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HSC116 > Module 7: Cardiovascular (Hypertension and Diuretics) > Flashcards

Module 7: Cardiovascular (Hypertension and Diuretics) Flashcards

1
Q

What is the order of blood flow in the heart?

A
  1. Vena cava (in to heart)
  2. Right atrium
    — tricuspid valve —
  3. Right ventricle
    — pulmonary valve —
  4. Pulmonary artery
  5. Lungs
  6. Pulmonary veins
  7. Left atrium
    — mitral valve—
  8. Left ventricle
    — aortic valve —
  9. Aorta (to arteries - out to body)
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2
Q

What is hyperlipidemia?

A

Increased levels of fats (lipids) in the blood

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3
Q

What is angina?

A

Chest pain due to decreased blood fow to heart

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4
Q

What is acute coronary syndrome?

A

Sudden reduced blood flow to heart causing myocardial infarction (heart attack)

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5
Q

What is hypertension?

A

High BP

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6
Q

What is heart failure?

A

Weakened heart muscle (or atrophy) doesn’t pump blood as it should.

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7
Q

What is arhythmias?

A

Probelm with rate or rhythm of heart beat

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8
Q

What is Acute Ischemic Stroke?

A

Sudden loss of blood to brain, resulting in loss of neurological function.

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9
Q

What is the function of the right coronary artery?

A

Supplies blood to R atrium, R ventricle, bottom portion of L ventricle and septum

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10
Q

What is the function of the left coronary artery?

A

Spilts in Circumflex artery and Left anterior descending artery - supplies blood to L atrium and L ventricle

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11
Q

What is the function of coronary veins?

A

Take oxygen-poor (deoxygenated) blood that has been used by the muscles back to the heart and right atrium

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12
Q

What is the leading cause of death in Canada and what % of it accounts for mortality?

A

Cardiovascular disease - accounts for 40% of total mortality

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13
Q

What is high levels of cholesterol correlated with?

A

Coronary Artery Disease (CAD)

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14
Q

What does moderate CAD manifest itself as?

A

Angina (chest pain)

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15
Q

What does severe CAD manifest itself as?

A

Myocardial infarction (MI, Heart attack)

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16
Q

What does an acuumulation of cholesterol in the vessels lead to? (medical term)

A

Artherosclerosis

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17
Q

Explain how atherosclerosis evolve within the vessel?

A

Fatty streaks -> Fibrous stage -> Lesions (involving calcification, ulceration, hemorrhage and eventually thrombosis and occlusion of a vessel)

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18
Q

Is atherotherombosis clinically present?

A

No it is clinically silent

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19
Q

What does complicated lesion/rupture in atherothrombosis lead to?

A
  • unstable angina
  • MI (myocardial infarction)
  • Ischemic stroke
  • acute limb ischemia
  • cardiovascular death
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20
Q

What does fibrous plaque in vessels lead to?

A
  • stable angina

- intermittent claudication (muscle pain on mild exertion)

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21
Q

List the risks of Atherosclerotic CAD?

A
  • dyslipidemis (high LDL and low HDL)
  • hypertension
  • DM
  • smoking
  • family hx of CAD
  • obesity, lack of exercise
  • male sex and advanced age
  • others (homocysteinemia, C reactive protein (CRP), Lipoprotein a (Lpa), infection (?Chlamydia pneumonie)
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22
Q

What is LDL (low density protein) known to be?

What does it do?

A

“Bad” cholesterol

It causes formation of thick and hard plaques along blood vessel walls which clog arteries, completely or partially, resulting in less flexible blood vessels.

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23
Q

What is HDL (high densty protein) known to be? What does it do?

A

“Good cholesterol”

It scavenges LDL and helps recycle them in the liver, thus reducing the level of cholesterl in blood.

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24
Q

What are some important functions of HDL in our body?

A
  • builds/maintains cell membranes
  • manufactures bile
  • necessary for fat and vitamin absorption
  • insulates nerve fibers
  • aids in adrenal gland hormone production
  • aids in sex hormone productions
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25
Q

What risks does LDL pose on our body? (outcomes of high LDL)

A
  • clog arteries
  • lead to CAD (coronary artery disease)
  • lead to heart attack
  • lead to stroke
  • ultimately lead to death
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26
Q

What total components make up cholesterol? (3)

What should they be on blood test?

