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NS, CV and renal pharmacology > NS, CV and renal pharmacology > Flashcards

NS, CV and renal pharmacology Flashcards

1
Q

What is the treatment for second and third degree heart block?

A

Emergency treatment required - Atropine (IV) or Isoprenaline (IV)

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2
Q

Class I Anti-arrhythmic drugs

A

Sodium channel blockers

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3
Q

Class II anti-arrhythmic drugs

A

Beta blockers

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4
Q

Class III anti-arrhythmic drugs

A

K+ channel blockers/Prolong A.P duration

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5
Q

Class IV anti-arrhrhymic drugs

A

Calcium channel blockers

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6
Q

What are the differences between Class Ia,b and C anti-arrhythmic drugs?

A

Differences due to recovery/unbinding of drugs

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7
Q

What is the main affect of Class I anti-arrhrhymic drugs?

A

Block Na+ channels to decrease phase 0 - depolarisaiob

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8
Q

Dysopyramide

A

Sodium channel blocker (Class 1A anti-arrhythmic drug) used to treat ventricular arrhythmias

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9
Q

Lidocaine (IV)

A

Sodium channel blocker (Class 1b anti-arrhrhymic drug) used in treatment prevention of ventricular tachycardia and fibrillation during and immediately after myocardial infarction

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10
Q

Flecainide

A

Sodium channel blocker (Class 1c anti-arrhrhymic drug) used to prevent paroxysmal atrial fibrillation and recurrent tachyarrythmias associated with abnormal conduction pathways

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11
Q

Amiodarone, sotalol, Bretylium

A

K+ channel blockers, prolong A.P depolarisation

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12
Q

What is Amidarone used to treat?

A

Tachycardia associated with WPW syndrome

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13
Q

What is Sotalol used to treat?

A

used in paraxysmal supraventricular dsyrthmias and suppresses ventricular ectopic beats, and short runs of ventricular tachycardia

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14
Q

outline the mechanism of CCB’s

A

act on L-type channels, shorten the plateau of the AP and reduce the force of contraction. Reduced Ca2+ entry reduces after depolarisation and thus suppresses premature ectopic beats

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15
Q

Veramapil

A

CCB

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16
Q

Diltiazem

A

CCB

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17
Q

outline the side effects of CCBs?

A

bradycardia, negative inotropic effect, constipation (verapamil), hypotension (diltiazem)

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18
Q

Loop diuretics, site of action

A

Act on thick ascending limb (TAL) of loop of Henle to inhibt Na+/K+/Cl-

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19
Q

Furosemide, Butetamide

A

Loop diuretics

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20
Q

Thiazides site of action

A

Distal tubule

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21
Q

Why might thiazides be preferred over loop diuretics?

A

Thiazides are less powerful than loop diuretics so preferred in treating uncomplicated hypertension. In contrast to loop diuretics thiazides reduce Ca2+ excretion and so is favourable in elderly patients

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22
Q

Thiazides mechanism of action

A

Bind to the Cl- site of distal tubular Na+/Cl- cotransport system inhibiting its action causing natriuresis with loss of Na+ and Cl-, results in reduced blood volume.

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23
Q

Clinical uses of thiazide diuretics

A

Hypertension, mild heart failure (loop diuretics preferred), severe resistant oedema, nephrogenic diabetes insipidus

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24
Q

Adverse effects of loop diuretics and thiazides

A

hypotension, gout, hypokalemia (caues dysrhythmias, increased digoxin toxicity and hyperglycaemia)

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25
Q

Potassium sparing diuretics- site of action

A

Act exclusively on distal parts of nephron: collecting tubule and collecting duct

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26
Q

Aldosterone antagonist - mechanism of action

A

Competitive inhibtion of intracellular aldosterone receptors, decreases the numbre of luminal Na+ channles and decreases number of basolateral Na+-K+-ATPases. This inhibits Na+ retention and K+ secretion

