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ESUN MS2Unit4 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is the 60/40/20 rule for body water?

A

60% of body weight is total body fluid
40% of BW is intracellular fluid
20% of BW is extracellular fluid

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2
Q

What are the 2 compartments within ECF?

A

Intravascular—>blood (7% of BW/25% of ECF)

Extravascular—>interstitial fluid (75% of ECF)

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3
Q

Where and how does diuretics work on? ICF or ECF? and it is equivalent to?

A

Force renal output—>shrink intravascular volume (ECF)—>decrease CO—>decrease BP
Equivalent to decrease Na intake

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4
Q

Total body fluid increase or decrease as ones ages?

A

Decrease from 75% of BW to 50% (most shrinkage occurs in ECF)

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5
Q

Is the osmolarity of ICF and ECF same or different?

A

Same

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6
Q

What are the equations for BP or CO?

A 
BP = TPR x CO
CO = HR x SV
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7
Q

How large are the CO going through kidneys/RBF/RPF/GFR?

A

20% of CO perfuses the kidneys
1/2 of RBF is RPF
20% of RPF is GFR (125 ml/min)—>filtration fraction (FF)

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8
Q

Is there urine production if RBF is zero?

A

NONE

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9
Q

What happened when you drink a lot of water or sodium?

A

ECF expands—>increase renal output of water and sodium

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10
Q

In healthy individual, renal output of Na matches?

A

Dietary intake of Na

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11
Q

Edema is a shift of fluid from ___ to ___?

A

Intravascular to extravascular

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12
Q

Hydrostatic pressure does? oncotic pressure does?

A

Push fluid out of the capillaries/push fluid into the capillaries

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13
Q

The ultrafiltrate of glomerulus has similar composition to plasma except?

A

Without protein

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14
Q

What is the equation for excretion? and what is the fraction of excretion of water and Na(FEwater/FEsodium)?

A

Excretion = filtration - reabsorption + secretion

1%

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15
Q

___ and ___ of kidney are impermeable to water, which results in?

A

Thin and thick ascending limb—>reabsorb solute w/o water—>dilute the tubular fluid (osmolarity decreases)

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16
Q

___ drives the solute transport and maintain the counter current multiplication

A

Thick ascending limb

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17
Q

The clearance rate of ___ is the GFR? and it is similar to endogenous __?

A

Inulin (amount filtered = amount excreted)/creatine

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18
Q

What does it mean when FEwater > or

A

> 1%—>positive water balance

negative water balance

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19
Q

Fractional reabsorption is = ?

A

1 - FE

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20
Q

Is sodium ever secreted in the kidney?

A

Never

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21
Q

Aldosterone increase __ reabsorption and ___ secretion?

A

Na/K

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22
Q

We have normally a high or low K diet? which results in?

A

High K diet/aldosterone secretes K into the tubule

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23
Q

How does hypokalemia happens during alkalosis?

A

Proton comes out of the cells and K goes into the cell—->increase K secretion in kidneys

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24
Q

The faster the flow through the collecting duct, the ___ of the rate of secretion of K into the tubule

A

Higher

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25
Q

If creatine excretion is going up, what does that tell you about the GFR?

A

It is going down (kidney is sick)

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26
Q

Reabsorption of Na increases or decreases as Na goes from Loop of Henle to the Collecting duct? and what happens if a diuretics is used?

A

Decrease/diuretics blocks Na reabsorption—>different part of the tube will try to compensate by reabsorbing more Na

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27
Q

Na reabsorption is coupled with ___ in the late distal tubule and early collecting duct?

A

K secretion

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28
Q

Diuretics (non K sparing) cause hyper/hypokalemia?

A

Hypokalemia

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29
Q

What drives the Mg and Ca from the tubular fluid into the blood at thick ascending limb of loop of Henle? what if you block the Na/K/Cl channel with a diuretics?

A 
The positive (+7) voltage difference in the tubular fluid created by the Na/K/Cl channel--->push Mg and Ca out of the tubular fluid
Increase Mg and Ca in the tubular fluid for excretion
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30
Q

What does it mean when U/P (urine osmolarity over plasma osmolarity) >1 or

A

> 1—>urine is hypertonic—>free water clearance is negative—>kidney is retaining water
urine is hypotonic—>free water clearance is positive—>kidney is eliminating water

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31
Q

ADH increases when plasma osmolarity rises or falls?

A

Rises

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32
Q

What transporter is responsible for Na reabsorption in early distal tubule? and what blocks it?

