Cardiology- Anti Hypertension Drugs

Front 1

WHat percent of people with HTN are under control?

Back 1

34%

Front 2

Name the classic two Thiazide diuretic

Back 2

HCTZ
metolazone

Front 3

Name the four classic Loop diuretics.

Back 3

furosemide
bumetanide
torsemide
ethacrynic acid

Front 4

Name the classic two thiazide-like duiretics

Back 4

chlorthalidone
indapamide

Front 5

Name the classic 4 K+ sparing diuretics

Back 5

triamterene
amiloride
spironolactone
eplerenone

Front 6

ending for ACE inhibitors

Back 6

-pril

eg. lisonopril

Front 7

ending for ARBs

Back 7

-sartan

Front 8

1) ending for Ca++ channl antagonists

2) two exceptions to this nomenclature

Back 8

1) -ipine
eg. nifedipine

2) diltiazem, verapamil

Front 9

Two classic vasodilators

Back 9

hydralazine
minoxidil

Front 10

ending for Alpha1 antagonists

Back 10

-osin

i.e. prazocin

Front 11

Two common alpha2 agonists

Back 11

clonidine
methylodpa

Front 12

ending for Beta Blockers

Back 12

-lol

i.e. porpranolol, metoprolol

Front 13

Two classic sympatholytics

Back 13

Reserpine
Guanethidine

Front 14

1)How do Diuretics change the pressure-natriuresis curve?
2) how does this effect systemic vascular tone?

Back 14

1) shift to the left
2) long term vasodialtion

Front 15

Thiazide Diuretics:
1) inhibit what?
2) Where?

Back 15

1) Na/Cl cotansporter
2) DCT

Front 16

Loop Diuretics:
1) inhibit what?
2) Where?

Back 16

1) Na/K/2Cl co transporter
2) TALH

Front 17

K+ Sparing diuretics:
1) What does Amiloride inhibit?
2) Where?
3) How does spironolactone act?
4) Where?

Back 17

1) ENaC channels
2) DCT
3) Competitive inhibitor of aldosterone, preventing insertion of aldo-sensitive Na+ Channels
4) DCT

Front 18

Actions of Aldosterone on:
1)Na+
2) volume
3) vascular compliance
4) Endothelium
5)Pressor Responses of AII
6) Vasc. Smooth Muscle Cells
7)Kidneys, heart, vasculature
8) Coagulation
9) Effect on AII signalling
10) growth
11)ROIs
12) Hypertrophy of?
13)blood lipids
14) ___kalemia
15) ____Magnesemia

Back 18

1) Retention
2) Volume expansion
3) Reduction in vascular compliance
4)Endothelial Dysfunction
5) Potentiation of Pressor Responses from AII
6) Increase SM Na|+ influx
7) kidney, heart, vessel fibrosis
8) actiate plasminogen activator INHIBITOR (pro-thrombotic)
9) Upregulate AII receptors
10) stim. TGF-B1
11) increase ROIs
12) Hypertrophy of VSMC and myocardium
13) increased blood lipids
14) Hypokalemia
15) HypoMagnesemia

Front 19

1) what does renin do?
2) What blocks this directly?

Back 19

1) converts Angiotensiogen to angiotensin
2) Renin receptor blockers

Front 20

1) What does ACE do?
2)What blocks this directly
3) What alternate pathwat can circumvent this blockage

Back 20

1) Convert AI to AII
2) ACE inhibitors
3) Non-ACE conversion with CAGE, chymase, Cathepsin G

Front 21

1)What does AII bind?
2)What blocks this?
3What are the three downstream events of this binding event?

Back 21

1) AT1 receptor
2) ARBS
3) Vasoconstriction, Aldosterone secretion, sympathetic activation

Front 22

ACE inhibitors:
1) Cause lowered BP how?

Back 22

1) Decreased AII- vasodialtion
Decreased Aldo- Natriuresis
Less sympathetic activation
Decreas endothelin and inmprove endothelial function

Front 23

terminal elimination phase of ACE-inhibitors

Back 23

renal or renal/hepatic

Front 24

ACE-inhibitor dosing

Back 24

multiple regimens with variable trough to peak ratios

Front 25

Racial variation of ACE-inhibitor actvity
1) doesnt work as well in...
2) Why?
3) solution?