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27
Q

Spironolactone

A

Potassium sparing diuretic - aldosterone antagonist

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28
Q

Na+ channel blockers - mechanism of action

A

Inhibit Na+ re-absorption by blocking lumenal sodium channels and decreasing K+ excretion

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29
Q

Triameterene, Amiloride

A

Potassium sparing diuretic - Na+ channel blockers

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30
Q

Clinical uses of potassium sparing drugs

A

used with K+ losing diuretics, heart failure, primary aldosteronism (conns syndrome), resistant essential hypertension, secondary hyperaldosteronism caused by hepatic cirrhosis complicated by ascites

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31
Q

Osmoitic diuretics - site of action

A

Main effect is exerted on parts of the nephron that are FREELY permeable to water: proximal tubule, descending limb of the loop and collecting tubules

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32
Q

Osmotic diuretics - mechanism of action

A

Increase filtrate osmolairty, passive water reabsoprtion is reduced by the presence of non reabsorbable solute within the tubule

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33
Q

Clinical use of Osmotic diuretics

A

Used in emergency treatment of acutely raised intraocular or intracranial pressure

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34
Q

Clinical uses of carbonic anhydrase inhibitors

A

Glaucoma, altitude sickness, little use as a diuretic drug due to rapid tolerance

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35
Q

What is nephrotic syndrome?

A

Increased permeability of the glomerular basement membrane to proteins leading to proteinuria. Increases volume of interstitial fluid leading to tissue swelling and activation of RAAS.

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36
Q

Treatment of glomerular nephritis

A

Antihypertensive, loop diuretic, immunosuppresive

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37
Q

Consquences of glomerular nephritis

A

Acute renal failure, chronic renal failure, dialysis or transplantation

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38
Q

Acute Kidney Injury

A

Abrupt reduction in kidney function resulting in failure to maintain fluidm electrolye, and acid-base homeostasis. Decreased urine production and fluid-electrolyte imbalance.

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39
Q

Pre-renal causes of AKI

A

Causes that decrease effective blood flow to the kidney e.g. reduced cardiac output - heart failure, MI, bradycardia. Drugs - ACE inhibitors, NSAIDS

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40
Q

Renal causes of AKI

A

Blockage of renal vasculature = uric acid crystals, cholesterol emboli, vasculitis, endothelial damage (blood clots). Glomerulonenephritis Interstitial nephritis

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41
Q

Post renal causes of AKI

A

Urinary tract obstruction, benign prostatic hypertrophy, cancers/tumours, stones, non-emptying bladder, crystal deposition

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42
Q

Disopyramide, procainamine, quinidine

A

Class 1a antiarrythmic drugs - sodium channel blockers. Intermediate dissociation rate, leading to moderate decrease in phase 0 and increased QRS and QT interval Used to treat AF (triggered by vagal overreactivity) and VT

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43
Q

lidocaine, mexiletine

A

Class 1b anti-arrhythmic drugs -sodium channel blockers. Fast dissociation rate, decreased AP duration and QT interval. Used to treat and prevent VT and VF immediatley after Myocardial infarction

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44
Q

Flecainide, Moncizine, propafenone

A

Class 1c anti-arrhythmic drugs, blocks with slow dissociation rate causing large decrease in phase 0, leading to increased QRS and QT interval. Used to treat AF and recurrentt tachycardias associated with adnormal conduction pathways and WPW syndrome

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45
Q

Class 1a anti-arrhythmic drugs side effects

A

Atropine like (urinary retention, dry mouth, blurred vision, constipation) and Quinide causes syncope (due to triggering torsades de pointes)

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46
Q

Class 1b anti-arrhythmic drugs side effects

A

CNS, drowsiness, disorientation and convulsions

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47
Q

Beta blockers mechanism

A

Block cardiac B1 adrenoreceptors to reduce sympathetic drive to the heart, decreasing heart rate

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48
Q

Propranolol

A

Non selective B antagonist, long acting, oral

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49
Q

Timolol

A

Non selective B antagonist, used to treat glaucoma (decreases AH formation)

