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Year 1 > Pharmacology Cardio > Flashcards

Pharmacology Cardio Flashcards

1
Q

Class 1a Antiarrhythmic

(Class 1 = Na+ channel blockers

A

Quinidine
Procainamide
Disopyramide

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2
Q

Class 1b Antiarrhythmic
(Class 1 = Na+ channel blockers

A

Lidocaine

Hydrochloride

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3
Q

Class 1c Antiarrhythmic

(Class 1 = Na+ channel blockers)

A

Felcainide

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4
Q

Class 1c Antiarrhythmic

(Class 1 = Na+ channel blockers)

A

Felcainide

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5
Q

Class 2 Antiarrhythmic
(class 2 = β blocker)

(olol)

A

Bisoprolol
Atenolol
Propanalol
Timolol

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6
Q

Class 3 Antiarrhythmic

(class 3 = K+ channel blocker

A

Amiodarone

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7
Q

Class 3 Antiarrhythmic

(class 3 = K+ channel blocker)

A

Sotalol

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8
Q

Class 4 antiarrhythmic

Non-dihydropyridines

(class 4 = Ca2+ channel blocker)

A

Verapamil
Diltiazem

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9
Q

peripheral hypertensive calcium channel blockers

A

Amlodipine
Nifedipine

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10
Q

‘other antiarrhythmic’ need to know

A

Adenosine

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11
Q

‘other’ anti-arrhythmic

A

Digoxin

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12
Q

what is Quinidine
Procainamide
Disopyramide used for

A

Treats tachyarrhythmia caused by reentry circuit

Ventricular Fibrillation

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13
Q

what are Lidocaine , Hydrochloride used for

A

Treats tachyarrhythmia caused by reentry circuit

Local anesthetic

Ventricular Arrhythmias

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14
Q

Felcainide what is it used for

A

Treats tachyarrhythmia caused by reentry circuit. *tachyarrhytmia = tachycardia

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15
Q

Bisoprolol
Atenolol what is it used for

A

Tachyarrhythmias caused by increased sympathetic activity
Atrial Flutter
Atrial Fibrillation
AV nodal re-entrant tachycardia
In atrial fibrillation, the atria beat irregularly. In atrial flutter, the atria beat regularly, but faster than usual and more often than the ventricles

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16
Q

what is binding site for Quinidine
Procainamide
Disopyramide

A

Na+ channels

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17
Q

what is binding sites for Lidocaine

Hydrochloride

A

Na+ channels

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18
Q

what is binding site for felcainide

A

Na+ channels

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19
Q

what is bisoprolol and atenolol binding site

A

B1 receptor, Gs

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20
Q

what is propanolol and timolol binding site

A

β1 receptor
(non-selective)

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21
Q

what is amiodarone binding site

A

K+ channels

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22
Q

what is sotalol binding site

A

K+ channels and Beta receptors

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23
Q

what is verampil and diliazem binding site

A

Ca2+ channels (L type)

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24
Q

what is amlodipine and nifedipine binding site

A

Ca2+ channels

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25
Q

what is adenosine binding site- other arrhythmitic

A

alpha 1 purinergic receptors

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26
Q

what is digoxin binding site-other antiarrhythmic

A

Na+/K+, ATPase

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27
Q

what is digoxin used for

A

Used to control ventricular response rate in:
1. Atrial Fibrillation
2. Atrial Flutter

only given really if they’re bed bound otherwise use bisoprolol.

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28
Q

what is adenosine used for

A

Paroxysmal SVT
supraventicular tachyardia

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29
Q

what is verapamil and dilitazem used for

A

Stable angina
Supraventricular arrhythmias (supraventricular tachycardia, atrial flutter, atrial fibrillation)
Hypertension (Diltiazem)

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30
Q

what is sotalol used for

A

Inhibit reentrant tachycardias

Maintenance of sinus rythms in patients with:
1. Atrial Fibrillation
2. Atrial Flutter
3. Refractory paroxysmal SVT
4. Ventricular arrhythmias

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31
Q

what is amiodarone used for

A

Inhibit reentrant tachycardias

Tachycardias:
1. Atrial fibrillation,
2. Atrial flutter
3. Refractory ventricular fibrillation

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32
Q

what is the mechanism of action of Quinidine
Procainamide
Disopyramide

A

Moderate Na+ channel blocker
Decrease slope of phase 0

  1. They bind to the Na+ channels in the inactivate state (refractory period)
  2. This prevents more Na+ influx , thus slowing down the rapid upstroke during phase 0 - this causes a delay in the depolarisation
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33
Q

what is the mechanism of action of felcainide

A

Strong Na+ channel blocker
Decrease slope of phase 0

Flecainide suppresses phase 0 upstroke in Purkinje and myocardial fibers. This causes marked slowing of conduction in all cardiac tissue, with a minor effect on the duration of the action potential and refractoriness. Automaticity is reduced by an increase in the threshold potential, rather than a decrease in slope of phase 4 depolarization.

