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Pharmacology > Drugs > Flashcards

Drugs Flashcards

1
Q

Beta Blockers effects

A
  • May block beta-adrenoceptors non-selectively or selectively
  • During exercise, or stress, RATE, FORCE and CO are depressed
  • Reduced maximal exercise tolerance
  • Myocardial O2 requirement falls, thus better oxygenation of the myocardium
  • Decrease excessive sympathetic drive and help restore normal sinus rhythm
  • Delay conduction through AV node and help restore sinus rhythm
  • Increase amount of time spent in the diastole, improving perfusion to left ventricle
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2
Q

Beta blockers - Used for

A

Used to treat//

  • Arrhythmia
  • Angina
  • Heart failure (compensated, chronic - start low and go slow)
  • Hypertension (no longer first line unless comorbidities are present like angina)
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3
Q

Beta Blockers - Side effects

A
  • Bronchospasm
  • Bradycardia
  • Hypoglyceamia
  • Fatigue
  • Cold extremities (beta 2 adrenoceptor mediated vasodilation in cutaneous vessels is prevented)
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4
Q

Propranolol

A
  • Non selective beta blocker
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5
Q

Atenolol

A

Beta-1 selective beta blocker

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6
Q

Bisoprolol

A

Beta-1 selective beta blocker

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7
Q

Atropine

A
  • Non selective muscarinic ACh receptor antagonist
  • Increase in HR
  • No effect upon arterial BP
  • No effect upon response to exercise

Treatment for//

  • Severe bradycardia (following M.I.) + monitoring as given cautiously
  • In anti cholinesterase poisoning
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8
Q

Digoxin

A
  • Cardiac glycoside
  • Increases CONTRACTILITY of the heart
  • Positive inotrope (also dobutamine)

> blocks SARCOLEMMA ATPase
causes increase of Ca2+ in the cell and that is subsequently stores
Increased calcium induced calcium release
INCREASED CONTRACTILITY

> stimulates vagal activity
slows conduction and prolongs refractory period in AV node and bundle of His

> AV Node

> narrow therapeutic window

1.0 - 2.6 nmol/L

Treatment//

  • IV in acute heart failure where CO is insufficient in providing adequate tissue perfusion
  • Orally in chronic heart failure
  • Heart failure with AF
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9
Q

Digoxin - side effects

A
  • Narrow therapeutic window
  • excessive depression of AV node conduction
  • can cause arrythmias
  • nausea
  • vomiting
  • diarrhoea
  • disturbance of colour vision
  • can be dangerously enhanced in hypokalaemia
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10
Q

Organic nitrates

A
  • relax all types of smooth muscle
  • venorelaxation
  • arteriolar dilatation
  • Blood is redirected towards ischaemic zone in angina

> In angina - benefit derives from decreased myocardial oxygen requirement via

i) decreased preload
ii) decreased afterload
iii) improved perfusion to the ischaemic zone

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11
Q

Arterial Pulse Wave Reflection

A

Blood collides with Y shaped junction of artery bifurcation.

Pressure in the other direction (negative pressure wave going back to the heart) – more work for the heart to do.

Organic nitrates decrease this effect

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12
Q

GTN (glyceryltrinitrate)

A

> Short acting
Sublingual (as it has extensive first pass metabolism)
more sustained if transdermal patch

Treatment//

  • Angina
  • Acute coronary syndrome

Tolerance/adverse effects//

  • repeated administration of GTN/organic nitrates can lead to diminished effects
  • postural hypotension
  • headaches
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13
Q

Isosorbide Mononitrate

A
  • Organic Nitrate
  • longer lasting than GTN
  • resistant to first pass metabolism
  • orally as prophylaxis fro angina
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14
Q

Renin release stimulated by

A
  • renal sympathetic nerve activity increased
  • renal artery hypotension
  • decreased sodium delivery to distal tubules of kidney (decreased glomerular filtration)
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15
Q

ACE inhibitor (-prils)

