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PHARMACOLOGY > EXAMS 2 > Flashcards

EXAMS 2 Flashcards

1
Q

functional unit of the kidney

A

The nephron

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2
Q

5 mains regions of the nephron

A
  • Glomerulus
  • Proximal convoluted tubule
  • Loop of Henle
  • Distal convoluted tubule
  • Collecting duct
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3
Q

three basic function of the renal

A
  • Cleansing of extracellular fluid (ECF) and maintenance of ECF volume and composition
  • Maintenance of acid-base balance
  • Excretion of metabolic wastes (drugs/toxins)
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4
Q

renal filtration

A
  • Occurs at the glomerulus

- All small molecules get filtered

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5
Q

renal absorption

A
  • 99% of water, electrolytes and nutrients undergo reabsorption via active transport
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6
Q

renal active tubular secretions

A
  • Located in proximal convoluted tubule

- Excrete products into lumen of nephron

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7
Q

where in the regions of the nephron does filtration occur

A

glomerus

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8
Q

where in the regions of the nephron does active tubular secretion occur

A
  • Located in proximal convoluted tubule

- Excrete products into lumen of nephron

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9
Q

what are the most abundant electrolytes in filtrate

A

sodium and chloride.

SODIUM AND CHLORIDE ARE ABSORBED IN DIFFERENT AMOUNTS based on the location in the nephron

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10
Q

how does diuretics work?

A

Diuretics work by disrupting reabsorption of electrolytes (Na and Cl)

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11
Q

proximal convoluted tubule (PCT)

A
  • High reabsorptive capacity

= 65% of filtered Na+ and Cl- reabsorbed here
= 100% of filtered K+ and bicarbonate reabsorbed here

  • Water flows freely
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12
Q

what percentage of filtered sodium and chlorine are rebasorbed in the proximal convoluted tubule

A

65%

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13
Q

what percentage of filtered potassium and bicarbonate are rebasorbed in the proximal convoluted tubule

A

100%

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14
Q

where does water flow freely in the nephron?

A

proximal convoluted tubule

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15
Q

which of the limbs of the loop of henle is freely permeable to water

A

descending limb

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16
Q

which of the limbs of the loop of henle IS NOT permeable to water

A

ascending limb

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17
Q

which of the limbs of the loop of henle does filtrate become VERY concentrated

A

descending limb

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18
Q

which of the limbs of the loop of henle does filtrate become LESS concentrated

A

ascending limbs

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19
Q

what does not leave the descending limb

A

sodium and chloride

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20
Q

….% of sodium and chloride are rebasorbed in the ………. whereas …..% of sodium and chloride are rebabsorbed in the ……..

A

65% of sodium and chloride are reabsorbed in the proximal convoluted tube, whereas the 20% of Na and Cl rebasorbed in the ascending limb

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21
Q

early segment of distal convulated tubule (DCT)

A
  • Freely permeable to water

- 10% of Na and Cl reabsorbed here

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22
Q

late segment of distal convulated tubule (DCT)

A
  • Na can be exchanged for K
  • Process stimulated by hormone called aldosterone
  • Part of Renin-angiotensin-aldosterone system
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23
Q

where can sodium be exchanged for potassium

A

late segment of distal convoluted tubule (DCT)

THIS PROCESS IS STIMULATED BY ALDOSTERONE HORMONE which is part of the renin-angiotensin-aldosterone system

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24
Q

what are direutics

A

drugs that increase urine output

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25
Q

what diurectics are more effective

A

Diuretics that work EARLIER in the nephron are more effective

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26
Q

Increases in urine are directly related to??

A

Increases in urine are directly related to how much reabsorption of Na and Cl are blocked

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27
Q

most diuretics work by….

A

Most work by blocking reabsorption of Na and Cl at some point in the nephron. Remember, water follows salt!

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28
Q

Applications of diurectics

A
  • Treatment of hypertension

- Edema associated with heart failure, kidney failure, and cirrhosis

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29
Q

classes of diuretic

A
  • loop diuretics
  • thiazide diuretics
  • potassium-sparing diuretics
  • osmotic diuretics
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30
Q

what are the potassium-sparing diuretics

A
  • Aldosterone antagonists

- Non-aldosterone antagonists

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31
Q

Most effective class of diuretics

A
  • loop diuretics
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32
Q

mechanism of action of loop diuretics

A
  • Block sodium and chloride reabsorption in the ascending Loop of Henle
  • 20% of Na and Cl typically reabsorbed here, inhibition leads to profound diuresis
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33
Q

loop diuretics drugs

A
  • Furosemide
  • Torsemide
  • Bumetanide
  • Ethacrynic acid
Oral= 60 mins
IV= 5 minutes
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34
Q