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34
Q

what is the mechanism of action of Bisoprolol and atenolol- CLASS 2

A

Decrease HR & conduction velocity
Indirectly alter conduction velocity

  1. Beta blocker will bind to the B1 receptor competitively
  2. The amount of cAMP is reduced
  3. This decreases the amount of L-type channels that open
  4. Less Ca2+ will enter the cell, therefore less Na+ will be pumped into of the cell

Less Ca2+ in the cell = less Ca2+ efflux = less Na+ influx = slower depolarisation = slows down the heart rate + contractility

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35
Q

what is the mechanism of action for propanolol and timolol- CLASS 2

A

Decrease HR & conduction velocity
Indirectly alter conduction velocity

  1. Beta blocker will bind to the B1 receptor competitively
  2. The amount of cAMP is reduced
  3. This decreases the amount of L-type channels that open
  4. Less Ca2+ will enter the cell, therefore less Na+ will be pumped into of the cell

Less Ca2+ in the cell = less Ca2+ efflux = less Na+ influx = slower depolarisation = slows down the heart rate + contractility

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36
Q

what is the mechanism of action of amiodarone- CLASS 3

A

Increase ERP

Class III agents block K+channels and, thus, diminish the outward K+current during repolarization (phase 4) of cardiac cells. These agents prolong the duration of the action potential and increased the refractory period

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37
Q

what is the mechanism of action of sotalol- CLASS 3

A

Increase ERP

Sotalolblocks a rapid outward K+current, known as the delayed rectifier current. This blockade prolongs both repolarization and duration of the action potential, thus lengthening the effective refractory period.

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38
Q

what is the mechanism of action of verapamil and diltiazem- CLASS 4

A

Decreases slope of phase 2
Slow down conduction velocity
Decrease contractility
Adjusts refactory period.

  1. The L-type Ca2+ channels on the T-Tubule are now blocked
  2. There is now little outflux of Ca2+ from the sarcoplasmic reticululm - no “Ca2+ induced Ca2+ release”
  3. Ca2+ cannot bind to troponin and therefore they’ll be less contraction - reducing the force and speed of contraction
  4. Little Ca2+ will leave the cell meaning little Na+ will enter the cell
  5. This means less K+ enters the cell

*They slow down the conduction of the AV nodes and the automaticty
* They supress the cardiac conduction down the Bundle of His - this slows down the ventricular rate and reduces cardiac contractility

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39
Q

how do amlodopine and nifedipine work -

A

act on blood vessels as calcium channel blockers to prevent dilation, reduces TBR by causing vasodilation. NOT CLASS 4 ANTIARRHYTHMICS . DECREASE BP BY DECREASE TPR.

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40
Q

what is adenosine mechanism of action

A

Decrease SAN firing and conductivity
Increase ERP

  1. Has potent effects on the SA node - resulting in sinus bradycardia
  2. Slows cardiac action thru the AV node
  3. Inhances the flow of K+ out of the cell - hyperpolarising the resting

acts on receptors in the cardiac AV node, significantly slowing conduction time. [3] This effect occurs by activation of specific potassium channels, driving potassium outside of cells, and inhibition of calcium influx, disrupting the resting potential of the slow nodal cardiac myocyte

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41
Q

how does digoxin work

A

Cardiac glycosides inhibit Na+/K+ pump, increase Ca2+ exchange, increase vagus effects
Increase contractile force
Decrease HR, AV conduction

