Cardiac medications & hypertension Flashcards

1
Q

What are the 2 types of HTN?

A
  1. Primary (essential)
  2. Secondary (caused by something)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

List some examples of causes of secondary HTN

A

OSA (overweight); Renal impairment; Diet; certain meds

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

HTN causes _____ injury leading to impaired ____ & release of ______ ______

A

endothelial injury; impaired synthesis; nitric oxide

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

Hypertension promotes what type of mediators?

A

inflammatory mediators

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

People with HTN will have accelerated development of ____

A

atherosclerosis

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

HTN can be known as the ____ _____ ____

A

“silent killer disease”

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

HTN causes increased ____ _____ & ____ ____

A

cardiac afterload & ventricular hypertrophy

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

If HTN is left untreated it can lead to end-organ damage affecting:

A
  1. heart
  2. brain
  3. kidneys
  4. arteries
  5. eyes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the strong vasoconstrictor hormone?

A

Norepinephrine

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

What other hormone is a part of the SNS stimulation?

A

Epinephrine

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

The stimulation fo SNS during stress or exercise causes …

A

local constriction of veins & arterioles b/c of release of norepinephrine from sympathetic nerve endings

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

Sympathetic stimulation causes the adrenal medulla to secrete _____

A

BOTH norepinephrine & epinephrine into the blood

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

Angiotensin II is a ___

A

very strong vasoconstrictor from RAAS
will increase PVD & BP

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

Histamine has a ____

A

vasodilator effect on arterioles (inflammatory response)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Serotonin is released by ____

A

the platelets, causing vasoconstriction & can cause vascular spasm (inflammatory response)

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

What hormone comes from the globulin (kininogen) that is present in body fluids?

A

bradykinin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Bradykinin causes ____

A

intense dilation of arterioles, increased capillary permeability, & constriction of venules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Kinins play a special role in ___

A

regulating blood flow & capillary leakage in inflamed tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Bradykinins help regulate BF in what 3 body sites?

A
  1. skin
  2. salivary
  3. GI tract
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are prostaglandins made from?

A

arachidonic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How are prostaglandins related to tissue injury?

A

Tissue injury leads to release of AA from cell membranes, which initiates prostaglandin synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Some prostaglandins cause ____ while others cause _____

A

vasoconstriction; vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What role do corticosteroids play in prostaglandin synthesis?

A

They produce anti-inflammatory response by blocking release of AA & preventing prostaglandin synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

HTN is not just about the heart but about what else?

