Exam 2: Hypertension Flashcards
1
Q
How many Americans have hypertension
A
76 million Americans
2
Q
If uncontrolled, HTN can lead to serious heart problems like
A
- Damage to heart and vessel
- Kidney damage
- Stroke
- erectile dysfunction
- Vision loss
3
Q
Examples of damage to heart and vessel from HTN
A
Angina
Peripheral artery disease
4
Q
What is the number one cause of stroke
A
Hypertension
5
Q
Essential hypertension
A
Chronic elevation in BP with no clearly identifiable etiology (except genetics/environmental)
6
Q
Essential hypertension accounts for ____% of hypertension
A
90-95%
7
Q
Onset age for essential hypertension
A
40’s to 50’s
8
Q
Blood pressure =
A
(Peripheral vascular resistance)(Cardiac output)
9
Q
Cardiac output =
A
(Heart rate) (stroke volume)
10
Q
Stroke volume =
A
End diastolic volume - end systolic volume
11
Q
Genetic predisposition/ _____ of patients have family history of essential hypertension
A
70-80
12
Q
Goal of treatment for essential hypertension
A
BP < 140/90 and minimizing morbidity and mortality
13
Q
Secondary hypertension has a
A
Identifiable etiology
14
Q
For secondary hypertension. many factors influencing CO, SVR, and BP can be disrupted by disease processes that impact:
A
Volume status
Adrenergic tone
Peripheral Vascular resistance
15
Q
goal of treatment for secondary hypertension
A
Treat underlying cause and minimizing morbidly and morality
16
Q
Symptoms, when present, are caused
A
By long term effects of HTN on susceptible organs
17
Q
Essential hypertension complications/target organ damage
A
RENAL disease Heart Brain Peripheral vasculature Eyes
18
Q
examples of heart complications due to essential hypertension
A
Left ventricular hypertrophy
Angina
Myocardial infarction
Heart failure
19
Q
examples of brain complications due to essential hypertension
A
Stroke or transient ischemic attack
20
Q
examples of peripheral vasculature complications due to essential hypertension
A
Peripheral arterial disease
21
Q
examples of eyes complications due to essential hypertension
A
retinopathy
22
Q
Classifications of antihypertensives
A
Ace inhibitors ARBs Aldosterone inhibitors Renin inhibitors Vasodilators Diuretics CCBs Sympatholytics
23
Q
Acronym to remember antihypertensive classifications
A
Always Accept A Red Valentine's Day Card Surprise
24
Q
Ace inhibitors end in
A
-Prils
25
All Ace inhibitors are administered
PO
26
Which ace inhibitor is not administered PO
Enalaprilat
27
All ace inhibitors are prodrugs besides
Captopril and lisinopril
28
Indications for ace inhibitor/ captopril
hypertension
heart failure
Diabetic nephropathy
Left ventricular dysfunction following MI
29
MoA of ACE inhibitors/ CaptoPRIL
Blocks ACE from converting angiotensin I to angiotensin II, leading to decreased
- vasoconstriction
- Peripheral vascular resistance
- Aldosteron production
- Fluid volume
- -- Overall decreased BP
30
Adverse effects of captopril (& other ACE inhibitors)
Hypotension: Especially in 1st dose due to abrupt lowering of angiotensin II
Dry, persistent cough (ACE COUGH; secondary to increase bradykinin)
Hyperkalemia: secondary to inhibition of aldosterone; rare, but increase risk if also taking potassium-sparing diuretic, potassium supplements
Swelling of tissues (angioedema)
31
Hyperkalemia
High potassium levels
32
Most common reason for discontinuing ACE inhibitor therapy
Dry, persistent cough: ACE cough
33
Advise individuals to not take ____ during ACE inhibitors
Do not take K+ supplements or salt substitutes
34
Ace inhibitors are good antihypertensives for diabetics because
they limit damage to renal blood vessels often seen in diabetic patients and other patients with renal disorders
35
Black box warning for ACE inhibitors
Drugs that act on RAAS can cause injury/death to developing fetus
36
Should ACE inhibitors be given to pregnant women
No!
37
Angiotensin II receptor blockers (ARBs) end with
-sartans
38
All angiotensin II receptor blockers (ARBs) are given how?
All PO
39
Indications for Angiotensin II receptor blockers (ARBs) / Iosartan
Hypertension
Congestive Heart Failure
Myocardial infarction
Stroke Prevention
40
MoA ARBs
```
Blocks actions of angiotensin II which causes vasodilation and decreased
- peripheral vascular resistance
- aldosterone production
- fluid volume
and overall decreased BP
```
41
All anihypertensives can cause what adverse effect
hypotension
42
Adverse effects for angiotensin II receptor blockers (ARBs)
Hypotension
| Hyperkalemia
43
Rare adverse effects for ARBs
Thrombocytopenia
Rhabdomyolysis
Angioedema
44
Black boxed warnings for ARBs
drugs that act on RAAS can cause injury/death to developing fetus
45
Should ARBs be given to pregnant women
No!