  1. Digoxin binds to the Na⁺/K⁺ ATPase on the myocyte membrane and partially inhibits it. This increases the intracellular Na⁺ concentration and decreases the Na⁺ concentration gradient, the effect is downregulation of the Na⁺/Ca²⁺ transporter so excess Ca²⁺ remains in the cell to be stored in
  2. This enhances contractility
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42
Q

what is phenylephrine

A

a1 agonist

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43
Q

what is clonidine

A

a2 antagonist

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44
Q

what is dobutamine in

A

B1, B2, A1 agonist

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45
Q

what is salbutamol in

A

B2agonist

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46
Q

what is norepinephe

A

a1. a2 agonist

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47
Q

what is epinephrine in

A

a1, a2, b1, b2 agonist

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48
Q

what is doxazosin and prazosin in

A

a1 antagonists

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49
Q

what is atenolol, bisoprolol and metopralol

A

B1 antagonist

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50
Q

what is phenoxybenzamine in

A

a1 + a2 antagonists

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51
Q

what is propanolol and timolol in

A

B1 + B2 antagonist

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52
Q

what does phenylephrine used for

A

reduced nasal conjestion

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53
Q

what is clonidine used for

A

resistant hypertention

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54
Q

what is dobutamine used for

A

cardiogenic shock

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55
Q

what is salbutamol used for

A

bronchodilation

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56
Q

what is epinephrine used for

A

anaphylaxis and MI

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57
Q

what is dozasin used for

A

resistant hypertension

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58
Q

what is prazosin used for

A

resistant hypertension and benign prostatic hyperplasia

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59
Q

what is phenoxybenzamine used for

A

phaeochromocytoma

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60
Q

what is atenolol, bisoprolol and metoprolol used for

A

primarily hypertension, heart failure after MI (cardio selective B1 ONLY)

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61
Q

what is propanolol used for

A

hypertension, angina (non-selective, B1 and B2)

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62
Q

when can b blockers be used for angina and why

A

at rest they cause little change in HR, BP, and CO but decrease effects of excercise

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63
Q

what do non selective B blockers antagonise (meaning it binds to and competitibely antagonises both B1 and B2 receptors, likely causing bronchoconstriction, excaserbating patient’s asthma

A

B1 and B2

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64
Q

work calcium channels work best in the heart

A

diltiazem and verampamil

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65
Q

where are doxazosin and prazosin found

A

vascular smooth muscle

66
Q

what is MOA of doxason + prozasoin ( alpha adrenoreceptor antagonists)

A

Prevents agonists such as epinephrine, norepinephrine and phenylepinephrine from binding to the α1 receptor and so prevents their MOA from occuring. This in turn causes vasodilation

67
Q

what does clonidine do (a2 agonist)

A

cause vasodilation

68
Q

what does phenoxybenzamine do a1 + a2 antagonist

A

Non-selective α antagonist that causes an irreversible blockade of all α adrenoreceptors

69
Q

what does epinephrine do, a +B agonist

A

Causes increased HR, increased force of contraction & central shunting of blood

70
Q

what does dopobutamine do , b1 receptor agonist

A

ionotropic effect increases contractility, leading to decreased end-systolic volume and, therefore, increased stroke volume.

71
Q

what is aliskerin

A

renin inhibitor competitive antagonist

72
Q

what is aliskirin used for

A

hypertension

73
Q

what is normal MOA of renin, and what does aliskerin do

A

renin= Renin catalyses the conversion of angiotensin to ANG1
aliskerin= Aliskerin compeitively antagonises renin and prevents the formaiton of ANG1, which is needed for the prouction of ANG2

74
Q

what is ramipril (any prils)

A

ACE inhibitor- competitively antagonise

75
Q

what is ramipril used for

A

hypertension and heart failure

76
Q

what is ACE normal MOA and what does ramipril do

A

ACE- ACE normally converts Angiotensin 1 into Angiotensin 2
In hypertension we can ventricular hypertrophy, which contributes to the diastolic component of heart failure via imparied diastolic filling
Ramipril- competitively antagonise the ACE enzyme to prevent the conversion of ANG1 to ANG2.
BP=COxTPR
↓ANG2 leads to vasodilation and ↓TPR
↓ANG2 reduces further hypertrophy
Results in CO from heart becoming sufficient for perfusion

77
Q

what is losartan and valsaratan

A

Angiotensin 2 Receptor Blockers - ARBs
(sartans)- bind at AT2R competitive antagonist

78
Q

what is losartan and valsartan used for

A

Hypertension

79
Q

how does ANG2 and AG1 MOA usually work, and how does ARB stop this

A

-ANG2 normally binds to AT1 receptors, causing increased aldosterone levels
-ARBs competitively antagonise AT1 receptors in vascular, adrenal and neuronal tissue.