indication of loop diuretics

A
  • Congestive heart failure
    Pulmonary edema
    Peripheral edema
  • Hypertension
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35
Q

adverse effects of loop diuretics

A
  • Hypovolemia/dehydration
  • Electrolyte abnormalities
    Hyponatremia, hypochloremia, hypokalemia, hypomagnesemia, hypocalcemia
  • Hypotension
  • Ototoxicity
  • Hyperuricemia
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36
Q

drug interactions of loop diuretics

A
  • Digoxin
  • Ototoxic drugs
  • Potassium-sparing diuretics
  • Lithium
  • Anti-hypertensive drugs
  • NSAIDs
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37
Q

monitoring points for loop diuretics

A
  • Avoid taking before bedtime
  • Monitor urine output
  • Watch for signs of dehydration
  • Give IV doses SLOWLY to avoid ototoxicity
  • Caution in patients with a sulfa allergy
  • Monitor urine output
  • Can be given safely to patients with a sulfa allergy
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38
Q

Thiazide Diuretics

A

Lesser diuretic effect than loop diuretics

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39
Q

mechanism of actions of thiazide diuretics

A
  • Block reabsorption of Na+ and Cl- at the early segment of the distal convoluted tubule (DCT)
  • 10% of Na and Cl reabsorbed from DCT; inhibition leads to diuresis
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40
Q

drugs of thiazide diuretics

A
  • Hydrochlorothiazide (HCTZ)
  • Chlorothiazide
  • Chlorthalidone
  • Metolazone
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41
Q

indication of thiazide diuretics

A
  • Hypertension (first-line)
  • Edema
  • Diabetes insipidus
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42
Q

drugs interactions of thiazide diuretics

A
  • Digoxin
  • Potassium-sparing diuretics
  • Lithium
  • Anti-hypertensive drugs
  • NSAIDs
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43
Q

adverse effects of thiazide diuretics

A 
- Electrolyte abnormalities
	Hyponatremia, hypochloremia, hypokalemia, hypomagnesemia
- Dehydration
- Hyperglycemia
- Hyperuricemia
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44
Q

route for thiazide diuretics

A

oral EXCEPT chlorothiazide

chlorothiazide = IV

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45
Q

monitoring points for thiazide diuretics

A
  • Avoid dosing before bedtime
  • All agents equally effective
  • Monitor for ADEs especially related to electrolyte abnormalities
  • Caution in patients with a sulfa allergy
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46
Q

therapeutic effects of potassium-sparing diuretics

A
  • Small amount of diuresis
  • DECREASE potassium excretion
  • Reduce cardiac remodeling
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47
Q

Aldosterone Antagonists drug of potassium-sparing diuretic

A

Spironolactone

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48
Q

Non-aldosterone Antagonists drug of potassium-sparing diuretic

A
  • Amiloride

- Triamterene

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49
Q

mechanism of spironolactone

A

Blocks aldosterone in the distal convoluted tubule

  • Aldosterone typically causes sodium retention and potassium excretion.
  • Increased excretion of sodium and retention of potassium
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50
Q

indications of spironolactone (PO)

A
  • Hypertension and edema
  • Heart failure
  • Acne
  • Polycystic ovarian syndrome
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51
Q

adverse effects of spironolactone

A
  • Hyperkalemia

- Endocrine effects

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52
Q

drug interaction of spironolactone

A
  • Thiazide and loop diuretics

- Agents that raise potassium

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53
Q

mechanism of action of amiloride and triamterene (PO)

A
  • Direct inhibitor of the Na/K ion exchange transporter

- Increased excretion of sodium and retention of potassium

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54
Q

indications of amiloride and triamterene

A
  • hypertension

- Edema

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55
Q

adverse effect of amiloride and triamterene

A

hyperkalemia

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56
Q

drug interactions of amiloride and triamterene

A
  • Thiazide and loop diuretics
  • Agents that raise potassium

same as spironolactone

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57
Q

implications with mannitol

A

ONLY GIVEN BY IV

  • Inspect the product prior to administration
  • Mannitol can crystalize
  • Must be administered through a 0.22 micron filter to remove microcrystals
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58
Q

what is mannitol

A

Osmotic diuretic made of a 6-carbon sugar

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59
Q

mechanism of action of mannitol

A
  • Filtered by the glomerulus
  • Does NOT undergo reabsorption and remains in the lumen
  • Increased osmotic pressure keeps water from being reabsorbed
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60
Q

indications of mannitol

A
  • Reduce elevated intracranial pressure

- Reduce elevated intraocular pressure

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61
Q

adverse effect of mannitol

A
  • Edema

- Electrolyte imbalances

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62
Q

Drugs Impacting the Renin-Angiotensin-Aldosterone-System (RAAS)

