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OU Module Cardio Spring 2018 > Hypertension - Sharpe > Flashcards

Hypertension - Sharpe Flashcards

1
Q

What is the primary function of renin?

A

increase blood pressure

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2
Q

What does renin cleave?

A

cleaves angiotensinogen to form AngI

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3
Q

What increases renin release?

A
  • loop diuretics
  • ACE inhibitors
  • ARBs
  • renin inhibitors
    (via disruption feedback)
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4
Q

What decreases renin release?

A
  • NSAIDs

- beta blockers

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5
Q

Renin release regulation

A
  • Renin release is regulated by beta 1 receptor activation
  • Increased levels of Na sensed by the macula densa inhibits renin production and release
  • Intravenal baroreceptor pressure increase = inhibits renin release
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6
Q

What does ACE do?

A
  • forms AngII from AngI which occurs primarily in the lungs
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7
Q

Where are AT1Rs the strongest?

A

kidney

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8
Q

AT1R actions

A
  • vasoconstriciton
  • fibrosis
  • VSMC inflammation
  • oxidative stress
  • cardiac hypertrophy
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9
Q

AT2R actions

A
  • vasodilation
  • antifibrotic
  • anti-inflammation
  • reduce oxidative stress
  • antiproliferation
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10
Q

AngII actions n

A
  • increase TPR -> increase BP
  • increase cardiac contractility by opening Ca channels
  • increase HR
  • antidiuretic; increase Na reabsorption
  • increase production and release aldosterone from adrenal cortex
  • constricts renal vascular smooth muscle
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11
Q

What does ACEI’s do?

A
  • keeps AngI from being converted to AngII -> lowers BP and enhances natriuresis
  • Reduces TPR by arteriolar dilation and increase compliance of large arteries which reduces systolic pressure
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12
Q

ACEI drugs

A
  • Benazepril
  • Captopril
  • Enalapril
  • Fosinopril
  • Lisinopril
  • Moexipril
  • Quinapril
  • Ramipril
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13
Q

What are the categories of ACEI’s?

A
  • Sulfhydryl-containing
  • Dicarboxyl-containing
  • Phosphorus-containing
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14
Q

Sulfhydryl-containing ACEI

A

Captopril

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15
Q

Dicarboxyl-containing ACEI

A
  • Enalapril
  • moexipril
  • benazepril
  • quinapril
  • Ramipril
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16
Q

Phosphorus-containing ACEI

A

Fosinopril

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17
Q

What are the effects of ACEI’s?

A
  • inhibits degradation of bradykinin
  • increase levels of natural stem cell regulator
  • increase renin prodction (due to loss of AngII feedback)
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18
Q

Who are ideal candidates for ACEI?

A

patients with elevates levels of plasma renin; they probably have too much AngII production because they have high levels of renin

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19
Q

Which patients are not ideal candidates for ACEI?

A

in patients with primary aldosteronism

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20
Q

Are ACEI’s a concern in patients who exercise or experience postural changes?

A

no

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21
Q

What can be combined with ACEI’s for additional management?

A

can be combined with thiazides or CCB for additional management

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22
Q

What does ARBs do?

A

blocks AT1R by binding to the AT1 receptor as a competitive antagonist but binding is almost irreversible

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23
Q

ARB drugs

A
  • Azilsartan
  • Candesartan
  • Irbesartan
  • Losartan
  • Olmesartan
  • Valsartan
  • Telmisartan
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24
Q

What is a special thing about ARBs?

A

renoprotective for type 2 diabetics

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25
Q

What does CCB’s do?

A

block entry for voltage-gated calcium channels; inhibit calcium entry into smooth muscle such as cardiac myocytes; this will cause decrease in TPR and relief of the HTN

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26
Q

CCB drugs

A
  • Amlodipine
  • Felodipine
  • Nifedipine
  • Diltiazem
  • Verapamil
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27
Q

What are the categories of CCB’s?