A

blood vessels; kidneys; vascular resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Increased resistance = _____ _____
increased BP
26
First line Tx begins with what?
non-pharmacologic interventions
27
list non-pharmacologic interventions
1. diet 2. exercise 3. life-style management
28
Patient education on non-pharmacologic interventions includes
1. diet 2. exercise 3. lifestyle management (ex. good sleep; smoking cessation; alcohol consumption)
29
What is the first step in HTN management?
Lifestyle management
30
List 3 first line medications used for HTN management
1. ACE inhibitors 2. ARBs 3. Thiazide diuretics
31
What type of medication is not considered a first line pharmacologic Tx of HTN?
beta blockers
32
What 3 things can be done if BP goal is NOT met?
1. increase dose 2. add 2nd or 3rd drug 3. change to different drug
33
pharmacologic management of HTN works to alter
the body regulatory mechanisms **NOT a cure**
34
What must be taken into consideration when choosing what med is used to Tx HTN?
A patient's comorbidities
35
What are 3 reasons a pt may require more than one medication to Tx HTN?
1. to avoid maxing out the dose 2. minimize/ avoid side effects 3. synergistic effects
36
List 3 examples of ACE inhibitors
1. Lisnopril 2. Enalapril 3. Ramipril
37
List 3 examples of ARBs (angiotensin II receptor blockers)
1. Losartan 2. Irbesartan 3. Valsartan
38
List 2 examples of Thiazide diuretics
1. Hydrochlorothiazide (HCTZ) 2. chlorthalidone
39
List 4 examples of beta blockers
1. metoprolol 2. atenolol 3. bisoprolol 4. labetalol
40
List 4 examples of calcium channel blockers
1. Amlodipine 2. Felodipine 3. Diltiazem 4. Verapamil
41
List one examples of renin inhibitor
**Rarely used** 1. Aliskiren (tekturna)
42
Pathophysiology of thiazide diuretics
1. inhibit reabsorption of Na & Cl from distal tubules in kidneys 2. ↓ peripheral resistance 3. ↓ preload 4. better for Na sensitive HTN as in African Americans & older adults
43
How are thiazide diuretics usually tolerated?
Generally well
44
List adverse effects of thiazide diuretics (5)
1. hypokalemia 2. hyperglycemia 3. exacerbation of gout 4. other electrolyte imbalances (i.e. Ca) 5. orthostasis
45
Adverse effects of thiazide diuretics: Can cause exacerbation of gout
1. increases uric acid 2. should not be given to patients with Hx of gout
46
Who should not take thiazide diuretics?
Anyone with renal impairment
47
Why do we need to keep a close eye on diabetic pts taking thiazide diuretics?
Can cause hyperglycemia
48
Nursing considerations for thiazide diuretics
1. use in caution/ contraindicated in those allergic to sulfa drugs 2. avoid in renal failure 3. digoxin toxicity 4. may see decrease effect of DM meds 5. lithium toxicity
49
What labs should be monitored in those taking thiazide diuretics?
potassium & glucose levels
50
What vitals should be checked in those taking thiazide diuretics?
BP & HR
51
Patient education for thiazide diuretics
1. minimize alcohol intake 2. stop smoking 3. avoid NSAIDs 4. diet changes 5. lifestyle changes: exercise
52
indications for taking ACE inhibitors
1. HTN 2. HF 3. Diabetes 4. Post MI & PCI
53
ACE inhibitors are typically ____ agents (& list examples)
oral agents → captopril → enalapril → lisinopril
54
Which ACE inhibitor can also be given IV
Enalapril
55
Suffix fro ACE inhibitors
"pril"
56
Pathophysiology of ACE inhibitors
1. ↓ aldosterone production 2. inhibit angiotensin II production 3. ↓ vasoconstriction 4. interfere with RAAS 5. keep vasodilation effects of bradykinin 6. ↓ both preload & afterload
57
How are ACE inhibitors usually tolerated?
Generally well tolerated
58
Adverse effects of ACE inhibitors
1. hyperkalemia 2. dizziness 3. Cough
59
The ACE cough is related to
Kinins & activation fo Arachidonic pathway & prostaglandin production
60
When does the ACE cough usually begin
within one to two weeks of initiation
61
How can you resolve the ACE cough
Typically resolves within a few days of stopping medication
62
What ethnicity do we see an increased incidence of the ACE cough in?
Chinese ethnicity
63
Why does angioedema occur from ACE inhibitors?
B/c of elevated bradykinin causing vasodilation
64
Angioedema from ACE inhibitors: What is responsible for inactivating bradykinin
Angiotensin II
65
Black box warnings of ACE inhibitors
1. Serious fetal abnormalities (do NOT give during preg & use cautiously in those in child bearing years) **Contraception is very important**
66
What can happen if ACE inhibitors are given during the 3rd trimester of pregnancy?
can dry up amniotic fluid
67
Nursing considerations for ACE inhibitors
1. be aware of renal function & K+ levels 2. Assess orthostasis 3. awareness of admin to childbearing women 4. NO NSAID use 5. should be taken on empty stomach
68
What labs should be checked for someone taking ACE inhibitors?
BUN/ Cr & potassium levels
69
What vitals should be checked for someone taking ACE inhibitors?
HR & BP
70
What is the nurse responsible for with patients taking ACE inhibitors?
Knowing when to give the med & when to hold it
71
Indications for giving ARBs
1. HTN 2. when ACEI can NOT be used
72
How do ARBs work?
Bind with AG-II receptors in vascular smooth muscle & adrenal cortex to stop vasoconstriction & aldosterone production
73
ARBs block AG-II from binding at receptor sites in what body sites?
Brain; kidneys; heart; periphery; & adrenal tissue
74
Suffix for ARBs
"Sartan"
75
Can ACEI & ARBs be given together?
NO
76
What kind of protection do ARBs provide in comparison to ACEI?
About same amount of protection w/o leading to the ACE cough
77
Adverse effects of ARBs
1. Cough (< an ACEI) 2. Hyperkalemia (< ACEI) 3. H/A 4. Dizziness & syncope 5. GI complaints 6. xerostomia 7. alopecia
78
Why is it important to monitor BUN/ Cr in patients taking ARBs?
They can increase Creatinine due to possible decreased GFR
79
List drug interactions of ARBs
1. Diltiazem 2. oral anti-fungals
80
Are ARBs okay to give during pregnancy?
NO → should not be given during pregnancy