A

Na-Cl cotransporter/thiazide diuretics

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33
Q

ADH acts on what parts of the kidney?

A

Late distal tubule and collecting duct

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34
Q

When you eat a lot of Na, your ADH is high or low?

A

Low

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35
Q

In the late distal tubule and collecting duct, increase ADH results in?

A

Increase Na reabsorption—>increase Na/K ATPase on the blood side of the luminal cell—>increase intake of K into the cell—>increase secretion of K out of the cell into the tubular fluid

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36
Q

Conductance equals to ?

A

1/resistance

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37
Q

Can AP opens an inactivated gate?

A

No

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38
Q

Which phase does the heart muscle contracts?

A

The plateau phase of the AP

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39
Q

What is the AP of pacemaker cells in the SA and AV node that is different from the rest of the heart muscle cells?

A

Slow response AP

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40
Q

Hypo/hyperkalemia causes hyper/depolarize?

A

Hypokalemia—>hyperpolarize (increase threshold)

Hyperkalemia—>depolarize (decrease threshold)

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41
Q

Threshold potential depends on?

A

Resting membrane potential/Na current availability/cell size

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42
Q

Resting membrane potential depends on which ion?

A

K

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43
Q

What is the level of hyperkalemia affect the excitability?

A

Moderate—>increase excitability

Severe—>decrease excitability (too much depolarization—>decrease K conduction)

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44
Q

What is effective/relative/functional refractory period?

A

Effective—>can’t be stimulated with an AP
Relative—>can be stimulated but need a bigger AP
Functional—>combination of effective and relative

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45
Q

Heart muscle cells and pacemaker cells depends on what ions for AP?

A

Heart muscle cells—>Na

Pacemaker cells—>Ca

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46
Q

Which cell has faster conduction speed, heart muscle or pacemaker cells?

A

Heart muscle cells

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47
Q

Sequence of conduction in the heart

A

SA node—>AV node—>purkinje fibers

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48
Q

Cardiac contract is dependent on?

A

AP duration

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49
Q

Tackycardia increases or decreases CO?

A

Decreases

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50
Q

Stretching sarcomere length increase ___ but over stretching causes?

A

Increase contractility/decrease in contractility

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51
Q

SV = ?

A

end diastolic volume - end systolic volume

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52
Q

Ejection fraction = ?

A

SV/EDV

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53
Q

How does diuretics work?

A

Increase urine output by decreasing active reabsorption of the solutes
Initial affect—>maintenance of the new baseline (body fights back)

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54
Q

Which kind of diuretics mimic diabetes insipidus? and how does it work?

A

Aquaretics—>decrease the ability of ADH to increase the water permeability of the late distal tubule and collecting duct

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55
Q

How does saluretics work?

A

Decrease solute reabsorption

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56
Q

How does osmotic diuretics work?

A

Raise osmolarity of tubular fluid—>oppose water reabsorption

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57
Q

What are diuretics used for?

A

HTN/edema/hyper or hypocalcemia or kalemia

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58
Q

Where is bicarb reabsorbed in the kidney?

A

Proximal tubule

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59
Q

What is the affect of loop diuretics on water regulation of the kidney?

A

Keeping the osmolarity of the urine close to that of the plasma—>decrease both + and - free water clearance—>takes the pt longer to get rid of/conserve water when he is volume overloaded/dehydrated

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60
Q

Thiazide diuretics only affect + or - free water clearance?

A

+

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61
Q

Which has a higher chance to cause hyponatremia, loop or thiazide diuretics?

A

Thiazide diuretics

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62
Q

What diuretics work on proximal tubule?

A

Carbonic anhydrase inhibitor/osmotic diuretics/aminophylline

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63
Q

Excess glucose is like what kind of diuretics?

A

Osmotic

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64
Q

What diuretics work on thick ascending limb?

A

Loop

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65
Q

What diuretics work on early distal tubule?

A

Thiazide

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66
Q

What diuretics work on late distal tubule/collecting duct?

A

K sparing/vaptans

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67
Q

How is bicarb and Na reabsorbed in the proximal tubule and what block this?

A

Na comes in and H+ goes out to the lumen—>bicarb + H+ becomes carbonic acid—>then disassociate into H2O and CO2—>CO2 comes into the cell and combine with water to form carbonic acid and then disassociate into H+ (goes out again) and bicarb—>bicarb is transported into the blood/carbonic anhydrase inhibitor (carbonic anhydrase facilitate the disassociation and association of bicarb and carbonic acid)

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68
Q

What is carbonic anhydrase does to ammonia excretion?