A
  • Angiotensin converting enzyme inhibitors (ACE-i)
  • Angiotensin II receptor blockers (ARB)
  • Direct renin inhibitors (DRI)
  • Aldosterone antagonists
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63
Q

role of the RAAS system

A
  • The RAAS system plays critical role in regulating blood pressure, blood volume and fluids and electrolytes
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64
Q

key compounds of the RAAS

A
  • Angiotensin
  • Aldosterone
  • Renin
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65
Q

what is renin of the RAAS

A

Enzyme that starts the whole RAAS pathway

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66
Q

renin are produced by the kidney in response to?

A
  • Low blood pressure
  • Low blood volume
  • Low blood sodium content
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67
Q

renin release is suppressed when……

A
  • Low blood pressure, volume and sodium content return to normal
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68
Q

three subtypes of angiotensin

A

angiotensin I, II, III

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69
Q

Angiotensin I:

A

inactive; converted into angiotensin II by angiotensin-converting enzyme (ACE)

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70
Q

Angiotensin II:

A
  • Powerful vasoconstrictor (increases blood pressure)
  • Stimulates release of aldosterone (increases blood pressure)
  • Causes remodeling and hypertrophy of the myocardium
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71
Q

Angiotensin III

A

effects incompletely understood

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72
Q

function of aldosterone

A
  • Stimulates Na+ retention and K+ excretion in the distal convoluted tubule
  • Na+ retention leads to water retention which increases blood pressure
  • Causes pathologic remodeling and hypertrophy of the myocardium
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73
Q

what does Na+ leads to? and causes what?

A

Na+ retention leads to water retention which increases blood pressure

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74
Q

Angiotensin Converting Enzyme Inhibitors (ACE-i) drugs

A
  • Lisinopril (PO)
  • Enalapril (PO)
  • Enalaprilat (IV)
  • Captopril (PO)
  • Benazepril (PO)
  • Generally well-tolerated
  • All agents are equally efficacious
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75
Q

Angiotensin Converting Enzyme Inhibitors (ACE-i) are very effective for treating?

A
  • Hypertension
  • Heart failure
  • Diabetic nephropathy
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76
Q

mechanism of action Angiotensin Converting Enzyme Inhibitors (ACE-i)

A
  • inhibit angiotensin converting enzyme (ACE) from converting angiotensin I to angiotensin II
  • Inhibit kinase II from converting bradykinin to an inactive form
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77
Q

increase in bradykin results in

A
  • vasodilation
  • cough
  • angioedema (RARELY)
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78
Q

decrease in angiotensin II results in

A
  • vasodilation
  • decrease blood volume
  • decrease cardiac and vascular remodeling
  • potassium retension
    fetal injury
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79
Q

pharmacokinetics of ACE- inhibitors

A
  • All administered orally (EXCEPTION: enalaprilat is IV)
  • Long half-lives (EXCEPTION: captopril)
  • Renally excreted
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80
Q

adverse effects of ACE-inhibitors

A
  • First-dose hypotension
  • Dry cough
  • Hyperkalemia (high potassium levels)
  • Renal failure in patients with bilateral renal artery stenosis
  • Fetal injury
  • Angioedema
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81
Q

ACE-Inhibitors indication

A
  • hypertension
  • heart failure
  • myocardial infarction
  • diabetic nephropathy
  • Prevention of MI, stroke and death in patients at high risk for CV disease
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82
Q

Angiotensin II Receptor Blockers mechanism of actions

A

block angiotensin II from binding to its receptor

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83
Q

Angiotensin II Receptor Blockers physiologic effects

A
  • Vasodilation
  • Decrease production of aldosterone
  • Reduce cardiac remodeling
  • Dilation of renal blood vessels
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84
Q

Angiotensin II Receptor Blockers drugs

A
  • Losartan
  • Valsartan
  • Telmisartan
  • Olmesartan

all PO

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85
Q

Angiotensin II Receptor Blockers (ARB) therapeutic uses

A
  • Hypertension
  • Heart failure
  • Diabetic nephropathy
  • Myocardial infarction
  • Prevention of MI, stroke and death in high risk patients
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86
Q

adverse effects of Angiotensin II Receptor Blockers (ARB)

A
  • Angioedema
  • Fetal harm
  • Renal failure
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87
Q

Direct Renin Inhibitors (DRI) drug

A

Aliskiren (PO)