80
Q

what class is mannitol

A

osmotic diuretic

81
Q

what is usage of mannitol

A

cerebral oedema, reduce ischameia, cerabral damage, acute traumatic brain injury

82
Q

what is mannitol MOA vc normal MOA

A

normal MOA: 1. Na+ is actively pumped across basolateral membrane via Na+/K+ ATPase
2. Decreased Na+ conc, activates Na+ pumps on apical membrane
3. Na+/H+ transporter & Na+/glucose transporter move Na+ from the nephron lumen into the ICF.
mannitol MOA: Osmotic diuretics increase the concentration of solute in the nephron lumen, pulling water back into the lumen to dilute the concentration of the solute and so more water remains In the nephron lumen to be excreted

83
Q

what is furosemide class

A

loop diueretic

84
Q

what is furosemide usage

A

Oedema
Pulmonary oedema due to LVHF & Chronic HF
Resistant Hypertension

85
Q

what is furosemide binding site

A

Na+/K+/2CL- receptor anatgonist

86
Q

where are furosemide receptors found

A

ascending loop of henle

87
Q

furosemide MOA vs normal MOA

A

NORMAL:
1. Na+ is actively pumped across basolateral membrane via Na+/K+ ATPase
2. Decreased Na+ conc, activates Na+ pumps on apical membrane
3. Na+/K+/2Cl- pumps ions across the apical membrane from the nephron lumen into the ICF

DRUG MOA:
Thiazide diuretics are antagonists of the Na+/Cl- receptor, so more sodium remains in the nephron lumen and is excreted. The water remains with the sodium and is excreted.

88
Q

Bendroflumethiazide class

A

thiazide diuretic

89
Q

bendroflumethiazide usage

A

Hypertension - lower doses
Oedema due to chronic HF - higher doses

90
Q

bendroflumethiazide binding site and where

A

na/cl receptor antagonist distal convuluted tube

91
Q

bendroflumethiazide MOA and normal MOA

A

normal MOA: 1. Na+ is actively pumped across basolateral membrane via Na+/K+ ATPase
2. Decreased Na+ conc, activates Na+ pumps on apical membrane
3. Na+/Cl- receptor pumps ions across the apical membrane from the nephron lumen into the ICF

drug MOA:
Block Na+/Cl- cotransporter so more Na+/Cl- excretion
Water loss

92
Q

indapamide class

A

thiazide like diuretics

93
Q

indepamide binding site and where

A

na/cl antagonist in distal convuluted tubule

94
Q

indempamide MOA and normal MOA

A

normal MOA- 1. Na+ is actively pumped across basolateral membrane via Na+/K+ ATPase
2. Decreased Na+ conc, activates Na+ pumps on apical membrane
3. Na+/Cl- receptor pumps ions across the apical membrane from the nephron lumen into the ICF
indampemide MOA- Block Na+/Cl- cotransporter so more Na+/Cl- excretion
Water loss

95
Q

amiloride class

A

potassium sparring diuretic

96
Q

amiloride binding side and where found

A

ENaC-Na+ cotransporter antagonist in cortical collecting tubule

97
Q

amiloride MOA and normal MOA

A

normal MOA - 1. Na+ is actively pumped across basolateral membrane via Na+/K+ ATPase
2. Decreased Na+ conc, activates Na+ pumps on apical membrane
3. Na+ channels are activated

amiloride MOA- Block Na+ cotransporter so more Na+ excretion
Water loss

Amiloride is an antagonist of the Na+ channel, so more sodium remains in the nephron lumen and is excreted. The water remains with the sodium and is excreted.

98
Q

what is amiloride usually used in conjuction with

A

This drug is used for fine tuning and so is normally used in cojunction with another diuretic (usually thiazide)

99
Q

what is spironalactone class

A

aldosterone antagonist

100
Q

what is spironolactone binding site

A

mineralcoricoid receptor antagonist

101
Q

what is spironalactone MOA vs normal MOA

A

normal MOA- 1. Aldosterone is a steroid hormone that binds to mineraloorticoid receptor and acts principally by modulating gene transcription
2. Aldoseterone increases the activity of several key proteins involved in Na+ transport it does this by:
* increasing the amount of Na+/K+ ATPase - this causes more Na+ reabsorption on the apical membrane
* Increases the expression of the apical Na+ channels and the Na+/K+/Cl- cotransporters - this increases the Na+ reabsorption and water follows (less is secreted in the urine)

drug MOA-
Aldosterone antagonist so blocks MR so decrease in AIP so fewer Na+/K+ pumps, Na+ channels and K+ channels so increased Na+ excretion
Water loss