A

Total cholesterol (below 5.2) = LDL (below 2.6), HDL (above 1.5), and triglycerides (bwloe 1.7)

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27
Q

List the drug classes used for Dyslipidemia?

“He fell behind Nancy & Edward”

A
  • HMG -CoA Reductase Inhibitors (Statins)
  • Fibrates
  • Bile Acid Asequestrants (Resin)
  • Nicotinic Acid (Niacin, Vit 3)
  • Ezetmibe
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28
Q

How do HMG-CoA Reductase Inhibitors (Statins) work on Dyslipidemia?

A

They reduce HMG-CoA enzyme which is the final enzyme needed in creation of cholesterol

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29
Q

What are the main therapeutic uses of Statins?

A
  • Hyperlipidiamia
  • Primary (before 1st heart attack)
  • Secondary ( to prevent 2nd heart attack)
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30
Q

What are the side effects of Statins?

A

Myopathy (elevated CPK levels in body indicating injury)

Liver dysfunction

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31
Q

Describe myopathy

A

myopathy is a disease of the muscle in which the muscle fibers do not function properly. This results in muscular weakness.

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32
Q

What is CPK?

A

creatinine phosphokinase (enzyme in body that is important for muscle function and is indicative of muscle disease)

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33
Q

Are there an any drug interactions with Statins and what do they do?

A

Fibrates - increases chances of myopathy (pain or breakdown of muscles)

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34
Q

What is Hypercholesterolemia?

A

Hypercholesterolemia, also called high cholesterol, is the presence of high levels of cholesterol in the blood.

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35
Q

What is steatorrhea?

A

the excretion of abnormal quantities of fat with the feces owing to reduced absorption of fat by the intestine

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36
Q

What drug class do Gemfbrozil and Fenofibrate belong to?

A

Fibrates for Hyperlipidimia

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37
Q

How do fibrates work?

A

reduces VLDL (carry triglycerides to blood) production in liver and speed up removal of triglycerides from blood

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38
Q

What is the clinical use for fibrates?

A

For pts with hypertriglyceridemia

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39
Q

What are the side effects of fibrates?

A

gallstones, liver dysfunction

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40
Q

Are there any drug interactions with fibrates?

A

Statins (myopathy)

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41
Q

Should fibrates with taken empty stomach?

A

NO with food.

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42
Q

What drug class do Prevalite and questran (cholestyramine) belong do?

A

Bile Acid Sequestrants

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43
Q

What is the clinical use of Bile Acid Sequestrants?

A

Hypercholesterolemia

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44
Q

How do Bile Acid Sequestrants work?

A

convert cholesterol to bile acids in liver

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45
Q

What are the side effects of Bile Acid Sequestrants?

A

Bad taste, GI upset (including steatorrhea), cause deficiency of lipid-soluble vitamins (A, D, E K), gall stones, increased VLDL and increased triglycerides

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46
Q

When are Bile Acid Sequestrants contraindicated?

A

With pts with hypertriglyceridemia (b/c side effect Bile Acid Sequestrants = raise triglycerides)

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47
Q

How does Nicotinic Acid work?

A

Helps increase HDL and decrease LDL from bloostream

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48
Q

What is the therapeutic use of Nicotinic Acid?

A

Hypertriglycerdemia

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49
Q

What drugs are taken for Hyperglycerdemia(2) ?

A

Nicotinic Acid and Fibrates

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50
Q

What does low doses of Nicotonic Acid vs. high doses do?

A

Low - increase HDL

High - decrease LDL

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51
Q

What are the adverse effects of Nicotinic Acid?

Frankie turned red and itchy, but could not itch her itch in public and could not drink with her friends either to avoid the itch.

A

Flushing
Rash
pruritis (anus itch)
hepatotoxity (liver damage due to drugs)

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52
Q

Are there any drug interactions with Nicotinic acid?

A

Statins (risk of liver damage)

Fibrate (risk of gallstones)

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53
Q

How does Ezetimibe work and how?