A

Decrease ammonia excretion—>causes hepatic encephalopathy

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69
Q

Which loop diuretics does not have a sulfamoyl group?

A

Ethacrynic acid

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70
Q

How does the body counter the increase of Na excretion created by diuretics?

A

Decrease GFR (decrease filtering load of Na)

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71
Q

How does hypokalemia happens with loop diuretics?

A

Late distal tubule and collecting duct trying to compensate for excess Na in the tubular fluid by reabsorbing Na—>increase K secretion—>hypokalemia

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72
Q

Thiazide decrease or increase Ca reabsorption and results in?

A

Increase/prevent Ca stone in the tubules

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73
Q

What is the pathology of nephrogenic diabetes insipidus?

A

Collecting duct and late distal tubule fail to response to ADH

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74
Q

What does Li do to the distal tubule and the collecting duct? what is used to treat that?

A

Make them fail to response to ADH (like diabetes insipidus)/K sparing—>might need to decrease Li dosage

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75
Q

Why do loop and thiazide diuretics cause hyponatremia?

A

Decrease + free water clearance

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76
Q

Response to volume contraction/expansion happen only at what part of the kidney?

A

Distal tubule and collecting duct

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77
Q

Where in the kidney do amiloride and triamterene secreted into the tubular fluid?

A

Proximal tubule

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78
Q

High or low Na diet is needed for spironolactone to work?

A

Low Na diet—>volume contracted—>ADH is released

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79
Q

Does the activity of spironolactone depends on GFR/tubular secretion and con.?

A

No (act inside of the cell)

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80
Q

Can we use diuretics for renal disease and nephrotic syndrome? and what should we be aware?

A

Yes/need to increase dose of diuretics

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81
Q

Hypokalemia can be an indication for ___ and ___?

A

Renal artery stenosis/hyperaldosteronism

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82
Q

Should you treat a younger HTN pt more aggressively or conservatively?

A

Mosre aggressively

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83
Q

HTN can causes LV hypertrophy, which is called ___?

A

End organ disease

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84
Q

What are the 5 factors associated with cardiac disease?

A

Smoking/diabetes/cholesterol/family history/HTN

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85
Q

How does alpha receptor decreases BP?

A

Alpha receptor—>vasoconstriction

Block alpa—>decreases peripheral resistance

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86
Q

What are the 3 factors that stimulate renin release?

A

Low CO/low volume/sympathetic tone (NE and epi)

87
Q

Potency of diuretics in descending order?

A

Loop>thiazide>K sparing

88
Q

What causes the dry cough from ACEI?

A

Bradykinin (prevent breakdown)

89
Q

Why can’t you use dihydropyridine Ca channel blocker for anti-angina?

A

It causes reflex tachycardia—>increase O2 demand—>worsen angina

90
Q

Couple Ca channel blocker with ___ to lessen leg edema

A

Diuretics

91
Q

Which Ca channel blocker decrease HR/AV node conduction/contractility?

A

Non-dihydropyridine

92
Q

Primary mechanism of beta blockers?

A

Reduce CO

93
Q

For otherwise healthy pt with HTN, give what first?

A

ACEI—>get cough—>switch to ARB

94
Q

For obese pt with HTN, give what first?

A

Thiazide

95
Q

Is the airway obstruction reversible for asthma? and it is driven by TH_ cells?

A

Yes/TH2

96
Q

Are allergen is only type of substance that can cause asthma?

A

No, cold air and exercise can also cause asthma

97
Q

Beta 2 binds to Gs or Gi protein?

A

Gs

98
Q

Most beta 2 agonist is a mix of R and S isomer, which isomer exerts beta 2 agonist effects?

A

R

99
Q

How is long acting beta 2 agonist long acting?

A

Highly lipid soluble and binds to a 2nd site

100
Q

How does paradoxical bronchospasm occurs?

A

Prolonged use of beta 2 agonist

101
Q

Which M receptor is responsible for the effect of antimuscarinic agents on COPD?

A

M3

102
Q

What is the first line treatment for chronic stable COPD?

A

Tiotropium

103
Q

What is the mechanism of methylxanthine?

A

Inihibit breakdown of cAMP—>increase intracellular cAMP—>bronchodilation

104
Q

Roflumilast mechanism?

A

Inhibit PDE4—>prevent neutrophil migration

105
Q

When to use anti-inflammatory corticosteroid for COPD? what is the risk for?

A

For severe COPD with frequent exacerbation/pneumonia

106
Q

Steroid sensitivity can be restored with low dose of ?

