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Pharmacology > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Basic functional unit of the kidney

A

Nephron

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2
Q

Four functionally distinct regions of the nephron

A

Glomerulus
Proximal convoluted tubule
Loop of Henle
Distal convoluted tubule

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3
Q

Where does filtration occur in the kidney?

A

Glomerulus

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4
Q

What is reabsorbed in the kidney?

A

99% of water, electrolytes, and nutrients

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5
Q

Where does reabsorption occur in the kidney?

A

Specific sites along the nephron:
- Proximal convoluted tubule
- Loop of Henle
- Distal convoluted tubule
- Collecting duct (distal nephron)

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6
Q

Through filtration and reabsorption, what is also regulated in the kidneys?

A

Sodium-potassium exchange
Regulation of urine concentration

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7
Q

Three basic functions of diuretics:

A
  • Cleansing of extra cellular fluid and maintenance of ECF volume and composition
  • Maintenance of acid-base balance
  • Excretion of metabolic wastes and foreign substances
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8
Q

Three main classifications of diuretics:

A

Loop diuretics
Thiazides
Potassium-sparing

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9
Q

Two types of potassium-sparing diuretics:

A

Aldosterone antagonists
Nonaldosterone antagonists

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10
Q

Definition of diuretics

A

Drugs that increase urinary output

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11
Q

Two major applications of diuretics

A

Treatment of hypertension
Mobilization of edematous fluid to prevent renal failure

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12
Q

Mechanism of action of diuretics

A

Blockade of sodium and chloride reabsorption

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13
Q

Best site of action of diuretics

A

Proximal tubule produces greatest diuresis

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14
Q

Adverse effects of diuretics

A

Hypovolemia
Acid-base imbalance
Electrolyte imbalances

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15
Q

Prototype drug for loop diuretics

A

Furosemide (Lasix)

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16
Q

Mechanism of action of Furosemide (Lasix)

A

Acts on ascending loop of Henle to block reabsorption

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17
Q

Pharmacokinetics of Furosemide (Lasix)

A

Rapid onset (PO 60 min; IV 5 min)

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18
Q

Therapeutic uses of Furosemide (Lasix)

A

Pulmonary edema
Edematous states
Hypertension

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19
Q

Adverse effects of Furosemide (Lasix)

A

Hyponatremia, Hypochloremia, dehydration
Hypotension (volume loss, relaxation of venous smooth
muscle)
Hypokalemia
Ototoxicity
Hyperglycemia
Hyperuicemia

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20
Q

Can Furosemide (Lasix) be used during pregnancy? Why or why not?

A

No, because too risky when balancing fluid/electrolytes of both mom and baby

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21
Q

Normal range of potassium levels

A

3.5-5.0

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22
Q

Drug interactions of Furosemide (Lasix)

A

Digoxin
Ototoxic drugs
Potassium-sparing diuretics
Lithium
Antihypertensive agents
Nonsteroidal anti-inflammatory drugs

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23
Q

Administration routes for Furosemide (Lasix)

A

Oral
Parenteral

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24
Q

Another name for Thiazides and related diuretics

A

Benzothiadiazides

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25
Q

Effects of Thiazides and related diuretics

A

Similar to those of loop diuretics:
- Increase renal excretion of sodium, chloride, potassium, and water
- Elevate levels of uric acid and glucose

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26
Q

How is diuresis of Thiazides and related diuretics compared to loop diuretics

A

Considerably lower than that produced by loop diuretics
Not effective when urine flow is scant (unlike loop diuretics)

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27
Q

Prototype for Thiazides and related diuretics

A

Hydrochlorothiazide (HydroDIURIL)

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28
Q

How long does it take for hydrochlorothiazide to peak?

A

4-6 hours

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29
Q

Therapeutic uses for hydrochlorothiazide

A

HTN
Edema
Diabetes insipidus

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30
Q

Adverse effects of hydrochlorothiazide

A

Hyponatremia, hypochloremia, and dehydration
Hypokalemia
Hyperglycemia
Hyperuricemia
Impact on lipids, calcium, and magnesium

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31
Q

Effects of hydrochlorothiazide on pregnancy

A

During lactation, enters breast milk

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32
Q

Drug interactions with hydrochlorothiazide

A
  • Digoxin
  • Augments effects of hypertensive medications
  • Can reduce renal excretion of lithium (leading to accumulation)
  • NSAIDs may blunt diuretic effect
  • Can be combined with ototoxic agents without increased risk of hearing loss
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33
Q

Potassium-sparing diuretics compared to other diuretics

A

Most modest increase in urine production
Decrease in potassium excretion
Rarely used alone for therapy

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34
Q

Two groups of potassium-sparing diuretics

A

Aldosterone antagonist
Nonaldosterone antagonist

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35
Q

Prototype drug for aldosterone antagonist potassium-sparing diuretics

A

Spironolactone (Aldactone)

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36
Q

Mechanism of action for Spironolactone

A

Blocks aldosterone in the distal nephron
Retention of potassium
Increased secretion of sodium

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37
Q

Therapeutic uses of spironolactone

A

HTN
Edematous states
Heart failure (decreased mortality in severe failure)
Primary hyperaldosteronism

Can be used for hormonal issues:
Premenstrual syndrome
Polycystic ovary syndrome
Acne in young women

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38
Q

Adverse effects of spironolactone

A

Hyperkalemia
Benign and malignant tumors
Endocrine effects

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39
Q

Drug interactions of spironolactone

A

Thiazide and loop diuretics
Agents that raise potassium levels

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40
Q

Prototype of osmotic diuretics

A

Mannitol (Osmitrol)

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41
Q

Action of Mannitol

A

Promotes diuresis by creating osmotic force within lumen of the nephron

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42
Q

Pharmacokinetics of mannitol

A

Drug must be given parenterally

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43
Q

Therapeutic uses of mannitol

A

Prophylaxis of renal failure
Reduction of intracranial pressure
Reduction of intraocular pressure

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44
Q

Adverse effects of mannitol

A

Edema
Headache
Nausea and vomiting
Fluid and electrolyte imbalance

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45
Q

How much does one liter of fluid weigh?

A

2.2 lbs

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46
Q

How much of the total body water is in intracellular fluid?

A

2/3

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47
Q

Where is extracellular fluid located?

A

Outside the cells:
Divided into the vascular compartment (blood vessels) and the interstitial space (the gaps between the cells)

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48
Q

Explain the renin-angiotensin-aldosterone system

A

Decreased renal perfusion initiates release of aldosterone.
Aldosterone is a mineral corticoid that retains sodium and where sodium goes, water goes.
Aldosterone also retains potassium.

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49
Q

Lab value for potassium

A

3.5-5.0 mEq/L

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50
Q

Lab value for sodium

A

135-145 mEq/L

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51
Q

Lab value for chloride

A

95-105 mEq/L

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52
Q

Lab value for magnesium

A

1.5 to 2.5 mEq/L

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53
Q

Lab value for serum creatinine

A

0.6 to 1.2 mg/dl

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54
Q

Lab value for BUN

A

10 to 20 mg/dl

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55
Q

Lab value for glucose

A

70 to 100

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56
Q

Lab value for platelets

A

150,000 to 400,000

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57
Q

Lab value for hemoglobin (Hgb)

A

F 12-16 g/dl
M 14-18 g/dl

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58
Q

Lab value for hematocrit (Hct)

A

F 37-47%
M 42-52%

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59
Q

What can cause an abnormal loss of fluids? And what symptoms would they have?

A

Vomiting, diarrhea, hemorrhage
Dehydration

Weak, low BP
Dry skin

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60
Q

What can cause someone to have fluid volume excess? And what symptoms would they have?

A

CHF, kidney failure
Crackles, dyspnea, edema

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61
Q

How would a pt be treated who has fluid volume excess?

A

Diuretics

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62
Q

What nursing interventions would be done for pts who have abnormal fluid volume?

A

Assess the pt
Daily weights
I & O
IV fluids

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63
Q

Types of drugs that act on the Renin-Angiotensin-Aldosterone System

A

Angiotensin-converting enzyme inhibitors (ACE inhibitors)
Angiotensin II receptor blockers (ARBs)
Direct renin inhibitors
Aldosterone antagonists

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64
Q

Main functions of the RAA system

A

All involved with blood pressure
Many involved with fluid volume
Many involved with electrolytes

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65
Q

How is the RAAS involved with blood pressure?

A

Actions of angiotensin II
Vasoconstriction
Release of aldosterone

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66
Q

Actions of aldosterone

A

Regulation of blood volume and blood pressure
Pathologic cardiovascular effects

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67
Q

How does aldosterone regulate blood pressure and blood volume?

A

When aldosterone is released form adrenal cortex, it acts on the distal tubular of the kidneys, causing release of sodium and potassium
Because of this BP and blood volume go down

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68
Q

How does the RAAS elevate BP?

A

Angiotensin II formed by renin and angiotensin-converting enzyme
- renin speeds up formation of angiotensin I from angiotensinogen
- Regulation of renin release
- Angiotensin-converting enzyme (kinase II) converts angiotensin I (inactive) to angiotensin II (highly active)

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69
Q

Main part of RAAS to increase BP or blood volume

A

Renin (its main purpose is to elevate BP)

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70
Q

Where are ACE enzymes (AKA kinase II) located?

A

On the surface of many blood vessels
In the lining of the vasculature of the lungs
(Even though we typically only think of it being involved with the renals)

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71
Q

Situations the RAAS helps to regulate BP in

A

Hemorrhage
Dehydration
Sodium depletion

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72
Q

When someone is experiencing low BP, how does the RAAS act on the body to fix it?