A

Block conversion of angiotensin 1 to angiotensin II (Angiotensin Converting Enzyme)

Inhibit metabolism of bradykinin

Cause venous dilatation

Fall in arterial blood pressure

  • produces a dry cough

Treatment//

> Hypertension - reduced TPR and MABP

> Cardiac Failure - decreasing vascular resistance

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16
Q

AT1 receptor Blockers (ARBs) (-sartans)

A

ARBs block angiotensin II at AT1 receptors in a competitive manner

indicated when patient cannot cope with dry cough associated with ACEIs

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17
Q

Bradykinin

A

Vasodilator

causes blood pressure to fall.

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18
Q

What are ARBs and ACEIs contraindicated in?

A

Pregnancy

Bilateral renal stenosis

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19
Q

Calcium Antagonists

A

Prevent opening of L-type channels in excitable tissues

Limit increase in calcium concentration

Arteriolar dilatation, reducing TPR and MABP

In nodes - can reduce rate of conduction through the AVN

In ventricular AP - can reduce force of contraction

Ventricular rate in rapid AF reduced by suppression of conduction through AV node

Interact preferentially with L-type calcium channels found
> in the heart
> in smooth muscle

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20
Q

What do L-type calcium channels mediate?

A

> UPSTROKE of AP in the nodes

> Phase 2 (plateau phase) of ventricular AP

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21
Q

Verapamil

A
  • Cardiac L-type selective calcium channel antagonist

used for//

hypertension

atrial flutter

cause coronary vasodilation - so suitable for patients with ANGINA and HYPERTENSION

adverse effects//

heart block in high doses

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22
Q

Amlodipine

A

Dihydropyridine - relatively selective for smooth muscle L-type calcium channels

Treatment//

Angina

Adverse Effects//

  • ankle oedema
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23
Q

Diltiazem

A

Intermediate activity calcium antagonist

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24
Q

Calcium Antagonists - adverse effects

A

Hypotension
Dizziness
Flushing
Ankle oedema

due to excessive vasodilation

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25
Q

Which calcium antagonist should be avoided in heart failure?

A

Verapamil - particularly in combination with a beta blocker

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26
Q

Potassium Channel Openers

A

Opening of potassium channel causes hyper polarisation - which switches off L-type Calcium channels

Hyperpolarisation - because more positive charge on outside of cell than inside, so membrane potential is very negative.

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27
Q

Minoxidil

A

Potassium channel opener

Drug of last resort in HYPERTENSION

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28
Q

What can minoxidil cause?

A

Reflex tachycardia (can be prevented by a beta blocker)

Salt and water retention

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29
Q

Nicorandil

A

Potassium channel opener

  • Used in angina refractory to other treatments
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30
Q

alpha1-adrenoceptor antagonists

A
  • cause vasodilation by blocking vascular alpha-1 adrenoceptors
  • ↓MABP

PRAZOSIN and DOXAZOSIN

Benign prostatic hyperplasia

Postural hypotension

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31
Q

Diuretics

A

Act on kidneys to increase the excrete of Na, Cl and H2O

Relaxant effects on vasculature

Thiazide and Loop diuretics

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32
Q

Thiazide diuretics

A

Inhibit NaCl reabsorption in the distal tubule by blocking the Na+/Cl- co-transporter

Cause up to 5% of filtered Na+ to be excreted along with H20 producing a moderate diuresis

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33
Q

Loop Diuretics

A

Inhibit NaCl reabsorption in the thick ascending limb of the loop of Henle by blocking the Na+/K+/2Cl- co-transporter
Cause up to 15-25% of filtered Na+ to be excreted with accompanying H20 producing a strong diuresis

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34
Q

What undesirable effect do diuretics have, and how can this be corrected?