A

Theophylline

107
Q

Which way is better for delivery, metered dose or dry powder?

A

Dry powder (no need to coordinate)

108
Q

What is the first line treatment for persistent asthma?

A

Inhaled corticosteroids

109
Q

What to give for COPD and asthma exacerbation?

A

Corticosteroid/short acting beta 2 agonist/antibiotics for COPD

110
Q

Shear stress on the coronary vessels causes vaso__?

A

Vasodilation

111
Q

Is angiographic test a diagnostic test for heart ischemia?

A

No/test to show the presence of coronary narrowing

112
Q

What happens to the extracellular K level during ischemia and how does it happens?

A

Extracellular K level goes up/increase K leak outwards during AP

113
Q

What happens to the extracellular phosphate/lactate/fatty acid?

A

Increases (MI causes symp activation—>increase fatty acid)

114
Q

What is systolic injury current (subendocardial injury) and what does that cause on EKG?

A

Shortening of AP in ischemic cells—>ischemic cells are more negative than normal cells—>positive current flow from normal cells to ischemic ones/ST depression on EKG

115
Q

What is stress test used for and what is the goal?

A

Diagnosis of ischemia/85% of max HR

116
Q

If baseline EKG is not normal then what should be added to diagnose ischemia?

A

Echo and nuclear tracers

117
Q

If the pts can not exercise, what should you do to diagnose ischemia?

A

Use dobutamine (beta 1 agonist) to stimulate the heart like it is exercising/use vasodilator to create perfusion mismatch and then detect using radioactive tracer

118
Q

Why clopidogrel is not used for long term use?

A

Stronger than aspirin—>more risk for bleeding (except for severe vascular disease pts)

119
Q

Which antiplatelet drugs can be used for pt with liver dysfunction?

A

Ticagrelor

120
Q

What is the box warning for ticagrelor?

A

Aspirin maintenance dose has to be under 100mg

121
Q

Which substance does ACE help degrading?

A

Bradykinin

122
Q

How does hyperkalemia caused by ACEI?

A

Decrease aldosterone

123
Q

How does beta blocker causes decreased exercise tolerance?

A

Not be able to reach high HR and CO

124
Q

Affect of nitrate on cardiac function?

A

Increase myocardial O2 supply/venous dilation—>decrease preload

125
Q

Difference between the 1st and 2nd gen dihydropyridines?

A

1st gen has negative inotropic effect (decrease heart contractility) and reflex tackycardia/2nd gen does not have those (less reflex tacky)

126
Q

Non-dihydropyridines have negative ___ effect

A

Inotropic (decrease contractility)

127
Q

What is the definition of congestive heart failure?

A

Inability to pump blood at a rate that required to supply tissues (inability for the heart to keep up)

128
Q

What are class I to IV of heart failure?

A

Class I—>pts with cardiac disease but w/o limitation in physical activity
Class II—>cardiac disease with slight limitation
Class III—>marked limitation
Class IV—>inability to carry out physical activities w/o discomfort

129
Q

___ reduce readmission with chronic heart failure pts

A

Exercise

130
Q

LV dysfunction w/o intervention will get?

A

Worse (cardiac remodeling)

131
Q

What is responsible for cardiac remodeling of heart failure?

A

neurohormonal (e.g. NE/aldosterone/angiotensin II)—>target these to prevent heart failure

132
Q

What are stage A and B of development of heart failure and how to manage?

A

Stage A—>high risk for HF w/o structural heart disease nor symptoms—>treat underlying conditions (use ACEI or ARB)
Stage B—>structural heart disease no symptoms of HF (ACEI or ARB)

133
Q

What are stage C and D of development of heart failure and how to manage?

A

Stage C—>structure disease with HF symptoms (ACEI/diuretics/beta blockers)
Stage D—>refractory HF (hospice)

134
Q

Main effect of ACEI?

A

Artery and vein dilation—>increase CO and exercise tolerance

135
Q

CHF/LV dysfunction, first line treatment? what about ischemic heart disease?

A

ACEI/aspirin, beta blockers, statin

136
Q

Mechanism and benefit of angiotensin receptor blockers over ACEI?

A

Block angiotensin II type 1 receptor (AT1)—->usually used to replace ACEI because of the cough
Inhibit angiotensin II’s effect on symp tone—>dilate vessels

137
Q

Treating HTN, use diuretics with combo of ___?

