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Blood pressure Flashcards

1
Q

Warfarin is what type/class of medication?

A

anticoagulant
- inhibits production of vitamin K

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2
Q

Dabigatran (Pradaxa) is what type/class of medication?

A

direct acting oral anticoagulant (DOAC)

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3
Q

Rivaroxban (Xarelto) is what type/class of medication?

A

direct acting oral anticoagulant (DOAC)
- factor Xa inhibitor

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4
Q

Apixaban (Eliquis) is what type/class of medication?

A

direct acting oral anticoagulant (DOAC)

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5
Q

Edoxaban (Lixiana) is what type/class of medication?

A

direct acting oral anticoagulant (DOAC)

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6
Q

What is the antidote/reversal agent for Warfarin?

A

Vitamin K

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7
Q

Heparin is what type/class of medication?

A

anticoagulant
- factor Xa inhibitor

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8
Q

What are the 5 ausculatory areas when assessing/listening to heart sounds?

A

APETM:
- aortic
- pulmonic
- erbs point
- tricuspid
- mitral

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9
Q

Which heart sound denotes the closure of the mitral and tricuspid valves?

A

S1 heart sound

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10
Q

What does the S1 heart sound represent?

A

closing of the mitral and tricuspid valves

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11
Q

Which heart sound denotes closure of the aortic and pulmonic valves?

A

S2 heart sound

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12
Q

The S2 heart sound represents what?

A

closing of the semilunar and pulmonic valves

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13
Q

Murmurs heard in early diastole are due to what?

A

incompetent semilunar valves
- aortic or pulmonic regurg
- aortic regurg if sound intensifies when patient sits forward and holds their breath

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14
Q

Mitral stenosis is associated with what conditions?

A
  • rheumatic heart disease
  • myxomas
  • congenital malformations
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15
Q

A friction rub or “scratchy” high-pitched sound heard when assessing the heart is a classic finding of what condition?

A

pericarditis

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16
Q

Hyperkalemia (K+ > 6 mEq/L) is associated with what ekg/cardiac?

A
  • tall, peaked T-waves
  • widening QRS complex
  • p-wave flattens/widens
  • prolongation of the PRI
  • slowed AV conduction
  • potential arrhythmias
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17
Q

Hypokalemia (< 3 mEq/L) is associated with what ekg/cardiac changes?

A
  • PVC’s (uni or multi-focal)
  • U-wave seen after T-wave
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18
Q

Hypercalcemia is associated with what ekg/cardiac changes?

A
  • increases cardiac contractility
  • shortens QT interval
  • AV block
  • BBB
  • bradycardia
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19
Q

Hypocalcemia is associated with what ekg/cardiac changes?

A
  • decreased cardiac contractiity
  • bradycardia
  • decreased CO
  • hypotension
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20
Q

Does hyper or hypokalemia potentiate the effects of digitalis toxicity?

A

hypokalemia

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21
Q

Does hyper or hypocalcemia potentiate the effects of digitalis toxicity?

A

hypercalcemia

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22
Q

Does hyper or hypocalcemia potentiate the effects of digitalis toxicity?

A

hypercalcemia

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23
Q

Does hyper or hypocalcemia decrease the efficacy of digitalis?

A

hypocalcemia

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24
Q

At what magnesium level would ECG changes occur?

A

ECG changes may occur at magnesium levels > 5 mEq/L

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25
Q

According to current guidelines when should antihypertensive medications be started on a patient at high CVD risk?

A

SBP > 130 or DBP > 80 measured on 2 separate occasions

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26
Q

What is the term for HTN of unknown cause?

A

essential or primary

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27
Q

What medication(s) should be used to treat Isolated systolic HTN?

  • SBP > 160 and DBP < 90
A
  • diuretics
    -Dihydropyridine calcium blockers
    • end in “dipine”
  • angiotensin receptor blockers
  • avoid beta blockers
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28
Q

What are the contraindications for the use of ACE inhibitors?

A
  • potassium > 5.5 mEq/L
  • pregancy
  • bilateral renal artery stenosis
  • not to be used with ARBs or renin inhibitors
  • not effective in African Americans
  • not to be used with lithium: Na stays and lithium is excreted
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29
Q

What are potential adverse effects of ace inhibitors?

A
  • cough
  • rash
  • hyperkalemia
  • angioedema
  • renal impairment
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30
Q

What are the indications for ACEi/ARBs use?