A

Lower LDL and it does so by blocking absorption of cholesterol in the small intestine

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54
Q

What is the therapeutic use of Ezetimibe?

A

For those with elevated LDL (used alone or with Statins)

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55
Q

What are the side effects of Ezetimibe?

A

Nausea, bloating

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56
Q

Are there any drug interactions for Ezetimibe?

A

None (mentioned by Bassam)

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57
Q

What are the main drugs used for Acute Coronary Syndrome?

A
  • thrombolytics
  • anti-thrombotic agents
  • anti-coagulant agents (warfarin, heparin, low molecular weight heparin)
  • beta blockers
  • calcium channel blockers
  • statins
  • ace inhibitors
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58
Q

What drug class do warfarin, heparin and low molecular weight heparin fall under?

A

Anti-coagulant

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59
Q

How do thrombolytics work/

A

They help open up clogged arteries

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60
Q

What drug category do TPA, RPA, and TNK fall under?

A

Thrombolytics

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61
Q

Out of the 3 thrombolytics, which is the only 1 used for strokes?

A

TPA (Alteplase)

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62
Q

What are the therapeutic uses of thrombolytics?

A

heart attack, stroke (TPA only)

63
Q

What are the side effects of thrombolytics?

A

bleeding, reperfusions dysrhythmias, hypotension

64
Q

What is reperfusion arrhythmias?

A

arrhythmias occurring as the result of increased myocardial perfusion are called reperfusion arrhythmias - blood entering back to organ

65
Q

What does are the 3 different thrombolytics given at?

A

TPA: loading then infusion
RPA: 2 bolus doses 30 mins apart
TNK: 1 bolus dose

66
Q

What drug category do ASA, Clopidogrel, Ticlopidine, IIb-IIa Antagonists fall under?

A

Anti-thrombotix agents

67
Q

What kind of antaagonists are Eptifibitide, Tirofiban, and Abciximab?

A

llb-llla Antagonists (Anti-thrombotic agents)

68
Q

How do Anti-thrombotic agents work?

A

They decrease the function of platelets

69
Q

What are the therapeutic uses of Anti-thrombotic agents?

A 
Prevent heart attack 
Prevent stroke (ASA, Clopidogrel, Ticlopidine)
70
Q

What are the side effects of Anti-thrombotic agents?

A

Bleeding, nausea, thrombocytopenia (decreased platelet count)

71
Q

What dosing are Anti-thrombotic agents used at?

A

Oral: ASA, Clopidogrel, Ticlopidine
Parentral: lllb-llla antagonist agents (loading dose then infusion)

72
Q

What is pulmonary embolism?

A

is a blockage in one of the pulmonary arteries in your lungs

73
Q

What drug category do warfarin, heparin, and low molecular heparin fall under?

A

Anti-coagulant agents

74
Q

How do Anti-coagulant agents work?

A

Inhibit clotting factors

75
Q

What are the therapeutic uses of Anti-coagulant agents?

A
  • clotting disorders
  • prevent/tx heart attack
  • tx pulmonary embolism (blockage of pulmonary artery to lung)
  • prevent/tx DVT
  • prevent stroke
  • atrial fibrilation (hearts 2 upper chambers beat chaotically)
76
Q

What are the side effects of warfarin?

A

bleeding, purple toes

77
Q

With what are the effects of warfarin reversed?

A

Vitamin K

78
Q

How long does it take warfarin to “kick in” and what is used alongside until warfarin kicks in?

A

5 days to kick in

Heparin/LMWH used until warfarin kicks in

79
Q

Is warfarin contraindicated for anyone?

A

Preg women

80
Q

How should the therapeutic effects of warfarin be monitored?

A

Blood test (INR)

81
Q

Explain the different administration routes for warfarin, heparin, ad LMWH?

A

warfarin - oral
heparin - IV or subcutaneous
LMWH - subcutaneous

82
Q

Explain the difference in monitoring between warfarin, heparin, ad LMWH?

A

warfarin - bloodtest (INR)
heparin - aPPT (not same as INR)
LMWH - no monitoring

83
Q

What are the side effects of Heparin and LMWH?