A

Loss of potassium.

corrected by potassium sparing diuretic/ K+ supplements

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35
Q

Bendroflumethiazide

A

Thiazide diuretic

  • Mild heart failure
  • Hypertension
  • Severe resistant oedema (+ loop)
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36
Q

Furosemide

A

Loop diuretic

acute pulmonary oedema IV)

Chronic heart failure

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37
Q

In vascular smooth muscle, how does contraction come about?

A
  • GPCR activation promotes release of Calcium from sarcoplasmic reticulum
  • Calcium combines with Calmodulin to form Ca2+-calmodulin
  • Ca2+-Cal activates Myosin light chain kinase
  • MLCK then phosphorylates myosin light chain
  • —> CONTRACTION
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38
Q

Relaxation in vascular smooth muscle cells?

A
  • cyclic GMP promotes the activation of protein kinase G (PKG)
  • PKG activates Myosin light chain PHOSPHATASE
  • This dephosphorylates myosin light chain leaving myosin light chain
  • RELAXATION
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39
Q

Anti-arrhythmic drugs

A

4 classes, 1 is split into 1a, b and c

Classes I: Ia, Ib, Ic
II
III
IV

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40
Q

Class Ia

A

Block voltage-activated Na+ channel

Slow rise of AP and prolong refractory period

Act on VENTRICLES, ATRIA, AV accessory pathways

Moderate rate of dissociation

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41
Q

Class Ib

A

Block voltage-gated Na+ channel

Prevents premature beats

Act on VENTRICLES

Rapid rate of dissociation

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42
Q

Class Ic

A

Voltage activated Na+ channel

Slow rate of dissociation

Act upon ATRIA, Ventricles and AV accessory pathways

Depress conduction

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43
Q

Disopyramide

A

Class Ia anti-arrhythmic

Moderate rate of block and unblock

Block open channels

If AP frequency is high, moderate dissociation results in insufficient time for blocking and unblocking

Used to prevent recurrent ventricular arryhthmias

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44
Q

Lignocaine

A

Class Ib anti-arrhythmic

rapid block/dissociation

prevents premature beats

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45
Q

Flecainide

A

Class Ic anti-arrhythmic

slow rate of block and unblock

strongly depresses conduction in myocardium and reduces contractility

Prophylaxis of paroxysmal atrial fibrillation

Negative inotropic action - may trigger ventricular arryhthmias

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46
Q

Class II

A

Beta-adrenoceptor antagonist (beta blockers)

Control SVT by suppressing impulse conduction through AV node

Suppress excessive sympathetic drive that may trigger VT

decrease rate of depolarisation in SA and AV nodes

Act on VENTRICLES and AV node

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47
Q

Class III

A

Voltage-activated K+ channels BLOCKERS

Prolong AP duration increasing refractory period

Act upon ATRIA

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48
Q

Class IV

A

Voltage Activated Ca2+ channels

Slow conduction in SA and AV nodes

Act on AV NODE

Decrease force of cardiac contraction

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49
Q

Amiodarone

A

Class III anti-arrhythmic

Potassium channel blocker

Prolongs the AP

Increases refractory period

suppresses reentry

effective against SVT and VT as it has Ia and IV actions and also blocks beta adrenoceptors

Effective when many other drugs have failed

Adverse effects//

  • pulmonary fibrosis
  • thyroid disorders
  • photosensitivity reactions
  • peripheral neuropathy
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50
Q

Where do class I agents bind?

A

They preferentially bind to areas of myocardium in which firing frequency is highest.

Channels which are in the OPEN and INACTIVATED states

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51
Q

Adenosine

A

> Activates A1 adenosine receptors coupled to Gi/o

– opens ACh-sensitive K+ channels

– Hyperpolarises the AV node briefly, suppressing impulse conduction

– Used to terminate paroxysmal supraventricular tachycardia caused by re-entry

Acts upon AV node

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52
Q

Anticoagulants

A

> Treatment of venous thrombosis and embolism

  • -DVT
    • Prevention of post-op thrombosis
    • patients with artificial valves