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88
Q

Direct Renin Inhibitors (DRI) mechanism of action

A

binds to renin and prevents it from cleaving angiotensinogen to angiotensin I

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89
Q

Direct Renin Inhibitors (DRI) physiologic actions

A
  • Vasodilation
  • Decrease production of aldosterone
  • Reduce cardiac remodeling
  • Dilation of renal blood vessels

same as Angiotensin II Receptor Blockers

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90
Q

adverse effects of Direct Renin Inhibitors (DRI)

A
  • Angioedema
  • Dry cough
  • Diarrhea
  • Hyperkalemia
  • Fetal injury
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91
Q

indications of Direct Renin Inhibitors (DRI)

A

Hypertension

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92
Q

Aldosterone Antagonists mechanism of action

A

blocks aldosterone from binding to receptors in kidney

93
Q

Aldosterone Antagonists physiologic effects

A
  • Decrease Na+ reabsorption and increase reabsorption of K
  • Decrease blood pressure and blood volume
  • Reduce pathologic remodeling of the heart
94
Q

drugs of Aldosterone Antagonists

A

Eplerenone (PO) =
Selective for aldosterone receptors

Spironolactone (PO) = NON-selective

95
Q

Aldosterone Antagonists indications

A

Hypertension

Heart failure

96
Q

Aldosterone Antagonists adverse effects

A

Hyperkalemia
Diarrhea
Gynecomastia

97
Q

Physiology of Calcium Channels

A

Calcium channels are gated pores in the cytoplasmic membrane

98
Q

locations of calcium channels

A
  • Vascular smooth muscle (stimulates contraction)
  • Heart
    Myocardium = increase force of contraction
    SA node = increase heart rate
    AV node = increase conduction velocity which increases heart rate
99
Q

Classification of Calcium Channel Blockers (CCBs)

A
  1. Dihydropyridines
    - several drugs
    - works only on vascular smooth muscle
  2. Non-dihydropyridines
    - two drugs
    - Work on heart and vascular smooth muscle
100
Q

Dihydropyridine Calcium Channel Blockers drugs

A
  • Amlodipine (PO)
  • Nifedipine (PO)
  • Felodipine (PO)
  • Nimodipine (PO)
  • Nicardipine (IV)
  • Clevidipine (IV)

IV 5 to 10 mins
PO= 12 to 24 hours

101
Q

Dihydropyridine Calcium Channel Blockers mechanism of action

A

block calcium channels in the vascular smooth muscle

MINIMAL effects on the heart

102
Q

indications of Dihydropyridine Calcium Channel Blockers

A

Angina pectoris

Hypertension

103
Q

hemodynamic effects if Dihydropyridine Calcium Channel Blockers

A
  • Vasodilation of the arteries and arterioles which decreases blood pressure
  • Vasodilation cardiac vasculature which increases myocardial perfusion
  • Reflex tachycardia
104
Q

first line iv medications for hypertension

A

Nicardipine

Clevidipine

105
Q

monitoring points for Dihydropyridine Calcium Channel Blockers

A
  • DDI with beta-blockers
  • Toxic doses can affect the myocardium
  • Nimodipine is ONLY indicated for SAH
  • Nicardipine and clevidipine are first-line IV medications for hypertension
106
Q

Non-dihydropyridine Calcium Channel Blockers drugs

A
  • verapamil ( both mouth and IV )
  • diltiazem ( both mouth and IV)

oral 1-2 hours
IV - 5 minutes

107
Q

Mechanism of action of Non-dihydropyridine Calcium Channel Blockers

A

block of calcium channels in the vascular smooth muscle AND heart

108
Q

Hemodynamic effects: of non-dihydropydrine calcium channel blockers

A
  • Vasodilation of the arteries and arterioles which decreases blood pressure
  • Vasodilation cardiac vasculature which increases myocardial perfusion
  • Blockade of the SA and AV node which decreases heart rate
  • Decreased force of myocardial contraction
109
Q

indications of non-dihydropydrine calcium channel blockers

A
  • Angina pectoris
  • Hypertension
  • Cardiac dysrhythmias
110
Q

monitoring points for non-dihydropydrine calcium channel blockers

A
  • DDI with digoxin and beta-blockers
  • Possible interaction with grapefruit juice
  • Monitor BP, ECG and heart rate
  • Do not crush or chew ER products
111
Q

adverse effects of non-dihydropydrine calcium channel blockers

A 
Constipation (verapamil)
Dizziness
Flushing
Headache
Bradycardia
AV nodal block
Peripheral edema
112
Q

Classification of Hypertension (HTN)

A
  • primary/essential = NO IDENTIFIABLE

- secondary = IDENTIFIABLE CAUSE

113
Q

Why is hypertension so dangerous?