81
Nursing considerations for patients taking ARBs
1. monitor renal function 2. know drug interactions related to cytochrome P450 3. can be given w/ or w/o foods
82
What is the correlation between ARBs and cytochrome P450 enzyme?
Patients may be an inducer or inhibitor → therefore you may need to adjust the dose
83
Indications for using calcium channel blockers
1. HTN 2. Angina 3. rate control in A-fib 4. supraventricular tachycardia (SVT) 5. Raynaud syndrome 6. Migraines (verapamil)
84
List the 2 types of calcium channel blockers
1. Dihydropyridine 2. non-dihydropyridine
85
Pathophysiology of calcium channel blockers (6)
1. ↓ cardiac workload & myocardial O2 consumption 2. inhibits movement of Ca across membranes of myocardial/ arterial muscle cells 3. alters action potential 4. blocks muscle cell contractions 5. ↓ contractility & slows AV conduction 6. Relaxes & dilates arteries
86
What should you think of with CCB?
coronary & peripheral arteries → leads to vasodilation which leads to ↓ BP (more blood getting into heart)
87
What type of CCB is more vascular selective?
Dihydropyridine
88
Dihydropyridine has a more direct effect on ______ & less reduction of _____
vasodilation; calcium
89
Dihydropyridine has no effect on ...
AV contraction & may increase HR due to vasodilation
90
Suffix for dihydropyridine drugs
"pine"
91
List 3 examples of dihydropyridines
1. amlodipine 2. felodipine 3. nifedipine
92
List 5 side effects of dihydropyrines
1. peripheral edema (common) 2. H/A 3. flushing 4. lightheadedness 5. dizziness
93
What VS is crucial to monitor in those taking dihydropyridine?
blood pressure → as it decreases BP
94
Does dihydropyridine have an effect on the kidneys?
Not really
95
What is important to teach patients to avoid if taking dihydropyridine?
Grapefruit juice → increases risk of hypotension
96
Adverse effects of dihydropyridine
1. pedal edema 2. flushing 3. can have increased HR 4. GI effects
97
Indications for giving non-dihydropyridine
1. HTN 2. Angina 3. Arrhythmias (i.e. A-fib or SVT)
98
Non-dihydropyridine has _____ inotropic effects
negative
99
Non-dihydropyridine slows...
AV conduction & the rate of the SA node
100
List 2 examples of non-dihydropyridines
1. verapamil 2. diltiazem **can both be given IV**
101
Adverse effects of non-dihydropyridine
1. bradycardia 2. decreased cardiac output 3. GI effects
102
What type of patients should not be taking non-dihydropyridines?
Patients with heart blocks
103
What VS should be monitored in someone taking CCB?
BP as well as HR → pt HR can drop into 30s
104
Nursing considerations for CCB
1. be aware of conduction issues 2. avoid use in those with HF 3. Grapefruit juice → esp. w/ diltiazem 4. always check apical HR prior to giving 5. check orthostasis 6. no lab monitoring
105
grapefruit juice can inhibit what type of medications
Drugs metabolized by CYP3A enzyme
106
Grapefruit juice increases risk of adverse effects & events due to
Increasing levels of CCBs in the blood
107
When CYP3A is inhibited from grapefruit juice it can decrease metabolism of what meds?
1. oral antifungals 2. Diltiazem 3. Statins
108
Indications for using beta blockers
1. HTN (not 1st line) 2. ↓ risk of sudden death after MI 3. all pts after MI or PCI 4. HR reduction in AF 5. palpitations 6. HF 7. Migraines 8. performance anxiety 9. hyperthyroidism
109
Pathophysiology of beta blockers
1. ↓ HR & BP 2. ↓ muscle contraction 3. ↓ SNS response (blocks it) 4. ↓ renin release 5. ↑ BF to the kidneys
110
Adverse effects of beta blockers
1. fatigue 2. depression 3. impotence 4. sleep issues 5. **Bradycardia**
111
Suffix for beta blockers
"olol"
112
Special uses of beta blockers: Metoprolol
HF & post MI
113
Special uses of beta blockers: Propanolol
Social anxiety, headaches
114
Cautions with taking Beta blockers: Chronic lung disease
May increase risk of asthma attacks (b/c beta 2 receptor plays a role)
115
Cautions with taking Beta blockers: Diabetics
May mask hypoglycemic episodes (keep eye on blood sugar)
116
Cautions with taking Beta blockers: In those with ____ arrhythmias
Brady arrhythmias
117
If a patient needs to stop taking a beta blocker can they stop it abruptly?
No they must be weaned
118
Nursing considerations of beta blockers
1. check apical before giving 2. check for orthostasis 3. monitor glucose (esp. if diabetic) 4. make sure pt is given med, even if NPO 5. assess for side effects 6. no major lab concerns
119
List examples of selective beta 1 blockers
1. metoprolol 2. atenolol 3. esmolol 4. bisoprolol
120
List examples of non-selective (effects both beta 1 & 2 receptors)
1. propanolol 2. carvedilol 3. nadolol 4. sotalol
121
Nonselective BB are contraindicated in patients with:
Asthma Bronchospasm HF
122
What is important to note about cardio-selective BB?
Less likely to have Sx but higher doses can cause lung Sx
123
What are the 2 types of metoprolol
1. succinate (LA) 2. tartrate (SA)
124
Metoprolol succinate (LA)
1. usually dosed daily 2. Tx of HF 3. TX of HTN
125
Metoprolol tartrate (SA)
1. used post MI 2. Used for rate control in arrhythmias 3. can be given IV
126
Can SA & LA metoprolols be used interchangeably?
No → work differently
127
Alpha blockers inhibit
alpha synapse at the alpha adrenergic receptors (blocks SNS)
128
Alpha blockers prevent feedback of ______
norepinephrine
129
What line of Tx are alpha blockers considered?
3rd or 4th line of Tx (not really used in BP control)
130
Why are alpha blockers not seen often for Tx
They almost work too well → they can block both alpha & beta receptors and can drop BP too much
131
Side effects of Alpha blockers
1. orthostatic hypotension 2. vertigo/ syncope/ dizziness 3. sexual dysfunction 4. tachycardia
132
Adverse effects are significant in what type of medication class?
Alpha blockers!!
133
List examples of alpha blocker medications
1. Doxazosin (cardura) 2. Prazosin (Minipress) 3. Catapress (clonidine)
134
Who should we avoid using alpha blockers in?
older adults due to increased sedation/ confusion