A

Constricts renal blood vessels
Acts on the kidney to promote retention of sodium & water, and the excretion of potassium

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73
Q

How do ACE inhibitors work?

A

By preventing Angiotensin II, which lowers the levels of angiotensin II, which can dilate vessels

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74
Q

Therapeutic uses of ACE inhibitors

A

Hypertension
Heart failure
MI
Diabetic and non diabetic nephropathy
Prevention of MI, stroke, and death in pts at high cardiovascular risk

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75
Q

How do ACE inhibitors help MI and heart failure?

A

By remodeling the heart and preventing more damage from happening

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76
Q

Adverse effects of ACE inhibitors

A

First dose hypotension (fall risk!)
Fetal injury (can’t take during pregnancy)
*Cough (due to increased bradykinin)
Angioedema (swollen face, need to be taken off)
Hyperkalemia
Dysgeusia and rash
Renal failure or **bilateral renal artery stenosis (contraindicated)
Neutropenia

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77
Q

Drug interactions for ACE inhibitors

A

Diuretics
Antihypertensive agents
Drugs that raise potassium levels
Lithium (b/c some cause lithium to accumulate in the body)
Nonsteroidal anti-inflammatory drugs

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78
Q

How should ACE inhibitors be administered?

A
  • All administered orally, except for Enalapril (Vasotec) which is given IV
  • May be administered without regard to meals, except for Captopril (capoten) and Moexipril
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79
Q

List 3 ACE inhibitors

A

Captopril (Capoten)
Enalapril (Vasotec)
Lisinopril (Prinivil)

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80
Q

Pharmacologic effects of ARBs

A
  • Block access of angiotensin II
  • Cause dilation of arterioles and veins
  • Prevent angiotensin II from inducing pathologic changes in cardiac structure
  • Reduce excretion of potassium
  • Decrease release of aldosterone
  • Increase renal excretion of sodium and water
  • Do not inhibit kinase II
  • Do not increase levels of bradykinin
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81
Q

Difference between ACE inhibitors and ARBs

A

ARBs do not increase bradykinin release in vasculature of the lungs. Because of this, they do not cause cough

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82
Q

Therapeutic uses of ARBs

A

HTN, heart failure, MI
Diabetic nephropathy
If unable to tolerate ACE inhibitors, next best protection against MI, stroke, and death from cardiovascular causes in high-risk patients

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83
Q

Adverse effects of ARBs

A

Angioedema
Fetal harm in pregnancy
Renal failure (**bilateral renal artery stenosis)

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84
Q

Administration of ARBs

A

All are given PO

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85
Q

List 3 ARBs

A

Losartan (Cozaar)
Valsartan (Diovan)
Telmisartan (Micardis)

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86
Q

Function of direct renin inhibitors

A

Binds tightly with renin and prevents the division of angiotensinogen to angiotensin I

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87
Q

Side effects of direct renin inhibitors

A

Angioedema
Cough
GI effects
Hyperkalemia
Fetal injury

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88
Q

Only drug approved for HTN in direct renin inhibitor class

A

Aliskiren (Tekturna)

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89
Q

Mechanism of action of aldosterone antagonists

A

Selective blockade of aldosterone receptors

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90
Q

Therapeutic uses of Eplerenone (Inspra)

A

HTN
Heart failure

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91
Q

Administration considerations for Eplerenone (Inspra)

A

Absorption is not affected by food

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92
Q

Adverse effects of Eplerenone (Inspra)

A

Hyperkalemia (can be severe)

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93
Q

Drug interactions of Eplerenone (Inspra)

A

Inhibitors of CYP3A4
Drugs that raise potassium levels
Use with caution when combined with lithium

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94
Q

Prototype for aldosterone antagonists

A

Spironolactone (Aldactone)

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95
Q

Mechanism of action for spironolactone (Aldactone)

A

Blocks aldosterone receptors, binds with receptors for other steroid hormones

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96
Q

Therapeutic uses of Spironolactone (Aldactone)

A

HTN
Heart failure

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97
Q

Adverse effects of Spironolactone (Aldactone)

A

*Hyperkalemia (b/c it is also a potassium sparing diuretic)
Gynecomastia
Menstural irregulatrities
Impotence
Hirsute said
Deepening of the voice

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98
Q

How do calcium channel blockers work?

A

*Prevent calcium ions from entering cells

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99
Q

Which parts of the body to calcium channel blockers have the greatest impact on?

A

Heart
Arteries
Arterioles

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100
Q

What are calcium channel blockers used to treat?

A

*HTN
*Angina pectoris
*Cardiac dysrhythmias

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101
Q

Other names for calcium channel blockers

A

Calcium antagonists
Slow channel blockers

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102
Q

What do calcium channels do?

A

Regulate the entry of calcium ions into cells

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103
Q

What are the 2 groups of CCBs?

A

Verapamil and diltiazem
Dihydropyridines

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104
Q

What are verapamil and diltiazem?

A

Agents that act on the vascular smooth muscle and the heart

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105
Q

What are dihydropyridines?

A

Agents that act mainly on vascular smooth muscle

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106
Q

How do calcium channel blockers work on vascular smooth muscle when they are open vs. blocked?

A

Open = contractile process
Blocked = *vasodilation

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107
Q

What do therapeutic doses of calcium channel blockers do?

A

Work selectively on peripheral arterioles and arteries, and arterioles of the heart
Do not have significant effect on veins

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108
Q

Why does blocking calcium channels cause vasodilation?

A

Calcium causes forceful contractions of the heart. If we relax the muscle by blocking some of the calcium, it makes contractions less forceful and allows smooth muscle to relax

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109
Q

Which receptor are calcium channels highly intertwined with?

A

Beta1 adrenergic receptors in the heart

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110
Q

Classifications of calcium channel blockers

A

Dihydropyridines
Non-dihydropyridines

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111
Q

Example of dihydropyridines group of calcium channel blockers

A

Nifedipine (Procardia)

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112
Q

Examples of non-dihydropyridines group of calcium channel blockers

A

Verapamil, Diltiazem (Cardizem)

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113
Q

Site of action for Dihydropyridines

A

Act primarily on arterioles

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114
Q

Site of action for verapamil and diltiazem

A

Act on arterioles and on the heart

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115
Q

Function of Verapamil (Calan, Covera-HS)

A

Agent that blocks calcium channels in blood vessels and acts on vascular smooth muscle and the heart

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116
Q

Hemodynamic effects of Verapamil

A

Direct effects on the heart and blood vessels (relaxes)
Reflex effects

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117
Q

Five direct hemodynamic effects of verapamil

A
  • Block at peripheral arterioles (reduces arterial pressure)
  • Block at arteries and arterioles of heart (increases coronary perfusion)
  • Block at SA node (reduces heart rate)
  • Block at AV node (decreases AV nodal contraction)
  • Block in the myocardium (decreases force of contraction)
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118
Q

Indirect (reflex) hemodynamic effects of Verapamil

A

Baroreceptor reflex (may cause BP to jump back up)

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119
Q

Net effects of verapamil

A

Little or no net effect on cardiac performance
*Vasodilation accompanied by reduced arterial pressure and increased coronary perfusion

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120
Q

Administration of Verapamil

A

Can be given PO or IV

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121
Q

Therapeutic uses of Verapamil

A

Angina pectoris (vasopastic angina and angina of effort)
Essential hypertension (first line agent)
Cardiac dysrhythmias

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122
Q

Types of cardiac dysrhythmias verapamil can be used for

A

Atrial flutter
Atrial fibrillation
Paroxysmal supraventricular tachycardia

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123
Q

How does verapamil help with dysrhythmias

A

If dysrhythmias are really fast, verapamil slows down contractions causing rhythm to be more regular

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124
Q

Adverse effects of Verapamil

A

*Constipation (most common complaint)
*Dizziness, facial flushing, headache (from lowered BP/HR)
Edema of ankles and feet
Gingival hyperplasia
Heart block

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125
Q

Drug interactions of Verapamil

A

Digoxin (doesn’t work well with other drugs)
Beta-adrenergic blocking agents (could lower BP too much or cause dysrhythmias)

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126
Q

When is Verapamil given IV?

A

Only for dysrhythmias and Pt must be on cardiac monitor with resuscitation equipment immediately available

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127
Q

Actions of Diltiazem

A

*blocks calcium channels in heart and blood vessels (similar to verapamil)
Lowers blood pressure

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128
Q

How does Diltiazem lower blood pressure?

A

Arteriolar dilation
Direct suppressant/reflex cardiac stimulation = little net effect on heart

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129
Q

Therapeutic uses for diltiazem

A

Angina pectoris
HTN
Cardiac dysrhythmias (atrial flutter, atrial fibrillation, paroxysmal tachycardia)

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130
Q

Adverse effects of diltiazem

A

(Similar to verapamil, but less constipation)
Dizziness
Flushing
Headache
Edema of ankles and feet
*Exacerbates bradycardia, sick sinus syndrome, heart failure, second- or third-degree heart block

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131
Q

Drug interactions of diltiazem

A

Digoxin
Beta-adrenergic blocking agents

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132
Q

What are Dihydropyridines?