A
  • Increases risk of heart disease and stroke
  • Increases risk of irreversible kidney damage
  • Often asymptomatic (the “silent killer”)
114
Q

overall management of hypertension

A
  • Diagnose (Primary vs Secondary)
  • Evaluate for factors that increase CV risk and target organ damage
  • Treatment Goals
  • Therapeutic Management
115
Q

drug therapy of hypertension

A
  • Many different options
    Treatment algorithms to guide decisions
  • Different mechanisms of action can be combined to have stronger effect or synergistic effect
  • Combine with lifestyle changes
116
Q

hypertensive emergency

A
  • end organ damage

Need to rapidly decrease BP over one hour

  • Requires IV medications
  • Sodium nitroprusside, labetalol, clevidipine, nicardipine
117
Q

hypertensive urgency

A
  • no end organ damage

Decrease BP gradually over 24 hours
- Can use IV or PO medications

118
Q

chronic hypertension

A 
- Discontinue all category X drugs
	ACE-i
	ARBs
	DRI
Preferred drugs: labetalol, methyldopa
119
Q

Preeclampsia and Eclampsia

A
  • Disorder characterized by HTN and proteinuria after 20 weeks gestation
  • Presence of seizures = eclampsia
  • Serious risks to the mother and fetus
  • Treatment
    Labetalol
    Magnesium(anticonvulsant)
    Deliver baby (if possible)
120
Q

pathophysiology of heart failure

A

Step 1: Myocardial dysfunction
Step 2: Activation of the RAAS system
Step 3: Activation of the neurohormonal system
Step 4: Remodeling of ventricular myocardium

121
Q

The normal compensatory systems of the body make the issue worse:

A
  • RAAS system → fluid accumulation

* Neurohormonal system → cardiac remodeling

122
Q

Angiotensin Receptor Neprilysin Inhibitor drugs

A
  • Valsartan/sacubitril
    Valsartan -> ARB
    Sacubitril -> neprilysin inhibitor
123
Q

what is neprilysin

A

Enzymes that break down natriuretic peptides

124
Q

ONLY 3 FDA-approved for HF

A

Bisoprolol
Carvedilol
Metoprolol

125
Q

inotropes

A

Added in very severe heart failure

126
Q

three agents of inotropes

A

Digoxin ( PO or IV)
Dobutamine (IV)
Milrinone (IV)

  • All inotropes are given IV
    EXCEPTION digoxin which can be given PO or IV
127
Q

digoxin mechanism of action

A
  • Inhibition of the Na/K/ATPase pump
    ↑ intracellular Ca concentrations
    ↑ force of contraction
128
Q

role of potassium digoxin

A
  • Competes with digoxin for binding to Na/K/ATPase
  • If K levels low = ↑ digoxin binding
  • If K levels high = ↓ digoxin binding
129
Q

low potassium levels impact on digoxin

A

↑ digoxin binding

130
Q

high potassium levels impact on digoxin

A

↓ digoxin binding

131
Q

digoxin physiologic effects

A
  • Increased cardiac output
  • Suppresses renin release in the kidneys → ↓ activation of the RAAS pathway
  • Alters electrical activity in the heart → ↑ vagal responses
132
Q

pharmakokinetics of digoxin

A
  • Well absorbed and distributed into tissues
  • High levels reached in cardiac tissues
  • Long half-life
133
Q

dosing of digoxin

A

Loading dose

Maintenance dose

134
Q

Monitoring points for digoxin

A

digoxin = last line defense

Narrow therapeutic index
DRUG LEVELS (0.5-0.8 mcg/mL)
135
Q

adverse effects of digoxin

A
  • Cardiac dysrhythmias
  • GI symptoms
  • Fatigue
  • Visual disturbances
136
Q

dobutamine mechanism of action

A
  • Beta-1 & beta-2 activation
    ↑ force of contraction
    ↑ heart rate
  • Place in therapy =
    Acute decompensated heart failure
137
Q

Adverse effects/ Monitoring parameters of dobutamine

A

Arrythmias

BP and HR monitoring

138
Q

Milrinone mechanism of action

A
  • Phosphodiesterase-3 inhibitor
    ↑ cyclic AMP → ↑ myocardial contractility
    Vasodilation

place in therapy = Acute decompensated heart failure

139
Q

Adverse effects/ Monitoring parameters of milrinone

A

Arrythmias

Hypotension

140
Q

two types of dysrhythmia

A
  • Tachydysrhythmia = Dysrhythmia where rate is increasing
  • bradydysrhythmia
    Dysrhythmia where rate is decreasing

Drugs are used to treat dysrhythmias BUT can also predispose patients to dysrhythmias