A

Bleeding, Heparin Induced thrombocytopenia (HIT - decreased platelet count)

84
Q

Whata drug class do Dabigatran and Rivaroxaban fall under?

A

Anti-coagulant agents

85
Q

Why is Dabigatran and Rivaroxaban used as an alternative to warfarin?

A

When it is hard to stablize pts to warfarin or when pt is porly compliant to monitoring (INR)

86
Q

What are the side effects of Dabigatran and Rivaroxaban?

A

bleeding, GI upset

87
Q

How is Dabigatran and Rivaroxaban administered?

A

Orally

88
Q

At what BP is a person considered to be hypertensive?

A

140/90 mm or higher

89
Q

Risk factors for hypertension? (that you have control over)

A

-smoking
-physical inactivity
-obesity (esp around waist)
-high fat diet
-excess salt intake
excessive alcohol consumption

90
Q

Risk factors for hypertension? (that you don’t have control over)

A
  • family hx
  • old age
  • ethnicity
91
Q

At what BP is a person considered to be hypotensive?

A

80/60 mmHg

92
Q

What are the medications used for initial therapy for hypertension?

A
  • Diuretics
  • ACEI
  • ARB
  • Long acting CCB
  • Beat blockers (not for pts over 65)

And (covered in hypertension module):

  • Alpha1 antagonists
  • Alpha 2 antagonists
  • Direct acting visodilators
93
Q

What should be consdered if initial therapy isn’t adhering to pts hypertension?

A

Dual therapy (2 drugs togethers) or triple/quadruple

94
Q

What are the 3 kinds of diuretics?

A

Thiazides, Loop, Potassium Sparing

95
Q

What is the function of Thiazides (diuretics)?

A
  • cause diuresis (decrease plasma volume_
  • reduce peripheral vascular resistance
  • works in distal part of the kidney
96
Q

What is the function of Loop (diuretics)?

A
  • cause more diuresis than thiazides
  • not for chronic management of hypertension
  • works in the “loop of Henle” in kidney
97
Q

What is the function of Potassium Sparring (duretics)?

A
  • weak diuresis

- usually combined with a thiazide to preent potassium loss

98
Q

How do diuretics work to treat hypertension

A

Diuretics help rid your body of sodium and water. Most work by making your kidneys release more sodium into the urine. The sodium then takes water with it from your blood decreasing the amount of fluid flowing through your blood vessels hence lowering blood pressure.

99
Q

What are the therapeutic uses of diuretics?

A

Hypertension

Heart Failure

100
Q

What are the adverse effects of Diuretics?

A
  • hypotension
  • electrolyte abnormalities
  • gynecomastis
  • NSAID reduce effectiveness of diuretics
101
Q

Why is monitoring important with use of diuretics and what should be monitored?

A
  • Electrolytes can range abnormally
  • kidney function
  • BP (hypotension can occur)
102
Q

How do the Angiotensin-converting enzyme (ACE) inhibitors to treat hypertension and Angiotension Receptor Bockers (ARBs)?

A

help relax your veins and arteries to lower your blood pressure. ACE inhibitors prevent an enzyme in your body from producing angiotensin II, a substance that narrows your blood vessels.

103
Q

What are the therapeutic uses of Angiotensin-converting enzyme (ACE) and Angiotension Receptor Bockers (ARBs)?

A

Hypertension
Heart failure
Heart attack
DM Nephropathy (diabetic kidney disease)

104
Q

What are the adverse effects of Angiotensin-converting enzyme (ACE) and Angiotension Receptor Bockers (ARBs)?

A

Hypotension
Abnormal electrolytes
Couch (ACEI only)
Angioedema (swelling of the lower layer of skin and tissue just under the skin or mucous membranes)

105
Q

What is the prefix for Angiotensin-converting enzyme (ACEI) drugs?

A

end in “pril”

106
Q

What is the prefix for Angiotension Receptor Bockers (ARBs) drugs?

A

end in “sartan”

107
Q

What is prostatic hypertrophy?

