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Pharmacology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Penicillin’s

  • MOA
  • SE
  • Coverage
A

Bactericidal–interfere with cell wall synthesis
SE: hypersensitivity, GI distress, seizures, encephalopathy
Mostly G+ coverage
Some G- coverage

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2
Q

Cephalosporins

  • Method of action
  • SE
  • Coverage
A

Bactericidal–interfere with cell wall synthesis
SE: hypersensitivity, GI distress
As you progress from 1st to 4th generation, has more G- and less G+ coverage

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3
Q

Aminopenicillins

  • Method of action
  • SE
  • Coverage
A

Amoxicillin (oral) and ampicillin (IV)
Bactericidal-interfere with cell wall synthesis
Good for G+ but also can treat some G-
Good for sinusitis, OM, lyme disease, H. Pylori, listeria meningitis

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4
Q

Monobactams

  • Method of action
  • SE
  • Coverage
A

Aztreonam
Bactericidal–interfere with cell wall synthesis
SE: GI distress, usually no cross-sensitivity with penicillin or cephalosporin
Primarily against G-

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5
Q

Carbapenems

  • Method of action
  • SE
  • Coverage
A 
Imipenem, meropenum, doripenum
most broad spectrum agents available
Bactericidal--interfere with cell wall synthesis 
SE: neurotoxicity, GI distress
G+ , G-,
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6
Q

Fluoroquinolones

  • Method of action
  • SE
  • Coverage
A

-Floxacin
Bactericidal–Inhibit DNA gyrase and topoisomerase IV
SE: GI distress, dizziness, confusion, tendon rupture, QT prolongation
G+ and G-

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7
Q

Macrolides

  • Method of action
  • SE
  • Coverage
A

Erythromycin, azithromycin, clarithromycin
Bacteriostatic–binds to 50S
SE: GI distress, hepatotoxicity, ototoxicity
May cause QT prolongation
DOC for atypical pneumonia/CAP and chlamydia
Broad spectrum: G+, G-, Atypical

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8
Q

Aminoglycosides

  • Method of action
  • SE
  • Coverage
A

entamicin, Neomycin, Streptomycin, Tobramycin
Bacteriostatic–binds to 30S
SE: Nephrotoxicity and ototoxicity
Mainly active against G-
Can combine with beta lactams for G+ coverage
Monitor renal function and levels

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9
Q

Tetracyclines

  • Method of action
  • SE
  • Coverage
A

Bacteriostatic–binds to 50S
SE: GI distress, gray-brown discoloration of the teeth, photosensitivity
Broad spectrum–G+, G-, atypical
Can be used for acne, walking pneumonia, chlamydial infections and PID, tick infections

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10
Q

Sulfonamides

  • Method of action
  • SE
  • Coverage
A

Bacteriostatic–inhibits folic acid
SE: GI distress, rash, fever, steven johnson syndrome and vasculitis
G+ and G- (except pseudomonas and GAS)

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11
Q

Vancomycin

  • Method of action
  • SE
  • Coverage
A

Bactericidal–inhibits d-alanyl-d-alanine portion of cell wall
SE: fever, chills, phlebitis, red man syndrome, nephrotoxicity
Active mostly against MRSA

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12
Q

Oxazolidinones

  • Method of action
  • SE
  • Coverage
A 
Linezolid + Tedizolid
Oral tx for MRSA 
Bacteriostatic--bind to 50S 
se: GI distress, thrombocytopenia, leukopenia 
G+ only--MRSA, VRE
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13
Q

Clindamycin

  • Method of action
  • SE
  • Coverage
A

Bacteriostatic–binds to 50S
SE: diarrhea and C. DIff colitis
Active against G+ and G- anaerobic
Used for anaerobic respiratory infections, skin infections, PID

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14
Q

Metronidazole

  • Method of action
  • SE
  • Coverage
A

Bactericidal–inhibition of DNA protein synthesis
SE: GI distress, seizures, peripheral neuropathy
G- coverage only
DOC for abdomen and GU system (H Pylori, C. Diff, bacterial vaginosis, trich)

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15
Q

Chloramphenicol

  • Method of action
  • SE
  • Coverage
A

Variably bactericidal–binds to 50S
SE: Gray baby syndrome, optic neuritis, fatal aplastic anemia
Broad spectrum: G+, G-, anaerobic

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16
Q

Rifampin

  • Method of action
  • SE
  • Coverage
A

Variably bactericidal–inhibits DNA
SE: GI distress, headache, fever, discolors body fluids to orange
Mostly against G+ with some G- coverage
DOC for TB

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17
Q

Nitrofurantoin

A

Variably bactericidal–interferes with cell wall synthesis
SE: N/V and pulmonary reactions, hepatotoxicity, peripheral neuropathy
Only used for uncomplicated UTI

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18
Q

First line treatment for HSV-1

A

Topical acyclovir or penciclovir

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19
Q

Second line treatment for HSV-1

A

Systemic acyclovir, famciclovir, valacyclovir

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20
Q

First line treatment for VZV

A

Systemic antiviral if <72 hours from outbreak or patient is immunocompromised

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21
Q

Treatment of warts

A

Salicyclic acid
Keratolytic peeling agent
CI in diabetes or impaired circulation

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22
Q

Medications that may cause an increase in blood pressure

A

Oral contraceptives, nicotine, steroids, appetite suppressants, TCA’s, cyclosporine, NSAID’s, some nasal decongestants

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23
Q

Diagnostic criteria for hypertension

A

> 150/90 in adults >60
140/90 in adults <60
Must have 3 readings at least 1 week apart