141
Q

SA node

A

pacemaker of the heart

142
Q

AV node

A

getaway for impulse to reach the ventricles; delays impulse travel

143
Q

His-Purkinje System

A

conduct electrical impulse to the ventricles

144
Q

Properties that Generate an Impulse

A

AUTOMATICITY

  • Heart’s ability to generate an electrical impulse
  • SA node has the fastest rate of automaticity

CONDUCTIVITY

  • Ability of cardiac tissue to transmit electrical impulses
  • Orderly, rhythmic transmission of impulses needed to generate effective contractions
145
Q

4 classifications of antidysrhythmic drugs

A 
Class I: Sodium Channel Blockers
Class II: Beta-blockers
Class III: Potassium Channel Blockers
Class IV: Calcium Channel Blockers
Other: digoxin and adenosine
146
Q

Class I; Sodium Channel Blockers

A

Class IA

  • Disopyramide
  • Quinidine
  • Procainamide

Class IB

  • Lidocaine
  • Mexiletine

Class IC

  • Flecainide
  • Propafenone
  • ↓ conduction velocity in the atria, ventricles and His-Purkinje system
  • Similar in action and structure to local anesthetics
  • Effects are secondary to sodium channel blockade
147
Q

adverse effect of quinidine

A

Diarrhea (33%)

Cinchonism = hearing loss, tinnitus, dizziness, flushing, and blurry vision

148
Q

Procainamide( CLASS IA) adverse effect

A
  • Systemic Lupus Erythematosus reaction
  • Blood dyscrasias
  • Arterial embolism
149
Q

adverse effect of lidocaine (CLASS IB)

A
  • CNS effects
  • Toxic doses:
    Seizure
    Respiratory arrest
150
Q

monitoring points of lidocaine (CLASS IB)

A
  • Narrow therapeutic index
  • Monitor: drug levels
  • Make sure you’re using the correct product!
151
Q

monitoring points for Flecainide (CLASS IC)

A

↑ mortality in post-MI patients with asymptomatic Vtach

152
Q

Class II: Beta-blockers DRUGS

A 
Propranolol
Acebutolol
Esmolol
Sotalol
= 4 approved

Metoprolol
Labetalol
Bisoprolol
Carvedilol

153
Q

physiological effects of Class II: beta-blockers

A

Physiologic effects:
↓ automaticity in SA node
↓ conduction velocity through AV node
↓ myocardial contractility

154
Q

indications of Class II: beta-blockers

A

Sinus tachycardia

Atrial fibrillation/flutter

155
Q

Propranolol adverse effect

A
  • AV block
  • Sinus arrest
  • Hypotension
  • Bradycardia
156
Q

monitoring points for Propranolol

A
  • Give IV SLOWLY to avoid hypotension

- Monitor: HR, BP, ECG

157
Q

adverse effect of esmolol

A
  • AV block
  • Sinus arrest
  • Hypotension
  • Bradycardia
158
Q

monitoring points for esmolol

A
  • VERY fast acting
  • Short half-life
  • Monitor: HR, BP, ECG
159
Q

monitoring points for sotalol

A
  • Also causes blockade of K channels; can be considered
  • Class III
  • Monitor: HR, BP, ECG
160
Q

Class III: Potassium Channel Blockers

A
  • amiodarone (PO/IV)
  • dronedarone (PO)
  • sotalol (PO)
  • Ibutilide
  • Dofetilide
161
Q

adverse effects of Amiodarone (CLASS III)

A
  • Toxicity – lungs, liver, eyes, thyroid

- Photosensitivity

162
Q

monitoring points for amiodarone (CLASS III)

A
  • Hypotension

- Give through 0.22 micron filter

163
Q

adverse effects of dronedarone (CLASS III)

A
  • Photosensitivity

- Hepatotoxicity

164
Q

monitoring points for dronedarone (CLASS III)

A

Contraindicated in pregnancy

165
Q

monitoring points for dofetilde (CLASS III)

A

Initiated therapy in the hospital

166
Q

Monitoring points for Sotalol (CLASS III)

A

Class II and III agent – do NOT use like a typical beta-blocker

167
Q

Adenosine mechanism of action

A
  • ↓ automaticity of SA node
  • ↓ conduction through the AV node
  • Prolonged PR interval
168
Q

indication of adenosine

A
  • Termination of supraventricular tachycardia (SVT)

- NOT for treatment of afib or aflutter

169
Q

pharmacokinetics of adenosine

A
  • EXTREMELY short half-life (2 to 10 seconds)

