5. HTN & Antianginal Flashcards

1
Q

What is the key diuretic?

A

HCTZ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is HCTZ?

A

Diuretic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Effects of HCTZ? Uses? Adverse effects?

A

Acutely decreases blood volume (baroreflex nuetralizes this effect long term)
Chronic Na depletion leads to decreased PR

Mild HTN or combo to prevent tolerance

K loss (drowsiness) & arrhythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Effects of beta blocker (or partial beta agonist)?

A

Decreased HR
Decreased renin release

partial ag has smaller effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Effects of alpha antag?

A

Decrease PR

May increase blood volume due to decrease perfusion of kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the ACE inhibitors? Difference between them?

A

Captopril (active)

Enalapril (prodrug)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is Captopril?

A

ACE inhib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is Enalapril?

A

ACE inhib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Effects of ACE inhibitor?

A

LEss Ang II –> decreaser PR & less aldosterone (lower blood volume)

Bradykinin buildup –> decreased PR [y works even in people with low renin levels]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

ACE inhibitors are still effective on some individual who are shown to have low renin levels. How?

A

Buildup of bradykinin –> decreased PR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the key Ang II receptor blocker?

A

Losartan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is losartan? Effects?

A

Ang II blocker

Decreased PR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the Ca Channel blockers? Difference?

A

Nifedipine
Diltiazem
Verapamil

Nife doesn’t effect the heart like the other 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the effects of Ca channel blockers?

A
Decreased PR
Decreased HR (not nife)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the key vasodilators? Difference?

A

Hydralazine (effects arteries more)

Nitroproside (effects arteries & veins the same)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is hydralazine? Effects?

A

Vasodilator

Decrease PR mainly in the arterioles (less so in the venoules)
Reflex increase in blood volume & CO

17
Q

Mechanisms of vasodilators?

A

NO release –> cGMP

18
Q

What is the adrenergic neuron blocker?

A

Reserpine

19
Q

What are the CNS acting drugs?

A

Alpha methyl dopa

Clonidine

20
Q

How is coronary circulation different than systemic circulation?

A

Flow during diastole instead of systole

Heart already extracts all O2 from blood, so during strenuous situations the blood flow must increase a lot to meet demand

21
Q

What % of CO goes to coronary circulation during rest? During stress?

A

5%

15%

22
Q

What determines O2 demand of heart? Supply?

A

how much work the heart is doing (= Contracility, HR, preload & afterload)

Coronary patency, diastolic BP, blood O2 capacity & collateral circulation

23
Q

What are the 3 types of Angina Pectoris?

A

Stable/typical
Unstable/Atypical
Variant/Prinzmetal

24
Q

How does stable/typical angina present? Cause? Best treatment?

A

Heavy substernal discomfort on exertion

Artherosclerotic narrowing (always narrow)

Nitro

25
Q

How does unstable/atypical angina present? Cause?

A

Discomfort no matter what

Plaque rupture & thrombosis

26
Q

What is Nitroglycerin? How does it work?

A

Selective venodilator

Venous dilation –> decreased cardiac return –> decreased preload –> decreased EDV –> decreased O2 demand

Smaller effect = coronary dilation –> more blood supply

27
Q

How is nitroglycerin administered? Why?

A

Sublingual or trandermal

Can’t be taken orally cuz metabolized really fast

28
Q

What is the effect of high dose of Nitro?

A

Big decreased in CO –> Reflex tachycardia to compensate –> increased O2 demand off sets desired decrease in O2 demand

29
Q

What is the normal nitro pathway? Pathway during NO administration?

A

Ach or histamine –> activation of nitro oxidase in endothelial cell –> Arginine split into NO & arginine

No diffuses into smooth muscle –> guanyl cyclase –> GTP –> cGMP –> muscle relaxation

Administered NO goes straight to smooth muscle cell

30
Q

How does Varient/Prinzmetal angina present? Cause? Best treatment?

A

“Random” chest pain

Coronary vasospasm due to autonomic stimulation or underlying plaque

Ca Channel blocker

31
Q

Uses of Isosorb mono-dinitrate?

A

oral prophylaxis for angina

32
Q

Adverse effects of nitrates?

A

headache, hypotension, tachycardia

33
Q

How is nitrate tolerance prevented

A

8 hour free period

If take patch, take it off while sleep

34
Q

Nitroglycerin uses?

A

Acute angina

35
Q

Beta blocker usage for angina?

A

Prophylaxis

36
Q

Drug combos for angina?

A

Nitrates plus beta blocker (decreased )2 demand without relfex tachycardia)

Nitrates & verapamil/diltazem (decrease O2 demand & increase supply)

Nitrates & nifedipine (hypotension & tachycardia)

Beta blocker & verapamil/diltazem (enhacned cardiac suppression)

Beta Blocker & nifedipine (blunter reflex)