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24
Q

When to initiate emergency BP treatment

A

If above 180 systolic

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25
Q

3 factors associated with resistant hypertension

A

Obesity, impaired renal function, diabetes

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26
Q

Hypertension in blacks

A

Occurs at an earlier age, more severe, results in organ damage more often

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27
Q

Isolated or predominant systolic hypertension is secondary to

A

Aorta artery stiffening secondary to advancing age

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28
Q

Main causes of secondary hypertension

A

CKD, renovascular hypertension, hypothyroidism, hyperparathyroidism, pheochromocytoma, sleep apnea, primary aldosteronism

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29
Q

Stimulation of alpha 1

A

Vasoconstriction of arterioles and veins

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30
Q

Stimulation of beta 2

A

Vaso dilation

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31
Q

Stimulation of beta 1

A

Increase in HR and contractility

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32
Q

What to avoid before BP readings

A

Smoking 30 minutes before and caffeine 1 hour before

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33
Q

Goals of BP treatment

A

<140/90 for general population
<130/80 for people with co-morbidities
Follow up every month until BP is at goal and then every 3-6 months

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34
Q

Tx for hypertension without compelling indications

A

Stage 1: thiazide diuretics for most; can consider ACEI, ARB, Beta blocker, calcium channel blocker
Stage 2: combination of drugs including a thiazide diuretic

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35
Q

Tx for hypertension for diabetics

A

ACEI or ARB

Can combine with calcium channel blocker, thiazide diuretic or beta blocker

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36
Q

Tx for hypertension for CKD

A

ACEI or ARB

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37
Q

Tx for hypertension for CAD

A

ACEI or ARB

+ Beta blocker if recent MI or angina

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38
Q

Tx for hypertension for heart failure

A

ACEI + beta blocker + loop diuretic

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39
Q

Tx for hypertension for African American

A

Thiazide diuretic or calcium channel blocker or combination

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40
Q

What to monitor with thiazide diuretics

A

Serum electrolytes, glucose, uric acid
Excessive fluid loss
Sexual dysfunction

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41
Q

What to monitor with calcium channel blockers

A

Headache, dizziness, peripheral edema, drug interactions (grapefruit juice, clarithromycin, erythromycin)

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42
Q

What to monitor with ACEI and ARBs

A

BUN, Cr, potassium

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43
Q

Thiazide diuretics

  • MOA
  • SE
  • CI
A

Hydrochlorothiazide
inhibit reabsorption of Na + Cl in distal tubules
Takes several days for effect
Causes potassium and bicarb excretion but decreased Ca excretion
Causes uric acid retention
CI: Allergy to sulfa, anuria
Preg Cat B
SE: hypokalemia, hypomagnesia, hypercalcemia, hyperuricemia, hyperglycemia, tinnitus, paresthesia, N/V, diarrhea, impotence, hyperlipidemia, anorexia

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44
Q

Loop diuretics

  • MOA
  • SE
  • CI
A

Bumetanide, furosemide, torsemide
Inhibits reabsorption of Na + Cl at proximal and distal tubules and loop of Henle
Indicated for edema d/t CHF, hepatic cirrhosis, renal disease
CI: anuric or severe electrolyte depletion and allergy to sulfa
Preg Cat C
SE: Hypocalcemia, hypokalemia, hypomagnesia
Reserved for patients with renal dysfunction over thiazide diuretics

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45
Q

Potassium sparing diuretics

  • MOA
  • SE
  • CI
A

Amiloride, Spirinolactone
Interfere with sodium reabsorption at distal tubule, decreasing K+ secretion
True benefit for HF patients
CI: severe renal impairment, K+>5, acute renal insufficiency, anuria, Addison’s disease
SE: gynecomastia, hyperkalemia, hyponatremia, hirsutism, menstrual irregularities, drowsiness, confusion, headache, rash

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46
Q

First line diuretic for uncomplicated hypertension

A

Thiazide

Loop is second (especially if renal dysfunction)

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47
Q

Treatment considerations of potassium sparing diuretics

A

Use in combination with thiazides to augment diuresis and blunt hypokalemic effects

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48
Q

Beta Blockers MOA

A

Block central and peripheral beta receptors–results in decreased cardiac output and sympathetic outflow

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49
Q

Selective beta blockers

A

A-M
Better for patients with asthma, COPD, and peripheral vascular disease
At higher doses, lose cardioselectivity and may aggravate bronchospasm

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50
Q

Beta blockers with intrinsic sympathomimetic activity

A

Pindolol and Acebutolol
Reduce HR and contractility during excessive sympathetic outflow, but in resting states HR and contractility are maintained

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51
Q

Beta blockers in CHF

A

Decreases mortality and decreases vascular remodeling

Discontinue if patient has acute decompensation

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52
Q

Tapering of beta blockers

A

Taper gradually over 14 days when discontinuing to prevent withdrawal symptoms–unstable angina, MI, death

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53
Q

Beta blockers are CI in

A

Sinus bradycardia, asthma, COPD, AV block, cardiac failure, Severe PVD

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54
Q

Pregnancy category for beta blockers

A

Cat C

But best for lactation

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55
Q

In diabetic patients, beta blockers

A

Can mask all symptoms of hypoglycemia with the exception of sweating

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56
Q

ACE Inhibitors MOA

A

-pril
Inhibits ACE enzyme, which decreases production of angiotensin II (decreases vasoconstriction and decreases aldosterone effects of water retention)
Also inhibits degradation of bradykinin and increases synthesis of vasodilating prostaglandins

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57
Q

ACEI CI in

A

Bilateral renal artery stenosis + pregnancy (cat d)