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50
Q

Atenolol, bisoprolo, metoprolol

A

B1 Selective antagonist

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51
Q

Pindolol

A

B1 Selective partial agonist

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52
Q

Nevbivolol

A

B1 selective antagonist and also increases NO (leading to less fatigue, bradycardia,and impotence)

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53
Q

Labetalol

A

Mixed alpha/beta adrenergic antagonist

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54
Q

Carvedilol

A

Mixed Alpha1/beta antagonist

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55
Q

Clinical uses of beta blockers

A

Rate control in SVT, rate and rhythm control in AF and flutter, VT

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56
Q

Adverse effects of B blockers

A

Bronchospasm (caution in asthma), negative inotropic effect, bradycardia, fatigue, increased risk of hypoglycaemia (diabetics)

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57
Q

Sotalol, amiodarone, bretylium

A

Class 3 anti-arrhythmic drugs-prolong AP duration by prolong phase 3 by blocking K+ channels

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58
Q

Amidarone

A

K+ channel blocker. Also a modest Na+ and Ca2+ blocker and alpha adrenergic receptor antagonist and decreases cardiac B1 adrenergic receptor expression. When given orally has slow onset (up to 3 weeks) and a very long plasma half life

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59
Q

Amidarone side effects

A

thyroid abnormalities, corneal deposits, pulmonary disorders, skin pigmentation

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60
Q

Class 3 anti-arrhythmic drugs clinical uses

A

SVTs, WPW syndrome, ventricular tachycardias

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61
Q

Sotalol

A

Class 3 anti-arrhythmic also a non selective B blocker. Lacks the adverse ADRs seen in amidarone

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62
Q

Verapamil, Diltiazen

A

Class IV anti-arrhythmic drugs. Calcium channel blockers to slow down AVN conduction

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63
Q

Therapeutic uses of Class IV anti-arrhythmic drug

A

paroxsmal SVT, AF (but NOT if due to WPW)

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64
Q

Class IV anti-arrhythmic drug side effects

A

bradycardias, negative inotropic effect, constipation (verapamil), hypotension (more with diltazem)

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65
Q

Ist line treatment for hypertension <55 years

A

ACE inhibitor or angiotensin receptor AT1 blockers

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66
Q

Captopril, Enalapril

A

ACE inhibitors

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67
Q

ACE inhibitors effects

A

reduce TPR with little effect on HR or cardiac output

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68
Q

ACE inhibitors adverse effects

A

Dry cough (due to accumulation of bradykinin)

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69
Q

Losortan, Candesartan

A

Angiotensin receptor (AT1) blockers

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70
Q

?Why mgiht AT1 blockers be preffered over ACE inhibitors

A

NO dry cough - no bradykinin accumulation

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71
Q

Aliskiren

A

Renin inhibitor

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72
Q

Renin inhibitors

A

e.g. Aliskiren. reduces plasma renin activity by binding and inhibiting activity

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73
Q

Contraindication of RAAS inhibitors

A

In pregnancy (due to fetotoxicity)

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74
Q

Common ADRs of RAAS inhibitors

A

hypotension (with thiazides), hypersemsitvity (head & neck angioedema), hyperkalaemia

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75
Q

1st line hypertension treatment in African/Carribbean and elderly (>55 years)

A

Calcium channel blockers

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76
Q

Nifedipine, Amlodipine

A

CCB, dihydropines, act preferentially on vascular smooth muscle, use in hypertension and angina

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77
Q

Phenylalkylamines

A

Verapamil - CCB act on cardiac preferentially

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78
Q

Benzothiazepines

A

Diltiazem, CCB with an intermediate effect on cardiac and smooth muscle

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79
Q

ADRs of Calcium channel blockers

A

Postural hypotension, flushes/tremors (nifedipine), AV block and negative ionotropic effects (verapamil, diltiazem)

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80
Q

Treatment for hypertension when ACEi/CCBs do not work?