A

Agents that act mainly on vascular smooth muscle
Create a significant blockade of calcium channels in blood vessels
And *Minimal blockade of calcium channels in the heart

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133
Q

Prototype of dihydropyridines

A

*Nifedipine (Procardia)

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134
Q

Actions of Nifedipine

A

Vasodilation by *blocking calcium channels
Blocks in vascular smooth muscle
Very little blockade of heart Ca channels
Cannot be used to treat dysrhythmias
Less likely than verapamil to exacerbate pre-existing cardiac disorders (used more for BP)

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135
Q

Direct effects of nifedipine

A

Limited blockade of Ca channels in vascular smooth muscle (no direct suppressant effects on: automaticity, AV conduction, or contractile force)

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136
Q

Indirect effects of nifedipine

A

Lowered BP activates baroreceptor reflex
(Primarily with fast-acting vs. sustained release)

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137
Q

Net effect of nifedipine blocking calcium channels and causing vasodilation

A

*Lowered BP
*Increased heart rate
*Increased contractile force
(HR and contractile force not affected as much as BP)

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138
Q

Therapeutic uses of nifedipine

A

Angina pectoris
HTN

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139
Q

Adverse effects of nifedipine

A

Flushing
Dizziness
Headache
Peripheral edema
Gingival hyperplasia
Chronic eczematous rash in older patients
Reflex tachycardia (= increased cardiac O2 demand)
- & can increase pain for anginal patients

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140
Q

What can nifedipine be combined with to prevent reflex tachycardia?

A

Beta blocker
(This is ok b/c nifedipine does not lower HR as much as beta blockers do)

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141
Q

Vasodilator that works selectively to dilate arterioles

A

Hydralazine

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142
Q

Vasodilator that works selectively to dilate veins

A

Nitroglycerin

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143
Q

Vasodilator that works to dilate both arterioles and veins

A

Prazosin

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144
Q

What occurs when a drug dilates resistance vessels (arterioles)?

A

Cause a decrease in cardiac Afterload

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145
Q

What occurs when a drug dilates capacitance vessels (veins)?

A

Decreased force with which blood is returned to the heart, so decreased preload

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146
Q

Therapeutic uses of vasodilators

A

*Essential HTN
*HTN crisis
*Angina pectoris
Heart failure
MI
Pheochromocytoma
Peripheral vascular disease
Pulmonary arterial hypertension
Production of controlled hypotension during surgery

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147
Q

Main adverse effects related to vasodilation

A
  • Postural hypotension
  • Reflex tachycardia
  • Expansion of blood volume
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148
Q

What should you tell a patient who first starts taking vasodilators?

A

*They may faint, feel dizzy or fatigued

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149
Q

Action of Hydralazine (Apresoline)

A

Selective dilation of arterioles
(Postural hypotension is minimal)

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150
Q

Therapeutic uses of Hydralazine (Apresoline)

A

Essential hypertension (PO)
Hypertensive crisis (IV)
Heart failure

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151
Q

Adverse effects of Hydralazine (Apresoline)

A

Reflex tachycardia
Increased blood volume
Systemic lupus erythematous-like syndrome
Headache
Dizziness
Weakness
Fatigue

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152
Q

Drug interactions of Hydralazine (Apresoline)

A

Other antihypertensive agents
Avoid excessive hypotension

(Combined with beta blocker to protect against reflex tachycardia and diuretics to prevent sodium and water retention and expansion of blood volume)

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153
Q

Action of Minoxidil (Loniten)

A

Selective dilation of arterioles
(More intense dilation than Hydralazine, but causes more adverse reactions)

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154
Q

Uses of minoxidil (Loniten)

A

Severe HTN that is unresponsive to safer drugs

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155
Q

Adverse effects of minoxidil (Loniten)

A

Reflex tachycardia
Sodium and water retention
Hypertrichosis (hair growth b/c can also be used topically as rogane)
Pericardial effusion

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156
Q

Fastest acting antihypertensive agent

A

Sodium Nitroprusside (Nitropress)

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157
Q

Action of sodium nitroprusside (Nitropress)

A

Causes venous and arteriolar dilation

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158
Q

Administration of Nitropress

A

*IV infusion (CCU)

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159
Q

Onset of Nitropress

A

Immediate (but BP returns to pretreatment level in minutes when stopped)

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160
Q

When is Nitropress used?

A

For hypertensive emergencies
(Pt must be hooked up to monitor b/c vasodilation effects are so strong)

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161
Q

Adverse effects of Nitropress

A

Excessive hypotension (Must lower pt’s bp slowly)
Cyanide poisoning (b/c of how it breaks down in body, creates cyanide build up)
Thiocyanate toxicity

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162
Q

Other vasodilators

A

ACE inhibitors
Angiotensin II receptor antagonists
Direct renin inhibitors
Organic nitrates
Calcium channel blockers
Sympathy lyrics
Nesiritide

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163
Q

What are nesiritides?

A

Drugs for pulmonary arterial hypertension

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164
Q

Prehypertension BP

A

120-130 / 80-89

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165
Q

Two categories of HTN

A

Primary (essential) HTN
Secondary HTN

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166
Q

Difference between primary and secondary hypertension

A

Primary (essential) HTN:
- no identifiable cause
- chronic, progressive disorder
- can be treated but not cured

Secondary HTN:
- identifiable primary cause
- possible to treat the cause directly
- some individuals can actually be cured

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167
Q

Who is more likely to have primary (essential) HTN?

A

Older adults
African Americans
Mexican Americans
Post menopausal women

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168
Q

Consequences of hypertension

A

Heart disease
- MI
- heart failure
- angina pectoris

Kidney disease
Stroke

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169
Q

Free lifestyle modifications for pts with HTN

A

Sodium restriction
DASH diet (fruits, veggies) & alcohol restriction
Aerobic exercise, smoking cessation
Maintenance of K+ and Ca+ intake

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170
Q

Formula for arterial pressure

A

Arterial pressure = cardiac output X peripheral resistance

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171
Q

What causes changes in cardiac output?

A

Heart rate
Myocardial contractility
Blood volume
Venous return

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172
Q

Systems that help regulate blood pressure

A

Sympathetic baroreceptor reflex
Renin-angiotensin-aldosterone system
Renal regulation of blood pressure

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173
Q

Patient education for taking BP medications

A

They must take them faithfully to bring BP down
If they don’t get BP under control, may have stroke or MI
Encourage them to get a BP cuff to check at home
Can cause impotence in men and makes them not want to take it

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174
Q

Drugs for hypertensive emergencies

A

Fenoldopam
Labetalol
Diazoxide
Clevidipine

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175
Q

Which BP meds are contraindicated during pregnancy?

A

ACE inhibitors
ARBS
Direct renin inhibitors (DRIs)

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176
Q

Which medications should be used for preeclampsia and eclampsia?

A

Labetalol
Magnesium sulfate (anticonvulsant)

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177
Q

Patho of heart failure

A

Cardiac remodeling (gets out of shape & bigger)
Physiologic adaptations to reduced cardiac output

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178
Q

Physiologic adaptations to reduced CO

A

Cardiac dilation
Increased sympathetic tone
Water retention and increased blood volume
Natriuretic peptides

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179
Q

Drugs that are used to treat heart failure

A

Diuretics
Drugs that inhibit the renin-angiotensin-aldosterone system
Beta blockers
Inotropic agents (Digoxin- cardiac glycoside, dopamine)
Vasodilators

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180
Q

Drugs that inhibit the RAAS

A

ACE inhibitors
ARBs (if ACE inhibitors are not tolerated)
Aldosterone antagonists
Direct renin inhibitors

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181
Q

What are inotropic agents?

A

Sympathomimetics

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182
Q

Types of sympathomimetics

A

Dopamine (Intropin)
Dobutamine
Phosphodiesterase inhibitors

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183
Q

How does dopamine work for heart failure?

A

Catecholamine
Activates beta1 adrenergic receptors in heart, kidney, and blood vessels
Increases heart rate
Dilates renal blood vessels
Activates alpha1 receptors

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184
Q

How does dobutamine work for heart failure?

A

Synthetic catecholamine
Selective activation of beta1 adrenergic receptors

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185
Q

Intravenous vasodilators used for acute care

A

*Nitroglycerin
*Sodium nitroprusside (Nitropress)
Nesiritide (Natrecor)

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186
Q

Principle adverse effects of nitroglycerin

A

Hypotension
Resultant reflex tachycardia

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187
Q

Principal adverse effect of Nitropress

A

Profound hypotension

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188
Q

Principle adverse effect of Nesiritide (Natrecor)

A

Sympatomatic hypotension

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189
Q

Functions of digoxin and cardiac glycosides

A

Positive inotropic actions:
- increase myocardial contractile force
- alter electrical activity of the heart
- favorable affect neurohormonal systems

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190
Q

What is Digoxin

A

A cardia (Digitalis) Glycoside

Naturally occurring compound

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191
Q

*Effects of Digoxin

A

Profound effects on the mechanical and electrical properties of the heart
Increases myocardial contractility
Increased cardiac output

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192
Q

Adverse effect of Digoxin

A

Can cause severe dysrhythmias

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193
Q

Relationship of potassium to inotropic action

A

Potassium levels must be kept in normal physiologic range

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194
Q

Hemodynamic benefits of Digoxin

A

Increased cardiac output
- decreased sympathetic tone
- increased urine production
- decreased renin release

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195
Q

*Heart rate of a pt taking digoxin that would cause you to hold the drug and call the provider

A
  • <60
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196
Q

Drug interactions of Digoxin

A

Diuretics
ACE inhibitors
ARBs
Sympathomimetics
Quinidine
Verapamil

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197
Q

Half life of digoxin

A

About 1.5 days

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198
Q

Stage A of heart failure

A

No symptoms of HF
Management directed at reducing risk

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199
Q

Stage B of heart failure

A

TX is same as for stage A with the addition of ACE inhibitors or ARBs

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200
Q

Stage C of heart failure

A

Relieve symptoms
Diuretics
BB
digoxin

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201
Q

Stage D of heart failure

A

Worse
Multiple drugs
Diuretics
Repeated hospitalizations
Fluid management is constant

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202
Q

What does ASCVD stand for?