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58
Q

SE ACEI

A

Chronic dry cough, rashes, dizziness, angioedema

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59
Q

ACEI decreases mortality in patients with

A

CHF, post MI, and systolic dysfunction

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60
Q

ARB’s MOA

A

-sartan

Block vasoconstriction and aldosterone secreting effects of angiotensin II by blocking angiotensin receptor

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61
Q

ARBs indicated for

A

Hypertension, nephropathy in type 2 DM, heart failure, those who can not tolerate ACEI

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62
Q

SE ARBs

A

Dizziness, upper respiratory tract infections, cough, viral infection, fatigue, pharyngitis, rhinitis

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63
Q

Red flags with ACEI or ARB’s

A

Swelling, SOB, difficulty swallowing, hives, uritcaria, fainting, cloudy urine ,sore throat, abdominal pain, irregular HR, leg weakness, numbness and tingling, extreme nervousness

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64
Q

Renin Inhibitors

A

Aliskiren
Blocks conversion of angiotensinogen to angiotensin I
CI in pregnancy (Cat X)
SE: diarrhea and rare angioedema

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65
Q

Ca channel blockers MOA

A

Inhibits movement of Ca ions across the cell membrane, which causes cardiovascular relaxation and vasodilation
CI in pregnancy Cat C

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66
Q

Non-dihydropyridine Ca Channel blockers

A

Verapamil + Diltiazem
Decrease HR + slow conduction at AV node
Avoid in patients with AV block and caution with heart failure
SE: GI upset, peripheral edema, hypotension

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67
Q

Dihydropyridine Ca channel blockers

A

-dipine
Potent vasodilators
SE: headache, flushing, palpitations, peripheral edema, gingival hyperplasia (nifedipine)

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68
Q

Recommended for use of ca channel blockers

A

Blacks, hypertension associated with ischemic heart disease, prinzmetal angina

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69
Q

Special factors of nifedipine

A

Cause potent peripheral vasodilation–most likely to cause peripheral edema

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70
Q

Special factors of amlodipine

A

Best for blacks, elderly, people with high cholesterol

Not likely to cause peripheral edema

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71
Q

Peripheral alpha 1 blockers

A

-zosin
Effective in BPH and not usually prescribed for htn
Dilates arterioles and veins
CI in presence of cardiovascular disease
Relaxes smooth muscle in bladder neck + prostate
SE: first dose phenomenon, vivid dreams and depression

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72
Q

Central alpha 2 agonists

A

Clonidine, methyldopa, guanabenz, guanfacine
Decreases release of NE
May cause fluid retention (can combine with diuretic)
Usually used in STAT management of htn
Do not abruptly stop
SE: fluid retention, sedation, dry mouth, dizziness, syncope

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73
Q

Direct vasodilators

A

Hydralazine + Minoxidil
Arteriolar smooth muscle relaxation
Reserved for essential or severe hypertension
May cause fluid retention and reflex tachycardia (combine with beta blocker and diuretic)
SE: dermatitis, drug fever, peripheral neuropathy

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74
Q

Direct vasodilators CI in

A

CAD, acute MI, aortic aneurysm

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75
Q

Adrenergic antagonists

A

Resperine, guanethidine, guanadrel
Inhibits SANS by decreasing NE stores
May cause depression

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76
Q

DOC for htn in pregnancy

A

Methyldopa

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77
Q

Medications used in hypertensive emergency

A 
Hydralazine
Nitrates 
Nicardipine + Clevidipine
Labetalol + Esmolol
Phentolamine
Enalapril
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78
Q

Contributing factors to hyperlipidemia

A

Beta blockers, oral contraceptives, diabetes, pregnancy, diets high in fat and cholesterol, lack of exercise, obesity, smoking, hypertension, age

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79
Q

Chylomicrons

A

largest lipoproteins, composed mainly of triglycerides

Produced in the guy from dietary fat and cholesterol

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80
Q

VLDL

A

Composed of cholesterol and triglycerides

Converted to LDL when triglyceride content decreases

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81
Q

LDL

A

Contains mostly cholesterol

50% taken up by the liver and 50% taken up by the peripheral cells

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82
Q

Primary symptom of atherosclerosis

A

Angina–due to compromised blood flow

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83
Q

4 major statin benefit groups

A
  1. Have clinical atherosclerotic cardiovascular disease
  2. No disease but LDL >190
  3. No disease, 40-75 yo, DM, LDL 70-189
  4. No disease, 40-75 yo, LDL 70-189, 10 year risk of disease >7.5%
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84
Q

If patient is not having an expected response to statins…

A

Monitor every 3-12 months for continued assessment

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85
Q

Most common complaint with statins

A

Muscle related–increases risk of myopathy
If symptoms resolve after discontinuation and patient has no other CI, Restart the same statin at a lower dose or different statin at a low dose

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86
Q

Statin MOA

A

Block conversion of HMG-CoA to mevalonate–rate limiting step in production of cholesterol by the liver
Increases number of LDL receptors on liver
Decreases triglyceride levels and moderately increases HDL
Maximum effect after 4-6 weeks
Best to take at night time

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87
Q

Statin CI

A

Pregnancy, breastfeeding, active liver disease

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88
Q

Ezteimibe

A

Cholesterol absorption inhibitor at the brush border of small intestine; decreases delivery of cholesterol to liver and increases clearance of cholesterol from blood
Complements statins

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89
Q

Cholestytramine

A

Bile acid resins
Bind bile acids in the intestines to be excreted in feces–decreases return of cholesterol to the liver and increases LDL receptors
Increases triglyceride levels
Max effect seen in 3 weeks
Adjunct therapy to diet therapy
Not absorbed systemically–do not need to monitor liver levels
SE: bloating, abdominal pain, heartpain, constipation