A

Also give patient diuretics

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81
Q

Treatment in resistant hypertension

A

B Blockers and alpha antagonists

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82
Q

Statins, fibrates, bile-acid binding resins

A

Lipid lowering drugs

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83
Q

Statins mechanism

A

inhibits HMG-CoA reductase (key enzyme in cholestrol production)

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84
Q

Simvastatin, Atorvastatin, Pravastatin

A

Statins

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85
Q

Clinical uses of Statins

A

Primary and secondary prevention of CHD, (in patients with chronic kidney disease, diabetes type 1 and 2) familial hypercholesterolaemias, in children (>10years)

86
Q

Contraindications in statins

A

In pregnancy

87
Q

Statins ADRs

A

Muscle. (more serious: myopathies, hepatotoxicity)

88
Q

Fibrates mechanism and effects

A

activator of peroxisomal proliferator activator receptor (PPARalpha) leads to increasedity, lipoprotein lipase activity and increase HDL synthesis

89
Q

Clinical uses of Fibrates

A

In combination with statins/ in various dyslipidaemias

90
Q

Fenofibrate, gemfribrozil

A

Fibrates (lipid lowering drugs)

91
Q

Colestyramine, cholestipol

A

Bile acid binding resins (lipid lowering drugs)

92
Q

Bile acid binding resins mechanism and effects

A

Enhance plasma cholesterol clearance via enterohepatic circulation. Get decrease in LDL (but no increase in HDL and triglyceride :( )

93
Q

Clinical uses of bile acid binding resins

A

In patients with liver disease/pregnancy (with caution) when statins are not recommended

94
Q

Ezetimibe

A

Lipid lowering drug, decreases cholesterol absoroption

95
Q

Nicotinic acid/Niacin

A

Lipid lowering drug

96
Q

Aspirin

A

COX-1 Inhibitors (antiplatlet agent)

97
Q

Clopidogel mechanism

A

Antagonists of ADP Receptors (antiplatlet drug). Reduced expression of GPIIb/IIIa leads to platlet aggregation

98
Q

Dipyridamole

A

Phosphodisterase inhibitors

99
Q

ABCIXIMAB, Eptifibatide, tirofiban

A

Glycoprotein IIb/IIIa receptor inhibitors

100
Q

Aspirin therapeutic uses

A

Primary prevention of ACS (in stable angina):Low dose Aspirin 75-150mg/day

In unstable angina: higher loading doses 150-300mg

Secondary prevention of MI = in combination with ACEI, statins and B blockers

101
Q

Aspirin Side Effects

A

GI bleeding, Cerebral Haemorrhage

102
Q

Clopidogrel clincial uses

A

Secondary prevention of MI (with aspirin or alone)

103
Q

Anticoagulant mechanism of Heparin

A

Binds reversibly to to antithrombin III (ATIII) and greatly accerlates the rate at which it inactivates coagulation enzymes thrombin and factor Xa

104
Q

Side effects of Heparin

A

Bleeding, immune thrombocytopenia, osteoporosis, hypersensitivity

105
Q

Protamine Sulfate

A

Herpain antagonist (IV admin) used to to stop bleeding caused by heparin

106
Q

Fondapariunux

A

Synthetic pentasaccheride inhibitor of activated factor Xa

107
Q

Fondaparinux clinical uses

A

Acute coronary syndromes (unstable angina, NSTEMI, STEMI), stroke, deep-vein thrombosis, pulmonary embolism, prophylaxis of venous, thromboembolism follwoing orthapedic surgery

108
Q

Enoxaparin

A

Low molecular weight Heparin

109
Q

Hirudin, Bivalirudin

A

Direct thrombin inhibitors

110
Q

Direct thrombin inhibitors therapeutic uses

A

Prevention of stroke and systemic embolism. Prophylaxis of venous thromboembolism (After hip or knee replacement surgery)

111
Q

Rivaroxaban

A

Selective factor Xa inhibitor

112
Q

Warfain

A

Oral anticoagulant. Inhibits Vitamin K reductase

113
Q

Warfain -drug interactions

A

Antibiotics (decreased vitamin K avalibilty) excess alcohol (increases warfain), drugs inhibiting hepatic drug metabolism, NSAIDS (increase internal bleeding) Hypothyroidism (decreases warfain) and Hyperthyroidism (ncrease warfain)

114
Q

Warfain: side effects and contraindication

A

Bleeding.