- Must be given IV push

170
Q

adverse effects of adenosine

A
  • Momentary asystole

- Chest discomfort

171
Q

Drug interactions of adenosine

A
  • Methylxanthines (E.g. theophylline) – block adenosine receptors
172
Q

Types of Angina

A
  • chronic stable
  • variant (prinzmetal’s)
  • unstable
173
Q

what is chronic stable angina

A
  • Caused by coronary artery disease (CAD), in which PLAQUES cause PARTIAL occlusion of the vessel
174
Q

what are chronic stable angina triggered by

A
  • Increase in physical activity (most common)
  • Emotional excitement
  • Large meals
  • Cold exposure
175
Q

treatment approach for chronic stable angina

A
  • Decrease myocardial oxygen demand

- Increase myocardial oxygen supply

176
Q

non-drug interventions of chronic stable angina

A
  • Avoid precipitating factors
  • Smoking cessation
  • Exercise
  • Healthy diet
177
Q

Therapeutic agents: chronic stable angina

A

All medications work by decreasing myocardial oxygen demand

  • Organic nitrates
  • Beta-blockers
  • Calcium channel blockers

-/+ ranolazine

178
Q

what is variant angina

A

Caused by coronary artery SPASM (VASOSPASM) which decreases blood flow resulting in decreased oxygen supply

179
Q

variant angina precipitating factors

A

NO precipitating factors

  • Can occur at rest, while sleeping, or during normal activity
180
Q

treatment approach for variant angina

A
  • Decrease Incidence and severity of attacks with drug therapy that increase oxygen supply
181
Q

therapeutic agents variant angina

A
  • Calcium channel blockers
  • Organic nitrates
  • Beta-blockers and ranolazine are INEFFECTIVE
182
Q

INEFFECTIVE Beta-blockers and ranolazine is part of what angina

A

variant angina

183
Q

what is unstable angina

A

CAD complicated by vasospasm.

  • a plaque ruptures causing a clot that partially occludes the vessel
  • Medical emergency with higher risk of death than stable angina
184
Q

Presentation of unstable angina

A
  • Symptoms at rest
  • New-onset exertional angina
  • Intensification of existing angina
185
Q

therapeutic approach unstable angina

A
  • Maintain oxygen supply

- Decrease oxygen demand

186
Q

Therapeutic Options unstable angina

A 
- Anti-ischemic therapy:
	Organic nitrates
	Beta-blocker
	Oxygen
	IV morphine
- Anti-platelet therapy:
	Aspirin
	Clopidogrel, ticagrelor or prasugrel
187
Q

Nitrates mechanism of actions

A
  • Converted to nitric oxide using sulfhydryl group

- Acts primarily on cells of vascular smooth muscle (VSM)

188
Q

nitrates physiologic effects

A
  • Vasodilation

GREATER EFFECTS ON VEIN than arteries

  • Nitroglycerin is the oldest and most commonly used
189
Q

nitroglycerin Mechanism of action in STABLE angina:

A
  • Vasodilates veins which REDUCES VENOUS RETURN to the heart and REDUCES preload leading to decreased oxygen demand
190
Q

nitroglycerin Mechanism of action in VARIANT angina:

A
  • Relaxes spasms in the coronary arteries which helps increase oxygen supply
191
Q

pharmacokinetics of nitroglycerin

A 
- Extremely lipid soluble
	Allows it be administered by uncommon routes (ie. transdermal, ointments, sprays, sublingual)
- Rapidly metabolized by the liver 
	Large first-pass effect
- Short half-life (5-7 minutes)
192
Q

adverse effect of nitroglycerin

A
  • Headache
  • Orthostatic hypotension
  • Reflex tachycardia
193
Q

drug interactions of nitroglycerin

A
  • Anti-hypertensive agents
  • Phosphodiesterase-5 (PDE5) inhibitors
    Sildenafil (Viagra), Tadalafil (Cialis) and Vardenafil (Levitra)
  • Beta-blockers
  • Non-dihydropyridine calcium channel blockers
194
Q

Isosorbide mononitrate (ER)

A

given twice daily

195
Q

Isosorbide dinitrate (IR)

A

given three times daily

196
Q

what are Ranolazine

A

first-line or add-on therapy to beta-blockers, CCBs or nitrates

197
Q

adverse effects of ranolazine

A
  • QT prolongation
  • Elevation in BP
  • Constipation, dizziness, nausea, headache
198
Q

drug interactions ranolazine

A
  • CYP3A4 inhibitors
  • QT prolonging drugs
  • CCB - can inhibit CYP 3A4 - ecept amlodipine
199
Q

myocardial infarction complete block

A

STEMI

200
Q

myocardial infarction incomplete block

A

NSTEMI

201
Q

routine therapy of STEMI

A 
M = morphine
O = oxygen
N = nitroglycerin
A = aspirin
B = beta- blockers
202
Q