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90
Q

Bile acid resins CI in

A

biliary obstruction, chronic constipation, triglycerides >300

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91
Q

Niacin

A

B vitamin–take in higher doses
Decreases VLDL synthesis, inhibits lipolysis in adipose tissue, increases lipoprotein lipase activity
Decreases triglycerides and LDL and increases HDL
Most people can not tolerate adverse effects–pruritus and flushing

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92
Q

Niacin CI

A

Hepatic dysfunction, severe hypotension, hyperglycemia, gout, A Fib, peptic ulcers

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93
Q

Baseline monitoring for niacin

A

Glucose and uric acid levels

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94
Q

Fibric acid derivatives

A

Gemfibrozil + Fenofibraic
Mainly affects triglycerides and HDL
CI in history of gallstones + severe hepatic/renal dysfunction
SE: Myopathy when combined with statins, hepatotoxicity, cholestatic jaundice, leukopenia, anemia, thrombocytopenia

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95
Q

First, second, third line for hyperlipidemia

A

First: statins
Second: cholesterol absorption inhibitors, niacin, bile acid resins
Third: fibric acid derivatives

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96
Q

S/S angina

A

Left sided chest pain, discomfort, heaviness or pressure, sensation radiating to back, jaw, neck, throat or arms lasting 1-15 minutes, SOB, fatigue

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97
Q

Modifiable risk factors for angina

A

Cigarette smoking, hypertension, dyslipidemia, diabetes, obesity, physical inactivity

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98
Q

Non-modifiable risk factors for angina

A

Age, heredity, men

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99
Q

Atherosclerosis pathophys

A

Fatty streak –> fibrous plaque –> complicated lesion

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100
Q

Nonpharmacologic therapy for angina

A

Decrease weight, smoking cessation, exercise

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101
Q

Drug choices for angina

A

ACEI/ARBs, nitrates, beta blockers, calcium channel blockers, antiplatelet therapy

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102
Q

What should you assess when starting someone on an ACEI or ARB

A

Renal function and serum potassium within 1-2 weeks of starting

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103
Q

ACEI + Lithium

A

Patients taking lithium and ACEI are at increased risk of toxicity due to decreased renal excretion

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104
Q

Nitrates MOA

A

Decreases preload through dilation of veins and decreases afterload by causing dilation of arteries
Increases blood flow and O2 supply to myocardium through artery dilation
SE: headache, flushing, dizziness, weakness, orthostatic hypotension, reflex tachycardia
Do not stop abruptly–can cause rebound hypertension

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105
Q

Sublingual nitroglycerine

A

Nitrol + Isordil
First line therapy for managing angina acutely
Relieves in 1-5 minutes

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106
Q

Long acting nitrates

A

Isosorbide Dinitrate, isosorbide mononitrate, nitroglycerine (transdermal)
Used for chronic prophylaxis of angina

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107
Q

Nitrate tolerance

A

Can occur in 7-10 days

Have one 10-12 hour nitrate free interval per day

108
Q

CI combo of nitrate +

A

Phosphodiesterase-5 inhibitors (viagra)

109
Q

Beta blockers particularly helpful for what type of angina

A

Exertional angina

Decreases HR + contractility which decreases the workload of the heart and decreases O2 demand

110
Q

Aspirin

A

Irreversible enzyme antagonism to block prostaglandin synthesis–blocks formation of TAX-2
Recommended to take 75-162mg daily for patients with acute/chronic ischemic heart disease
SE: dyspepsia, bruising, bleeding

111
Q

Clopidogrel

A

Decreases ADP induced platelet activation

112
Q

First line, second line, third line for chronic prophylaxis angina

A

All patients should receive daily aspirin and short acting nitrate for acute attacks
First: beta blockers
Second: beta blocker + calcium channel blocker or long acting nitrate
Third: 3 drug combination

113
Q

Highest risk factors for heart failure

A

CAD, hypertension, cardiomyopathy

Other risk factors: acute MI, arrhythmias, pulmonary embolism, sepsis

114
Q

Drugs that may worsen heart failure

A

NSAIDs, steroids, hormones, antihypertensives, sodium containing drugs, lithium, amphetamines, cocaine, alcohol

115
Q

S/S left sided heart failure

A

Cough, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, nocturia
Cardiomegaly, S3 heart sound, signs of pulmonary edema, tachycardia, increased RR

116
Q

S/S right sided heart failure

A

Peripheral pitting edema, abdominal pain, anorexia, bloating, constipation, nausea, vomiting
Hepatomegaly, distention of jugular veins, hepatojugular reflex, signs of portal htn, ascites, splenomegaly

117
Q

4 levels of heart failure

A
  1. No limitation of physical activity
  2. Slight limitation; comfortable at rest
  3. Marked limitation; less than ordinary activity causes dyspnea
  4. Unable to carry out physical activity without symptoms; symptoms present at rest
118
Q

In patients with a history of reduced ejection fraction, what can be used to prevent HF

A

ACEI or ARBs

119
Q

In patients with an MI and reduced ejection fraction, what should be given to prevent HF

A

Beta blockers

120
Q

Which ACEI have been shown to prolong survival for patients with LV dysfunction

A

Enalapril, Captopril, Lisinopril

121
Q

ACEI for heart failure

A

indicated for patients who present with fatigue or mild dyspnea on exertion and who do not have any other signs of symptoms of volume overload
Decreases preload and afterload, increases cardiac index and increases ejection fraction

122
Q

Diuretics for heart failure

A

Loop diuretics are more potent
Combine with ACEI and beta blocker
Decreases preload by reducing volume overload
Dose is increased until urine output increases and weight decreases
NSAIDs may decrease effects
May decrease lithium clearance