Back 25

1) blacks
2) Low renin levels
3) use a higher dose

Front 26

ACE-inhibitor with a short half live

Back 26

Captopril

Front 27

Indication for an ACE-inhibitor?

Back 27

Diabetic Nephropathy

Front 28

1)A pt. with diabetic nephropathy and HTN should get what class?
2) why?

Back 28

1)ACE-inhibitor (-pril)
2) Dilated efferent arteiole which drops GFR (increase creatinine by less than 30%)

Front 29

Contraindications to ACE-inhibitors as a class

Back 29

1) Angioedema
2) 2nd or 3rd trimester (teratogenic?)
3) Renal Artery Stenosis of stenosis in a solitary kidney (concerned if Creatinine goes up more than 30%)
Baseline serum creatinine elevation is NOT a contraindication

Front 30

One side effect of ACE-inihibitors eliminate a large age group from ever getting this drug, which group and why?

Back 30

Teens, because ACE-inhibitors are teratogens and teens will not tell you if they are pregnant.

Front 31

A pt. has baseline serum creatinine elevation, but no renal artery stenosis. Can this pt. have ACE inhibitors?

Back 31

Yes

Front 32

ACE- inhibitors:
6 side effects that are class effects:
1) BP
2) Respiratory
3) Immune
4) Renal
5) ___ Kalemia
6) Blood

Back 32

1) First does hypotension if volume depleted
2) COUGH
3) Angioedema
4) Functional Renal insufficiency
5) Hyperkalemia
6) Anemia due to erythropoetin chnages

Front 33

ACE- inhibitors:
Two side effect specific to captopril

Back 33

Taste disturbnces and Rash

Front 34

ACE-inhibitors:
1) If your patient develops a cough on this drug,what ca you switch them to?
2) Why did they develop this cough?
3) If a pt. on this drug develops functional renal insufficiency what do you do?

Back 34

1) ARB
2) Increased Bradykinin metabolism to cough inducing compounds
3) stop temporarily

Front 35

Effects of AII:
1) Kidney
2)CNS
3) adrenal
4) Vascular

Back 35

1) renal vasocnstriction; Increased Na and H20 reabsorption; Inhibits Renin secretion
2) Sympatheic ouflow: ADH Secretion
3) Increases Aldo synthesis and secretion
4) Vasoconstriciton, Decreases NE reuptake

Front 36

Mechanism of ARB action:
Decreases three parameters which all sum to lower BP. Name them.

Back 36

Decreases Aldo secretion
Decreases Vasoconstriction
Decreaed Sympathetic activation

Front 37

How do the AT1 and AT2 receptors differ?
1) expression
2) Absorbtion of sodium
3) Vascular tone
4) cell growth regulation

Back 37

1) AT1 Always expressed, T2 only expresed during stress or injury
2) AT1 increases, AT2 decreases
3) AT1- vasoconstrict; AT2- vasodilate
4) AT1- activate AT2- inhibit

Front 38

Limitation of ARB usage?

Back 38

Price

Front 39

1) Alliskerin (Tekturna) is what kind of drug?
2) Why is it not widely used yet?

Back 39

1) Direct Renin Inhibitor
2) very new, not much outsomes data out yet

Front 40

Vasopeptidase inhibitors:
1) Upside?
2) downside?

Back 40

1) VERY effective
2) Large rate of angioedema especilly in AAs

Front 41

1) What kind of Ca++ channels doe Ca++ channel blockers work at?
2) What normally activates these channels?
3) What substrates can cause Ca++ influx in other types of ligand gated channels?

Back 41

1) L-type
2)Voltage
3) endothelin, AII, NE

Front 42

There are three classes of Ca++ blockers. Two of them only contain one drug that is relevant, and the last one is a larger class. Name all of them and give an example.

Back 42

1) Phenylalkylamines: verapamil
2) Benzothiazeprines; Diltiazem
3)dihydropyridines; -ipine ending

Front 43

What is a major effect of the non DHP (verapamil, diltiazem) Ca++ channel blockers that is not present in the DHP drugs?
2) Which one does this more?