Spironolactone blocks the following actions:
Aldosterone on the apical membrane causes:
More ENaC channel phosphorylation meaning they stay open for longer allowing more sodium entry to the cell from the lumen
Less ENaC channels to be endocytosed so more remain in the membrane

Aldosterone on the basolateral membrane causes:
More Na+/K+ pumps to be inserted into the membrane increasing the Na+ extrusion from the cell, increasing the driving flux for Na+

102
Q

what is spironolactone usually used in conjunction with

A

usually used with a thiazide diuretic

103
Q

what class is unfractionated heparin

A

heparin

104
Q

what is usage of unfractionated heparin

A

Prevention of VTE - following an operation, in patients with angina and following acute MI
Treatment of VTE

105
Q

what is MOA of unfractionated heparin

A

Increase affinity of ATIII to to clotting factors

Heparin increases the affinity og antithrombin III (ATIII) to clotting factors XIIa (12a), XIa (11a), IXa (9a), Xa (10a) and IIa (thrombin)

This interupts the coagulation cascade and no fibrinogen is converted to fibrin and no clotting can occur

106
Q

what class is enoxaparin

A

low molecular weight heparin(LMWH)

107
Q

what is enoxaparin usage

A

Prevention of VTE - following an operation, in patients with angina and following acute MI
Treatment of VTE

108
Q

what is enoxabin moa

A

LMWH inhibit Xa (10a), via increasing afinity of ATIII

This will inhibit the conversion of II (prothrombin) to Iia (thrombin)

109
Q

what is fondaparinux MOA

A

inhibits factor Xa

110
Q

what class is warfarin

A

anticoagulant antagonists

111
Q

what is warfarin usage

A
  • Prevention of venous thrombosis or pulmonary embolus
  • Prevention of arterial thromboemboli (in patients with AF or a cardiac disease)
112
Q

what is warfarin binding site

A

vitamin K reductase

113
Q

where are warfarin receptors found

A

blood

114
Q

what is warfarin MOA and normal MOA

A
  1. Vitamin K is reduced to form its reduced form (hydroquinone)
  2. This activates the clottings factors (II, VI, IX, X)

normal MOA
1. Warfarin inhibits vitamin K epoxide reductase
2. This prevents the reactivation of Vitamin K to its reduced form
3. Inactives vitamin K dependent clotting factors (II, VII, IX and X) can’t bind stable to the blood vessel endothelium and so can’t activate clotting

115
Q

what class is dibigratran

A

anticoagulant competetive antagonist

116
Q

what is dibitgatran usage

A
  • Prevention of stroke and embolism in patients with AF
  • Prophylaxis of venous thromboembolism after hip or knee replacement surgery
117
Q

what is dibigatran binding site

A

Factor IIa

118
Q

where is dibigatran receptors found

A

blood

119
Q

what is dibigatran MOA

A

Competitively binds (reversibly) to the free and fibrin bound factor Iia which inhibits the production of fibrin

120
Q

what is rivaroxaban/apixaban class

A

anticoagulant competitive antagonist

121
Q

what is rivaroxaban/apixaban usage

A

Prophylaxis of VTE after hip or knee replacement surgery

122
Q

what is rivaroxaban/aprixaban binding site

A

factor Xa

123
Q

what is rivoroxaban/apixaban where are the receptor found

A

blood

124
Q

what is the MOA of rivaroxaban /apixaban

A

Competitively antagonsises factor Xa, which inhibits thrombin (Iia) production from prothromin (II)

125
Q

what class is aspirin

A

antiplatelet

126
Q

what is usage of aspirin

A

Used prophylactically to prevent arterial thrombosis leading to:
Transient ischaemic attack
Stroke
MI

127
Q

what is binding site of aspirin

A

COX-1
(cyclooxygenase-1)

128
Q

where a aspirin receptors found

A

platelets

129
Q

what is aspirin MOA and normal MOA

A

aspriin- 1. Aspirin irreversibly inhibits COX-1 , therefore the synthesis of TXA2 is inhibited.
2. The TXA2 cannot recruit more platelets

Because platelets do not contain RNA or DNA they cannot synthesise new COX-1 - making this reaction irreversible

normal MOA - Activated platelets cover and adhere to exposed subendothelial surface of damaged endothelium