A

Atherosclerotic Cardiovascular Disease

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203
Q

What is cholesterol?

A

A component of all cell membranes and membranes of intracellular organelles

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204
Q

What is cholesterol required for?

A

Synthesis of certain hormones and bile salts

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205
Q

Where does cholesterol come from and what is it manufactured by?

A

Comes from dietary sources
Manufactured by cells, primarily in the liver

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206
Q

What are apolipoproteins?

A

Recognition sites for cell-surface receptors

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207
Q

Function of apolipoproteins

A

Activate enzymes that metabolize lipoproteins
And increase the structural stability of lipoproteins

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208
Q

What are the 3 classes of plasma lipoproteins that are relevant to coronary atherosclerosis?

A

Very-low-density lipoproteins (VLDLs)
Low-density lipoproteins (LDLs)
High-density lipoproteins (HDLs)

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209
Q

Which class of lipoprotein are triglycerides in?

A

VLDLs

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210
Q

Which category of lipoproteins is the greatest contributor to CHD?

A

LDLs

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211
Q

Which class of lipoproteins is cholesterol in?

A

HDLs

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212
Q

What happens with the inflammatory process of atherogenesis?

A

Infiltration of macrophages, T lymphocytes, and other inflammatory mediators

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213
Q

How old/often should you have cholesterol screened?

A

Every 5 years for adults over 20

214
Q

What do we want HDL cholesterol levels to be?

A

> or equal to 45 mg/dL

215
Q

What do we want LDL cholesterol levels to be?

A

< 100 mg/dL

216
Q

What do we want triglycerides levels to be?

A

< 90 mg/dL

217
Q

Factors in risk assessment of cholesterol

A

Identifying CHD risk factors
Identifying CHD risk equivalents:
- diabetes, atherosclerotic disease other than CHD
Identifying an individual’s CHD risk category

218
Q

Therapeutic lifestyle changes for High-LDL cholesterol

A

Smoking cessation
Diet
Exercise

219
Q

Three medication categories for high cholesterol

A

HMG-CoA reductase inhibitors
Bile-acid sequestration
Fibrates

220
Q

Secondary treatment targets of cholesterol medication

A

Metabolic syndrome (increases risk for CHD & T2DM)
High triglycerides (levels above 150 mg/dL)

221
Q

Factors of metabolic syndrome

A

High blood glucose
High triglycerides
High apolipoprotein B
Low high-density lipoprotein (HDL)
Prothrombotic state
Proinflammatory state
Hypertension

222
Q

Treatment goals for metabolic syndrome

A

Reduce the risk for atherosclerotic disease
Reduce the risk for T2DM
Increase physical activity

(Want to make sure pts know that they have to turn this disease around otherwise they will have diabetes and heart problems)

223
Q

Most effective drugs for lowering LDL

A

HMG-CoA Reductase Inhibitors (Statins)

224
Q

What do Statins do?

A

Lower LDL cholesterol
Raise HDL cholesterol
Lower triglyceride levels

225
Q

Nonlipid beneficial cardiovascular actions of statins

A

Promote plaque stability
Reduce the risk for cardiovascular events
Increased bone formation

226
Q

Prototype for statins

A

Lovastatin/Mevacor

227
Q

When is the best time to take a drug that lowers cholesterol?

A

In the evening
Because a lot of cholesterol synthesis takes place at night while sleeping

228
Q

What happens if you stop taking statins?

A

Cholesterol goes back up to where it was before starting the drug

229
Q

Mechanism of action for statins

A

Cholesterol reduction

230
Q

Therapeutic uses of statins

A

Hypercholesterolemia
Primary and secondary prevention of CV events
Post MI therapy (bc it helps prevent plaque from building up in vessel walls)
Diabetes

231
Q

Another popular statin drug

A

Rouvastatin (Crestor)

232
Q

Nursing consideration for patients taking Crestor

A

If pt is Asian, may get very high levels of this drug and have to decrease dose to lower levels

233
Q

Adverse effects of statins

A

Common:
- headache
- rash
- GI disturbances

Rare:
- *Myopathy/rhabdomyolysis
- hepatotoxicity

234
Q

What is myopathy and rhabdomyolysis?

A

A rare side effect of stating drugs
Myopathy - injured muscle tissue and can develop into:
Rhabdomyolysis - muscle tissue breaks down and increased levels of creatinine kinase floats around and could get into renals

235
Q

Which severe side effects should you watch for in a pt taking statins?

A

Muscle tenderness and weakness (could indicate myopathy/rhabdomyolysis

Jaundice, pt saying they don’t feel good (could indicate hepatotoxicity)
Need to draw liver enzymes to see if they’re elevated

236
Q

Drug interactions of statins

A

Most other lipid-lowering drugs (except bile acid sequestration)
Drugs that inhibits CYP3A
*Use in pregnancy (Category X = contraindicated)

237
Q

Dosing of statins

A

*should be once daily, in the evening

238
Q

What should the patient have done before they start taking a cholesterol lowering medication?

A

We need to get a lipid profile on them

239
Q

Function of Bile-Acid sequestrants

A

Primarily used as adjuncts to statins
Lowers LDLs

240
Q

Prototype bile-acid sequestrant

A

Colesevelam/Welcol

241
Q

Difference between Colesevelam/Welchol and other bile-acid sequestrants

A

Does not increase uptake of fat-soluble vitamins as other bile sequestrants do
Does not significantly reduce the absorption of statins, warfarin, digoxin, and most other drugs studies

242
Q

Two other drugs in the bile-acid sequestrants group

A

Cholestyramine
Colestipol

243
Q

Function of Colesevelam (Welchol)

A

Decrease in LDL cholesterol
(Increased VLDL levels in some patients)

244
Q

Mechanism of action of Colesevelam (Welchol)

A

Increases LDL receptors on hepatocytes
Prevents reabsorption of bile acids

245
Q

Use of Colesevelam (Welchol)

A

Reduces LDL cholesterol (with modified diet and exercise)

246
Q

Adverse effects of Colesevelam (Welchol)

A

Constipation

247
Q

Function of Ezetimibe (Zetia)

A

Inhibits cholesterol absorption

248
Q

Which type of cholesterol drug is Ezetimibe (Zetia)?

A

Bile-Acid Sequestrant

249
Q

Uses of Ezetimibe (Zetia)

A

Lower total cholesterol
LDL cholesterol
Apolipoprotein B

250
Q

Adverse effects of Ezetimibe (Zetia)

A

Myopathy
Rhabdomyolysis
Hepatitis
Pancreatitis
Thrombocytopenia

251
Q

Drug interactions of Ezetimibe (Zetia)

A

Statins
Fibrates
Bile-acid sequestrants
Cyclosporine

252
Q

Most effective type of drug available for lowering TG levels

A

Fabric Acid Derivatives (Fibrates)

253
Q

Main functions of Fibrates

A

Most effective drug for lowering TG levels
Can raise HDL cholesterol
Little or no effect on LDL cholesterol

254
Q

Drug interactions for Fibrates

A

Warfarin (can increase risk for bleeding)
Statins (can increase risk for rhabdomyolysis)

255
Q

3 Fibrates used in the United States

A

*Gemfibrozil (Lopid)
Fenofibrate (Tricor)
Fenofibric acid (TriLipix)

256
Q

Prototype for Fibrins

A

Gemfibrozil (Lopid)

257
Q

Effects of Gemfibrozil (Lopid) on plasma lipoproteins

A

Decreased plasma TG content
Decreased VLDL levels
Can increase HDL cholesterol

258
Q

How does Gemfibrozil (Lopid) interact with warfarin?

A

Displaces warfarin from plasma albumin
Must measure INR frequently

259
Q

Uses of Gemfibrozil (Lopid)

A

Reduces high levels of plasma triglycerides (VLDLs)
(Treatment reserved for pts who have not responded to diet modification)
Less effective than statins in reducing LDL
Can raise HDL but not approved for this use

260
Q

Adverse of Gemfibrozil (Lopid)

A

Rashes
GI disturbances
Gallstones
Myopathy
Liver injury (hepatotoxic)

261
Q

Other products that are used to alter plasma lipid levels

A

Lovaza - omega 3 acid
Fish oil - diet
Plant stanol and sterol esters
Cholestin

262
Q

What are GP2B3A receptors?

A

Receptors on platelets (50,000-80,000 on each platelet)
Where anticoagulation medications go in and attach to decrease platelet aggregation

263
Q

Stage 1 of hemostasis

A

Formation of platelet plug
Platelet aggregation

264
Q

Stage 2 of hemostasis

A

Coagulation
Intrinsic and extrinsic coagulation pathways

265
Q

Three major groups of drugs for thromboembolic disorders

A

Anticoagulants
Antiplatelets
Thrombolytics

266
Q

What do anticoagulants do?

A

Reduce the formation of fibrin

267
Q

Two mechanisms of action of anticoagulants

A

Inhibit the synthesis of clotting factors
Inhibit the activity of clotting factors

268
Q

Two drugs in anticoagulant group of drugs for thromboembolic disorders

A

Heparin
Coumadin

269
Q

Function of heparin

A

Enhances antithrombin
Rapid-acting anticoagulant

270
Q

How is heparin administered?

