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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
What does CCB's do?
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
26
CCB drugs
- Amlodipine - Felodipine - Nifedipine - Diltiazem - Verapamil
27
What are the categories of CCB's?
- Dihydropyridine | - Nondihydropyridine
28
Dihydropyridine CCB's
- Amlodipine - Felodipine - Nifedipine
29
Nondihydropyridine CCB's
- Diltiazem | - Verapamil
30
Dihydropyridine CCB's effects
- 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
31
Nondihydropyridine CCB's effects
- Greater effects on cardiac myocytes and AV | - Have effects on both vasodilation and negative inotropy and chronotropy
32
CCB's effects
- 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
α1-blocker drugs
doxazosin
34
α1-blocker effects
- 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
What is added with α1-blockers?
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
β-blocker drugs
- Atenolol - Bisoprolol - Carvedilol - Labetalol - Metoprolol tartrate - Metoprolol succinate - Propranolol
37
β1 receptor blockade effects
- 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
β2 receptor blockade effects
- Increased airway resistance - Inhibit lipolysis -> can impair ability to cope with hypoglycemia - Reduce intraocular pressure (used to treat glaucoma)
39
When do we reach lipolysis ?
- 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
What is the β-blocker prototype?
- propranolol | - long acting form available
41
Which β-blockers are β1-selective?
- metoprolol - atenolol - nebivolol
42
Why are β1-selective blockers important?
- less respiratory issues | - less lipolysis issues
43
Which β-blockers also have some α1-blocker effects?
- labetalol | - carvedilol
44
Which β-blocker is the most β1-selective?
nebivolol
45
nebivolol actions
- Causes vasodilation via NO synthase activation | - Increases insulin sensitivity, no lipid effects
46
Central α2-agonist drugs
clonidine
47
Central α2-agonist effects
- 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
Where is the α2 receptor located?
brainstem
49
ACE inhibitors adverse effects
- hypotension especially on first dose for patients who have high renin levels - dry persistent cough - hyperkalemia - angioedema
50
In ACEI's, how is the dry persistent cough produced and what can you do to manage it?
- 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
What is a contraindication for ACEI's?
- pregnant women - teratogenic - can cause renal development issues in 3rd trimester
52
ARB's adverse effects
Half the incidence of cough and angioedema compares to ACE inhibitors
53
What is a contraindication for ARB's?
- pregnant women - teratogenic - can cause renal development issues in 3rd trimester
54
Which patients is most likely to experience hyperkalemia using ACEI's?
patients on potassium supplements or potassium-sparing diuretics
55
Which patients is most likely to experience hyperkalemia using ARB's?
patients with renal disease, on potassium supplements or potassium-sparing diuretics
56
CCB's adverse effects
- Cardiac depression - Flushing, fizziness, nausea (associated with exaggerated vasodilation) - Peripheral edema (swollen ankles; gravitational problem) - Constipation - Can aggravate GERD
57
CCB's adverse effects: cardiac depression
- bradycardia, AV block, cardiac arrest, heart failure | - Nondihydropyridine are going to be at greater risk of this
58
α1-blocker adverse effects
- Postural hyper/hypotension | - Risk of congestive heart failure (CHF) with doxazosin (monotherapy)
59
β-blockers adverse effects
- 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
What are possible withdrawal symptoms following the abrupt discontinuation of β-blockers?
- hyperglycemia | - vasoconstriction
61
If β-blockers cause impaired AV conduction, what is the patient at risk for?
bradyarrhythmia
62
Central α2-agonist adverse effects
- Postural hypotension - Erectile dysfunction - Nightmares/vivid dreams - Bradycardia - Withdrawal syndrome
63
What are possible withdrawal symptoms following the abrupt discontinuation of Central α2-agonists?
- headache - tremors - sweating - tachycardia
64
Bradycardia is a problem in which patients taking a Central α2-agonists?
patients with AV dysfunction (disease or drug-induced)
65
Central α2-agonists poses a risk for which type of patients?
- for congestive heart failure patients - due to decreased SNS tone to heart - can worsen CHF
66
ACE inhibitors kinetics
- 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
ARBs kinetics: Candesartan cilexetil
- Inactive prodrug hydrolyzed into active form in GI tract | - clearance is RENAL and hepatic
68
ARBs kinetics: Olmesartan medoxomil
- Inactive prodrug | - hydrolyzed into active form in GI tract
69
ARBs kinetics: Azilsartan medoxomil
- Inactive prodrug hydrolyzed into active form in GI tract | - Metabolized by CYP2C9 into inactive metabolites
70
ARBs kinetics: Losartan
- 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
ARBs kinetics: Irbesartan
Clearance is renal and liver, not affected by mild to moderate failure
72
ARBs kinetics: Telmisartan
Clearance mostly HEPATIC
73
ARBs kinetics: Valsartan
- Food decreases EXTENT of absorption significantly | - Clearance is HEPATIC
74
CCB’s kinetics
- 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
α1-blocker kinetics
- Long t1/2 (22h) | - Metabolized extensively by kidney and liver
76
β-blockers kinetics
- 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
Which β-blockers is lipophilic?
- metoprolol - bisoprolol - carvedilol - propranolol
78
Which β-blockers is hydrophilic?
- atenolol | - labetalol

OU Module Cardio Spring 2018 (16 decks)

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