05.15 - HTN (Gosmanova) - PP, No reading Flashcards by Ryan Lee

Increase NaCl delivery to MD increases ___ production

Adenosine

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Wet HTN

Essential with Low Renin

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

Cortisol excess activates ENaC (same as aldosterone)

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Gordon Syndrome is characterized by

Salt-sensitive HTN, HyperK, Metabolic Acidosis

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Individuals from INTERSALT had higher ___ compared to rural populations

Average systolic and Diastolic BP

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Tx for Genetic PseudoHypoAldosteronism

Triamterene Amiloride

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

B1 and PG activate, Adenosin2 inhibits

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Activating WNK-1 and Inactivating WNK-4 both cause

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

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Gene mutation leading to Aldosterone Synthetase responsive to ACTH

Glucocorticoid Remediable Aldosteronism

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Ouabain acts on

Na/K ATPase

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Infusion of Saline in normal kidney patient vs anephric

Small changes of BP in normal; rapid rise in anephric

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Dry HTN

Essential with High Renin

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Pressure-Natriuresis: ___ is mediator

Changes in interstitial medullary pressure

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% of HTN and Normotensive individuals with salt sensitivity

50 and 26

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Gordon Syndrome is due to

Constitutive activation of Thiazide-Sensitive NaCl channels in DCT

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Inability of kidneys to appropriately excrete Na load

Guyton’s theory

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Increase in CO in Essential HTN

does not persist

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Effect of Ouabain on SVR and Venous Tone

Increases SVR and Venous Tone

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Brenner’s Hypothesis

Reduction in Nephron Mass

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Decrased NaCl delivery to MD increases ___ production

NO and PG

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All forms of Secondary HTN are characterized by

Salt-sensitive HTN

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

Cons of Guyton’s Theory

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Mechanisms of Salt’s role in HTN

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

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Laragh’s Hypothesis

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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Tx for Liddle's

Triamterene or Amiloride

Does salt-sensitivity change with age

Yes, increases

Renin and Aldosterone in Secondary HTN

Low Renin and Aldosterone, except Aldosterone Excess obv

Liddle's disease is due to

Activating ENaC mutation

Psuedohypoaldosteronism Type 2 is aka

Gordon Syndrome

Cause of Liddle's Syndrome

Constitutive activation of ENaC in DT due to mutaiton in subunit

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

Incr SVR and BP

Causes of PseudoHypoAldosteronism (non-Liddle's)

11B-HSD-2 Defiency of Inhibition

Action of 11B-HSD-2

Breaks down Cortisol

Volume and Renin in Goldblatt Model 1

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

Change in Pressure-Natriuresis curve with salt-sensivity

Decrease in slope

Worsening condition after ACEi =

Highly suggestive of Bilteral RAS

How does Pseudohypoaldosteronism cause Hypokalemia

Incr Na reabsorption in CD creates favorable gradient for K secretion

Ouabain is activated by

Incr PV

What channel is upregulated in Aldosterone excess that contributes to HTN

ENaC channel reabsorbs Na in CD

Role of Genetics in HTN

70-80% of individuals have positive family history

Channel upregulated in Cushing's that contributes to BP increase

ENaC channel reabsorbs Na in CD

Goldblatt Model 1

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

Inc Pre-Load can be due to

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

What inhibits 11B-HSD-2

Chronic licorice ingestion (candies, chewing tobacco)

ACEi's in Goldblatt Model 1

Reduce BP b/c stenotic kidney is secreting renin

As CKD progresses, revalance of HTN \_\_\_

rises

ACEi's in Goldblatt Model 2

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

Renin levels in Essential HTN

20% high, 30% low, 50% normal

MAP = CO x SVR =

DBP + 1/3(SBP-DBP)

Guyton's theory

Inability of kidneys to appropriately excrete Na load

Pressure-Natriuresis: Changes in Na excretion occur without

changes in GFR

Deficiency in 11B-HSD-2 leads to excess

Cortisol

Activating ENaC mutation

Liddle's disease is due to

2 mutations that cause Gordon's

Activation of WNK-1, Inactivaiton of WNK-4

Volume and Renin in Goldblatt Model 2

Both high

Goldblatt Model 2

Biltateral RAS - No off-setting pressure natriuresis

Reduction in Nephron Mass --\> ___ --\> \_\_\_

Systemic/Glomerular HTN --\> Acquired Glomerular Sclerosis

Cause of Hyperkalemia in Gordon's

Reduced distal Na delivery, so decreased K secretion

No salt, no \_\_\_, even with \_\_\_\_

No salt, no HTN, even with aging

Age of onset for primary HTN

40s and 50s

Aloows for normal BV despite elevated pressure

Pros of Guyton's Theory

Pressure-Natriuresis: ___ is the principal site

Outer Medulla (TALH)

What is necessary to maintain GFR in Goldblatt Model 2

RAAS, so ACEi's are contraindicated

Most common causes of RAS

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

K and Acid-Base in Secondary HTN

All associated with Hypokalemia and Metabolic Alkalosis except Gordon Sydnrome

Inactivating mutations in 11B-HSD-2 gene

Apparent Mineralocorticoid Excess is due to

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

Decr afferent artiolar stretch, Decr NaCl delivery to Macula Densa

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

FALSE

SV can be increased by

Incr in Pre-Load or Contractility

Pros of Guyton's Theory

Aloows for normal BV despite elevated pressure

What normally degrades Cortisol

11B-HSD2

Is peripheral edema common in essential HTN

Does Adenosine vasoconstrict or dilate

Vasoconstrict

Apparent Mineralocorticoid Excess is due to

Inactivating mutations in 11B-HSD-2 gene

Prevalence of RAS is higher with

age, DM, PVD, DBP \>125

Gordon's Syndrome mimics

Gitelman's

How does PseudoHypoAldosteronism cause Metabolic Alkalosis

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

What is Pressure Natriuresis

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

Local factor autoregulation is mediated primarily by

Tx of Gordon's Syndrome

Thiazide Diuretics

Cons of Guyton's Theory

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