Back 43

1) Negative Inotropy
2) Verapamil

Front 44

Mechanism of Ca++ channel blocker action:

Back 44

Decreased Ca++ entry
Negative inotropy (non-DHP)
Dec. PVR
Natriuresis
Interference with AII, alpha1, and alpha2 mediated vasoconstriction

Front 45

How does the mechanism of Ca++ channel blockers intersect with the RAAS system and sympthetic nervous system

Back 45

Interference with AII, alpha1, and alpha2 mediated vasoconstriction

Front 46

Indications for Ca++ channel blocker usage (any class):

Back 46

All forms of hypertension
Salt sensitive hypertension

Front 47

Indications for Ca++ channel blocker usage (Non-DHP):

Back 47

HTN with diastolic dysfunction ( poor relaxation) will benefit from the negative inotropy of the non-DHPs

Front 48

Indications for Ca++ channel blocker usage (DHP specifically):

Back 48

To prolong half-life of cyclosporine

Front 49

One Absolute Contrandication for Ca++ channel blocker usage (non-DHP):

Back 49

1) Partial AV nodal block because of negative inotropy, could put then in complete heart block

Front 50

One relative contraindication for Ca++ channel blocker usage (non-DHP):

Back 50

Comcomitant use of Beta-blockers because of synergistic negative inotropy

Front 51

these are side effects of what class?
Headache
Peripheral Edema
Gingival hyperplasia

Back 51

Ca++ channel blockers

Front 52

SIde effects for Ca++ channel blocker usage (DHP only):

Back 52

Tachycardia (especialy with Nifedipine

We do not know why this happens

Front 53

Side effects for Ca++ channel blocker usage (Verapamil only [phenylalkylamine]):

Back 53

Constipation

Front 54

Side effects for Ca++ channel blocker usage (non-DHP only):

Back 54

CHF

Front 55

Side effects for Ca++ channel blocker usage (short acting DHP only):

Back 55

Acute MI

Front 56

Peripheral edema is a side effect of all Ca++ channel blockers. Why does this happen?

Back 56

Caused because these drugs are more effective arterial vasodilators rather than venous vasodilators.

Not a function of volume retention

Front 57

1) Name the two Direct vasodilators
2) Mechanism of action?

Back 57

1)Hydralazine
Minoxidil

2) unknown

Front 58

Reflex response from body to Direct vasodilators?

Back 58

activation if sympathetic NS, and RAAS loop

Front 59

1)Direct vasodilators Indicated for what group of patients?
2)Minoxidil indicated for what more specific subset?

Back 59

1) Pt. needing multidrug therapy with resistant hypertension
2) Refractory pateints with RENAL INSUFFICIENCY

Front 60

Direct vasodilators as a first line therapy?

Back 60

Really never, should be the 5th or 6th drug tried

Front 61

Direct Vasodilator Contraindication

Back 61

Pericardial Effusion

Front 62

Side effects of Direct Vasodilators
1) as a class
2) just for minoxidil

Back 62

1) Fluid retention
Tachycardia
Lupus-like syndrome

2) Pericardial effusion/tamponade
Hyypertrichois

Front 63

Why must vasodilators only be used in multi-drug therapy?

Back 63

Need others to combt all of the side effects

Front 64

Answer is a diagram of the side effects of direct vsodilators and how they are countered by two drugs. This about the diagram, and name the two drugs and the side effects they counter.

Back 64

Propranolol (Beta-blocker) counters Tachycardia, and renin activity (this is just beta1 activity, so could probably use metoprolol)

Diuretics counter the sodium and volume retention

Front 65

1) 140/90 is the target BP when:
2) 130/80 is the target BP when:

Back 65

1) no evidence if complication (except high cholesterol
2) HTN with increased CV risk (i.e diabetes, Hx of MI; LVH; nphropathy; CHF, TIA/CVA)

Front 66

1) Alpha1 antagonists mechanism?
2) Reflex reaction of the body?