Adjuncts to Reperfusion Therapy ANTICOAGULANTS

A
  • heparin
  • fondaparinux
  • bivalirudin
203
Q

Adjuncts to Reperfusion Therapy ANTIPLATELETS

A
  • thienopyridines
  • glycoprotein IIb/IIa inhibitors
  • Aspirin
204
Q

lipoprotein class

A 
VLDL = probably contribute to atherosclerois 
LDL = bad cholesterol = contribute to atherosclerosis
HDL = protect against atherosclerosis

VLDL is triglyceride
LDL AND HDL are cholesterol

205
Q

HMG-CoA Reductase Inhibitors drugs

A
  • Atorvastatin
  • Rosuvastatin
  • Lovastatin
  • Pravastatin
  • Simvastatin
206
Q

HMG-CoA Reductase Inhibitors pharmacokinetics

A
  • Administered orally

- Metabolized by the liver (CYP3A4

207
Q

drug-drug interaction HMG-CoA Reductase Inhibitors

A
  • other lipid-lowering drugs
  • Drugs that inhibit CYP3A4

CONTRAINDICATED IN PREGNANCY

208
Q

counseling points for HMG-CoA Reductase Inhibitors

A
  • Take medication in the evening at bedtime
  • Maximal effects seen in 4 to 6 weeks
  • Continue treatment lifelong
209
Q

adverse effects of HMG-CoA Reductase

A 
Mild headache, rash, GI disturbances 
Myopathy and rhabdomyolysis
	Possible with ALL statins
	Measure CK at baseline and repeat if patient complains of muscle pain and weakness
Hepatotoxicity
	Rare
	Measure LFTs at baseline 
Memory Loss
	Transient
	True incidence and correlation unclear
Cataracts
210
Q

Bile Acid Sequestrants mechanism of action

A
  • Bile acids are needed for re-uptake of cholesterol into the blood stream
  • BAS binds to bile acids and prevent their physiologic action
211
Q

Bile Acid Sequestrants

A
  • Decrease LDL (15-30%)
  • Increase HDL
  • Possible transient increase in TG
212
Q

Ezetimibe mechanism of action

A
  • Decrease reabsorption of cholesterol in the small intestines
213
Q

Ezetimibe effects on lipids

A
  • Decrease Total cholesterol
  • Decrease LDL (19%)
  • Decrease TG (5-10%)
  • Possible modest increase in LDL
214
Q

indication of Ezetimibe

A
  • Adjunct therapy for decrease LDL
215
Q

adverse effects of ezetimibe

A
  • well tolerated

- rare - myopathy and rhabdomyolis, hepatitis

216
Q

drug to drug interactions of ezetimide

A
  • Statins
  • Fibrates - increase risk of gallstones
  • Bile acid sequestrants
217
Q

drugs of bile acid sequenstants

A
  • Colesevelam
  • Cholestyramine
  • Colestipol
218
Q

Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9 Inhibitors)

A
  • Alirocumab

- Evolocumab

219
Q

Mechanism of action: Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9 Inhibitors)

A
  • PCSK9-inhibitors PREVENT the binding of PCSK9 to LDLRand enhances clearance of LDL
220
Q

adverse effects of Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9 Inhibitors)

A
  • Hypersensitivity reactions

- Immunogenicity = Body may develop antibodies to the drug itself

221
Q

Niacin

A
  • B2 vitamin, also called nicotinic acid
  • As a vitamin, products are not regulated by the FDA
  • Thought to it may help decrease LDL and TG levels
  • Niacin has not been shown to improve CV outcomes in patients, thus no longer recommended for use
222
Q

niacin adverse effects

A

flushing

223
Q

DDI fibric acid derivatives

A

increase risk of myopathy when combined with a statin

224
Q

fibric acid derivatives drugs

A

Gemfibrozil
Fenofibrate
Fenofibric acid

Most effective drugs for lowering TG levels
Also known as ‘fibrates’
No proven mortality benefit
Third-line agents for lowering lipid levels

225
Q

fish oil drugs

A
  • Lovaza
  • Vascepa

Goal to have 1 gram/day minimum beneficial oils to maintain a healthy heart:
Docosahexaenoic acid (DHA)
Eicosapentaenoic acid (EPA)
Effective for lowering TGs (20-50%)
Used as adjunct therapy for lowering TGs
Counseling points:
Can cause fishy burps, can freeze capsules to help prevent this

226
Q

Stage C heart failure

A

Symptoms AND structural heart damage

227
Q

drugs of stage C and D heart failure

A

ACE-i/ ARB/ARNI drugs

  • Beta-blocker diuretics
  • /+ digoxin or aldosterone antagonist
228
Q

stage D heart failure

A

Refractory HF requiring specialized intervention

PHARMACOLOGY (7 decks)

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