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Phase 2A HT > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Give three examples of TNF blockers

A

Etanercept
Infliximab
Adalimumab

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2
Q

adverse effects of TNF Blockers

A

Increased susceptibility to TB/activation of dormant TB through blunted TH1 response
Increased cancer incidence

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3
Q

give three examples of ACE inhibitors

A

ramipril, lisinopril, perindopril

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4
Q

mechanism of ACEI

A

block ACE - prevent conversion of angiotensin I to angiotensin II
ang II = vasoconstrictor and stimulates aldosterone secretion
blocking it reduces periph vasc resistance –> lowers BP
esp dilates efferent glomerular arteriole –> decreases glom P and slows progression of CKD
reduced aldosterone promotes Na and H2O excretion

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5
Q

adverse effects of ACEIs

A

hypotension
persistent dry cough
hyperkalaemia (due to low aldosterone)
worsen renal failure

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6
Q

aspirin - mechanism of action

A

aspirin irreversibly inhibits COX –> reduces production fo thromboxane from arachadonic acid –> reduced platelet aggregation

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7
Q

adverse effects of aspirin

A

GI irritation/ulceration–>haemorrhage
bronchospasm
tinnitus

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8
Q

aspirin overdose features

A

hyperventilation, hearing changes, metabolic acidosis, confusion
followed by convulsions, CV collapse and resp arrest

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9
Q

give three examples of Beta blockers

A

propanolol, bisoprolol, atenolol, metoprolol

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10
Q

mechanism of beta blockers

A

B1 adrenoceptors found mainly in hear, B2 adrenoceptors found mainly in SM of blood vessels and airways
B1 - BB reduce force of contraction and speed of conduction in heart
–> slow ventricular rate in AF by prolonging refractory period pf AV node
Also reduces renin secretion –> reduced vasoconstriction

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11
Q

adverse effects of BBs

A

fatigue, cold extremities, headache and Gi disturbance (nausea)
sleep disturbance and impotence in men can also occur

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12
Q

mechanism of clopidogrel

A

prevents platelet aggregation by binding irreversibly to ADP receptors on platelet surface
(independent of COX therefore actions are synergistic with aspirin)

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13
Q

adverse effects of clopidogrel

A

BLEEDING, GI upset (dyspepsia, abdo pain, diarrhoea)

rarely - thrombocytopenia

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14
Q

give two examples of fibrinolytic drugs

A

alteplase, streptokinase

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15
Q

mechanism of fibrinolytic drugs

A

= thrombolytic drugs, catalyse conversion of plasminogen into plasmin, which acts to DISSOLVE FIBRINOUS CLOTS and re-canalise occluded vessels

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16
Q

adverse effects of fibrinolytic drugs

A

N and V, bruising, hypotension
those requiring tx to be stopped = serious bleeding, allergic reaction, cardiac arrest
(transexamic acid is a antifibrinolytic drug)
cerebral oedema and arrhythmias due to reperfusion

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17
Q

2 examples of nitrates

A

glyceryl trinitrate, isosorbide mononitrate

18
Q

mechanisms of nitrates

A

nitrates converted into NO which increases cGMP synth and reduces intracellular Ca in vascular SM cells–> relaxation –> venous (and arterial) dilation
therefore reducing cardiac preload and ventricular filling –> reduced cardiac work and 02 demand

19
Q

AEs of ntirates

A

flushing, headaches, light-headedness, hypotension

sustained use can lead to tolerance

20
Q

2 examples of strong opioids

A

morphine, oxycodone

21
Q

AEs of strong opioids

A

resp depression, neurological depression, N and V, pupillary constriction, constipation, itching
continued use leads to tolerance and dependence
can experience withdrawal reactions

22
Q

3 examples of statins

A

simvastatin, atorvastatin, pravastatin, rosuvastatin

23
Q

mechanism of statins

A

reduce serum cholesterol levels - inhibit 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG CoA) reductase
decrease cholesterol prod by liver and increase clearance of LDL-cholesterol from blood
indirectly reduce triglycerides and slightly increase HDL
slow/reverse atherosclerotic processes

24
Q

AEs of statins

A

headache and GI distrubance

aches and myopathy

25
Q

3 examples of corticosteroids

A

prednisolone, hydrocortisone, dexamethasone

26
Q

mechanism of corticosteroids

A

= MODIFY IMMUNE RESPONSE - upregulate anti-inflam genes and downregulate pro-inflam genes

27
Q

AEs of corticosteroids

A

IMMUNOSUPPRESSION, DM and osteoporosis, proximal muscle weakness, skin thinning, easy bruising and gastritis
mood and behavioural changes
LT –> adrenal atrophy –> decreased cortisol secretion –> acute Addisonian crisis –> CV collapse
WITHDRAWAL = fatigue, WL and arthralgia

28
Q

give two examples of antiemetics

A

prochlorperazine, chlorpromazine

29
Q

list three benzodiazepines

A

diazepam, lorazepam, temazepam

30
Q

ferrous sulfate AEs

A

GI upset - nausea, epigastric pain, constipation and diarrhoea
black bowel motions

31
Q

name 3 CCBs

A

amlodipine, nifedipine, verapamil, diltiazem

32
Q

mechanism of CCBs

A

decrease Ca entry into vascular and cardiac cells (decrease Ca intracellular conc) causing relaxation and vasodilation in arterial SM decreasing arterial P
reduce myocardial contractility - suppress cardiac conduction and slow ventricular rate
leading to reduced cardiac demand therefore preventing angina

33
Q

AEs of CCBs

A

ankle swelling, flushing, headache, palpitations

verapamil - constipation, bradycardia, heart block and HF

34
Q

SSRIs indications

A

= antidepressants, used in:
moderate to severe depression
panic disorder
OCD

35
Q

mechanism of SSRIs

A

inhibit neuronal reuptake of seretonin (5-HT) from synaptic cleft, –> increases its availability for neurotransmission
differ from anticyclics in that theyy dont inhibit noradrenaline uptake and cause less blockade of other receptors
SSRIs preferred due to less AEs

36
Q

AEs of SSRIs

A

GI upset, appetite and weight disturbance
hypersensitivity incl rash
SUICIDAL THOUGHTS AND BEHAVIOUR
lower seizure threshold and can predispose to arrhythmias
Bleeding

37
Q

what is serotonin syndrome

A

triad of autonomic hyperactivity, altered mental state and neuromuscular excitation
due to high dose SSRIs/overdose/in combo with other antidepressants

38
Q

SSRIs contraindicated in:

A

epilepsy, peptic ulcer disease, young people (assoc w poorer efficacy and increased thoughts about self harm and suicide risk)

39
Q

name 2 tricyclics

A

amitriptyline, lofepramine

40
Q

indications for tricyclics

A

moderate to severe depression

neuropathic pain

41
Q

mechanism of tricyclics

A

inhibit reuptake of serotonin (5-HT) and noradrenaline, increasing their ability for neurotransmission
extensive adverse effects as they block a wide range of receptors

42
Q

AEs of tricyclics

A 
block antimuscarinic -- dry mouth, constipation, urinary retention, blurred vision
H1 and a1 - hypotension and sedation
arrhythmias and ECG changes
convulsions, hallucinations, mania
breast changes and sexual dysfunction
dangerous in overdose!

Phase 2A HT (11 decks)

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