A

ACEI or beta blockers

138
Q

___ dose of aldosterone antagonist is used for class III and IV of CHF to reduce death

A

Low (because the side effect of hyperkalemia)

139
Q

Eplerenone does not have side effect of ___ comparing with spironolactone?

A

Gynecomastia

140
Q

Why is beta blockers used for reduction of mortality in CHF?

A

Anti arrhythmic/inhibit negative cardiac remodeling

141
Q

Digoxin increases intracellular ___ and ___ level and has a ___ inotropic effect?

A

Na and Ca/positive

142
Q

What is the toxic effect of digoxin?

A

Cardiac arrhythmia

143
Q

When is digoxin used?

A

For pt who is admitted into the hospital and had a previous decompensation episode

144
Q

What does diuretics aim to and does it inhibit negative cardiac remodeling?

A

Treat symptoms/no

145
Q

Low dose dobutamine stimulate ___ receptor and high dose stimualte ___ receptor?

A

beta 2—>vasodilation/alpha—>vasoconstriction

146
Q

What is the effect of milrinone similar to?

A

Dobutamine—>increase HR/contractility/vasodilation

147
Q

Dobutamine and milrinone, which drugs develop tolerance?

A

Dobutamine

148
Q

Management of acute decompensated heart failure?

A

Diuretics for symptoms, use inotropic to improve CO and symptoms but long term worsen outcomes

149
Q

Which surface protein of chylomicron activates plasma lipoprotein lipase (or CPL) that hydrolyze chylomicron?

A

ApoCII

150
Q

Where is VLDL produced and how it is degraded?

A

Endogenously produced by liver/hydrolyzed from VLDL to IDL to LDL (mainly cholesterol by now)

151
Q

Which ligand on the surface of LDL is responsible for taking LDL back into the liver?

A

Apo B100

152
Q

What are the 3 effects of free cholesterol in the hepatocyte recycled by the liver from LDL?

A

Decrease HMG CoA reductase—>decrease cholesterol synthesis
Increase ACAT—>for storage of cholesterol esters
Decrease LDL receptor—>decrease uptake of LDL

153
Q

What is the enzyme used by HDL to get cholesterol from peripheral tissues and bring them back to liver?

A

LCAT

154
Q

How does atherosclerosis plaque developed?

A

Endothelial damage (HTN)—>inflammation response—>LDL deposition—>LDL oxidation—>macrophages swallow LDL—>foam cells—>smooth muscle cell joins—>plaque

155
Q

Serum cholesterol increases with __?

A

Age

156
Q

3 major risk factors for atherosclerosis?

A

Age/BP/smoking (decrease HDL)

157
Q

3 major factors that increase HDL level?

A

Estrogen/exercise/alcohol

158
Q

How to manage pt with moderate high lipid level?

A

Lifestyle and diet change first

159
Q

What is the mechanism of nicotinic acid?

A

Lower VLDL secretion from liver and increase HDL

160
Q

Fibric acid derivatives enhance ___ that stimulate ___ clearance?

A

LPL (or CPL)/TG-rich lipoprotein (like VLDL/chylomicron)

161
Q

Possible beneficial effects of statins?

A

Counteract osteoporosis/cardioprotective

162
Q

Statin is given with __ to have synergistic effect?

A

Ezetimibe

163
Q

Statin should not be given with ___ due to ___?

A

Fibrates/increased risk of myositis

164
Q

Electrolyte imbalance causes ___ and ___ waves in ECG?

A

U and J

165
Q

What are the 2 mechanisms of arrhythmia?

A

Automaticity and conduction

166
Q

Where is the ectopic activity usually located in the heart?

A

Purkinjie

167
Q

Which 2 phases do pacemaker cell AP lack?

A

phase 1 and 2

168
Q

How does early afterdepolarization occur?

A

Inhibit K current/inhibit Na inactivation current/increase Ca current—>another AP might be generated after depolarization

169
Q

What are the 2 triggered activity of abnormal automaticity?

A

EAD and DAD

170
Q

What are the 2 major factors that decrease conduction velocity and cause arrhythmia?

A

Low Na current/increase gap junction resistance

171
Q

What are the 3 general mechanism for cardiac arrhythmia?

A

Enhanced automaticity/triggered activity/reentry

172
Q

What is reentry arrhythmia?

A

A propagating impulse fail to die out and travel back in a circular path to re-excite the heart after refractory period is ended

173
Q

What is the concept behind class I anti arrhythmic drug?

A

Block the unidirectional block of reentry to a full block and break the circular path of reentry

174
Q

Hyper or hypokalemia causes bradycardia?