A
  • HTN (not very effective in AA)
  • CAD
  • previous MI
  • heart failure
  • nephroprotective in DM patients
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31
Q

Which antihypertensive meds should not be used in African Americans because they are not effective?

A
  • ACE inhibitors
  • ARBs
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32
Q

What are the 2 types of calcium channel blockers?

A
  • dihydropyridine: causes peripheral vasodilation
  • non dihydropyridine: directly relaxes the heart
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33
Q

Diltiazem and verapamil are what type of CCB?

A
  • non dihydropyridine
  • directly relax the heart
  • avoid in patients with heart failure with reduced ejection fraction
  • watch for bradycardia
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34
Q

Which class of BP medication is recommended for patients with aortic disease?

A

Beta-blockers

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35
Q

Which class of BP medication is recommended for patients with HF?

A
  • Ace inhibitors
  • Arb’s
  • beta blockers
  • aldosterone antagonists
  • diuretics if fluid overloaded
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36
Q

Which class of BP medication is recommended for patients with BPH?

A

Alpha-1-blockers

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37
Q

Which class of BP medication is recommended for patients with peripheral artery disease?

A
  • Diuretics
  • ace inhibitors
  • ARB’s
  • CCB’s
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38
Q

Captopril is what class of medication?

A
  • ACE inhibitor
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39
Q

Clonidine is what type of medication?

A
  • centrally acting Alpha-2 adrenergic agonist
  • anti-hypertensive
  • inhibits NE release
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40
Q

Labetolol is what type and class of medication?

A
  • alpha and beta adrenergic antagonist
  • used to treat:
    • HTN
    • angina
    • sympathetic over activity
      syndrome
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41
Q

Which class of BP med is the 1st line option when starting therapy?

A

Thiazide diuretics
- hydrochlorothiazide

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42
Q

What is the MOA for hydrochlorothiazide?

A
  • inhibits sodium absorption in the distal convoluted tubules causing increased sodium and water excretion
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43
Q

What affect does angiotensin II have on the body?

A

Increases BP by:
- stimulating aldosterone release for
adrenal cortex which increases Na and H20 reabsorption
- vasoconstriction of vascular smooth muscle
- triggers thirst center in hypothalamus
- stimulates ADH release from posterior pituitary

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44
Q

Which BP med(s) can be used in patients with heart failure with reduced ejection fraction?

A

Amlodipine and felodipine

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45
Q

Which diuretic class is preferred in patients with symptomatic HF and with GFR -30 ml/min?

A

Loop diuretics

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46
Q

Spironolactone is what Class/drug type?

A

Aldosterone antagonist
- diuretic

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47
Q

What is Clonidine’s MOA?

A

centrally acting alpha-2-agonist
- inhibits release of norepinephrine to reduce BP

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48
Q

How do hydralazine and minoxidil reduce BP?

A

BP reduction through arterial vasodilation

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49
Q

What medications should be considered to be given together with hydralazine or minoxidil and why?

A
  • diuretic due to Na and H2O retention
  • beta-blocker due to reflex tachycardia
50
Q

What classes of medication is Aliskiren?

A
  • direct renin inhibitor
  • very long acting
51
Q

Nicardipine (cardene) is what class of medication?

A

dihydropyridine CCB

52
Q

Nitroglycerin gtt should be started on which patients during a hypertensive emergency?

A

only in patients with acute coronary syndrome and/or acute pulmonary edema

53
Q

How do you calculate pulse pressure?

A

systolic BP minus diastolic

54
Q

Cholesterol screening should begin at what age and be done how often?

A

start at 20 and retest q5 yrs

55
Q

What is the normal triglyceride range?

A

TG < 150 mg/dl

56
Q

When should statin therapy be initiated?

A
  • LDL greater than or equal to 190 mg/dl
  • 40-75 y/o with DM
57
Q

What is the criteria needed to diagnose metabolic syndrome?

A

3 of the following:
- abdominal obesity
- TG > 150
- HDL < 40 males; < 50 females
- Systolic BP > 130
- Diastolic BP > 80
- taking anti-HTN med
- fasting glucose > 100 mg/dl

58
Q

What is the mechanism of action and classification of Heparin?

A

Class: anticoagulant
MOA: inhibits factor Xa

59
Q

A summation gallop (S3 and S4 heard together) is highly suggestive of what?