A

By injection only (Cannot be absorbed so can’t be PO)
IV (Continuous and intermittent)
Deep SubQ

271
Q

Therapeutic uses of Heparin

A

Preferred anticoagulant during pregnancy when rapid anticoagulation is required

Pulmonary embolism
Stroke evolving
Massive DVT
Open heart surgery
Renal dialysis
Low-dose therapy postoperatively
Disseminated intravascular coagulation (DIC)
Adjunct to thrombolytic therapy

272
Q

Adverse effects of heparin

A

Hemorrhage
Heparin-induced thrombocytopenia
Hypersensitivity reactions

273
Q

What is heparin-induced thrombocytopenia?

A

HIT syndrome: wipes out pt’s platelets

274
Q

How do we know HIT syndrome is occuring?

A

Get a base line lab value before starting pt on the drug and compare after starting. If platelets keep decreasing, will know they are being wiped out

275
Q

When is heparin contraindicated?

A

Thrombocytopenia, uncontrolled bleeding
During and immediately after surgery of the eye, brain, or spinal cord (could cause hematomas and put too much pressure in these areas)

276
Q

*Antidote for overdose of Heparin

A

*Protamine sulfate

277
Q

What is aPTT? When is it drawn, and why?

A

Activated partial thromboplastin time
Gives an indication of how effective the heparin is working.
Need to draw pt’s levels every 6-8 hours while they’re taking heparin

278
Q

Normal levels of aPTT and what happens to the levels when a pt is taking heparin?

A

Normal is around 40 seconds. Want it to increase when they are on heparin

279
Q

Difference between unfractioned heparin and low-molecular-weight heparins

A

Unfractioned heparin has a different molecular structure and can be given IV
Low-Molecular-Weight heparins are composed of molecules that are shorter than those found in unfractioned heparin

280
Q

Therapeutic uses of Low-Molecular-Weight heparins

A

Prevention of DVT after surgery (including replacement of hip, knee)
Treatment of established DVT
Prevention of ischemic complications

281
Q

What types of ischemic complications does Low-Molecular-Weight heparin prevent?

A

Pts with unstable angina
Non-Q wave MI
STEMI

282
Q

How is Low-Molecular-Weight heparin administered?

A

SubQ
Dosage is based on body weight

283
Q

Antidote for toxicity of Low-Molecular-Weight heparin

A

Protamine sulfate

284
Q

Benefits and down-sides of Low-Molecular-Weight heparin

A

Costs more than unfractionated heparin
Does not require monitoring, can be given at home

285
Q

Adverse effects and interactions of Low-Molecular-Weight heparin

A

Bleeding (but less than with unfractionated heparin)
Immune-mediated thrombocytopenia
Severe neurologic injury for pts undergoing spinal puncture or spinal epidural anesthesia

286
Q

Types of Low-Molecular-Weight heparins

A

*Enoxaparin (Lovenox)
Dalteparin (Fragmin)

287
Q

What is *Warfarin (Coumadin)?

A

*An oral anticoagulant

288
Q

Uses of Warfarin (Coumadin)

A

Oral anticoagulant with delayed onset
Vitamin K antagonist
Blocks biosynthesis of factors 7, 9, 10 and prothrombin in coagulation cascade

Not useful in emergencies (since it’s PO)

Long term prophylaxis of thrombosis

289
Q

Which patients would use Warfarin as a long-term prophylaxis of thrombosis?

A

For prevention of:
- Venous thrombosis and associated pulmonary embolism
- prevention of thromboembolism (in pts with prosthetic heart valves)
- prevention of thrombosis during atrial fibrillation

290
Q

How to monitor treatment with warfarin:

A

*Prothrombin time (PT) - normal is 12 seconds
* Internal normalized ratio (INR)

291
Q

Adverse effects of warfarin

A

Hemorrhage (give Vitamin K for toxicity)
Fetal hemorrhage and teratogenesis during pregnancy

Pts will bruise easily

292
Q

Drug interactions of warfarin

A

Drugs that increase anticoagulant effects
Drugs that promote bleeding
Drugs that decrease anticoagulant effects
Heparin
Aspirin
Acetaminophen

293
Q

Antagonist for Coumadin

A

Vitamin K

294
Q

What should you educate a pt on when they begin taking Warfarin?

A

Don’t want them to eat too much vitamin K in their diet to cancel it out
Should wear a bracelet that says they’re on Coumadin
Will bruise easily

295
Q

Difference between how direct thrombin inhibitors and heparin work

A

Direct thrombin inhibitors directly inhibit thrombin and heparin enhances the activity of antithrombin

296
Q

Drugs that are direct thrombin inhibitors

A

Dibigatran etexilate (Pradaxa) (not important)
Hiruden Analog: Bivalirudin (Angiomax)
Lepirudin (Refludan)

297
Q

Function of Angiomax

A

Prevents clot formation (combined with aspirin) in pts with unstable angina who are undergoing coronary angioplasty

298
Q

Mechanism of action of Angiomax

A

Facilitates the actions of antithrombin
Prevents conversion of fibrinogen to fibrin
Prevents activation of factor XII

299
Q

Adverse effects of Angiomax

A

Bleeding
Back pain
Nausea, headache

300
Q

Use of lepirudin (Refludan)

A

Prophylaxis and treatment of thrombosis in pts with HIT
(Direct inhibition of thrombin)

301
Q

Drug that is a selective factor Xa inhibitor

A

Rivaroxaban (Xarelto)

302
Q

Function of Xarelto

A

Binds directly with factor Xa to cause inactivation

303
Q

Use of Xarelto

A

Retention of DVT and PE after ortho surgery
Prevention of stroke in pts with atrial fibrillation

304
Q

Adverse effects of Xarelto

A

Bleeding

305
Q

How does aspirin function as an anti platelet drug?

A

Inhibition of cyclooxygenase

306
Q

Adverse effect of aspirin

A

Increases risk for GI bleeding

307
Q

How does Clopidogrel (Plavix) work as an anti platelet drug?

A

P2Y12, adenosine diphosphate receptor antagonist

308
Q

How does Vorapaxar (Zontivity) work as an antiplatlet drug?

A

Protease-activated receptor-1 (PAR-1) antagonist

309
Q

Therapeutic uses of aspirin

A

Ischemic stroke
Transient ischemic attack
Chronic stable angina
Unstable angina
Coronary stunting
Acute MI
Previous MI
Primary prevention of MI

310
Q

Adverse effects of aspirin

A

Bleeding
GI bleeding and hemorrhagic stroke
(Enteric coated tablets may not reduce risk for GI bleeding)

311
Q

Therapeutic uses of plavix

A

Prevents blockage of coronary artery stents
Reduces thrombotic events in pts with acute coronary syndromes:
- MI
- Ischemic stroke
- Vascular death

312
Q

Adverse effects of Plavix

A

Similar to those of aspirin

313
Q

How does Vorapaxar (Zonitivity) work as an antiplatlet drug?

A

Protease-activated receptor-1 PO

314
Q

Emergency drugs used in chest pain situations via IV

A

Aggrastat
Integrilin

315
Q

How does Eptifibatide (Integrilin) work?

A

Small peptide that causes reversible and highly selective inhibition of GP IIb/IIIa receptors

Effects reverse within 4 hours of stopping the infusion

316
Q

Which type of drug is Alteplase (tPa)?

A

Thrombolytic Fibrinolytic Drug

317
Q

Therapeutic uses of Alteplase (tPa)

A

Strong emergency critical care drug
MI
Ischemic stroke
PE

318
Q

Major adverse effects of Alteplase (tPa)

A

*Bleeding
(Minor oozing to life-threatening amount)
Risk for intracranial bleeding higher than with streptokinase

319
Q

Likely sites of bleeding in pts taking Alteplase (tPa)

A

Recent wounds
Needle puncture sites
Invasive procedure sites

320
Q

What increases the risk of bleeding for a pt taking Alteplase (tPa)?

A

Anticoagulants increase risk for hemorrhage
(Blood replacement may need to be considered)

321
Q

How can nurses minimize the risk of bleeding in pts taking Alteplase (tPa)?

A

Minimizing physical manipulation of the pt
Avoiding subQ and IM injections
Minimizing invasive procedures
Minimizing concurrent use of anticoagulants
Minimizing concurrent use of anti platelet drugs

322
Q

How is Alteplase (tPa) administered?

A

IV
Pt must be hooked up to 2 IVs. One for the tPa and one for a regular drip (like NS)
Weight based and requires careful assessment

323
Q

Where does pain from angina occur?

A

Sudden pain beneath the sternum, often radiating to left shoulder and arm

324
Q

What causes angina?

A

*Oxygen supply to the heart is insufficient to meet oxygen demand

325
Q

Two goals of angina drug therapy

A

Prevention of MI and death
Prevention of myocardial ischemia and anginal pain

326
Q

What controls cardiac oxygen demand

A

Heart rate
Myocardial contractility
Intramyocardial wall tension (preload/Afterload)

327
Q

What controls oxygen supply?

A

Myocardial blood flow
Myocardial perfusion only in diastole

328
Q

Three forms of angina pectoris

A

Chronic stable angina (exertional angina)
Variant angina (Prinzmetal’s or vasospastic angina)
Unstable angina

329
Q

Three families of antianginal agents

A

*Organic nitrates
*Beta blockers
*Calcium channel blockers

330
Q

What can cause chronic stable angina?