123
Q

ARBs for heart failure

A

Decreases blood pressure, decreases vascular resistance, decreases pulmonary capillary wedge pressure, decreases HR, and increases cardiac index
Decreases HF exacerbation

124
Q

Beta blockers for heart failure

A

Metoprolol, Bisoprolol, Carvedilol
All patients with stage 2-4 HF should receive
Should not be used in unstable patients or acutely ill patients
Symptomatic improvement may not be seen for 2-3 months

125
Q

Digoxin

A

Can prevent clinical deterioration in patients with heart failure but does not decrease mortality
Mild inotropic effect by inhibiting cell membrane Na/K ATPase, increases Ca entry into the cell, and increases force and velocity of contraction
Must monitor renal function

126
Q

Signs of digoxin toxicity

A

N/V, anorexia, headache, fatigue, disorientation, confusion, seizures, arrhythmias

127
Q

Digoxin should be discontinued if the following occur

A

Elevated digoxin level, substantial reduction in renal function, toxicity symptoms, conduction abnormality, increase in arrhythmias

128
Q

Drugs that will increase digoxin levels

A

Quinidine, amiodarone, flexainide, propafenone, spironolactone, verapamil, antibiotics, anticholinergics

129
Q

Drugs that decrease digoxin levels

A

Antacids, cholestyramine, neomycin, kaolin-pectin

130
Q

First, second, third line for HF

A

First: ACEI with or without a diuretic depending on fluid retention
Second: ACEI + beta blocker + diuretic (loop preferred)
Third: ARB + beta blocker + aldosterone antagonist + diuretic + digoxin

131
Q

Pediatrics tx of HF

A

Class I: IV inotropes (not digoxin) + IV diuretics
Class II: + Digoxin
Class III: + O2

132
Q

Monitoring for heart failure

A

Serum electrolyte levels, renal function, blood pressure, weights

133
Q

Conditions that may cause arrhythmias

A

myocardial ischemia, chronic HF, hypertension, valvular heart disease, hypoxemia, thyroid abnormalities, electrolyte disturbances, drug toxicity, increased caffeine, increased alcohol, anxiety, exercise

134
Q

Phases of cardiac AP

A

Phase 0: Rapid depolarization due to influx of Na
Phase 1: brief initial repolarization due to inactivation of inward Na and activation of outward K
Phase 2: plateau period no change in potential
Phase 3: repolarization due to K efflux
Phase 4: depolarization of cell with Na leaking into cell as K leaves

135
Q

Catecholamine stimulation leads to

A

Shorter AP duration

136
Q

Vagal stimulus and endogenous purines leads to

A

Inhibition of depolarization

137
Q

After-depolarization

A

Abnormal impulse formation due to intracellular calcium overload
May occur in response to hypothermia, electrolyte imbalance, catecholamine excess, or stress

138
Q

Supraventricular arrhythmias

A

Atria, SA and AV nodes
Not usually life threatening but can lead to decreased ventricular filling and decreased CO
Ex: sinus tachy, PSVT, sinus brady, A fib, A tach

139
Q

Ventricular arrhythmias

A

Originate in ventricles or bundle of His
Usually symptomatic and require immediate intervention
Ex: Premature ventricular contractions, v tach, v fib, tdp

140
Q

Risk factors for arrhythmias

A

Previous CAD, MI, cardiomyopathy, hypertension, valvular heart disease, alcohol or drug use

141
Q

Class 1 AAD’s

A

Na channel blockers

142
Q

Class 1A

A

Procainamide, quinidine, disopyramide
Intermediate onset/offset
Treatment of supraventricualr and ventricular arrhythmias
Widens QRS complex, prolongs QT and PR
Potent anticholinergic effects
Blocks alpha 1- can cause vasodilation and hypotension
SE: GI distress, tdp, hemolytic anemia, AV block, hypotension

143
Q

Class 1B

A

Lidocaine + Mexiletine
Fast onset/offset
Decreases automaticity + conduction velocity + shortens refractoriness
Primarily effects ventricular myocardium–selective to ischemic tissue
Eliminated via liver
SE: CNS dizziness, paresthesia, disorientation, tremor, agitation

144
Q

Class 1c

A

Flecainide + Propafenone
Slow onset and offset
Most used for supraventricular arrhythmias
Potent negative inotropic effects
SE: blurred vision, dizziness, headache, tremor, nausea, vomiting, bronchospasm, heart block, ventricular arrhythmias

145
Q

Class 2 AAD

A

Beta blockers
Useful for ventricular and supraventricular arrhythmias
Helpful when combined with other AAD’s
Decreases O2 consumption, decreases HR, decreases BP, decreases contractility and CO

146
Q

Class 3 AAD

A

Amiodarone, dronedarone, sotalol, dofetilide, ibutilide
K+ channel blockers
Used to treat a Fib primarily
Prolong QT interval

147
Q

Amiodarone

A

Has characteristics of all 4 AAD classes
no negative inotropic effects
Approved for life threatening recurrent ventricular arrhythmias
Requires loading dose, large Vd and high lipophilicity–potential to accumulate and cause adverse effects in numerous organs
Perform thyroid function tests every 6 monyhs and assess pulmonary function annually
SE: optic neuritis, GI distress, tdp

148
Q

Dronedarone

A

Shorter half life than amiodraone
CI in HF
No loading dose needed

149
Q

Sotalol

A

Reverse use dependence effects
Can maintain SR in patients with A Fib
Eliminated by kidneys–assess renal function routinely
Most SE due to beta blocking ability

150
Q

Class 4 AAD

A

Non-dihydropyridine calcium channel blockers
Verapamil + Diltiazem
Used for supraventricular arrhythmias
Slows conduction and prolongs refractoriness
Negative inotropic and chronotropic effect
CI in HF