46
Aldosteron inhibitors in this unit end in
-one
47
Indications for aldosterone inhibitors (spironolactone)
Hypertension
Heart failure
and following Myocardial infarction
48
MoA for aldosterone inhibitors
Blocks the release of aldosterone, leading to the urinary excretion of Na and H2O, also causes retention of K+
49
Retention of K+ or hyperkalemia can be due to
no exchange of Na, this can be done from urinary excretion of Na or reuptake of Na as oppose to Na/K exchange
50
Side effects of aldosterone inhibitors
Hypotension and Hyperkalemia
51
The only Direct Renin Inhibitor (DRI) currently on the market
Aliskiren
52
Aliskiren drug class
Renin inhibitors
53
Aliskiren is given
PO only
54
Aliskiren MoA
Binds to renin to inhibit conversion of angiotensinogen to angiotensin I, thereby suppressing the RAAS
55
When aliskiren is administered with high fat meals, it
decrease absorption
56
Adverse effects of aliskiren
Hypotension and hyperkalemia
57
are long term benefits and safety of aliskiren known?
No, they are not known yet
58
As a drug that affects RAAS, should aliskiren be given to pregnant women
No!
59
Vasodilator examples
Fenoldopam
Hydralazine
Minoxidil
Nitroprusside
60
Indications for vasodilators
Hypertension
Heart failure
Pulmonary Hypertension
61
MoA vasodilators
Vasodilation leads to decreased arterial pressure and decreased peripheral vascular resistance, as a result, we also see an increase heart rate and increase contractility of the heart
62
Adverse effects of vasodilators
Hypotension
Palpitations
Tachycardia
W/ high doses---> fluid retention edema, systemic lupus erythematous like S/S
63
systemic lupus erythematous like symptoms and signs
Facial rash, joint pain, fever, nephritis, and pericarditis
64
Nitroprusside (nitropress) drug class
Vasodilator, antihypertensive
65
MoA for nitroprusside
produces peripheral dilation by direct action on both arteriolar and venous smooth muscle, which caused decreased peripheral vascular resistance
66
Black box warning for nitroprusside
Never inject directly!! dilute first!
67
Indications for nitroprusside
Lower blood rapidly in hypertensive emergencies
| Controlled hypotension during surgical procedures
68
Continuous BP monitoring of nitroprusside should be done by
experienced personnel
69
Extensive hypotension from nitroprusside can result in
hypo perfusion of vital organs may occur
70
Adverse effects of nitroprusside
Hypotension: if administration is too rapid, it can cause a precipitous fall in BP
Sodium and water retention
Cyanide toxicity
71
How to combat sodium and water retention from nitroprusside
Furosemide
72
Cyanide toxicity and nitroprusside
nitroprusside contains 5 cyanide groups which are split free in the 1st step of nitroprusside metabolism
73
Nitroprusside gives rise to large cyanide quantities except when
used briefly or at low infusion rates
74
Hydralazine drug class
Hypertension, pre-eclampsia/eclampsia, heart failure
75
MoA hydralazine
Direct vasodilation of arterioles (little effects on veins) which cause decreased systemic resistance
76
Nursing considerations/adverse effects of hydralazine
Hypotension: orthostatic precautions should be observed
| Peripheral neuritis
77
Peripheral neuritis (from hydralazine) symptoms
Numbness, paresthesia, tingling
| Secondary to antipyridoxine effect
78
Types of diuretics
Thiazide diuretics
Loop diuretics
Potassium Sparing diuretics
79
Thiazide diuretics include
Chlorthiazide, hydrochlorothiazide
80
Thiazide diuretics indications
Hypertension
Heart failure
Liver Cirrhosis
Renal failure
81
MoA of thiazide diuretics
In the DISTAL CONVOLUTED TUBULE of the nephron, block NA and Cl reabsorption, leading to increase excretion of Na, Cl, H2O, K+
82
Adverse/side effects of thiazide diuretics
```
F/E imbalances such as
-Hyponatremia
-Hypochloremia
-Hypokalemia
-Dehydration
-Hyperglycemia
and increased uric acid
```
83
F/E imbalances refer to
loss of both water and solutes in the same proportion from the extracellular fluid space
84
Loop diuretics include
Bumethanide
Furosemide
Ethacrynic acid
Torsemide
85
Loop diuretics indications
Hypertension
Heart failure
Edema
86
Loop diuretics MoA
in the ASCENDING LOOP OF HENLE, blocks Na, Cl, K+ and water reabsorption, leading to increase excretion of Na, Cl, H2O and K+
87
Loop diuretics' effect is much more