A

Emotional excitement
Large meals
Cold exposure
CAD

331
Q

Treatment strategy for chronic stable angina

A

Increase cardiac oxygen supply
Decrease oxygen demand

332
Q

Therapeutic agents for chronic stable angina

A

Organic nitrates
Beta blockers
Calcium channel blockers
Ranolazine (newer drug with limited indications, can be combined with other drugs)

333
Q

Non drug therapy for chronic stable angina

A

Avoid factors that can precipitate angina
Decrease risk factors

334
Q

What causes variant angina?

A

Coronary artery spasm

335
Q

Treatment for variant angina

A

Increasing cardiac oxygen supply

336
Q

Therapeutic agents for variant angina

A

Calcium channel blockers
Organic nitrates

337
Q

How can you tell if someone is having unstable angina?

A

Symptoms of angina at rest
New onset of exertional angina
Intensification of existing angina

338
Q

Treatment strategy of unstable angina

A

Maintain oxygen supply
Decrease oxygen demand

339
Q

Therapeutic agents for acute management of unstable angina

A

Anti-ischemic therapy
Antiplatelet therapy
Anticoagulant therapy

340
Q

Types of angina nitroglycerin is used for

A

Stable and variant angina

341
Q

Action of nitroglycerin

A

Vasodilator

342
Q

Adverse effects of nitroglycerin

A

Headache
Orthostatic hypotension
Reflex tachycardia

343
Q

Drug interactions with nitroglycerin

A

Hypotensive drugs
Phophodiesterase type 5 inhibitors (Viagra)
Beta blockers, verapamil, and diltiazem

344
Q

Which group of antianginal meds does nitroglycerin fall into?

A

Organic nitrates

345
Q

What should you know about a pt’s tolerance to nitroglycerin?

A

Can develop rapidly, and will cause cross tolerance to all other nitrates

To minimize, use the lowest effective dose
For long acting formulas, do 8 drug-free hours per day

346
Q

Preparations and routes of nitroglycerin

A

Sublingual tablets
Sustained release oral capsules
Transdermal delivery systems
Translingual spray (most common)
Topical ointment
IV infusion

347
Q

What should a pt do if they are having chest pain and have nitro with them at home?

A

Take one sublingual nitro and wait 5 mins. If they are still having chest pain, call 911 and take another tablet

348
Q

Nursing considerations for nitroglycerin

A

If using long acting preparations, they should be discontinued slowly

349
Q

All uses for nitroglycerin

A

Acute anginal therapy
Sustained anginal therapy

IV for perioperative control of BP
Treatment of heart failure with MI
Unstable angina
Uncontrolled exacerbations of chronic angina

350
Q

Critical care organic nitrates

A

Isosorbide mononitrate (Imdur) & isosorbide dinitrate (Isordil)

Amyl nitrate

351
Q

Beta blockers that can be used for angina

A

*Propranolol (Inderal)
*Metoprolol(Lopressor)

352
Q

Function of propranolol and metoprolol for anginal pain

A

Decrease cardiac oxygen demand

353
Q

Adverse effects of propranolol and metoprolol

A

Bradycardia
Decreased AV conduction
Reduction of contractility
Asthmatic effects
Use with caution in pts with diabetes
Insomnia
Depression
Bizarre dreams
Sexual dysfunction

354
Q

Calcium channel blockers that can be used for angina

A

*Verapamil
*Diltiazem
*Nifedipine

355
Q

Function of calcium channel blockers for angina

A

Block calcium channels in vascular smooth muscle

356
Q

Types of angina calcium channel blockers can be used for

A

Stable and variant angina

357
Q

Adverse effects of calcium channel blockers

A

Dilation of peripheral arterioles
Reflex tachycardia
Hypotension
Beta blockers
Bradycardia
Heart failure
AV block

358
Q

Drug in new class of antianginal agents

A

Ranolazine (Ranexa)

359
Q

How does Ranexa work?

A

Benefits are modest, works better in men
Does not reduce heart rate, BP, or vascular resistance

360
Q

Side effects of Ranexa

A

Can prolong QT interval, and can lead to Vtach
Multiple drug interactions

361
Q

Drugs used to prevent MI and death

A

Antiplatelet drugs
Cholesterol-lowering drugs
Angiotensin-converting enzyme (ACE) inhibitors
Antianginal agents
(All of these can be used in combination to help with angina or to prevent MIs, etc.)

362
Q

Risk factors for angina

A

Smoking
High cholesterol
Hypertension
Diabetes
Physical inactivity

363
Q

Management of variant angina

A

Calcium channel blocker, or long acting nitrate
If either of these alone is inadequate, add a nitrate
If combination fails, CABG may be indicated
(Beta blockers not effective with vasospastic angina)

364
Q

Antiplatelet therapy for angina:

A

Aspirin (indefinitely)
- Clopidogrel (Plavix)
- Abciximab (ReoPro)
- Eptifibatide (Integrilin)

365
Q

Anticoagulant therapy for angina

A

Subcutaneous LMW heparin or IV
Unfractionated heparin

366
Q

Anti-ischemic therapy for angina

A

Nitroglycerin
Beta blockers
Supplemental O2
IV morphine
ACE inhibitor

367
Q

Revascularization therapy for angina

A

Coronary artery bypass graft (CABG) surgery
Percutaneous transluminal coronary angioplasty (PTCA)
Comparison of CABG surgery with percutaneous coronary intervention (PCI)

368
Q

Two types of myocardial infarctions

A

MI
STEMI (ST-Elevation MI)

369
Q

Difference between a MI and a STEMI

A

MI: necrosis of the myocardium resulting from ischemia
STEMI: acute IM, causes elevation of the ST segment on the ECG

370
Q

Pathophysiology of a STEMI

A
  • Blood flow to a region of myocardium is stopped (by platelet plugging and thrombus formation)
  • Hydrogen ions accumulate
  • Local metabolic changes occur
  • Myocardial injury triggers ventricular remodeling
  • Degree of residual cardiac impairment depends on amount/location of damage
371
Q

Pain symptoms of STEMI

A

Severe sub sternal chest pain
Crushing/constricting pain
Radiates down arm and jaw

372
Q

Things to look for to determine if someone has had a STEMI

A

Chest pain
Characteristic ECG changes
Sweating, weakness, sense of impending doom
(But 20% of pts experience no symptoms)
Biochemical markers for MI

373
Q

Routine drug therapy for management of STEMI

A

Oxygen
Aspirin (not NSAIDs) (have pt chew it)
Morphine (IV to relieve pain & decrease anxiety)
Beta blockers (give right after)
Nitroglycerin (to vasodilate)

374
Q

What is reperfusion therapy for when managing STEMI

A

Pt will go to cath lab for reperfusion therapy.
To dissolve clots, and convert plasminogen to plasmin

375
Q

Types of reperfusion therapy to manage STEMI

A

Primary percutaneous coronary intervention
Fibrinolytic (thrombolytic) therapy

376
Q

Adjuncts to reperfusion therapy when managing an MI

A

Heparin
Antiplatelet drugs

377
Q

What type of Fibrinolytic drugs are used for management of STEMI?

A

Alteplase (a tissue plasminogen activator)
Reteplase
Tenecteplase

378
Q

What is primary percutaneous coronary intervention?

A

Primary = use of angioplasty rather than fibrinolytic therapy
Stents may be placed

379
Q

What is the goal of primary percutaneous coronary intervention?

A

Primary PCI within 90 minutes of patient contact

380
Q

What should all patient undergoing PCI receive?

A

An anticoagulant (IV heparin, bivalirudin) combined with
Antiplatelet drugs: aspirin plus either Clopidogrel, ticagrelor, or prasugrel

381
Q

Function of fibrinolytic (thrombolytic) therapy?

A

Dissolves clots

382
Q

How does fibrinolytic therapy dissolve clots?

A

Converts plasminogen to plasmin (proteolytic enzyme)
1. Alteplase, a tissue plasminogen activator
2. Reteplase
3. Tenecteplase

383
Q

When is fibrinolytic therapy most effective?

A

When patient presents early
(Best for patients younger than 75 years)

384
Q

Goal of fibrinolytic therapy

A

To improve ventricular function and reduce mortality

385
Q

Adjuncts to reperfusion therapy when managing a STEMI

A
  • Unfractionated heparin (used for treatment lasting less than 48 hours)
  • Low-molecular-weight heparin (used for treatment lasting longer than 48 hours)
  • Antiplatelet drugs:
  • Low dose aspirin
386
Q

Types of Antiplatelet drugs used adjunct to reperfusion therapy when managing a STEMI

A

Clopidogrel (plavix)
Glycoprotein (GP) IIb/IIIa inhibitors

387
Q

Considerations when giving a pt aspirin adjunct to reperfusion therapy when managing a STEMI

A

May use aspirin concurrently with clopidogrel
Should take indefinitely
Higher dose should be given for PCI patients

388
Q

How should ACE inhibitors and ARBs be used while managing STEMI

A

They decrease short-term mortality in all patients
Start treatment within 24 hours

389
Q

Why should calcium channel blockers be used when managing STEMI

A

Antianginal, vasodilation, and antihypertensive actions

390
Q

Complications that can occur due to STEMI

A

Ventricular dysrhythmias
Cardiogenic shock

391
Q

What occurs with ventricular dysrhythmias after STEMI

A

Develop frequently and are major cause of death after MI
Prophylactic antidysrhythmics not successful

392
Q

What causes cardiogenic shock after a STEMI

A

Results from tissue perfusion reduction
7-15% of post MI patients develop shock in first few days

393
Q

How can patients who have had a STEMI improve their chances of having another one

A

Cholesterol control
Smoking cessation
Exercise
Blood pressure control
Diabetes control

394
Q

*Which medications should post MI patients take?

