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Cardio Exam 1 > RAS HTN > Flashcards

RAS HTN Flashcards

1
Q

RAS is important regulator of?

A

BP and hydromineral balance

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2
Q

RAS has a key role in?

A

HTN
Heart failure
Vascular Disease
Renal Failure

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3
Q

Define Renin

A

Enzyme stored and released by the juxtaglomerular cells

Converts angiotensinogen to Ang1

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4
Q

Define Angiotensinogen

A

Glycoprotein

Synthesized and released form the liver

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5
Q

Define Angiotensin I

A

Inactive protein

Formed in systemic circulation

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6
Q

Define ACE

A

Angiotensin converting enzyme

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7
Q

Define Angiotensin II

A

Active peptide

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8
Q

Define Angiotensin 1-7

A

Peptide

Opposite effect to angiotensin II via Mas receptors

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9
Q

What is the rate limiting step in the angiotensinogen to angII pathway?

A

Angiotensinogen to Ang1 via renin

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10
Q

Define AT1 Receptor

A

Mediator of pressor effects of angiotensin II

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11
Q

Define NEP

A

Neutral Endin Peptidase

Makes Angiotensin 1-7 from Ang1

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12
Q

Increased release of renin leads to?

A

Increased Ang II

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13
Q

Increased Ang II leads to?

A

Increased blood pressure!

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14
Q

Regulation of renin release via? Increase release?

A

↓ NaCl flux across macula densa
↓ BP in afferent arterioles
Activation of B1-receptors on juxtaglomerular cells
↓ circulating ang II

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15
Q

Increase in the macula densa pathway means?

A

Increased filtration and more sodium being absorbed

DECREASED RENIN

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16
Q

Increased intraarenal baroreceptor pathway means?

A

Increased blood pressure in the afferent arteriole

DECREASED RENIN

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17
Q

Decrease in beta-adrenergic receptor pathway means?

A

Decrease release of NE from synaptic terminals leading to a decreased activation of beta receptors
DECREASED RENIN

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18
Q

Short loop negative feedback on renin?

A

Stimulate angiotensin receptors on juxtaglomerular cells

DECREASED RENIN

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19
Q

Long loop negative feedback on renin

A

Increased circulating AngII which increase BP
Through the macula densa pathway, intrarenal baroreceptors pathway, beta-adrenergic receptor pathway
DECREASED RENIN

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20
Q

In vasculature, AT2 receptors mediate?

A

Vasodilation

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21
Q

Adult tissues have much less of which type of receptors?

22
Q

AT1 receptors in the vasculature cause?

A 
Vasoconstriction
SM hypertrophy (chronic)
23
Q

AT1 receptors in the adrenal cortex cause?

A

Synthesis and secretion of aldosterone

24
Q

AT1 receptors in the adrenal medula cause?

A

Epinephrine release

25
Q

AT1 receptors in the Kidney cause?

A

Efferent Arteriole vasoconstriction
Inhibition of renin release
Increased sodium reabsorption

26
Q

AT1 receptors in the heart cause?

A

Myocardioal hypertrophy and collagen synthesis

27
Q

AT1 receptors in the brain cause?

A

Release of vasopressin (ADH), stimulation of thirst and salt appetite, increased central sympathetic outflow

28
Q

Define Bradykinin

A

Potent vasodilator peptide

29
Q

ACE does what?

A

AngI to Ang II

Breaks down bradykinin

30
Q

ACE Inhibitors Mechanisms of Action?

A

Decrease formation of AngII
Increased levels of bradykinin
Increased (indirectly) formation of Ang1-7

31
Q

ACE Inhibitor Drugs

A

End in -pril
Lisinopril (Privinil; Zestril)
Benazepril (Lotensin)
Etc

32
Q

Sensitivity of ACEI is increased in pts with?

A

Activated RAS (low salt diet, heart failure)

33
Q

HTN pts and ACEI?

A

Decreased vascular resistance and BP
Increase the compliance of large arteries
Slight decrease in GFR

34
Q

Constriction of the afferent arteriole causes? Dilation?

A

Decreased GFR bc not as much blood can get through; increased

35
Q

Constriction of the efferent arteriole causes? Dilation?

A

Increased GFR; decreased GFR

36
Q

Increased Ang II means what for the glomerulus?

A

Constriction of both afferent and efferent but preference for efferent first

37
Q

ACEI Therapeutic Uses?

A 
HTN
Left ventricular systolic dysfunction
Acute MI
Prevention of CAD event and stroke
Chronic renal failure
38
Q

ACEI Adverse Effects

A 
HYPOtension
Cough 
HYPERkalemia
Acute renal failure
Modest elevation of serum creatinine
\+ NSAIDs = ↓ GFR
Teratogenic!!!
39
Q

What causes a cough?

A

Accumulation of bradikynin, substance P and PGs in lung

40
Q

How do NSAIDs ↓ GFR?

A

Inhibit formation of PGs which are potent vasoconstrictors

41
Q

Most severe adverse reaction of ACEI?

A

ANGIOEDEMA: rapid swelling of nose, throat, and mouth

Occurs suddenly and unexpected (no time frame

42
Q

AT1 Receptor Antagonists

A

All end in -sartan
losartan (Cozaar)
candesartan (Atacand)

43
Q

AT1 Receptor Antagonists Result in?

A 
Arterial vasodilation and decrease peripheral resistance
Reduction of aldosterone
Inhibition of peripheral SNS
Increased renin release and activity
Increased Ang II levels
44
Q

Another name for AT1 Receptor Antagonists is?

A

Angiotensin Receptor Blockers

45
Q

Differences between ARBs and ACEI

A

ARB reduce AT1 receptor activity more
ACEI increase renin levels but not ang II
ARBs generate AngII can act on AT2 (opposite effect of AT1)
ACI increase Ang1-7 more than ARBs and levels of bradykinin

46
Q

ARBs Main therapeutic effects

A

HTN
Heart Failure
Stroke Prophylaxis
Diabetic Nephropathy

47
Q

ARBs adverse effects

A

HYPOtension (salt depleted pts)
HYPERkalemia (renal disease or supplements)
Teratogenic potential

48
Q

ARBs have less?

A

Angioedema potential

And don’t cause cough

49
Q

Aliskiren is a ?

A

3rd generation renin inhibitor

50
Q

Aliskiren Indications

51
Q

Aliskiren adverse effects?

A 
Headache, fatigue, dizziness
Diarrhea
Nose bleeds
HYPERkalemia
HYPERuricemia
Teratogenic

Cardio Exam 1 (7 decks)

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