A

Hyperkalemia

175
Q

What does sick sinus syndrome cause?

A

Bradycardia

176
Q

What is 1st/2nd/3rd degree AV block?

A

1st—>prolonged PR interval
2nd: not every P wave is followed by QRS
mobitz type I—>PR interval prolongs till QRS beat is dropped (Wenchebach)
mobitz type II—>constant PR interval prolongation
3rd—>complete block (ventricular pacemaker)

177
Q

What is normal PR interval?

A

0.12 to 0.2 s

178
Q

What is hemiblock?

A

Block of either left anterior or posterior fascicle of left bundle branch

179
Q

What causes an inverted P wave?

A

Beat starts from AV node then travels back to SA node/may block a sinus beat and produce compensatory pulse

180
Q

What can cause prolonged QRS?

A

Bundle block/conduction starts in either left or right ventricle

181
Q

2/3 of supraventricular tachycardia is caused by ?

A

AV node reentry

182
Q

Paroxysmal (sudden onset and termination) is characteristics of what kind of SVT?

A

Atrial or junctional

183
Q

How to terminate AV node reentry SVT?

A

Vagal tone/adenosine/beta or Ca blocker

184
Q

What is Wolff-Parkinson-White syndrome?

A

Special kind of SVT—>higher risk for sudden death/treat with amiodarone and procainamide

185
Q

More than __ PVC is defined as ventricular tachycardia

A

3

186
Q

Difference between spontaneous and sustained VT?

A

Spontaneous VT—>less than 30 sec

Sustained VT—>more than 30 sec

187
Q

What is torsades de pointes and how does it occur?

A

It is a polymorphic VT—->long QT syndrome/caused by EADs via inhibition of K current (caused by many drugs)

188
Q

What is catecholamine induced polymorphic VT and what causes it and how do we treat it?

A

It is a one kind of PVT/defect in Raynodine receptor causes Ca overload—>DADs/beta blocker

189
Q

How does CPVT usually triggered?

A

Exercise induced

190
Q

What is atrial flutter?

A

Rapid atrial rate/e.g. every 4 P waves follows 1 QRS/saw tooth pattern

191
Q

When is atrial flutter dangerous?

A

When it causes Wolff-Parkinson-White syndrome

192
Q

How to manage chronic A fib?

A

Anticoagulant and rate control of ventricles

193
Q

What are ventricular flutter/fib what do they look like on ECG?

A

lethal/dysfunctional ventricular contraction/no QRS or T on ECG—>just up and down waves

194
Q

What does torsades de pointes ECG look like?

A

A sin wave

195
Q

What are class I anti-arrhythmic drugs? and which one is the strongest?

A

Block Na—>thus phase 0/Ic is the strongest

196
Q

What is special about class Ib anti-arrhythmic drug?

A

Block Na in ischemic tissues—>treat arrhythmia caused by ischemia

197
Q

Sotalol induces ____ strongly?

A

LQT

198
Q

Quinidine may increase ___ and interact with ___ ?

A

AVN transmission/Digoxin (displace it—>increase free Digoxin level)

199
Q

Which class Ia drug causes lupus like syndrome?

A

Procainamide

200
Q

Lidocaine is used for what kind of arrhythmia?

A

Ventricular fib/tachy

201
Q

What is the oral version of lidocaine?

A

Mexiletine

202
Q

Beta blockers decrease mortality in ___ pts?

A

CHF/MI

203
Q

Sudden withdraw of beta block in angina pt may cause?

A

MI

204
Q

What anti-arrhythmic drugs are strong proarrhythmic?

A

Class Ic and Class III

205
Q

Class III drugs are mainly used for ? (except for amiodarone)

A

Atrial arrhythmia because of their induction of ventricular arrhythmia

206
Q

Don’t use amiodarone for ___ pt?

A

Pregnant

207
Q

Which drug causes blue gray skin?

A

Amiodarone

208
Q

What other drugs interact with Digoxin like Quinidine?

A

Class IV

209
Q

What antiarrhythmic drugs are contraindicated in AV block pts?

A

Beta blockers/Ca channel blockers/Digoxin

210
Q

Adenosine does not work on ___?

A

Atrial arrhythmia

211
Q

What are the first line treatment for acute and chronic A fib/flutter/SVT?

A

Non dihydropyridine/beta blocker/digoxin

212
Q

What is given for unsustained VT and sustained VT?

A

Beta blocker/amiodarone or ICD

213
Q

What is given for V fib?

A

Amiodarone or ICD

ESUN MS2Unit4 (5 decks)

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