151
Q

Digoxin as AAD

A

Stimulates PANS–Increases vagal tone and slows conduction

Used primarily to slow ventricualr rate in supraventricular arrhythmias

152
Q

Electrolyte imbalances that can precipitate digoxin toxicity

A

Hypokalemia, hypomagnesia, hypercalcemia

153
Q

Adenosine

A

Converts PSVT to SR

Activates potassium channels – hyperpolarizes membrane, which decreases spontaneous nodal depolarization

154
Q

Atropine

A

Enhances both sinus nodal automaticity and AV nodal conduction for use in symptomatic bradycardia

155
Q

First line treatment for A Fib

A

Goal: control ventricular rate
If hemodynamically unstable, immediate DCC
If hemodynamically stable:
-Normal LV systolic function: IV diltiazem, verapamil or beta blocker
-EF<40%: IV beta blocker or digoxin
-IV amiodarone for ventricular rate control

156
Q

Second line treatment for A Fib

A

If it persists, DCC or give warfarin as anticoagulant for 2-3 weeks and then cardioversion
PO diltiazem or verapamil or beta blocker or digoxin

157
Q

Treatment of paroxysmal supraventricular tachycardia

A

If hemodynamically unstable: DCC or vagal maneuvers
DOC is adenosine
If persistent, try IV diltiazem, verapamil or beta blocker

158
Q

Treatment of non-sustained ventricualr tachycardia

A 
Terminates within 30 seconds; drugs not necessary if asymptomatic 
If symptomatic: beta blockers, non-dihydropyridine calcium channel blockers, class 1C AAD
159
Q

Treatment for ventricular tachycardia

A

If unstable DCC
If stable: IV amiodarone, procainamide, or sotalol
After acute episode is terminated, ICD is indicated

160
Q

Treatment for pulseless VT/VF

A

CPR + AED
If persists, vasopressor therapy with epinephrine
If persists, DOC is IV amiodarone

161
Q

Treatment of bradycardia

A

IV atropine if s/s poor perfusion

If not effective, give dopamine or epinephrine through continuous infusion

162
Q

Pediatrics and arrhythmias

A

Usually due to respiratory origin
PSVT is most common–occurs in children with congenital heart disease
Bradycardia is ominous sign in seriously ill children

163
Q

What should you avoid when being treated with AAD

A

Licorice (Can cause hypokalemia), alcohol, excessive salt intake, caffeine

164
Q

Venous thromboembolism

A

Venous thrombi form due to venous stasis, vascular endothelial wall injury, and hypercoagulability (virchow triad)

165
Q

Risk factors for venous thromboembolism

A

Prolonged immobility, varicose veins, obesity, pregnancy, recent surgery, thrombophilia, central venous catheters, oral contraceptives, age >40

166
Q

Source of 90% of pulmonary embolisms

A

Lower extremity DVT

167
Q

Where do proximal DVT’s develop

A

in the popliteal, femoral or iliac veins above the knee

168
Q

Atrial fibrillation

A

Loss of coordination of electrical and mechanical activity in the atria
Thrombi can form in the left atrial appendage due to impaired ventricle filling and incomplete emptying of the atria
Clot may travel to brain–stroke

169
Q

Goals of tx of A Fib

A

Prevent TIA with anticoagulants, restore SR, control ventricular HR

170
Q

Risk factors for developing stroke with A Fib

A

History of stroke, increased age, hypertension, HF with impaired systolic function, DM

171
Q

Indications for prosthetic valve

A

Mitral stenosis, mitral regurgitation, aortic stenosis, aortic regurgitation
Valves in the mitral position are more thrombogenic than aortic
Mechanical prosthetics require lifelong anticoagulation

172
Q

Final step in clotting cascade

A

Formation of thrombin (IIa), which converts fibrinogen to fibrin to form a clot

173
Q

Platelets in clotting

A

Adhere to the site of injured blood vessels, attracting other platelets and forming large platelet aggregates that help stabilize the platelet-fibrin clot
When platelets are activated, receptors for clotting factors are exposed; this provides a stable environment for the initiation of the clotting cascade

174
Q

Extrinsic pathway

A

Initiated by components from blood

Factor 7 is initiating factor

175
Q

Intrinsic pathway

A

When blood comes into contact with a foreign surface, such as a prosthetic device
Factor 11 is initiating factor

176
Q

Both clotting pathways converge at

A

Factor 10

Converts prothrombin to thrombin

177
Q

Antithrombin III

A

Inhibits active clotting factors 2a, 7a, 9a, 10a, 11a, 12a

178
Q

Protein C, S, Z

A

Prevent excess clot formation by inactivating 5a and 8a

Deficiency in these proteins creates a predisposition to pathologic thrombosis

179
Q

Venous thrombi

A

Form in areas of sluggish blood flow and contain primarily red cells held together with fibrin

180
Q

Arterial thrombi

A

Form in areas of high blood flow and are composed primarily of platelets bound with fibrin strands

181
Q

S/S venous thromboembolism

A

Erythema, pain, swelling, venous distention, warmth
50% have no symptoms
Increased D-dimer >500

182
Q

Diagnostic method of choice for DVT

A

Compression ultrasonography

183
Q

S/S A fib

A

Palpitations, chest pain, SOB, weakness, decreased BP, dizziness, syncope, irregular pulse, irregular jugular venous pulsations
Absence of P waves

184
Q

Diagnostic tests for ischemic stroke

A

Blood glucose, electrolytes, CBC with platelets, ECG, cardiac enzymes, prothrombin time, INR, aPTT, O2 saturation
Non contrast CT or MRI to diagnose