A

severe myocardial failure

60
Q

What is the MOA for dihydropyridine CCBs?

A
  • block binding to and blocking voltage-gated L-type calcium channels found on smooth muscle cells of arterial blood vessels causing vasodilation
  • nifedipine
  • nicardipine
  • nimodipine
  • amlodipine
61
Q

What is the MOA for the following meds:
- nifedipine
- nicardipine
- nimodipine
- amlodipine

A
  • dihydropyridine CCB
  • bind to and block voltage-gated L-type calcium channels in smooth muscle cells of arterial blood vessels causing vasodilation
62
Q

What is the MOA for the nifedipine?

A
  • dihydropyridine CCB
  • bind to and block voltage-gated L-type calcium channels in smooth muscle cells of arterial blood vessels causing vasodilation
63
Q

What is the MOA for the nicardipine?

A
  • dihydropyridine CCB
  • bind to and block voltage-gated L-type calcium channels in smooth muscle cells of arterial blood vessels causing vasodilation
64
Q

What is the MOA for the nimodipine?

A
  • dihydropyridine CCB
  • bind to and block voltage-gated L-type calcium channels in smooth muscle cells of arterial blood vessels causing vasodilation
65
Q

What is the MOA for the amlodipine?

A
  • dihydropyridine CCB
  • bind to and block voltage-gated L-type calcium channels in smooth muscle cells of arterial blood vessels causing vasodilation
66
Q

What is the MOA for the verapamil?

A
  • non-dihydropyridine CCB
  • blocks L-type calcium channels in the SA and AV node
  • slows SA node = reduced HR
  • decreased AV node conduction
  • decreased contractility
67
Q

What is the MOA for the diltiazem?

A
  • non-dihydropyridine CCB
  • blocks L-type calcium channels in the SA and AV node
68
Q

Indications for CCB use?

A
  • Arrhythmias:
    • atrial fibrillation
    • atrial flutter
    • symptomatic PAC’s
  • stable angina
  • prinzmetal/vasospastic angina
  • chronic HTN
  • hypertensive emergencies
  • HTN in pregnancy
  • Raynaud’s disease
  • vasospasm d/t SAH
69
Q

Adverse effects of Non-Dihydropyridine CCB use?

A
  • bradycardia
  • AV block
  • hypotension d/t reduced CO
70
Q

Contraindications for CCB use?

A
  • Wolf Parkinson White syndrome (may cause VT/VF)
  • don’t use with Beta Blockers
  • heart block
  • HFrEF
  • aortic valve stenosis
71
Q

What is the reversal agent for CCB?

A
  • give Calcium
    • calcium gluconate
    • calcium chloride
72
Q

Adverse effects of Dihydropyridine CCB use?

A
  • drugs end in -pine
  • reflect tachycardia
  • orthostatic hypotension
  • peripheral edema
  • flushed/red skin
73
Q

Where is renin produced?

A
  • in the Juxtaglomerular cells of the kidneys
  • released d/t decreased blood flow through the renal arteries
74
Q

What does renin do?

A

converts angiotensinogen to angiotensin I

75
Q

Where is angiotensinogen produced?

A

in the liver

76
Q

Where is Angiotensin Converting Enzyme produced?

A

in capillary endothelium of the lungs

77
Q

What does ACE do?

A

converts angiotensin I in to angiotensin II

78
Q

What is the MOA of Hydrochlorothiazide (HCTZ)?

A
  • inhibits sodium reabsorption in the distal convoluted tubule causing increased sodium and H2O in the urine which decreases blood volume = reduced BP
  • increases Calcium reabsorption from DCT
79
Q

What causes the cough related to ACE inhibitors?

A

ACE usually breaks down Bradykinin, inhibition of ACE leads to increased levels of bradykinin which causes bronchoconstriction and cough

80
Q

Indications for thiazide diuretic use?

A

1) HTN
2) fluid retention:
- peripheral edema r/t CHF or AKI
- pulmonary edema r/t CHF or AKI
- ascites r/t cirrhosis
3) osteopenia - since it increases Ca2+ absorption

81
Q

What are adverse effects of thiazide diuretics?

A
  • hyperuricemia d/t decreased uric acid excretion in the urine = gout
  • hyponatremia
  • hypochloremia (low chloride)
  • hypercalcemia
  • hypokalemia d/t increased urine loss
  • metabolic acidosis r/t to increased hydrogen loss in urine
  • hyperglycemia (d/t hypokalemia)
82
Q

How does hypokalemia lead to hyperglycemia?