Risk of haemorrhage

53
Q

Warfarin

A

> Anticoagulant
Competes with vitamin K for binding hepatic vitamin k reductase
renders factors II, VII, IX and X inactive
Oral
Slow onset of action

Disadvantages//

> low therapeutic index
Effects of warfarin must be monitored regularly

54
Q

LMWHs

A 
> Anticoagulant 
> Inhibit factor Xa via antithrombin III
> SC
> Elimination is of first order 
> Renal excretion - so not used in renal failure
55
Q

Enoxaparin

A

LMWH
Anticoagulant
given SC

not used in renal failure

56
Q

Dalteparin

A

LMWH
Anticoagulant
Given SC

Not used in renal failure

57
Q

Fondaparinux

A

LMWH
Anticoagulant
Given SC

Inactivates Xa via antithrombin III

Short duration of action

Not used in renal failure

58
Q

Idrabiotaparinux

A

LMWH
Anticoagulant

Long duration of action

59
Q

Heparin

A

Anticoagulant

Inactivates Thrombin (IIa) via antithrombin III

Inactive Xa via antithrombin III

Administered IV or SC

In vitro clotting test required to determine dosage

Zero order elimination

Used in renal failure (is not excreted renally)

60
Q

LMWHs and Heparin - Adverse effects

A

> Haemorrhage
Osteoporosis
Hypoaldosteronism
Hypersensivity reactions

61
Q

Dabigatran

  • what does it directly inhibit?
A

Orally active inhibitor (anticoagulant)

Direct inhibitor of THROMBIN (IIa)

Convenience of administration

Predictable degree of anticoagulation

Prevent venous thrombosis (hip and knee replacements)

No antidote in case of overdose

62
Q

Rivaroxaban

A

Orally active inhibitor (anticoagulant)

Directly inhibits Factor Xa

Taken orally - convenient

Predictable degree of anticoagulation

Used to prevent venous thrombosis in hip and knee replacements

No antidote in case of overdose

63
Q

“Antidote” for heparin?

A

Protamine sulfate

64
Q

Anti-platelet Drugs

A

Treatment of arterial thrombosis

65
Q

Aspirin

A

> Antiplatelet (main one)

> Irreversibly blocks cyclooxyrgenase (COX) in platelets, preventing TXA2 synthesis

> Inhibits COX in endothelial cells inhibiting production of anti-thrombotic prostaglandin I2
- anti-thrombotic effect

> THROMBOPROPHYLAXIS

> Used in ACUTE MI

66
Q

Clopidogrel

A

> Antiplatelet drug
Prodrug requiring hepatic metabolism

> Links to P2Y12 receptor producing irreversible inhibition

> Used when patient is INTOLERANT to aspirin

> Has synergistic effect when combined with aspirin

> Used in Acute MI with ST elevation

67
Q

Tirofiban

A

> Antiplatelet
Given IV

> Short term treatment to prevent M.I. in high risk patients WITH angina (+ aspirin and heparin)

68
Q

Fibrinolytics (thrombolytic)

A

> Opposes coagulation cascade

> Used to reopen occluded arteries in acute M.I. or stroke

> IV administered

> PCI is superior if available

Adverse effects//

haemorrhage

69
Q

Streptokinase

A

> Fibrinolytic

> May cause allergic reaction

> Extracted from cultures of streptococci

> Reduces mortality in acute M.I.

70
Q

Alteplase (and duteplase)

A

> FIbrinolytics
Show selectivity for clots

> No allergic reactions

> IV infusion

71
Q

Haemorrhage caused by fibrinolytics can be controlled by?

A

Oral TRANEXAMIC ACID - inhibits plasminogen activation

72
Q

Antithrombin III

A

> ATIII inhibits coagulation

> Neutralises all serine proteases (Xa, IXa etc) in coagulation cascade

> Heparin binds to ATIII, increasing its affinity for clotting factors to greatly increase their inactivation (hence less coagulation)

73
Q

Proton Pump Inhibitors

A

Irreversible inhibition by covalent modification of the gastric gland parietal cell H+/K+-ATPase (the ‘proton pump’) present in the apical (canalicular) membrane.

