

11B-HSD-2 Defiency of Inhibition

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24
Q

Action of 11B-HSD-2

A

Breaks down Cortisol

25
Q

Volume and Renin in Goldblatt Model 1

A

Renin is high, but volume is normal b/c contralateral kidney is able to excrete excess Na

26
Q

Change in Pressure-Natriuresis curve with salt-sensivity

A

Decrease in slope

27
Q

Worsening condition after ACEi =

A

Highly suggestive of Bilteral RAS

28
Q

How does Pseudohypoaldosteronism cause Hypokalemia

A

Incr Na reabsorption in CD creates favorable gradient for K secretion

30
Q

Ouabain is activated by

A

Incr PV

31
Q

What channel is upregulated in Aldosterone excess that contributes to HTN

A

ENaC channel reabsorbs Na in CD

32
Q

Role of Genetics in HTN

A

70-80% of individuals have positive family history

32
Q

Channel upregulated in Cushing’s that contributes to BP increase

A

ENaC channel reabsorbs Na in CD

33
Q

Goldblatt Model 1

A

Unilateral RAS w/ 2 normal kidneys - Incr SVR and Right shift in pressure natriuresis - Normal volume

35
Q

Inc Pre-Load can be due to

A

Incr Venous Tone or Incr Volume (and therefore total Na)

36
Q

What inhibits 11B-HSD-2

A

Chronic licorice ingestion (candies, chewing tobacco)

37
Q

ACEi’s in Goldblatt Model 1

A

Reduce BP b/c stenotic kidney is secreting renin

38
Q

As CKD progresses, revalance of HTN ___

A

rises

38
Q

ACEi’s in Goldblatt Model 2

A

Will not help - In fact, they’ll reduce GFR - RAAS necessary to maintain GFR in this scenario

40
Q

Renin levels in Essential HTN

A

20% high, 30% low, 50% normal

42
Q

MAP = CO x SVR =

A

DBP + 1/3(SBP-DBP)

43
Q

Guyton’s theory

A

Inability of kidneys to appropriately excrete Na load

45
Q

Pressure-Natriuresis: Changes in Na excretion occur without

A

changes in GFR

46
Q

Deficiency in 11B-HSD-2 leads to excess

A

Cortisol

47
Q

Activating ENaC mutation

A

Liddle’s disease is due to

48
Q

2 mutations that cause Gordon’s

A

Activation of WNK-1, Inactivaiton of WNK-4

49
Q

Volume and Renin in Goldblatt Model 2

A

Both high

51
Q

Goldblatt Model 2

A

Biltateral RAS - No off-setting pressure natriuresis

52
Q

Reduction in Nephron Mass –> ___ –> ___

A

Systemic/Glomerular HTN –> Acquired Glomerular Sclerosis

53
Q

Cause of Hyperkalemia in Gordon’s

A

Reduced distal Na delivery, so decreased K secretion

55
Q

No salt, no ___, even with ____

A

No salt, no HTN, even with aging

57
Q

Age of onset for primary HTN

A

40s and 50s

58
Q

Aloows for normal BV despite elevated pressure

A

Pros of Guyton’s Theory

59
Q

Pressure-Natriuresis: ___ is the principal site

A

Outer Medulla (TALH)

60
Q

What is necessary to maintain GFR in Goldblatt Model 2

A

RAAS, so ACEi’s are contraindicated

62
Q

Most common causes of RAS

A

Atherosclerosis (85%), Fibromuscular Dysplasia (15%)

63
Q

K and Acid-Base in Secondary HTN

A

All associated with Hypokalemia and Metabolic Alkalosis except Gordon Sydnrome

64
Q

Inactivating mutations in 11B-HSD-2 gene

A

Apparent Mineralocorticoid Excess is due to

65
Q

2 factors that activate renin release from JGA in response to Renal hypoperfusion

A

Decr afferent artiolar stretch, Decr NaCl delivery to Macula Densa

67
Q

T/F: We are all salt-sensitive to some degree

A

FALSE

68
Q

SV can be increased by

A

Incr in Pre-Load or Contractility

69
Q

Pros of Guyton’s Theory

A

Aloows for normal BV despite elevated pressure

70
Q

What normally degrades Cortisol

A

11B-HSD2

71
Q

Is peripheral edema common in essential HTN

A

No

72
Q

Does Adenosine vasoconstrict or dilate

A

Vasoconstrict

73
Q

Apparent Mineralocorticoid Excess is due to

A

Inactivating mutations in 11B-HSD-2 gene

74
Q

Prevalence of RAS is higher with

A

age, DM, PVD, DBP >125

75
Q

Gordon’s Syndrome mimics

A

Gitelman’s

76
Q

How does PseudoHypoAldosteronism cause Metabolic Alkalosis

A

Hypokalemia causes shift of H+ into tubular cells and then secretion into lumen; Also incr H+ secretion by H pump

77
Q

What is Pressure Natriuresis

A

When perfusion press incr., renal Na output incr and ECFV and BV contract to return MAP to baseline

79
Q

Local factor autoregulation is mediated primarily by

A

NO

80
Q

Tx of Gordon’s Syndrome

A

Thiazide Diuretics

81
Q

Cons of Guyton’s Theory

A

Ignores role of ANS: Fails to explain incr BP in pre-HTN, where CO incr is mainly driven by SNS activaiton

Renal (31 decks)

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