A

potassium is needed for insulin to be released from pancreatic cells. Low levels of potassium results in less insulin being released into the blood which leads to increased BG levels

83
Q

What are causes of essential/primary HTN?

A

1) vessel thickening r/t
- advanced age
- smoking
- DM
2) vasoconstriction
- stress
- obesity
- high sodium diet

84
Q

What are the causes of secondary HTN?

A

(RENALSS)
Renal vascular disease
Endocrine
Neurological
Aortic diseases
Little people (pregnant)
Substances
Sleep Apnea

85
Q

HTN in the upper extremities and low blood pressure in the lower extremities is a sign of what condition?

A

coarctation of the aorta, a narrowing of the aorta causing the heart to pump harder (HTN in UE) to get blood out to the body

86
Q

What are potential renal causes for secondary HTN?

A

Renal vascular disease
- CKD
- renal artery stenosis
above causes low renal perfusion which activates the RAAS leading to increase in BP

87
Q

What are potential Endocrine causes for secondary HTN?

A
  • hyperthyroidism = systolic HTN
  • hypothyroidism = diastolic HTN
  • hyperaldosteronism
  • Cushing’s (high cortisol levels)
  • high EPI/NE levels
88
Q

What are potential neurological causes for secondary HTN?

A
  • increased intracranial pressure
89
Q

What are potential aortic vessel disease causes for secondary HTN?

A
  • coarctation of the aorta
90
Q

Where are Beta 1 receptors located?

A
  • cardiac conduction system (SA, AV), activation increases HR
  • contractile cells of the cardiac tissue, activation increases stroke volume/CO
  • juxtaglomerular cells in kidneys, stimulation causes renin release
91
Q

Where are Beta 2 receptors located?

A
  • ciliary body in eye
  • lungs, stimulation causes bronchodilation
  • liver, increases glucose levels by stimulating gluconeogenesis and glycogenolysis
  • pancreatic alpha cells, stimulates glucagon release, which tells liver to make more glucose through gluconeogenesis and glycogenolysis
  • vessels supplying the brain and muscles, causes vasodilation
  • GIT, slows motility and secretions of GIT
92
Q

How do beta blockers reduce HTN?

A
  • blocks beta-1 receptors of the SNS:
  • slows cardiac conduction and decreases contractility which reduces HR and stroke volume, which reduces CO = reduction in BP
  • inhibits renin release from the kidneys, preventing the formation of angiotensin II through the RAAS = lower BP
93
Q

What are the 1st generation beta blocker medication names?

A
  • propanolol
  • sotalol
  • non-selective beta blockers bind to both B1 and B2 receptors
94
Q

Propanolol and sotalol are what class of medication?

A
  • 1st generation non selective beta blockers
  • bind to both B1 and B2 receptors
95
Q

What are the 2nd generation beta blocker medication names?

A
  • Atenolol
  • bisoprolol
  • esmolol
  • metoprolol
  • primarily B1 selective, but will bind to B2 receptors at high doses
96
Q

What are the 3rd generation beta blocker medication names?

A
  • labetolol
  • carvedilol
  • non selective, bind to B1, B2 and Alpha-1 receptors
97
Q

Atenolol is what class of medication?

A
  • 2nd generation beta blocker
  • primarily B1 selective, but will bind to B2 receptors at high dose
98
Q

bisoprolol is what class of medication?

A
  • 2nd generation beta blocker
  • primarily B1 selective, but will bind to B2 receptors at high dose
99
Q

metoprolol is what class of medication?

A
  • 2nd generation beta blocker
  • primarily B1 selective, but will bind to B2 receptors at high dose
100
Q

esmolol is what class of medication?

A
  • 2nd generation beta blocker
  • primarily B1 selective, but will bind to B2 receptors at high dose
101
Q

What class of medication is labetolol?

A
  • 3rd generation beta blocker
  • non selective, bind to B1, B2 and Alpha-1 receptors
102
Q

What class of medication is carvedilol?

A
  • 3rd generation beta blocker
  • non selective, bind to B1, B2 and Alpha-1 receptors
103
Q

What are the indications for beta-blocker use?

A
  • CAD, decreases O2 demand by reducing HR and contractility
  • SVT (Afib/Afl)
  • HTN, reduces CO
  • medical management of aortic dissection or aneurysm by lowering BP
104
Q

Which HTN medication is contraindicating in patients with pheochromocytoma or cocaine use?