Treatment of peptic ulcer disease

Dyspepsia

Eradication of H pylori

74
Q

Omeprazole

A

PPI

Treatment of peptic ulcer disease
Dyspepsia
Eradication of H pylori

75
Q

Lansoprazole

A

PPI

76
Q

What is used to eradicate H pylori?

A

Omeprazole + amoxicillin/ metronidazole/ clarithromycin

77
Q

Side effects of PPIs

A

Headache, diarrhoea, abdo pain, nausea, fatigue, dizziness

78
Q

What should not be used in peptic ulcer disease?

A

NSAIDs

79
Q

H2 receptor antagonists

A

Ranitidine

Competitive antagonism of the H2 receptor located on the basolateral membrane of acid secreting parietal cells of the gastric glands

Reduces gastric acid production

Less effective than PPIs

80
Q

Ranitidine

A

H2 receptor antagonist

Reduces gastric acid secretion

81
Q

What may histamine receptor antagonists and PPIs disguise?

A

The symptoms of gastric cancer

82
Q

Anti-motility drugs

A

Overall effect is constipating

> Treatment of acute diarrhoea
Symptomatic relief of diarrhoea (IBS)
Analgesia for acuter, moderate pain (codeine)

83
Q

Loperamide

A

Anti-motility

84
Q

Do not use anti-motility drugs in…

A

> Acute ulcerative colitis
Acute bloody diarrhoea
Clostridium difficile colitis

85
Q

Bulk forming laxatives

A

i) Used for constipation and faecal impaction. Viral/bacterial gastritis
ii) Mild chronic diarrhoea

do not use in intestinal obstruction

indigestible polysaccharide

86
Q

Methylcellulose

A

Bulk forming laxatives

87
Q

Osmotic Laxatives

A

Water is attracted to the stool, increasing the bulk and stimulating peristalsis

1) Constipation and faecal impaction

2) Bowl prep
3. Hepatic encephalopathy

Do not use in intestinal obstruction

88
Q

Lactulose

A

Osmotic laxative

89
Q

Macrogols

A

Osmotic laxative

90
Q

Stimulant laxative

A

Increase water and electrolyte secretion from the colonic mucosa. Colonic content is increased stimulating peristalsis

1) Constipation (PO)
2) Faecal impaction (suppository)

91
Q

Senna

A

Stimulant laxative

92
Q

Glycerol suppository

A

Stimulant laxative

93
Q

Faecal softners

A

Detergent-like action.
Arachis oil (enema)
Docusate sodium

Increased H2o and electrolyte secretion, increased peristalsis.

94
Q

Dopamine D2 Receptor Antagonist

A

Antiemetic

Nausea and vomiting associated with neoplastic disease; radiation sickness and drug induced emesis.

Prochlorperazine
Droperidol
Trifluoperazine
Chlorpromazine
Haloperidol
Levomepromazine
95
Q

Prokinetic drugs

A

Metoclopramide (antiemetic, GORD, migraine)

DOMPERIDONE (does not cross the BBB)

Increase gastric peristalsis
Increase LOS tone

Block D2 receptors in CTZ

96
Q

5HT3-receptor antagonists

A

-SETRONS

Granisetron
Ondansetron
Palonosetron

Block 5HT3 receptors in the GI tract and CNS

Chemotherapy induced N&V
Radiation induced emesis
Post-op N&V

97
Q

H1 Antihistamine

A

Promethazine
Cyclizine
Cinnarizine

Block H1 receptors in vestibular nuclei and NTS (nucleus tracts solitarius)

Additional anti-muscarinic effect

Useful in motion sickness, morning sickness, post op N&V

98
Q

Anticholinergics

A

Hyosine
Dycyclomine

Block muscarinic receptors in vestibular nuclei, NTS and vomiting centre

Motion sickness

99
Q

Predominant receptors in vomiting centre?