185
Q

CI to anticoagulation

A

Recent hemorrhagic stroke, active major bleeding, recent trauma or surgery, immediate postop after CNS/ocular surgery, spinal catheters, aneurysms
Warfarin CI in pregnancy

186
Q

Heparin indications

A

Treatment of acute venous or arterial thrombosis and prophylaxis of VTE

187
Q

Un-fractionated Heparin MOA

A

Inhibits reactions that lead to clotting but does not alter concentration of normal clotting factors
Binds to antithrombin III and increases inactivation rate of intrinsic clotting cascade pathway (12, 11, 10, 9) and thrombin (2)
Prevents conversion of fibrinogen to fibrin
Can not inactivate clot-bound thrombin or activated factor X
Immediate onset
Must be given IV or SC

188
Q

Limitations of un-fractionated heparin

A

Variability in size, highly bound to plasma proteins, some people have heparin resistance, can cause heparin induced thrombocytopenia

189
Q

Lab monitoring for un-fractionated heparin

A

aPTT

190
Q

Low molecular weight heparin

A

Dalteparin, enoxaparin, tinzaparin
Produce major effect via thrombin and factor X
Long half life than un-fractionated
SC administration
Less binding to proteins
Less intense lab monitoring and more predictable effect than un-fractionated

191
Q

Lab monitoring for LMWH

A

Anti-Xa activity

192
Q

Warfarin MOA

A

Inhibits activation of clotting factors in liver than depend on vitamin K: 2, 7, 9, 10 and protein C, Z, S
Does not affect function of existing clotting factors or thrombus
Long offset of effect–8-14 days for full effect (must heparinize initially)
Causes a quick fall in protein C–temporary hypercoagulable state
Long half life

193
Q

Lab monitoring for warfarin

A

INR every 4-6 weeks
Narrow therapeutic index
Multiple drug-drug interactions

194
Q

Direct acting oral anticoagulants

A

Dabigatran, rivaroxaban, apixaban, edoxaban
Faster onset than warfarin
Adv: Fixed dosing, no dietary interaction, no intense monitoring
Disadv: No antidote, more expensive, faster offset

195
Q

Antidote of warfarin

A

Oral vitamin K, fresh frozen plasma, four factor prothrombin complex concentrates

196
Q

Antidote of heparin

A

Protamine sulfate

197
Q

Heparin induced thrombocytopenia

A

Anti-body mediated prothrombotic reaction
Diagnosed by ELISA antibody test
Discontinue heparin and give alternative anticoagulant

198
Q

Anti-platelet agents indications

A

Prevention and treatment of stroke, add on therapy to anticoagulants, prevent CV death, MI, or stroke following acute coronary syndrome

199
Q

Asprin MOA

A

Prevents prostaglandin synthesis in platelets by irreversibly inhibiting COX, which usually catalyzes conversion of arachidonic acid to TXA2)
Onset of effect is within 5 minutes
Effect lasts 7-10 days after discontinuing

200
Q

Clopidogrel

A

Inhibits ADP, which is a promoter of platelet receptor binding
Extensively metabolized by liver from prodrug
Common SE is diarrhea

201
Q

First line therapy for DVT or PE

A

Bolus IV of unfractionated heparin followed by continuous IV infusion
Injectable UFH/LMWH followed by warfarin or direct thrombin inhibitor for at least 3 months

202
Q

First line therapy for prophylaxis of DVT or PE

A

For patients undergoing orthopedic surgery

LMWH, Warfain, direct oral anticoagulants, aspirin

203
Q

First line for prevention of non-cardioembolic ischemic stroke and transient ischemic attack

A

First: aspirin
Second: Clopidogrel

204
Q

First line therapy for stroke prevention in nonvalvular atrial fibrillation

A

Warfarin or direct acting oral anticoagulant

205
Q

First line therapy for prophylaxis against systemic embolism in patients with prosthetic heart valves

A

Long term anticoagulation with warfarin alone or in combination with aspirin

206
Q

Potential causes of anemia

A

Blood loss, nutritional deficiency, malabsorption syndromes, sickle cell disease, thalassemia, hemoglobinopathy, treatment of cancer, HIV, hepatitis C

207
Q

Normal Hgb and MCV values

A

MCV: 80-96
Men Hgb: 13
Women Hgb: 12

208
Q

S/S of rapid onset of anemia

A

Tachycardia, light headedness, breathlessness

209
Q

S/S of chronic anemia

A

Fatigue, weakness, headache, vertigo, faintness, sensitivity to cold, pallor, loss of skin tone

210
Q

Smokers normal RBC values

A

Higher than normal levels of RBC’s

211
Q

Microcytic anemias

A

Thalassemia, iron deficiency, chronic disease, sideroblastic

212
Q

Normocytic anemias

A

Acute blood loss

213
Q

Macrocytic anemias

A

Folate or vitamin B12 deficiency

214
Q

Immediate therapy for acute post-hemorrhagic anemia/chronic blood loss

A

Hemostasis, restoration of blood volume, treatment of shock with blood transfusion

215
Q

Patients with sickle cell anemia are susceptible to

A

Infection, particularly strep pneumoniae and haemophilus influenzae

216
Q

Important education for patients with sickle cell anemia

A

Folic acid supplementation and vaccinations

217
Q

Hydroxyurea

A

Can be used for prophylaxis of sickle cell crises
Increases Hgb F, Increases water content of RBC, increases deformability of sickled cells and alters RBC adhesions
Do not use if pregnant

218
Q

SE of hydroxyurea

A

Myelosuppression, risk of cancer, cutaneous hyperpigmentation, alopecia, xerosis, nail pigmentation, leg ulcers