A
  • 1st and 2nd generation beta blockers
  • causes unopposed Alpha 1 agonism, medication blocks beta 2 receptors on artery, resulting in increased binding of catecholamines (EPI, NE) to Alph 1 receptors resulting increased vasoconstriction and BP
  • doesn’t inhibit catecholamine release
105
Q

Which beta blocker is used to anxiety?

A
  • propranolol
  • inhibits SNS to reduce symptoms
106
Q

Which beta blocker is used in the treatment migraines?

A
  • propranolol
  • decrease blood flow to the brain which reduces the intracranial pressure
107
Q

Why would a beta-blocker be used in the treatment of a patient experiencing thyrotoxicosis?

A
  • increased levels of T3 and T4 increase the sensitivity and activation of the SNS, beta blockers will reduce the symptoms by inhibiting the SNS
  • reduce BP
  • slow HR
108
Q

What are adverse effects r/t beta blocker use?

A
  • AV block d/t slowed conduction
  • syncope r/t low BP
  • diarrhea r/t increased GIT motility and secretion production
  • HLD r/t reduced conversion of triglycerides to FFA d/t inhibition of lipoprotein lipase release from capillary endothelium
  • hypoglycemia d/t inhibition of glycogenolysis and gluconeogenesis in liver
  • hypoglycemia d/t inhibition of glycogen release from the alpha cells of the pancreas
  • Hypoglycemia unawareness r/t inhibition of SNS symptoms
  • fatigue
109
Q

Where are alpha-1 receptors located?

A
  • stimulated by catecholamines (EPI/NE)
  • peripheral vessels, causes vasoconstriction = increase BP
  • smooth muscle of the prostate, causes prostate contraction
  • urethral sphincter, causes contraction of the internal urethral sphincter = urine retention
110
Q

What do the alpha-1 blocker medications names end with?

A
  • osin
  • terazosin
  • tamsulosin
  • prazosin
  • doxazosin
111
Q

What are the indications for Alpha blockers?

A
  • 4th line med for HTN
  • urine retention r/t BPH
  • kidney stone in ureter, relaxes/dilates ureter to help pass the stone (tamsulosin)
112
Q

Methyldopa is what type/class of medication?

A
  • anti-hypertensive
  • centrally acting Alpha-2 adrenergic agonist that inhibits NE release
113
Q

What BP reading is defined as a hypertensive emergency?

A

> 180 / >120 with new or worsening organ damage
- intracranial hemorrhage
- acute ischemic stroke or MI
- unstable angina pectoris
- dissecting aortic aneurysm
- eclampsia
- acute renal failure

114
Q

What is the goal of therapy for a patient experiencing a hypertensive crisis?

A
  • goal is systolic BP = 160-180 and/or diastolic BP 105 or less
  • BP should be lowered no more than 25% within mins to 2hrs, then gradually lower over several days with oral meds
115
Q

Beta blockers should be used as first line anti-HTN medications in what patient population?

A

patients with
- ischemic heart disease
- HFrEF

116
Q

Why does clonidine need to be tapered down when discontinuing the medication?

A

may induce a hypertensive crisis d/t rebound HTN

117
Q

What type/class of med is hydralazine?

A
  • anti-HTN
  • causes arterial vasodilation
118
Q

What type/class of med is mynoxidil?

A
  • anti-HTN
  • causes arterial vasodilation
119
Q

What conditions could cause low diastolic pressures (< 80) that would result in widening pulse pressures (sys - dia > 40mmHg)?

A
  • aortic regurgitation, blood flows back into LV which lessens the volume and pressure in the artery
  • anemia, less volume
  • sepsis, causes vasodilation and fluid shift = less blood in vessels
120
Q

What are the potential causes of systolic HTN (> 120) that would result in widening pulse pressures (sys - dia > 40mmHg)?

A
  • atherosclerosis, systolic pressure needs to push through narrowed vessels
  • hyperthyroidism, causes increased inotropic effects
  • sepsis, compensatory increase in HR and contractility cause high systolic pressures
121
Q

What are the potential causes of narrowing pulse pressures (sys - dia < 40mmHg)?

A
  • cardiogenic shock
  • bleeding = less volume
  • aortic stenosis = less CO
  • cardiac tamponade

NP School (19 decks)

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