A

Beta blocker
ACE inhibitor
Antiplatelet drug or anticoagulant

395
Q

Symptoms of Diabetes Melkite’s

A

Sustained hyperglycemia
Polyuria
Polydipsia
Ketonuria
Weight loss

396
Q

Other names for T1DM

A

Insulin dependent
Juvenile onset

397
Q

Primary defect of T1DM

A

Destruction of pancreatic beta cells

398
Q

What percentage of diabetes cases is type 1?

A

5-10%

399
Q

Another name for T2DM

A

*Non-insulin dependent diabetes
Adult onset

400
Q

What causes type 2 diabetes?

A

Insulin resistance and impaired insulin secretion

401
Q

Short term complications of diabetes

A

Hyperglycemia and hypoglycemia

402
Q

Long term complications of diabetes

A

Macrovascular damage
- Heart disease
- HTN
- Stroke
Hyperglycemia
Altered lipid metabolism

403
Q

What can Macrovascular damage from diabetes cause?

A

Retinopathy
Nephropathy
Neuropathy
Gastroparesis
Amputation secondary to infection

404
Q

What causes gestational diabetes?

A

Placenta produces hormones that antagonize the actions of insulin
Glucose can pass freely from the maternal to the fetal circulation (fetal hyperinsulinemia)

405
Q

What can happen if proper glucose levels are not maintained during pregnancy?

A

To prevent teratogenic effects

406
Q

How is someone diagnosed with diabetes?

A

Excessive plasma glucose is diagnostic of diabetes.
Patient must be tested in two separate ways, and both tests must be positive

407
Q

Tests that can be used to diagnose diabetes

A

Fasting plasma glucose (FPG)
Casual plasma glucose
Oral glucose tolerance test (OGTT)

*Hemoglobin A1C

408
Q

What does glucose level have to be to diagnose diabetes from a fasting plasma glucose test?

A

126 mg/dL or higher

409
Q

What does glucose level have to be to diagnose pt with diabetes for a casual plasma glucose test?

A

200 mg/dL or greater

410
Q

What does a pt’s glucose level have to be to diagnose with diabetes during an oral glucose tolerance test?

A

200 mg/dL or higher

411
Q

What does hemoglobin A1C measure?

A

Measures the glucose that’s bound to the hemoglobin molecules in the blood
Gives snapshot of what glucose levels have been over last 3 months

412
Q

What level of A1C is indicative of diabetes?

A

6.5% and above

413
Q

Criteria for pts to be diagnosed with pre diabetes

A

Impaired fasting glucose between 100 & 125 mg/dL
Impaired glucose tolerance test

414
Q

What happens when someone is diagnosed with pre diabetes

A

They are at an increased risk for developing T2DM
(Many people who meet prediabetes criteria never develop diabetes)

May reduce risk with diet changes and exercise and possibly with certain oral anti diabetic drugs

415
Q

Primary goal of diabetes treatment

A

To prevent long-term complications

416
Q

What needs to be controlled during diabetes treatment?

A

Tight control of blood glucose level
Control blood pressure
Control blood lipids

417
Q

Treatment plan for T1DM

A

Integrated program of diet, self-monitoring of blood glucose, exercise, and insulin replacement

418
Q

Dietary measures for T1DM

A

Total number of carbohydrates is more important than the type
Glycemic index

419
Q

Treatment plan for T2DM

A

Requires comprehensive plan:
- modified diet and exercise
- drug therapy

Should be screened and treated for:
- HTN
- Nephropathy
- Retinopathy
- Neuropathy
- Dyslipidemias

420
Q

Common target values while self monitoring blood glucose:

A

*80-130 mg/dL before meals
*<180 mg/dL 1-2 hours after meals

421
Q

Goal for A1C for diabetic patients

A

Below 7%
But below 8% may be appropriate for pts with a history of severe hypoglycemia

422
Q

How is insulin synthesized?

A

In the pancreas by beta cells within the islets of langerhans

423
Q

What stimulates insulin release

A

A rise in blood glucose, usually by eating food

424
Q

*Types of rapid acting insulins

A

Insulin lispro (Humalog)
Insulin aspart (NovoLog)
Insulin glulisine (Apidra)

425
Q

*Types of short acting insulin

A

Regular insulin: Humulin R
Regular insulin: Novolin R

426
Q

*Type of intermediate duration insulin

A

Neutral Protamine Hagedorn (NPH) insulin

427
Q

*Types of long duration insulin

A

Insulin glargine (Lantus)
Insulin detemir (Levemir)

428
Q

*Types of ultra long duration insulin

A

Insulin glargine (toujeo)
Insulin degludec (Tresiba)

429
Q

Prototype for short-duration, rapid-acting insulin

A

Insulin lispro (Humalog)

430
Q

Time frames of Humalog

A

Rapid onset (15-30 mins)
Peak: .5-2.5 hrs
Short duration (3-6 hrs)

431
Q

When should Humalog be administered

A

Before (or even after eating)
Should be injected 5-10 minutes before meals

432
Q

Routes of Humalog

A

Usually subQ
Or insulin pump

433
Q

Time frames of NovoLog

A

Rapid onset 10-20 minutes
Peak: 1-3 hours
Short duration 3-5 hours

434
Q

When should NovoLog be administered?

A

5-15 minutes before meals

435
Q

Time frames of Apidra

A

Rapid onset 10-15 minutes
Peak: 1-1.5 hours
Short duration 3-5 hours

436
Q

When should Apidra be administered

A

Close to the time of eating

437
Q

Routes for regular insulin

A

SubQ injection
SubQ infusion
IM injection (used rarely)
IV

438
Q

Time frames for regular insulin

A

Onset: 30-60 mins
Peak: 1-5 hours
Duration: 10 hours

439
Q

Color of regular insulin

A

Clear

440
Q

Time frames of NPH insulin

A

Onset: 60-120 hours
Peak: 6-14 hours
Duration: 16-24 hours

441
Q

What can NPH insulins be mixed with?

A

Short acting insulins (to give more coverage)

442
Q

What color are NPH insulins?

A

Cloudy
And must be rotated before admin

443
Q

Administration of NPH insulin

A

SubQ injection only
Must be rotated before admin

444
Q

Time frames of lantus

A

Onset: 70 minutes
Duration 18-24 hours

445
Q

Time frames of levemir

A

Onset 60-120
Duration: 12-24 hours

446
Q

Color of long duration insulin

A

Clear solutions

447
Q

How long does Toujeo last?

A

24 hours
(Very concentrated)

448
Q

How are toujeo and tresiba typically administered?

A

Usually come in prefilled pens

449
Q

*Rules for mixing insulin

A

NPH with short-acting insulins
Short-acting insulin is drawn first (clear to cloudy)

450
Q

How can insulin be administered through subcutaneous infusion?

A

Portable insulin pumps
Implantable insulin pumps

451
Q

How should insulin be stored?

A

*unopened vials should be refrigerated until needed
Not frozen!
Can be used until expiration date if refrigerated.
Keep out of direct sunlight and extreme heat

452
Q

How should mixtures of insulin be stored?

A

Mixtures in vials: stable for 1 month at room temp and for 3 months under refrigeration

Mixtures in pre-filled syringes: stored in refrigerator for at least 1 week, stored vertically with needle pointing up

453
Q

*Therapeutic uses of insulin?

A

Principle use: diabetes mellitus
(Required by all type 1 and some type 2 pts)
IV insulin for DKA

Hyperkalemia (can promote uptake of potassium)
AIDS in the diagnosis of GH deficiency

454
Q

Complications of insulin treatment

A

Hypoglycemia
Lipohypertrophy (lumpy looking skin from injecting in same spot)
Allergic reactions
Hypokalemia

455
Q

Drug interactions with insulin

A

Hypoglycemic agents
Hyperglycemic agents
Beta-adrenergic blocking agents

456
Q

Glucose level of hypoglycemia

A

*below 70 mg/dL

457
Q

Treatment for a pt who has a blood glucose below 70

A

Rapid treatment for hypoglycemia is mandatory

Conscious pts: fast-acting oral sugar (OJ, glucose tabs, soda)

If swallowing or gag reflexes are suppressed: IV glucose or parenteral glucagon

458
Q

Medication group for T2DM

A

Oral hypoglycemics

459
Q

Prototype of oral hypoglycemics

A

Metforman (Glucophage)

460
Q

What type of oral hypoglycemic is metformin?

A

Biguanides

461
Q

Most common side effects of metformin

A

GI disturbances
Lactic acidosis (potentially fatal but rare)

462
Q

Uses of metformin

A

T2DM
Prevention of T2DM
Gestational diabetes
PCOS

463
Q

What are Sulfonylureas used for?

A

Oral hypoglycemic for T2DM only
Promote insulin release

464
Q

Major side effects of Sulfonylureas

A

Hypoglycemia
Weight gain

465
Q

Why does rosiglitazone (Avenida) have restricted use?

A

Can cause cardiac side effects

466
Q

How do alpha-glucosidase inhibitors work?

A

Oral hypoglycemics that act on the intestine to delay absorption of carbohydrates

467
Q

Two alpha-glucosidase inhibitors

A

Acarbose (Precose)
Miglitol (Glyset)

468
Q

Adverse effects of alpha-glucosidase inhibitors

A

Flatulence
Cramps
Abdominal distention
Diarrhea
Liver dysfunction

469
Q

How do DPP-4 inhibitors (AKA gliptins) work?

