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Renal > Lecture 10: ACEIs + ARBs > Flashcards

Lecture 10: ACEIs + ARBs Flashcards

1
Q

What are 4 renin secretion regulators?

A

Sympathetic division

Renal baroreceptors

Macula densa

Hormones
(AngII, ANP = dec. secretion)

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2
Q

Differentiate between AT1 and AT2 receptors

A

AT1 =
Widespread
Mediate: pressor effects, deleterious changes in CV morphology

AT2 =
More prominent in fetus; higher expression in patients with CV disease
Mediate: vasodilation, protective CV effects

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3
Q

Describe the rapid pressor and slow pressor effects of AngII

A

Rapid pressor =
Vasoconstriction

Slow pressor =
Salt/water retention
Plasma/volume expansion

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4
Q

What are two enzymes that can convert AngI to AngII?

A

ACE

Chymase (CHYM)

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5
Q

Describe the direct mechanisms for AngII mediated salt/water retention

A

AngII @AT1 =

Inc. Na reabsorption in PT by stimulation of NHE

Inc. Na reabsorption in DCT and CNT/CD via stimulation of NCC and ENaC, respectively

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6
Q

Describe indirect mechanisms for AngII mediated salt/water retention

A

AngII @AT1 =

Inc. Aldosterone secretion = inc. Na reabsorption in CNT/CD via ENaC

Constriction of AA and EA (EA > AA) = changes in Starling forces in PTCs = inc. sodium/water reabsorption in PT

CNS effects

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7
Q

Describe CNS effects at higher levels of AngII

A

Inc. ADH secretion = more water reabsorbed in CNT/CD

Inc. thirst = more water ingested

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8
Q

Does AngII decrease RPF?

A

Yes

AngII = inc. resistance of EA > AA = inc. RVR = dec. RBF = dec. RPF

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9
Q

Does AngII decrease GFR?

A

Hard to predict b/c of flow-dependence of GFR

AngII = dec. RPF = dec. Kf = dec. GFR

Or

AngII = Inc. resistance of EA > AA = inc. in hydraulic pressure of glomerular capillaries = Inc. GFR

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10
Q

Describe the renovascular effects (indirect mechanism for salt/water reabsorption in PT) of AngII

A

AngII increases resistance in afferent and efferent (more so!!) arterioles, resulting in increase in renal vascular resistance (RVR) = dec. in RPF

Filtration fraction always increases (indirect relationship with RPF) and leads to increase in oncotic pressure inside peritubular capillaries b/c of proteins staying behind = inc. reabsorption of sodium/water in PT

Inc. in resistance of EA = inc. RVR = dec. hydraulic pressure of PTC = inc. reabsorption of Na/H2O in PT

GFR can:
+ inc. from inc. hydraulic pressure in GC
+ dec. from dec. RPF (flow dependence)
+ not change (from balancing forces)

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11
Q

Define equation for filtration fraction (FF)

A

FF = GFR / RPF

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12
Q

In the Starling equation, what do the hydraulic pressure and oncotic pressure differences represent?

A

hydraulic pressure =
Pushing out fluid

oncotic =
Pulling in fluid

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13
Q

What changes in Starling forces in the PTCs occur that lead to indirect mechanism of inc. reabsorption of sodium and water in PT in presence of AngII?

A

Hydraulic pressure drops = difference in P decrease = pushing out fluid is low

Oncotic pressure increases with proteins that stayed behind = difference in Pi increases = pulling fluid IN is high

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14
Q

Describe differences in hydraulic and oncotic pressure along

AA
GC
EA
PTC

A

AA =
Hydraulic > Oncotic (difference = NFP)

GC =
Hydraulic > oncotic until eventually fluid filters out, oncotic inc. and filtration equilibrium achieved

EA =
Oncotic > Hydraulic
(No loss of fluid in EA so Pi stays the same, but P dec. from resistance)

PTC =
Oncotic > hydraulic
Means that fluid is being pulled into PTC (normal reabsorption in PT)

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15
Q

How does presence of AngII affect reabsorption in PT?

A

In glomerular capillaries =
+ Inc. hydraulic pressure = higher plateau
+ more rapid inc. in oncotic pressure due to dec. RPF

In PTC =
Higher oncotic pressure and lower hydraulic pressure = more driving force for reabsorption/pulling fluid in

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16
Q

How does RAAS respond in a volume-depleted patient?

A

(1) sympathetic division
Volume depletion = dec. stretch of arterial baroRs = inc. symp tone to kidneys via stimulation of beta1 on granular cells = inc. renin secretion

(2) renal baroreceptors
Volume depletion = dec. stretch = inc. renin secretion

(3) macula densa
Volume depletion = dec. NaCl delivery to macula densa = inc. renin secretion
(TGF will be on guard and the dec. in Adenosine/inc. PGE2 will counteract AngII mediated AA resistance inc.

17
Q

What are drug classes that antagonize the RAAS?

A

Inhibitors of renin secretion = beta antagonists = propranolol, metoprolol

Renin inhibitors = aliskiren

Aldosterone antagonists = K+ sparing diuretics

ACEIs = “prils”

ARBs = “sartans”

18
Q

What are indications for ACEIs and ARBs?

A

HTN
(Particularly pt’s with additional CVD or CKD w/ proteinuria)

MI and post-MI

HF

CKD
(Diabetic or non-diabetic)

19
Q

What are AEs associated with ACEIs and ARBs?

A

Cough + angioedema
(ACEI)

Hypotension
(common in pt’s with inc. renin)

Hyperkalemia

20
Q

Describe the mechanism for hyperkalemia side effect of ARBs and ACEIs

A

AngII stimulates inc. aldosterone, which can:

Directly: inc. K secretion in CNT/CD via ROMK, Na-K ATPase in principal cells

Indirectly: inc. Na reabsorption in CNT/CD via ENaC, Na-K ATPase in principal cells = lumen negative transepithelial potential (TEP) in CNT/CD = inc. K secretion

21
Q

What are contraindications for ACEIs and ARBs?

A

Pregnancy

22
Q

For which patients should ACEIs and ARBs be used with caution?

A

Poor renal perfusion
Renal a. Stenosis
Severe dehydration

Dec. renal perfusion = inc. renin secretion = inc. AngII, which could potentially inc. GFR….. but ACEI/ARB to these patients would decrease GFR by blocking

23
Q

How can increases in serum creatinine be explained while using ACEI?

A

Volume depletion from diuretic = dec. GC hydraulic pressure

Atherosclerotic lesions in renal a. = dec. renal perfusion pressure

Blocking RAAS is important for maintaining GC hydraulic pressure = dec. P(GC) = dec. GFR = inc. plasma creatinine

24
Q

What medication combinations should be avoided for patients with poor renal perfusion, etc?

A

Diuretic + ACEI or ARB

Diuretic + ACEI or ARB + NSAID
Each has own mechanism for decreasing GFR

25
Q

Briefly compare ACEI and ARBs

A

ACEIs = block BK metabolism

ARBs block AT1 but not AT2
And since no negative feedback, increased renin = inc. AngII to stimulate AT2 receptors

26
Q

What are kinin AEs and potential benefits?

A

AE = cough, angioedema

Potential benefits =
Vasodilation
CV protective effects

Renal (17 decks)

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