A
  • Dihydropyridine

- Nondihydropyridine

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28
Q

Dihydropyridine CCB’s

A
  • Amlodipine
  • Felodipine
  • Nifedipine
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29
Q

Nondihydropyridine CCB’s

A
  • Diltiazem

- Verapamil

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30
Q

Dihydropyridine CCB’s effects

A
  • Vascular smooth muscle effects are more than cardiac effects
  • May have tachycardia initially
  • Have predominant effect on vasodilation and afterload reduction; have less effect on the heart
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31
Q

Nondihydropyridine CCB’s effects

A
  • Greater effects on cardiac myocytes and AV

- Have effects on both vasodilation and negative inotropy and chronotropy

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32
Q

CCB’s effects

A
  • Blocking smooth muscle all over the body such as GI tract
  • Decreases arterial resistance, blood pressure, and cardiac afterload
  • Decrease contractility comes from cardiac myocytes causing negative inotropic effects
  • Causes decrease pacemaker rate and AV node conduction velocity
  • Are antianginal, antiarrhythmic, and antihypertensive
33
Q

α1-blocker drugs

A

doxazosin

34
Q

α1-blocker effects

A
  • have effect on vascular smooth muscle
  • Will decrease arteriolar resistance -> decrease TPR -> increase venous capacity -> decrease BP -> body will initially have a reflex to fix the BP and increase heart rate and renin activity but this eventually goes away and vasodilation stays keeping the BP down
35
Q

What is added with α1-blockers?

A

Diuretic added with these medications because when BP drops, body will try to renally compensate -> retention of salt and water -> add diuretic to help offset the compensation

36
Q

β-blocker drugs

A
  • Atenolol
  • Bisoprolol
  • Carvedilol
  • Labetalol
  • Metoprolol tartrate
  • Metoprolol succinate
  • Propranolol
37
Q

β1 receptor blockade effects

A
  • Decreases stroke volume & heart rate -> decreased cardiac output
  • Decreases renin release
  • Partial agonist/intrinsic sympathomimetic activity: peripheral vasoconstriction, bronchoconstriction, hypoglycemia
  • initial reaction -> decreased cardiac output and increased (reflexive) peripheral resistance
38
Q

β2 receptor blockade effects

A
  • Increased airway resistance
  • Inhibit lipolysis -> can impair ability to cope with hypoglycemia
  • Reduce intraocular pressure (used to treat glaucoma)
39
Q

When do we reach lipolysis ?

A
  • lipolysis: breaking down fat for energy

- when we haven’t eaten in a while or if you do heavy endurance activity; type I DM reach this fairly quickly

40
Q

What is the β-blocker prototype?

A
  • propranolol

- long acting form available

41
Q

Which β-blockers are β1-selective?

A
  • metoprolol
  • atenolol
  • nebivolol
42
Q

Why are β1-selective blockers important?

A
  • less respiratory issues

- less lipolysis issues

43
Q

Which β-blockers also have some α1-blocker effects?

A
  • labetalol

- carvedilol

44
Q

Which β-blocker is the most β1-selective?

A

nebivolol

45
Q

nebivolol actions

A
  • Causes vasodilation via NO synthase activation

- Increases insulin sensitivity, no lipid effects

46
Q

Central α2-agonist drugs

A

clonidine

47
Q

Central α2-agonist effects

A
  • Decrease SNS outflow
  • Decrease peripheral NE
  • Decrease heart rate & stroke volume (supine)
  • Decrease vascular resistance (standing)
  • If dose is too high, also agonize α2b receptors -> vasoconstriction
48
Q

Where is the α2 receptor located?

A

brainstem

49
Q

ACE inhibitors adverse effects

A
  • hypotension especially on first dose for patients who have high renin levels
  • dry persistent cough
  • hyperkalemia
  • angioedema
50
Q

In ACEI’s, how is the dry persistent cough produced and what can you do to manage it?

A
  • cause by accumulation of bradykinin / PG / substance P in the lungs
  • ASA or iron supplements can reduce cough
  • Can lower dose or switch to ARB
51
Q

What is a contraindication for ACEI’s?

A
  • pregnant women
  • teratogenic
  • can cause renal development issues in 3rd trimester
52
Q

ARB’s adverse effects

A

Half the incidence of cough and angioedema compares to ACE inhibitors

53
Q

What is a contraindication for ARB’s?

A
  • pregnant women
  • teratogenic
  • can cause renal development issues in 3rd trimester
54
Q

Which patients is most likely to experience hyperkalemia using ACEI’s?

A

patients on potassium supplements or potassium-sparing diuretics

55
Q

Which patients is most likely to experience hyperkalemia using ARB’s?