219
Q

Pain management for sickle cell crises

A

Hydration, aggressive pain relief with analgesics and opiates–NSAIDs, acetaminophen, morphine, hydromorphone

220
Q

Causes of iron deficiency anemia

A

Deficient diet, decreased absorption, pregnancy and lactation, blood loss, chronic alcoholism
Can be exacerbated by chronic intestinal blood loss due to parasitic and malarial infections

221
Q

Drugs that may cause iron deficiency

A

Fluoroquinolones, tetracyclines, H2 blockers, proton pump inhibitors, calcium supplements

222
Q

Diagnostic lab findings in iron deficiency anemia

A

Decreased serum iron, decreased ferritin, increased TIBC, decreased Hgb, decreased Htc
Low ferritin is earliest and most sensitive indication

223
Q

Treatment of iron deficiency anemia

A

Dietary supplementation and iron preparation

May take 6-8 weeks for hemaglobin to improve and 6 months to completely restore iron stores

224
Q

SE iron supplements

A

Discolored feces, anorexia, constipation or diarrhea, N/V

225
Q

What affects absorption of iron supplements

A

Vitamin C will increase
Milk and tea will decrease
Antacids, proton pump inhibitors and H2 antagonists will also decrease

226
Q

Indications for use of IV iron

A

Chronic bleeding, intestinal malabsorption, intolerance to oral iron, nonadherence, hemoglobin <6 with signs of poor perfusion

227
Q

Anemia of chronic renal failure

-Causes and Tx

A

Decreased EPO production by kidney due to decreased GFR

Give iron supplementation first, then treat reversible causes of decreased renal function, then give recombinant EPO

228
Q

Diagnostic lab findings in anemia of chronic disease

A

Decreased serum iron, decreased transferrin, decreased TIBC

229
Q

Tx of anemia of chronic disease

A

Increased doses of EPO administered subcu

230
Q

Tx of thalassemia

A

If severe, regular transfusions and folate supplementation

231
Q

Tx of vitamin B12 deficiency

A

Parenteral administration of B12–must receive every month for rest of life

232
Q

Tx of folate deficiency

A

Oral folate replacement until numbers are restored

233
Q

Tx for aplastic anemia

A

RBC transfusions and platelets given for bleeding, antibiotics given for infections
Severe forms may require hematopoietic stem cell transplant and immunosuppression therapy

234
Q

Geriatric Hgb <10

A

Negative outcomes–decreased physical performance, increased number of falls, increased frailty, decreased cognition, increased dementia, increased hospitalizations, increased mortality

235
Q

What makes fibric acid derivatives ineffective?

A

Alcohol

236
Q

Antidote to dabigratran (direct acting oral anticoagulant)

A

Idarucizumab

237
Q

Different types of iron supplements

A

Ferrous gluconate has less iron in it but causes less constipation than ferrous sulfate

238
Q

Sickling causes patients to be at high risk for

A

Pain, infection, gall stones, renal failure

239
Q

How long can you store B12 for

A

3 years
Deficiency is not an acute condition
Deficiency can cause permanent neurological issues

240
Q

How long can you store folate for

A

3 months

241
Q

Distinguish between folate and B12 deficiency

A

B12: increase in homocysteine and MMA
Folate: Increase in homocysteine onlu, normal MMA

242
Q

What do antiretrovirals do

A

Inhibit transcriptase

243
Q

Normal total cholesterol

A

Less than 200

244
Q

Normal LDL

A

Less than 130

245
Q

Normal triglyceride

A

Less than 150

246
Q

Normal HDL

A

Over 40

247
Q

Statins + calcium channel blocker requires

A

PT/INR monitoring due to risk of bleeding

248
Q

What cholesterol medication should not be dosed with a statin

A

Fibric acid derivatives

Unless under the care of a cardiologist

249
Q

Patient education for digoxin

A

Check HR before taking, routine lab work to check levels (dig toxicity and potassium)

250
Q

1st line agent for heart failure

A

ACEI

251
Q

Labs for hypertensive medications

A

Liver + renal, electrolytes

252
Q

If experiencing bad peripheral edema with nifedipine, switch to

A

Amlodipine

253
Q

If a patient has an allergic reaction to penicillin, give

A

Macrolide

254
Q

What antibiotic to give if pregnant

A

Macrolide

255
Q

Adenosine

A

Converts PSVT to SR
Activates potassium channels by increasing outward K+
current and hyper-polarizing membrane, which decreases spontaneous SA node depolarization

256
Q

Amiodarone

A

Class 3 AAD: K+ channel blocking
Has properties from all 4 classes
Good for treating ventricular arrhythmias orimarily
Many toxic side effects: pulmonary toxicity, retinal toxicity, liver, and thyroid toxicity
Prolongs QT interval

257
Q

DOC for lyme disease

A

Doxycycline

258
Q

Where to place transdermal nitrate patch

A

Place away from the chest area–on the extremities

259
Q

SE of gentamycin (aminoglycoside)

A

Ototoxicity

260
Q

Furosemide may cause

A

Ototoxicity

261
Q

If patient has not responded to penicillin or doxycycline

A

Give a fluoroquinolone

262
Q

Concerns with levofloxacin

A

Neurotoxicity and tendon rupture

263
Q

If a beta blocker is making a patient tired…

A

Can decrease the dose

264
Q

Labs to monitor with statins

A

CK and kidney function

Liver function tests

265
Q

Always treat hypertension with what first

A

Thiazide diuretic

266
Q

Coronary artery spasm education

A

Give sublingual nitroglycerine up to 3 doses 5 minutes apart

Pharmacology (56 decks)

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