Teratogenic (avoid in 1st trimester in pregnancy)

115
Q

Clinical uses of anticoagulants

A

treatment of unstable angina (NSTEMI), Prophylaxis of venous thromboembolism,

116
Q

Alteplsae

A

fibrinolytic agent - recombinant tPA. Prevents conversion of plasminogen to plasmin

117
Q

Reteplase

A

Fibrinolytic agents- recombinant tPA prevents conversion of plasminogen to plasmin

118
Q

Streptokinase

A

fibronlytic agent

119
Q

Urokinase

A

fibrinolytic agents

120
Q

Tranexamic acid

A

anti-thrombolytic

121
Q

First line treatment of heart failure

A

ACE inhibitor +B-blocker + Diuretic

122
Q

Digoxin, Oubain

A

Cardiac glycosides

123
Q

Milrinone, Enoximone

A

Phoshodiesterase type 3-inhibitors cardiac selective

124
Q

Minoxidil, Diazoxide, Nicorandil

A

Potassium (ATP-sensitive) channel activators (openers)

125
Q

Uses and effects of phoshodiesterase inhibitors in CHF

A

Use: short term treatment in acute decompensation of CHF

Effects: increased CO, reduced right atrial pressure, reduced TPR, overall has little affect of HR and BP

126
Q

Phosphodiesterase inhibitors side effects

A

Nausea, vomiting, liver abnormalities, thrombocytopenia, lethal arrthymias (with prolonged use)

127
Q

Glyceral trinitrate, isosorbide dinitrate, isosorbide mononitrate, sodium nitroprusside

A

Nitrates, and nitric oxide releasing drugs

128
Q

Ivabradine

A

I (funny) current inhibitors (SA node)

129
Q

Ranolazine

A

blocker of persistent cardiac sodium channels

130
Q

Moxonidine

A

Imidazoline I1 receptor agonists

131
Q

Levosimendan

A

Calcium sensitising positive inotropes

132
Q

Loop diuretics. Site of action

A

Thick ascending limb of the loop of henle

133
Q

Loop diuretics. Mechanism

A

Inhbition of the luminal Na+ /K+/2Cl- cotransporter

134
Q

Furosemide, Bumetanide

A

Loop diuretics

135
Q

loop diuretics - therapeutic uses

A

For treatment of salt and water overload in: acute pulmonary oedema, CHF, renal failure, nephrotic syndrome.

Liver cirrhosis with ascites

Hypertension complicated by renal impairment

136
Q

Thiazides site of action

A

early distal tubule

137
Q

Thiazides mechanism

A

Inhibition of Na+/Cl- transporter

138
Q

Bendroflumethiazide, Chlorothiazide

A

Thiazides

139
Q

Chlortalidone, Indapamide, Metolazone

A

Thiazide-like drugs

140
Q

Thiazides therapeutic uses

A

hypertension, in mild heart failure, severe resistant odema, prevention of kidney stone formation in idiopathic hypercalcicuria, nephrogenic diabetes insipidus

141
Q

Adverse effects of loop diuretics and thiazides

A

Hypotension, Gout, Hypokalaemia (Dysrhythmias, increased digoxin toxicity, hyperglycaemia)

142
Q

Spironalactone, Epleronone

A

Aldoesterone antagonists (Potassium sparing diuretic)

143
Q

Amiloride, Triamterene

A

Na+ channel epithelial blockers

144
Q

Potassium sparing diuretics therapeutic uses

A

To prevent hypokalalemia, heart failure, resistant essential hypertension, aldosteronisms