A

patients with renal disease, on potassium supplements or potassium-sparing diuretics

56
Q

CCB’s adverse effects

A
  • Cardiac depression
  • Flushing, fizziness, nausea (associated with exaggerated vasodilation)
  • Peripheral edema (swollen ankles; gravitational problem)
  • Constipation
  • Can aggravate GERD
57
Q

CCB’s adverse effects: cardiac depression

A
  • bradycardia, AV block, cardiac arrest, heart failure

- Nondihydropyridine are going to be at greater risk of this

58
Q

α1-blocker adverse effects

A
  • Postural hyper/hypotension

- Risk of congestive heart failure (CHF) with doxazosin (monotherapy)

59
Q

β-blockers adverse effects

A
  • Peripheral vasoconstriction, Hypoglycemia, lipid abnormalities, Bronchoconstriction risk
  • Can cause bradycardia; only worry in patients that already have bradycardia; fine to use in patients that have a normal heart rate
  • Abrupt discontinuation leads to withdrawal syndrome
  • Possible: fatigue, insomnia, nightmares, depression
60
Q

What are possible withdrawal symptoms following the abrupt discontinuation of β-blockers?

A
  • hyperglycemia

- vasoconstriction

61
Q

If β-blockers cause impaired AV conduction, what is the patient at risk for?

A

bradyarrhythmia

62
Q

Central α2-agonist adverse effects

A
  • Postural hypotension
  • Erectile dysfunction
  • Nightmares/vivid dreams
  • Bradycardia
  • Withdrawal syndrome
63
Q

What are possible withdrawal symptoms following the abrupt discontinuation of Central α2-agonists?

A
  • headache
  • tremors
  • sweating
  • tachycardia
64
Q

Bradycardia is a problem in which patients taking a Central α2-agonists?

A

patients with AV dysfunction (disease or drug-induced)

65
Q

Central α2-agonists poses a risk for which type of patients?

A
  • for congestive heart failure patients
  • due to decreased SNS tone to heart
  • can worsen CHF
66
Q

ACE inhibitors kinetics

A
  • Eliminated primarily in kidney
  • fosinopril and quinapril are equally both kidney and liver
  • hydrolyzed in liver to active metabolite: enalapril, benazepril, fosinopril, quinapril, ramipril, moxepril
  • fosinopril, quinapril, ramipril: absorption decreased by food (extent the same)
67
Q

ARBs kinetics: Candesartan cilexetil

A
  • Inactive prodrug hydrolyzed into active form in GI tract

- clearance is RENAL and hepatic

68
Q

ARBs kinetics: Olmesartan medoxomil

A
  • Inactive prodrug

- hydrolyzed into active form in GI tract

69
Q

ARBs kinetics: Azilsartan medoxomil

A
  • Inactive prodrug hydrolyzed into active form in GI tract

- Metabolized by CYP2C9 into inactive metabolites

70
Q

ARBs kinetics: Losartan

A
  • Converted to active metabolite by CYP2C9 and CYP3A4
  • Clearance by liver and kidney
  • Bonus MOAs—also a competitive antagonist of thromboxane A2 receptor (decreases platelet aggregation)
  • metabolite decrease COX2 mRNA upregulation and PG production
71
Q

ARBs kinetics: Irbesartan

A

Clearance is renal and liver, not affected by mild to moderate failure

72
Q

ARBs kinetics: Telmisartan

A

Clearance mostly HEPATIC

73
Q

ARBs kinetics: Valsartan

A
  • Food decreases EXTENT of absorption significantly

- Clearance is HEPATIC

74
Q

CCB’s kinetics

A
  • CYP3A4—responsible for 1st pass metabolism of many CCB
  • Bioavailability increased by CYP3A4 inhibitors (macrolides & imidazole antibiotics, antiretroviral agents, grapefruit juice
  • Bioavailability reduced by CYP3A4 inducers (rifampin, carbamazepine, St. John’s wort)
  • Verapamil—inhibitor of intestinal and renal P glycoprotein -> can increase levels of digoxin, cyclosporine, and loperamide
75
Q

α1-blocker kinetics

A
  • Long t1/2 (22h)

- Metabolized extensively by kidney and liver

76
Q

β-blockers kinetics

A
  • Half life is variable
  • Lipophilic agents are more antiarrhythmic than hydrophilic agents
  • Metabolized and eliminated by liver
  • Metoprolol (most significant), carvedilol, nebivolol are CYP2D6 dependent
77
Q

Which β-blockers is lipophilic?

A
  • metoprolol
  • bisoprolol
  • carvedilol
  • propranolol
78
Q

Which β-blockers is hydrophilic?

A
  • atenolol

- labetalol

OU Module Cardio Spring 2018 (16 decks)

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