A

Oral hypoglycemics that promote glycemic control by enhancing the actions of incretin hormones

470
Q

Adverse effects of DPP-4 inhibitors

A

Upper respiratory infection
UTI
Headache

471
Q

Types of drugs other than insulin that can treat T2DM

A

GLP-1 receptor agonists (incretin mimetics)
Amylin mimetics

472
Q

2 GLP-1 receptor agonists

A

Exenatide (Byetta)
Liraglutide (Victoza)

473
Q

1 drug that is a amylin mimetic

A

Pramlintide (Symlin)

474
Q

Acute complications of poor glycemic control

A

Diabetic ketoacidosis (DKA)
Hyperglycemic hyperosmotic nonketotic syndrome (HHNS)

475
Q

*Characteristics of DKA

A

Hyperglycemia
Water loss
Altered fat metabolism
Ketoacids
Hemoconcentration
Acidosis
Coma

476
Q

Treatment for DKA

A

*Insulin replacement
Bicarbonate for acidosis
Water and sodium replacement
Potassium replacement
Normalization of glucose levels

477
Q

Symptoms of HHNS

A
  • Large amount of glucose excreted in urine
  • Dehydration and loss of blood volume
  • Increases blood concentration of electrolytes and non electrolytes (particularly glucose)
  • Increases hematocrit (blood thickens and becomes sluggish)
478
Q

How does HHNS occur?

A

With T2DM with acute infection, acute illness, or other stress

479
Q

What happens if HHNS is left untreated?

A

Can lead to coma or death

480
Q

Management of HHNS

A

Correct hyperglycemia and dehydration with IV insulin, fluids, and electrolytes

481
Q

Difference between DKA and HHNS

A

HHNS has little or no change in ketoacid levels and has little or no change in blood pH
HHNS also has no sweet or acetone smell to urine/breath

482
Q

Difference between treating DKA and HHNS

A

HHNS does not get treated with bicarbonate because there is no acidosis to treat

483
Q

How is severe hypoglycemia treated?

A

IV glucose to immediately raise blood glucose level is preferred

*Glucagon can be used if IV glucose is not available

484
Q

How does *glucagon work for treating hypoglycemia?

A

Delayed elevation of blood glucose (promotes glycogen breakdown)
Will not work in starvation (b/c malnourished have little glycogen left to break down)

485
Q

Patient teaching for pts with diabetes

A

Self glucose checks
Medications
Care of insulin
All the supplies
Syringes - put used ones in a container
Nutrition
S & S of hypo- and hyper- glycemic
If they’re sick, have surgery, run marathons, etc, will all require adjusting doses
Age of pt and family support

486
Q

What functions do thyroid hormones have a profound effect on?

A

Metabolism
Cardiac function
Growth (promotes maturation in infancy and childhood development)

487
Q

Hormones produced by the thyroid

A

Triiodothyronine (T3)
Thyroxine (T4, tetraiodothyronine)

488
Q

Synthetic T3

A

Liothyronine

489
Q

*Synthetic t4

A

*Levothyroxine

490
Q

What is a serum TSH test used for?

A

Screening and diagnosis of hyperthyroidism
(Elevated TSH is indication of hyperthyroidism)

491
Q

What are serum T3 or T4 tests used for?

A

Can measure total T4 or free T4
(Or total T3 or free T3)

492
Q

What is hypothyroidism called in adults?
And in infants?

A

Myxedema in adults
Congenital hypothyroidism in infants

493
Q

How is hypothyroidism treated in adults?

A

Replacement therapy with thyroid hormones
In almost all cases, treatment must continue lifelong

494
Q

How is hypothyroidism treated in infants?

A

Replacement therapy with thyroid hormones

495
Q

Clinical presentation of hypothyroidism in adults

A

Pale, puffy, and expressionless face
Cold and dry skin
Brittle hair or loss of hair
Lowered heart rate and temperature
Lethargy and fatigue
Intolerance to cold
Impaired mentality

496
Q

Causes of hypothyriodism

A

Malfunction of the thyroid (usual cause)
Hashimoto’s disease (Chronic autoimmune thyroiditis)
Insufficient iodine in diet
Surgical removal of thyroid and destruction of thyroid with radioactive iodine
Insufficient secretion of TSH and TRH

497
Q

Lifelong medications that are used to treat hypothyroidism

A

Levothyroxine (T4) (standard treatment)
*Liothyronine (T3) option

498
Q

What can occur if someone has hypothyroidism during pregnancy?

A

In first trimester can result in permanent neuropsychological defects in the child

499
Q

What can occur in infants who have hypothyroidism

A

May be permanent or transient
Can cause mental retardation and derangement of growth if not diagnosed and treated

500
Q

Two forms of hyperthyroidism

A

Graves’ disease (most common form)
Toxic nodular goiter (Plummer’s disease)

501
Q

Who does Graves’ disease most typically affect?

A

Women 20-40 years old

502
Q

Notable symptom of Graves’ disease

A

Exophthalmos

503
Q

Cause of hyperthyroidism

A

thyroid-stimulating immunoglobulins (TSIs)

504
Q

Treatment of hyperthyroidism

A

Surgical removal of thyroid tissue
Destruction of thyroid tissue
Suppression of thyroid hormone synthesis
Beta blockers (ex: propranolol)
Nonradioactive iodine

505
Q

Causes of thyrotoxic crisis (thyroid storm)

A

Patients with thyrotoxicosis who undergo significant stress (surgery, illness, etc.)
High levels of thyroid hormone
(Cannot be identified by laboratory testing)

506
Q

Signs of thyrotoxic crisis

A

Hyperthermia (105° or higher)
Severe tachycardia
Restlessness
Agitation
Tremor
Unconsciousness
Coma
Hypotension
Heart failure

507
Q

*Treatment of thyrotoxic crisis

A

*Potassium iodide, *Methimazole, and *Beta blocker
Sedation, cooling, glucocorticoids, IV fluids

508
Q

Prototype thyroid hormone preparation for hypothyroidism

A

*Levothyroxine (Synthroid)

509
Q

What is Levothyroxine (Synthroid)?

A

Synthetic preparation of thyroxine (T4) and drug of choice for *all types of hypothyroidism
Conversion to T3

510
Q

Half life of Levothyroxine (Synthroid)

A

7 days

511
Q

When should Levothyroxine be taken?

A

In the morning at least 30-60 minutes before breakfast

512
Q

Adverse effects of Levothyroxine

A

Tachycardia
Angina
Tremors
Can intensify effects of warfarin

513
Q

Drug interactions of Levothyroxine

A

Drugs that reduce Levothyroxine absorption
Drugs that accelerate Levothyroxine metabolism
Warfarin
Catecholamines (too much stimulation)

514
Q

First-line drug for hyperthyroidism

A

Methimazole (Tapazole)

515
Q

What type of drug is Methimazole (Tapazole)?

A

Thionamides

516
Q

How long does it take for Methimazole to work?

A

May take 3-12 weeks for euthyroid state (may need to add something to help sooner)

517
Q

Pros and cons of Methimazole

A

Does not cause liver damage associated with PTU
Does not destroy existing stores of thyroid hormone

More dangerous than PTU during lactation and during the first trimester of pregnancy
Considered a hazardous agent, handle with caution

518
Q

Applications of Methimazole in hyperthyroidism

A
  • Can be used alone for Graves’ disease
  • Adjunct to radiation therapy until the effects of radiation manifest
  • Suppress thyroid hormone synthesis in preparation for thyroid gland surgery (subtotal thyroidectomy)
  • Patients experiencing thyrotoxic crisis (although PTU is preferred)
519
Q

Function of propylthiouracil (PTU)

A

Inhibits thyroid hormone synthesis
Second line drug for Graves’ disease

520
Q

Half life of PTU

A

90 minutes

521
Q

How long does it take PTU to work?

A

6-12 months for full benefits

522
Q

Therapeutic uses of PTU

A

Graves’ disease
Adjunct to radiation therapy
Preparation for thyroid gland surgery
Thyrotoxic crisis

523
Q

Adverse effects of PTU

A

Agranulocytosis (most serious)
Hypothyroidism
Pregnancy and lactation
Can cause *severe liver damage

524
Q

PTU vs. Methimazole

A

PTU can cause severe liver injury, meth does not
PTU has shorter half life, hence it requires 2-3 daily doses
PTU crosses placenta less readily than meth and achieves lower concentrations in breast milk
PTU blocks conversion of T4 to T3 in the periphery, meth does not

525
Q

What is Radioactive Iodine-131?

A

Radioactive isotope of stable iodine
Emits gamma and beta rays

526
Q

Half life of radioactive iodine 131

A

8 days

527
Q

How long does it take radioactive iodine to work?

A

2-3 months for full effect

528
Q

When is radioactive iodine used?

A

In Graves’ disease
Cannot be used in children or during pregnancy

529
Q

Type of nonradioactive iodine

A

Lugol’s solution

530
Q

What is Lugol’s solution used for?

A

Strong iodine solution used to suppress thyroid function in preparation for thyroidectomy

531
Q

Adverse effects of Lugol’s solution

A

Brassy taste
Burning sensation in mouth and throat
Soreness of teeth and gums
GI injury
(These could all also be symptoms of mild toxicity)

532
Q

How can beta blockers be used for thyroid issues?

A

For hyperthyroidism
Can suppress tachycardia and other symptoms of Graves’ disease
(Benefits derive from beta-adrenergic blockade, not from reducing levels of T3 or T4)

Also beneficial in thyrotoxic crisis

Pharmacology (16 decks)

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