145
Q

Adverse effects of potassium sparing diuretics

A

Main= hyperkalaemia (more common in patients with renal diseases)

146
Q

Mannitol

A

Osmotic diuretic

147
Q

Mechanism of osmotic diuretics

A

Increase filtrate osmolarity. decreasing passive water reabsorption. Act of parts of the nephron freely permeable to water: Proximal tubule, descending limb of loop of henle, collecting tubule (in the presence of ADH)

148
Q

Osmotic diuretics therapeutic uses

A

In acute renal failure.

Non renal uses: in emergency treatment of raised intracranial and intraocular pressure (glaucoma)

149
Q

Acetazolamide

A

Carbonic anhydrase inhibitors

150
Q

Carbonic anhydrase inhibitors clinical uses

A

Glaucoma, alitude thickness - little use as a diuretic drug due to rapid tolerance

151
Q
A
152
Q

Phenylephrine - site of action

A

alpha 1 selective agonist

153
Q

Phenylephrine and Methoxamine uses

A

Selective Alpha 1 agonists cause smooth muscle constriction, used as nasal decongestants

154
Q

Methoxamine

A

Selective alpha 1 agonist

155
Q

Clonidine - site of action and effects

A

Selective alpha 2 agonist prevents NA release and hence reduces BP used as an antihypertensive

156
Q

Dobutamine - site of action

A

B1 agonist

157
Q

Dobutamine effects and uses

A

Dobutamine is an B1 agonist which increases cardiac contractility and so is used to treat cardiogenic shock

158
Q

Adrenaline - therapeutic uses

A

Cardiac arrest and anaphylatic shock

159
Q

Terbutaline -site of action

A

B2 agonist

160
Q

Carbidopa

A

Inhibits NA synthesis by inhibiting DOPA decarboxylase. Used to treat parkisons disease alongside Levodpa

161
Q

alpha-methyl-p-tyrosine

A

Inhibits tyrosine hyroxylase, inhibiting synthesis of NA - prossible us in phaechromocytoma

162
Q

Isoprenaline

A

NON SELECTIVE Beta agonists

163
Q

Oxymetazoline

A

NON SELECTIVE alpha agonist

164
Q

Doxazocin, Prazosin - site of action

A

Selective alpha 1 agonists

165
Q

Effects of Prazosin

A

Alpha 1 antagonist causing vasodilation and fall in aterial pressure (smooth muscle relaxation of bladder)

166
Q

Yohimbine - site of action

A

Selective alpha 2 antagonist

167
Q

Amphetamine, Tyramine

A

Indirectly acting sympathimimetic. Substrate for NET - rapidly displaces NA and increases NA in the synapse.

168
Q

Cocaine, impramine

A

Inhibits NET -and therefore NA uptake, increasing NA in synapse

169
Q

Guanethidine

A

Substrate for NET and VMAT. Displaces NA slowly (high doses will destory neurones)

170
Q

Reserpine

A

Inhibits VMAT and therefore vesicular NA uptake. Free NA is metabolised by MAO

171
Q

Side effects of Reserpine

A

Depression and parkinsonism

172
Q

NA is metabolised by what two enzymes

A

Monoamine Oxidase (MAO) and Catechol-O-methyl transferase

173
Q

Alpha-methyldopa

A

False NA precursor. Metabolised to methyl-NA acts as a alpha 2 agonist (this inhibits release of NA), used to treat pregnancy induced hypertension.

174
Q
A
175
Q

Carbachol

A

Muscarinic receptor agonists

176
Q

Bethanecol

A

Muscarinic agonist - use to assist bladder empyting or to stimulate GI

177
Q

Pilocarpine

A

Muscarinic receptor agonist - selectivity for constrictor pupillae, sweat, salivary, lacrimal. (minimal activity on smooth muscle and heart) Used to treat glaucoma. Stable compound actions last for one day.