Activated platelets release chemical mediators inclusive of
ADP promotes platelet adhesion
PAF promotes platelet activation
Serotonin promotes platelet aggregation
TXA2 recruits more platelets to the plug and causes platelet aggregation

130
Q

what class is clopidogrel

A

anti platelet

131
Q

what is usage of clopidogrel

A

Patients who have coronary artery stents
Stroke Prevention
Post MI - STEMI & NSTEMI
Unstable angina

132
Q

what is binding site for clipidogrel

A

P2Y12 (ADP) receptor

133
Q

where are clopidogrel receotors found

A

platelet

134
Q

what is clopidogrel MOA and normal MOA

A

normal MOA- Activated platelets cover and adhere to exposed subendothelial surface of damaged endothelium

Activated platelets release chemical mediators inclusive of
ADP promotes platelet adhesion
PAF promotes platelet activation
Serotonin promotes platelet aggregation
TXA2 recruits more platelets to the plug and causes platelet aggregation

clopidogral MOA- Prevents ADP-mediated P2Y12 depedent platelet activation and aggregation

Irreversible binding

135
Q

what class is tricagrelor

A

Anti-platelet

136
Q

what is tricargelor usage

A

Patients who have coronary artery stents
Stroke Prevention
Post MI - STEMI & NSTEMI
Unstable angina

137
Q

what is tricagretor receptor found

A

P2Y12 (ADP) receptor

138
Q

where are tricagrelor receptors found

A

platelets

139
Q

what is tricagrelor MOA and normal MOA

A

tricagrelor MOa- Prevents ADP-mediated P2Y12 depedent platelet activation and aggregation

Irreversible binding

normal MOA-
Activated platelets cover and adhere to exposed subendothelial surface of damaged endothelium

Activated platelets release chemical mediators inclusive of
ADP promotes platelet adhesion
PAF promotes platelet activation
Serotonin promotes platelet aggregation
TXA2 recruits more platelets to the plug and causes platelet aggregation

140
Q

what class is dypyridamol

A

antiplatelet

141
Q

what class is alteplase

A

fibronlytic agonist

142
Q

what is the usage of alteplase

A

Dissolve clots that result in MI and ischaemic stroke
Massive PE - high risk of bleeding so not first choice
Restoring catheter and shunt function - by lysing clots causing occlusions

143
Q

what is the binding site of alteplase

A

Plasminogen

144
Q

what is the receptor of alteplase found

A

blood

145
Q

what is alteplase MOA and normal MOA

A

alteplase MOA- Catalyses the conversion of plasminogen to plasmin
normal MOA- There is always a balance between the breakdown (fibrinolysis) and the formation of thrombosis

Fibrinolysis happens by plasminogen being converted to plasmin which breaks down the fibrin fibres formed during the coagulation cascade

146
Q

atropine what class

A

anti muscarinic receptor. M1, M2, M3, M4 and M5 antagonist

147
Q

atropine what is usage

A

first line SVT

148
Q

atropine MOA

A

Atropine binds to and inhibits muscarinic acetylcholine receptors, competitively blocking the effects of acetylcholine and other choline esters

149
Q

what receptors do atropine bind to

A

binds to M1, M2, M3

150
Q

what is the most importany plasma protein

A

albumin

151
Q

what is the most importany plasma protein

A

albumin * a high plasma protein bound drug will show slower acting and prolonged therapeutic effects

152
Q

why should tetracuclines not be used in children

A

they accumulate slowly in bones and teeth because HIGH AFFINITY FOR CALCIUM

153
Q

what is asprin hydrolysed to

A

salicyclic acid

154
Q

what do ACEi and thiazide diuretics together lead to

A

lead to fainting

155
Q

aspirin MOA

A

decrease formation of thromboxaneA2. reversible cox 1 and cox 2 inhibitor

156
Q

what receptors does adrenaline work on

A

a1, a2, b1, b2

157
Q

warfarin contrainsndications

A

Warfarin is contraindicated in hemorrhagic stroke, in patients with significant bleeding, and in pregnancy

158
Q

who shouyou not give beta blockersn

A

heart failuire and asthmatics

159
Q

When do you use mannitol

A

Only in cranial hypertension

160
Q

Where does mannitol work

A

Proximal convultaed tubule

161
Q

What does ivabradine moa

A

Ivabradine aims to inhibit funny current HCN channels ONLY ON PACEMAKER CELLS ON SAN AND AVN. Slows down heart rate

Year 1 (19 decks)

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