Back 66

1) Block peripheral α1-receptors causing direct arterial vasodilatation
2) Reflex activation of sympathetic nervous system in a dose-dependent fashion

Front 67

Alpha1 blockers:
1) effect on RAAS axis?
2) Positional effects?

Back 67

1) Minimal
2) More effective upright than supine

Front 68

Alpha1 blockers:
1) Especially indicated in what population in why?
2) Side effect in women?

Back 68

1) men with BPH because relaxes bladder neck
2) incontinence

Front 69

Prototypical Aplha-1 antagonist?

Back 69

Prazosin (-osin drugs)

Front 70

Indications for Alpha1 antagonist therapy?

Back 70

1)Pt. requiring multidrug therapy
2)HTN complicated by metabolic abnormality like diabetes, insuil resistance, and hypercholesterolemia
3) BPH

Front 71

Side effect of Alpha1 antagonists?

Back 71

Fluid retention, orthostasis, incontinence in women, lethargy, fatigue, dizziness, headache, first-dose hypertension

Front 72

2 prototypical Central Alpha-2 agonists

Back 72

clonidine, methyldopa

Front 73

Alpha-2 agonists mechanism of action

Back 73

Decreased sympathetic nervous system activity and lowered plasma renin activity by central α2-adrenergic receptor stimulation

Front 74

Indications for central alpha-2 agonist

Back 74

Resistant HTN
Anxiety driven HTN
Perioperative HTN (analgesia and anesthesia sparing property)

Front 75

What class would you use for anxiety driven HTN?

Back 75

aplha2 agonist

Front 76

What cal would you use for perioperative HTH and why?

Back 76

Central alpha-2 agonist- analgesia and anesthesia sparing property

Front 77

1) What is the only drug that is actually indicated for HTN in pregnancy?
2) What drug is ACTUALLY used by Obstetricians in this case?

Back 77

1) methyldopa
2) nifedipine (DHP Ca++ blocker)

Front 78

Central Nervous pathway of Alpha-2 agonist meidating BP reduction

Back 78

Front 79

1)Side effect of all central aplha-2 agonists?
2) Side effect of just Clonidine?
3) side effect just of Methyldopa?

Back 79

1) fluid retention- dose dependant
bradycardia- dose dependant
2) sedation, dry mouth, skin iritation (transdermal)
3) autoimmune hemolytic anemia and hepatitis

Front 80

1) Major danger of Clonidine perscription
2) When is the probelem even more dangerous than normal?
3) how do we handle this

Back 80

1) Rebound hypertension if the drug is stopped suddenly
2) concomitant B-blocker
3) wean 30% per week until .1 mg/day and do not prescribe to unreliable people

Front 81

Beta Blockers: mode of action
(this is just speculative, we dont REALLY know)

Back 81

Reduce CO
Inhibit Renin release
Direct CNS effect
Alteration of catecholamine release or response

Front 82

Beta blockers:
1) Labetelol and carvediol are special, why?
2) Nebibolol is special, why?

Back 82

1) Beta and aplha1 antagonism, so they also lower PVR
2)Cardioselective vasodilator as a result of increased NO levels

Front 83

ALL beta b lockers except Nebibolol do what?

Back 83

Decrease CO

Front 84

SOme beta blockers have Intrinsic Sympathomimetic acitivty. We call these ISA Beta-blockers.
1) Three ISA B-blockers
2)In what sense are these Beta-blockers sympathomimetics? antagonists?

Back 84

1) propranolol, acebutolol, pindolol
2)They have a partial agonist acitivity at Beta1 and/or Beta2. Thas has little consequece in the absence of SNS input, but can act as as antagonists when the strong agonists like Epi and NE are released here.

Front 85

1) The mixed alpha1 and Beta blocking carvediol make them useful in treating HTN complicated by_____.

2) This alpha activity has what effect on C.O.

Back 85

angina

2) reduces PVR, which maintains CO while lone beta antagonists drop CO.