178
Q

Oxotremorine

A

Muscarinic agonist

179
Q

Methacholine

A

Muscarinic receptor agonist

180
Q

Atropine

A

NON Selective muscarinic antagonist

181
Q

Clinical uses of Atropine

A

Adjunct anaesthia, treat anticholinsterase poisoning, bradycardia, GI hypermotility

182
Q

Atropine side effects

A

Urinary retention, dry mouth, blurred vision, constipation

183
Q

Scopolamine

A

Non selective muscarinic receptor antagonist.

184
Q

Pirenzipine

A

M1 selective antagonist - treatment for peptic ulcers

185
Q

Ipratropium

A

Non selective muscarinic antagonist

186
Q

What is Ipratripiom used to treat?

A

Irritant induced bronchospasm by inhilation/nebulisers, asthma, bronchitis, COPD

187
Q

Tioptropium

A

Simular to Iproatropium but with improved PK. Binds to all muscarinc receptors - but with so M3 selectivity

188
Q

Oxybutynin

A

M3 selective antagonist

189
Q

Nicotinine

A

Stimulates autonomic ganglia, leads to tachycardia, increased BP and increased secretions

190
Q

Trimetaphan

A

Blocks nicotinic receptors and therefore action of ACH. used for emergency lowering of blood pressure

191
Q

Hexamethonium

A

Blocks channels on autonomic ganglia - doesnt not compete with ACh

192
Q

Hemicholinium

A

Blocks the uptake of choline

193
Q

Botulinum toxin

A

Prevents vesicles fusing and releasing ACh (Botox)

194
Q

Vesamicol

A

Vesamicol acts presynaptically by inhibiting ACh uptake into synaptic vesciles leads to empty vesicles fusing with neuron membranes and reducing ACh release.

195
Q

Tubocurarine

A

non depolarising competitve nACh receptor antagonist

196
Q

Gallamine

A

Non depolarising competitive nACh antagonist - synthetic analogue of tubocuraine

197
Q

Pancuronium

A

non depolarisng competitive nACh antagonist - synthetic analogue of tubocuraine

198
Q

Suxamethonium

A

Nicotinic acetylcholine receptor agonist, depolarizing neuromuscular blocker, resulting in persistent depolarization of the motor end plate. Used to induce short term muscle relaxation and short term paralysis

199
Q

α-Bungarotoxin

A

Bind irreversibly and competitively to the nACh receptors causing paralysis and respiratory failure

200
Q

Triethylcholine

A

Acts presynaptically. It is a drug that mimics choline (false transmitter) and causes failure of cholinergic transmission by interfering with synthesis of acetylcholine in nerve endings.

201
Q

Streptomycin

A

Inhibits Ca2+ entry presynaptically

202
Q

Neomycin

A

Inhibits Ca2+ entry presynaptically

203
Q

ß-Bungarotoxin

A

Acts pre-synaptically to block ACh release

204
Q

Neostigmine

A

Parasympathomimetic that binds and inhibits acetylcholinesterase. Used in people with myasthenia gravis.

205
Q

Edrophonium

A

Anticholinesterase reversible inhibitor

206
Q

Physostigmine (Eserine)

A

Physostigmine is a parasympathomimetic, specifically, a reversible cholinesterase inhibitor which effectively increases the concentration of acetylcholine at the sites of cholinergic transmission. Physostigmine is used to treat glaucoma. Because it crosses the blood-brain barrier, it is also used to treat the central nervous system effects of atropine overdose and other anticholinergic drug overdoses

207
Q

Disopropyl fluorophosphate (DFP)

A

Diisopropyl fluorophosphate is a parasympathomimetic drug irreversible anti-cholinesterase and has been used in ophthalmology as a miotic agent in treatment of chronic glaucoma

208
Q

Sarin

A

Inhibitor of anticholinisterase

209
Q

Pralidoxime

A

Dyflos/Sarin antidote

210
Q
A

NS, CV and renal pharmacology (1 decks)

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