A

A benign (not cancer) condition in which an overgrowth of prostate tissue pushes against the urethra and the bladder, blocking the flow of urine.

108
Q

What do Alpha1 Antagonists do to treat hypertention?

A

they prevent the stimulation of alpha1 receptors (vasocontrictors)

109
Q

Along with hypertension, what else do Alpha1 antagonists do in men with prostatic hypertrophy?

A

relax smooth muscle in the prostate and bladder neck, thus decreasing blockage of urine flow

110
Q

What are the therapeutic uses of Alpha1 Antagonists?

A

Hypertension

Prostatic Hypertrophy

111
Q

What are the adverse effects of Alpha1 Antagonists?

A

Hypotension
dizzy
fluid retention
nasal congestion

112
Q

How do Alpha2 Agonists work to treat hypertension?

A

They act within the brain to suppress sympathetic (norepinephrine) outflow to heart and blood vessel, which results in vasodilaton and reduced cardiac output

113
Q

What are the therapeutic uses of Alpha2 agonists?

A

Hypertension

Pre-eclampsia (+proteinuria - protein in urine above 20 weeks gestation)

114
Q

What are the side effects of Alpha2 Agonists?

A

Hypotension
Fluid retention
Dry mouth
Sedation

115
Q

What kind of Alpha2 agonist is used for Pre-sclampsia pts?

A

Methlydopa

116
Q

What happens if you abruptly stop this Alpha2 agonist, Clonidine?

A

rebound hypertension therefore DO NOT

117
Q

What drug class do Clonidine and Methydopa belong to?

A

Alpha2 Agonists

118
Q

What drug class do minoxidil and hydralazine belong to?

A

Direct Acting Vasodilators

119
Q

How do direct acting vasodilators work to treat hypertension?

A

cause vasodilaton in arterioles

120
Q

Do direct acting vasodilators act on arteries and veins?

A

Only on arterioles

Limited effect on veins, therefore minimal orthostatic hypotension (postural hypotension)

121
Q

What are the therapeutic uses of direct acting vasodilators?

A

hypertension
baldness
pre-eclampsia

122
Q

What kind of direct acting vasodilator is used for pre-eclampsia?

A

hydralazine

123
Q

What are the side effects of direct acting vasodilators?

A

hypotension,
fluid retention

Hydralazine can cause systemic lupus erthromatosis

Minocidil can cause hypertrichosis (excessive hair growth)

124
Q

Along with diuretics, ACEIS, ARBs, alpha1 antagonist, alpha2 agonists, and direct acting vasodilators, what other drugs are also used to treat hypertension ?(2)

A

betablockers

calcium channel blockers

125
Q

What cells regulate the rhythm of the herat and where are they located?

A

pacemakers cells

located within sinoatrial (SA) node which is within the wall of the rght atrium

126
Q

What is an arrhythmia?

A

irregular heartbeat (either too fast, too slow, or mismath between frequency of atrial and ventricular beats)

127
Q

How are cardiac arrhythmias classified?

A
  • heart rate
  • heart rhythm
  • site of origin
  • complexes on ECG
128
Q

What is the most frequennt cause of arrhythmias?

Why?

A

Coronary artery disease

Cause it results in myocardial ischemia (decreased blood flow to heart) and infarction (muscle damage)

129
Q

Due to what cellular level reasions are there change sin the rhythm of a heart?

A
  • changes in pacemaker cells
  • abnormal generation of impulse at sites other than the SA node
  • ectopic foci (abnormal pacemaker sites within heart)
130
Q

What is the difference betwen tachyarrhythmias and bradyarrhythmias?

A

Tachy = Supraventricular or ventricular

Brady =Atrioventicular (block) or sinus node dysfunction

131
Q

What are the 3 main ions in charge of heart rhythm?

A

NA+, Ca2+, K+

132
Q

How do Anti-Arrhythmic Drugs work?

A

They act primarily by altering ion fluxes within the tissue of the myocardium

133
Q

How are antiarrhythmic drugs classified?

A

On their ability to directly or indirectly block flux of one of these ione (NA+, CA2+, K+)

134
Q

What medications are used for Arrhythmias?