potent than other diuretics
88
Adverse and side effect of loop diuretics
F/E imbalances such as hyponatremia, hypochloremia, hypokalemia, dehydration, orthostatic hypotension, hyperglycemia, AND
-Increase uric acid
ALSO- ototoxicity
89
Examples of potassium sparing diuretics
Amiloride
Spironolactone
Triamterene
90
Potassium sparing diuretics indications
```
Hypertension
Heart Failure
Edema
Cirrhosis
Nephrotic syndrome
HYPOkalemia
```
91
MoA Potassium Sparing Diuretics
```
in the DISTAL PORTION OF NEPHRON, blocks Na, Cl, and water reabsorption,
which leads to
- increased excretion of NA
- Smaller loss of H2O
- Decreased excretion of K+
```
92
Adverse/side effects of Potassium Sparing Diuretics
Hyperkalemia
| Gynecomastia in males
93
Gynecomastia
overdevelopment or enlargement of breast tissue in mens/boys
94
Calcium channel blockers prevent the
movement of calcium ions into cardiac and vascular smooth muscle cells
95
Calcium channel blockers have major
therapeutic effects on heart and arteries
96
Calcium channel blockers indication
Hypertension
Angina pectoris
Cardiac dysrhythmias
97
Calcium channels are
Gated pored in the plasma membrane that regulate the entry of calcium ions into cells
98
Calcium plays an important role in
function of vascular smooth muscle and heart
99
At therapeutic doses, calcium channel blockers act
SELECTIVELY on the peripheral arterioles and/or cardiac arteries/arterioles
100
When an action potential travels down surface of smooth muscle cells, what happens to calcium channels?
Calcium channels open and calcium ions flow inward, initiating contraction
101
Blockage of the calcium prevents
Contraction, resulting in vasodilation
102
Calcium entry into myocardium has a
Positive inotropic effect
103
Positive inotropic effects mean
strengthen the heart's contractions, so it can pump more blood with fewer heartbeats
104
Cardiac effects of calcium on the SA node
Open calcium channels in SA node cause an increase spontaneous discharge of SA node
105
Cardiac effects of calcium on the AV node
Open calcium channels in AV node cause AV node to fire more readily
106
Calcium Channel Blockers can be categorized as
Dihydropyridines
| Non-Dihydropyridines
107
Dihydropyridines
Work primarily on the smooth muscles of there arteries; vasodilation
108
Examples of Dihydropyridines calcium channel blockers
Amlodipine
Felodipine
Nicardipine
Nifedipine
109
Non-Dihydropyridines
Negative inotropic effect on the heart;
Slow conduction through AV node
Decrease rate of SA node firing
110
Examples of non-Dihydropyridines calcium channel blockers
Diltiazem
| Verapamil
111
non-dihydropyridines calcium channel blockers MoA
inhibits the movement of calcium ions across the membranes of cardiac & arterial muscle cells:
- coronary vasodilation
- peripheral vasodilation
- negative chronotrope
- negative inotrope
- negative fromotrope
- increased CO
- Decrease BP
- Decrease myocardial O2 consumption and increase blood supply to heart
112
Adverse effects of non-dihydropyridines calcium channel blockers
Hypotension
Bradycardia
Peripheral edema
Heart block (increased risk with concurrent digoxin)
Constipation
Headache
Cardriosuppressant effects of beta blockers intensified with concurrent CCB
113
When taking non-Dihydropyridines calcium channel blockers, patients should avoid
Grapefruit juice as it can delay CCB metabolism and produce toxic levels
114
examples of sympatholytics
Alpha-1 adrenergic blockers
Beta adrenergic blockers
Alpha and Beta adrenergic blockers
Centrally acting alpha-2 agonists
115
Examples of alpha 1 adrenergic blocking agents
Doxazosin
Prazosin
Terazosin
116
Alpha 1 adrenergic blocking agents end in
-zosin
117
Alpha 1 adrenergic blocking agent indication
Hypertension
Benign prostatic hyperplasia
-not listed treatment of PHEOCHROMOCYTOMA, extravasation
118
MoA of alpha 1 adrenergic blocking agents, antagonist
Blocks alpha 1 receptors along the walls of peripheral blood vessels,
Leading to VASODILATION
119
Side effects of alpha 1 adrenergic blocking agents
Orthostatic hypotension
Reflex tachycardia
Headache
120
Most therapeutic effects are due to
Blockage of alpha 1 receptors on the vasculature
121
Indications for alpha 1 adrenergic blocking agents