A

Muscarininc M1 & 3
5HT3
H1

100
Q

Predominatn receptos in CTZ?

A

Dopamine (D2)
5ht3
Opioid H1

outside BBB

more permeable to circulating substances

101
Q

Receptors in vestibular nuclei?

A

Muscarinic

Histamine type 1

102
Q

Adjuvant antiemetics

A

Role in Chemo-indcued nausea and vomiting

103
Q

NK1 (neurokinin 1) receptor antagonist ( adjuvant antiemetics)

A

Aprepitant

Antagonism of substance P

104
Q

Corticosteroids as adjuvant antiemetics

A

Dexamethasone

Methylprednisolone

105
Q

Benzodiazepines

A

Lorazepam
Diazepam

Sedative, anti-anxiety, amnesia-inducing

Unpleasant memories of chemo. These drugs bring about a state of forgetfulness so they have fewer memories and do not want to vomit pre-chemo.

106
Q

Cannabinoids

A

Nabilone
Dronabinol

sedation, hallucinogenic

107
Q

Drugs for IBD

A

> Aminosalicylates
Glucocorticoids
Immunosuppressants
Biological agents

108
Q

Aminosalicylates

A

Long term maintenance of remission of IBD

More useful in UC

109
Q

Sulfasalazine***

A

Aminosalicylate

5-ASA
reduces inflammation by inhibiting COX and LOX

Folic acid supplementation

110
Q

Mesalazine

A

aminosalicylate

111
Q

Olsalazine

A

Aminosalicyalate

112
Q

Balsalaside

A

Aminosalicylate

113
Q

IBD- glucocorticoids

A

Anti-inflammatory
For acute UC and Crohn’s

Prednisolone, Budesonide

Hydrocortisone

for acute flare ups

114
Q

Immunosuppressants in IBD

A

For disease that is unresponsive to corticosteroids

inhibit t lymphocyte function

Azathioprine***
Ciclosporin]
6 mercaptopurine
Methotrexate

115
Q

Biological agents in IBD

A

Monoclonal antibodies
Restricted to severe IBD

Block action of TNF alpha (except vedolizumab)

Infliximab
Adalimumab

any “-mab”

116
Q

What is C diff colitis treated with?

A

Metronidazole

Vancomycin

117
Q

Opioid Drugs in GI

A

Constipating effect.

Decreased peristalsis
increased segmentation
increased fluid absorption 
constriction of pyloric, ileocaecal and anal sphincters
increased tone of large intestine
118
Q

Loperamide

A

Opioid

one of the main ones

119
Q

Diphenoxylate

A

Opioid

Overdose produces disturbing side effects - nausea, headache, weakness, blurred vision.

120
Q

Codeine

A

Opioid

121
Q

Ursodeoxycholic Acid

A

May be used to dissolve non-calcified cholesterol gall stones

122
Q

Bile salt resins

A

Prevent reabsorption of cholesterol and lower plasma cholesterol

123
Q

Morphine

A

Opioid analgesic

Constricts the sphincter of oddi

Buprenorphine and pethidine are alternatives

124
Q

Atropine, or GTN

A

Biliary spasm relief

125
Q

Chemo Induced N&V Triple Therapy

A

5HT3 receptor antagonist
Dexamethazone
Aprepitant

126
Q

Post-op nausea & vomiting

A

5HT3 receptor antagonist
Droperidol
Cyclizine
Dexamethazone

127
Q

Pregnancy Associated N&V

caused by?

A

Caused by Human Chorionic Gonadotropin (placenta)

Change in diet
Use of ginger and pyridoxine
Wrist acupressure

128
Q

Hyperemesis Gravidarum

A

Intractable vomiting from pregnancy

1st line - Antihistamine
2nd line - Prochlorperazine, Metoclopramide

129
Q

When to use immunosuppressants in IBD?

A

For disease that is unresponsive to corticosteroids

Pharmacology (2 decks)

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