Front 86

Beta Blockers: Indications

Back 86

uncomplicated HTN
Isolated Systolic HTN
Pulse rate dependent HTN
HTN with symptomatic CAD
CHF
Essential Tremor

Front 87

Beta Blockers: Contraindications-- Tell me why these are contraindications:
1) Bronchospasm
2) Decompensated CHF
3) Heart block, Sick Sinus
4) Insulin Dependant DM (relative contraindication)

Back 87

1) B2 blocker cuses bronchoconstriction- dont use non-selectives or B2 selelctives at HIGH doses)

2) Decompensated CHF due to decrease in C.O.

3) A.V. Nodal blockers

4) Blunts the symptoms of hypoglycemia ( tachycardia, tremor)

Front 88

Beta Blockers: Side effects

Back 88

Bronchospasm
Heart Block
Worsening CHF
High triglycerides or Low HDL
Mask hypoglysemia in IDDM
Depression or nightmares
Poor sleep

Front 89

Sympatholytics mechanism of action

Back 89

Lower BP by depelting NE from presynaptic storage granules

Front 90

Sympatholytics: Indication

Back 90

Resistant HTN

Front 91

Sympatholytics: Drug-Drug interactions
1) MAOI
2) TCAs

Back 91

1) Hypertensive crisis
2) Decreased hypotensive effect

Front 92

Sympatholytics: Side effects
1) HEENT
2) stomach
3) GI
4) GU
5) Psych

Back 92

1) stuffiness
2) gastric acidity
3)diarrhea
4) retrograde ejaculation
5) depression

Front 93

Definition of resistant HTN

Back 93

BP which is not controlled despite pt. being on 3 drugs at maximal doses, one of which is a diuretic

Front 94

Most people require __ drugs to control HTN

Back 94

3

Front 95

Particularly effective combinations of Antihypertensives:
Use Diuretics with-

Back 95

B blockers
ACE-I/ARB

Front 96

Particularly effective combinations of Antihypertensives:
Use Beta Blockers with

Back 96

Diuretics
Ca++ Channel Blockers

Front 97

Particularly effective combinations of Antihypertensives:
Use Ca++ Channel blockers with

Back 97

B Blockers
ACE-I/ ARB

Front 98

PArticularly effective combinations of Antihypertensives:
Use ACE Inhibitors and ARBs with

Back 98

Diuretics
Ca++ Channel Blockers

Front 99

Fill in the blanks

Back 99

Front 100

Algoritihim for Treatment of HTN

Back 100

Front 101

Initial Drug Choice-
Uncompliated HTN

Back 101

thiazide

Front 102

Initial Drug Choices-
CHF

Back 102

ACE inhibitors
Diuretics (Loop)

Front 103

Initial Drug Choices-
1) HTN with MI
2) HTN with MI with systolic dysfunction

Back 103

1) Non ISA - beta blockers
2) ACE inhibitors

Front 104

Initial Drug Choices-
HTN with DM

Back 104

ACE inhibitors

Front 105

Initial Drug Choices-
ISH in elderly
1) preffered
2) other

Back 105

1) diuretics
2) Long acting DHP Ca++ channel blockers

Front 106

HTN drugs with favorable effects on Angina

Back 106

B-blockrs
Ca++ channel blokckers

Front 107

HTN drugs with favorable effects on
Atrial tach and Fib

Back 107

B- blockers
Non-DHP Ca++ channel blockers

Front 108

HTN drugs with favorable effects on CHF

Back 108

Carvedilol
Metoprolol
Losartan

Front 109

HTN drugs with favorable effects on
MI

Back 109

Non-DHP Ca++ Channel blockers

Front 110

HTN drugs with favorable effects on Cyclosporine induced hypertension

Back 110

Ca++ channel blockers

Front 111

HTN drugs with favorable effects on
DM I with proteinuria

Back 111

ACE inhibitor

Front 112

HTN drugs with favorable effects on DMII with proteinuria

Back 112

ARBs
ACE-inhibitors are used to cuz cheaper and may work as well

Front 113

HTN drugs with favorable effects on Dyslipidemia

Back 113

alpha1-blockers

Front 114

HTN drugs with favorable effects on BPH

Back 114

aplha1-blockers

Front 115

Renal Insuficiency

Back 115

ACE inhibitors