- Hypertension: blocks alpha 1 on arterioles and veins, leading decrease in peripheral vascular resistance, which causes a decrease in blood pressure
- reversal of sympathomimetic drug effects! (epinephrine) in cases of OD/toxicity
- Prevention of tissue necrosis following extravasation of drugs that produce vasoconstriction (phentolamine approved for use)
- Benign prostatic hyperplasia: selective blockage of alpha-1 receptors on bladder beck, prostatic capsule)
- Pheochromocytoma (catecholamine-secreting tumor)
122
Terazosin drug class
Alpha 1 adrenergic blockers
123
Terazosin administration
PO only
124
Terazosin MoA
Competitive antagonist that produces SELECTIVE blockage of alpha-1 adrenergic receptors
- Decrease in arterial tone, leading to decrease peripheral vascular resistance, which leads to DECREASE IN BP
- Relaxation of bladder neck & prostatic capsule (used for benign prostatic hyperplasia)
125
Adverse/side effects of terazosin
```
Orthostatic hypotension
Tachycardia
Syncope following 1st dose
Impotence, decreasing libido
Retention of sodium and water (often combined with diuretic to counteract this effect)
Nasal congestion
Dizziness
```
126
Beta adrenergic antagonists
Beta blockers
Nonselective - blocks beta 1 and beta 2
Selective - blocks only beta 1
127
Major therapeutic effects of beta adrenergic antagonists
Blockage of beta 1 receptors in the heart
128
**. Indications of beta adrenergic antagonists
Angina pectoris: decrease cardiac workload and decrease O2 consumption
Cardiac dysrhythmias: Decrease rate of sinus nodal discharge & suppress conduction of atrial impulses through AV node which prevents ventricles from being driven by excessive rate
Myocardial infarction: decrease infarct size, decrease risk on reinfarction, and decrease in mortality
Hypertension
Migraine prophylaxis
also used in pain management
129
Beta adrenergic blockers end in
- olol
130
Metoprolol drug class
Caridioselective Beta 1 adrenergic antagonist, beta blocker
131
Advantages of metoprolol
@ normal, therapeutic dosages, blocks Beta 1 receptor sites only (Although selectivity is not absolute)
- may be used in proteins with bronchospastic disease with caution
132
Metoprolol MoA
Selective inhibitor of B-1 adrenergic receptors leads to multiple therapeutic effects:
- Decrease in conduction through AV node (decrease heart rate)
- Decrease in force of cardiac contraction
- Decrease in renin secretion
133
Adverse effects and side effects of metoprolol
```
Hypotension
Bradycardia
Dizziness
Heart block
Heart failure
-Drowsiness
-Vertigo
- Contraindicated in patients with history of severe allergy
--- CAUTION IN DIABETICS
```
134
Black box warning for metoprolol
Not be withdrawn abruptly! gradually taper (over 1-2 weeks) to avoid acute tachycardia, hypertension, and/or ischemia
135
Alpha and beta adrenergic antagonists examples
Carvedilol
| Labetolol
136
Alpha and Beta Adrenergic antagonist MoA
Blocks both Alpha-1 and Beta adrenergic receptors
- Vasodilation
- Decrease Heart rate
- Decrease force of contraction
- Decrease release of renin from kidneys
137
Adverse and side effects of alpha and beta adrenergic antagonists
Dizziness
Hypotension
Bradycardia
138
Examples of centrally acting alpha-2 adrenergic agonists
Clonidine
Guanfacine
Methyldopa
139
MoA centrally acting alpha-2 adrenergic agonists
-inhibits innervation of sympathetic neurons in the CNS, leading to a
- Decreased outflow of NE,
- Decrease heart rate
- Decrease contractility
Vasodilation
140
Adverse/side effects of centrally acting alpha-2 adrenergic agonists
Drowsiness
Dizziness
Rebound hypertension if abruptly discontinued
141
Clonidine drug class
Alpha- 2 adrenergic agonist
142
MoA clonidine
- stimulates alpha-2 adrenoceptors in brain stem (in areas associated with autonomic regulating of CV system) LEADS TO
- activation on inhibitory neurons
- Decrease in sympathetic outflow from CNS to CV system
- Decrease in peripheral vascular resistance
- Decrease in cardiac output
- Decrease in blood pressure
143
Clonidine administration
PO or transdermal patch
144
Adverse effects of clonidine
Bradycardia, hypotension, CNS depression (causing drowsiness); discontinue by tapering slowly to avoid rebound hypertension
145
Clonidine can also be used to prevent
- Cancer pains ( can be used as a pain medication because it prevents pain signal transmission)
- indicated for ADHD