A

Class 1A (Procainamide), Class 1B (Lidocaine), Class 1C (Propafenone), Class III (Amiodarone)

135
Q

What 2 medications are used for both atrial and ventricular arhythmias?

A

Class 1A (Procainamide) and C III (Amiodarone)

136
Q

What impact does Class 1A (Procainamide) have on ions?

A

Moderate block of NA+

137
Q

What impact does Class 1B (Lidocaine) have on ions?

A

Mild block of Na+

138
Q

What impact does Class 1C (propafenone) have on ions?

A

Marked block of Na+

139
Q

What impact does Class III (amiodarone) have on ions?

A

Block of K+

140
Q

List the different administration routes for the 4 classes of anti-arrhythmic drugs?

A 
Class 1A (procainamide) - oral and parenteral
Class 1B (Lidocaine) - parenteral
Class 1C (propafenone) - Oral and IV (loading dose)
Class III (amiodarone) - oral and parenteral (loading dose for converson out of atrial fibrillation)
141
Q

What are the side effects of Class 1A (procainamide)?

A
  • hypotention (dizzy)
  • rash (drug induced systemic lupus erthromatosis)
  • bradycardia
    vision disturbances
142
Q

What are the side effects of Class 1B (Lidocaine)?

A

Hypotention (dizzy)

Bradycardia

143
Q

What are the side effects of Class 1C (propafenone)?

A

Hypotention (dizzy)
bradycardia
SOB (asthma pts)

144
Q

What are the side effects of Class III (Amiodarone)?

A
  • Hypotention (dizzy)
  • hypo + hyperthyroidism
  • BLUE SKIN
  • liver toxicity
    bradycardia
    nausea
    pumonary fibrosis (lung disease - tissue damaged and scarred - leads to SOB)
145
Q

What nursing implications need to be taken for all 4 classes of Anti-Arrhythmic drugs?

A

Monitor for tolerability, HR and response (ECG)

146
Q

Which class of anti-arrhythmic drug is safe to use for pts with CHF (congestive heart failure)?

A

Class III (Amiodarone)

147
Q

With which class of anti-arrhythmic drug should caution be taken for CHF and asthma pts?

A

Class 1C (propafenone)

148
Q

What 2 additional tests need to be done for pts using Class III (Amiodarone) anti-arrhythmic drug?

A

Thyroid function tests (b/c side effect = hypo/hyperthyroidism)
Chest x-ray (b/cside effects = pulmonary fibrosis)

149
Q

Which anti-arrhythmic drug class has a side effect of blue skin?

A

Class III (Amiodarones)

150
Q

What are the 2 main types of strokes?

A
  • Thrombotic (bloost blot blocks blood flow to brain)

- Embolic (plaque or clot breaks away and flows to brain where blocks arteries)

151
Q

What are the goals of stroke therapy (meds)?

A
  • minimize brain damage
  • prevent complication
  • reduce risk of recurrence
  • restore function of the individual
152
Q

Explain the difference between the hemorrhagics - intracerebral and subarachnoid

A
  • Intracerebral - bleed within brain tissue and ventricles

- subarachnoid - bleed between brain and surround membranes (life-threatening)

153
Q

What are the symptoms of Acute Ishemic Stroke?

A

Sudden:

  • weakness (numbness in face, arm, legs etc)
  • trouble speaking
  • vision problems
  • headaches
  • dizziness (loss of balance)
154
Q

Explain briefly the treatment/assessment of a stroke?

A
  1. identify signs of a possible stroke
  2. critical EMS assessment (ABCs -airway, breathing, circulation).
  3. Immediate general assessment and stabalization
  4. Immediate neurologic assessment by stroke team
  5. Does CT scan show any hemorrhage?
    Yes - consult neurosurgeon No - consider fibrinolytic therapy
  6. If pt remains a candiate for fibrinolytic therapy then review risk/benefits with pt and family and give tPA (no anticoagulants or antiplatelet tx for 24 hrs)
  7. If pt does not remain a candidate for fibrinolytic therapy then administer aspirin. (admit to stroke unit, monitor BP, monitor neurologic status, monitor blod glucose, initiate supportive therapy.

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