MRCEM primary > Pharmacology > Flashcards

Pharmacology Flashcards

(81 cards)

Study These Flashcards
1
Q

Ventricular AP

A

phase 0: rapid depolarisation by Na influx from -90 to +30
phase 1: initial K efflux
phase 2: prolonged inflow Ca, enables AP to be prolonged and prevents tetany
phase 3: further K efflux
phase 4: resting potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Nodal AP

A

Phase 4: sloping voltage gradually reduces until -60 where hits threshold for depolarisation, Ca enters through L type cells
Phase 3:

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Sodium channel blockers

A

Class 1
flecainide, lidocaine, disopyramide, phenytoin
prolongs QRS

block fast Na channels
slow depolarisation
widen QRS
pro-arrhythmic risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Beta blockers

A

block beta adrenoreceptors
B1 receptors in heart
Gs protein-coupled - chemical on outside (norad or adre) attaches to ligand which produces secondary messenger e.g. increases cAMP and protein kinase A

leads to increase L type Ca channel opening -> increase Ca in cardiac cells -> increased HR -> increased contractility

B1 blockade -> reduced cAMP -> less Ca entry -> AV nodal slowing -> reduced contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Amiodarone

A

potassium channel blockers

delays process of K coming back into cells
prolongs repolarisation and slows HR
prolong QT

doesn’t work in torsades du point
blocks most atrial and ventricular arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Calcium channel blockers

A

diltiazem and verapamil
block L type Ca channels
slows AV conduction
negatively inotropic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Adenosine

A

acts on A1 receptor
increases K+ out of cell
reduces Ca 2+ influx

transient AV blockade

acts on Gi protein-couple receptor -> inhibits cAMP -> reduces Ca influx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Digoxin

A

inhibits Na/K ATPase
intracelluar Na rises
affects Na/Ca exchanger leading to less Na movement in and less Ca leaves cell -> increased intracellular Ca -> more Ca release from SR during systole -> positive inotropic effect

potassium competes with digoxin for binding at Na/K ATPase
low K means less competition -> more dig binding -> greater pump inhibition -> more Ca accumulation -> more arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

RAAS

A

decrease in renal perfusion (low pressure in afferent arteriole) -> renin released from macula densa

renin acts on angiotensinogen, cleaves to angiotensin I

ACE concerts to angiotensin II in lungs

angiotenisn II:
- increase sympathetic activity
- tubular NaCl reabsorption and K+ excretion, H2O retention
- stimulates aldosterone sercretion
- arteriolar vasoconstriction
- stimulates ADH secretion from post lobe pit, increased water reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

ACE inhibitors

A
  • reduces circulating volume of angiotensin II

prevent bradykinin being broken down, inflammatory mediator

adverse effects:
- cough
- angiooedema
- hyperkalaemia
- renal impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Angiotensin Receptor Blockers

A

block AT1 receptors
don’t get adverse effects of bradykinin

AT1 receptors are where most angiotensin II acts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Aldosterone antagonists

A

block aldosterone receptor
potassium sparing
mild diuretic

spironolactone or eplerenone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Diuretics overview

A

loop: act on Na+-K+ co transporter

thiazide: Na+-Cl- co transporter

potassium sparing: ENaC and aldosterone antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Loop diuretics

A

acts on NKCC co transporter on loop of henle
particularly thick ascending limb
blocks Na/K/2Cl on apical membrane of cell so reduces movement of Na/K/Cl into cell from lumen of nephron -> lose Na -> increases tubular fluid -> diuresis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

thiazide

A

act on distal convoluted tubule
block NaCl symporter - loose NaCl (Na exchanged for K further down tubule so higher levels of Na lead to more K loss)

bendoflumethiazide
hypokalaemia
hyperuricaemia and hyperglycaemia

interaction with lithium - reduced circulating Na leads to increased reabsorption in proximal tubule - lithium also reabsorbed there -> less renal clearance of lithium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Potassium sparing diuretics

A

block ENaC in distal tubule
reduces Na reabsorption in distal tubule
amiloride, triamterene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Calcium Channel Blockers

A

block L type calcium channels
reduces Ca entry into cells
vascular smooth muscle relaxation -> vasodilation
reduced cardiac contractility
slowed AV node conduction

dihydropyridines - don’t act on heart, main action on SM e.g. amlodipine and nifedipine, predominantly vascular effects
adverse effects - peripheral oedema, flushing, headache, reflex tachycardia

non-dihydropyridines - verapamil and diltiazem
slows AV node conduction by blocking Ca uptake, used for arrhythmias
adverse effects: bradycardia, heart block (if used with beta blockers), reduced cardiac contractility, constipation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Severe Hypertension

A

malignant HTN and pre eclampsia
reduce BP gradually

labetalol - combined a1 and b blocker, reduces peripheral vascular resistance without large reflex tachycardia

nicardipine - CCB causing arterial vasodilation

GTN - veno and coronary vasodilation

hydralazine - arterial vasodilator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Inotropes and vasopressors

A

act on adrenoreceptors
G protein coupled - increase intracellular Ca

adrenaline:
- beta - increase HR, increase contractility, dilate coronary arteries, bronchodilation
- alpha - vasoconstriction of skin and splanchnic vessels

noradrenaline - acts on alpha receptors, a1 smooth muscle, a2 on pre synaptic receptor (causes inhibition of synapse)

dobutamine - B1 agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Coagulation cascade

A

intrinsic pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Factor Xa/antithrombins

A

catalyses prothrombin to thrombin
factor Xa blockers - unfractionated heparin, LMWH, fondaparinus

work through changing shape of antithrombin III which acts on factor Xa

LMWH - removed various weights of heparin, more predictable than unfractionated heparin (lots bound by plasma, requires APTT monitoring)

bleeding in LMWH or unfractionated heparin can be reversed by protamine

fondaparinux
synthetic, pentasaccharide related to heparin
binds antithrombin -> selective inhibition on factor Xa
lower risk of HIT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Warfarin

A

inhibits vit K recycling
reduced factors II, VII, IX, X
takes days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

DOACs

A

dabigatran factor IIa inhibitor, reversed by idarucizumab (monoclonal Ab)

factor Xa inhibitors e.g. apix or rivaroxaban
reversal agent andexanet alfa

Reversal in major bleeding:
- prothrombin complex concentrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

antiplatelets

A

aspirin:
- irreversible COX-1 inhibitor
- cannot form thromboxane
- platelet has no nucleus so cannot make more, blocked for life span (5-7 days)

clopidogrel, prasugrel and ticagrelor
- P2Y12 blockade
- block ADP mediated platelet activation

clopidogrel - prodrug (needs activation), irreversible P2Y12 receptor inhibitor, hepatic activation

prasugrel - prodrug, more potent and faster than clopi

ticagrelor - direct reversible P2Y12 inhibitor, rapid onset, stronger platelet inhibition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
NSAID prothrombotic effect
diclofenac inhibits cyclooxygenase, especially COX2, alters balance between prostcyclin and thomboxane prostacyclin - produced from endothelium, causes vasodilation, inhibits platelet aggregation thromboxane A2 - produced from platelets, causes vasoconstriction, promotes platelet aggregation by reducing prostacyclin, thromboxane activity unopposed leading to increased platelet aggregation and vasoconstriction
26
Lipid lowering - statin
block HMG-CoA reductase reduces intracellular cholesterol in hepatocytes liver binds LDL in liver and removes from circulation
27
Drugs prolonging QT
drugs blocking cardiac potassium channels e.g. amiodarone increases risk of torsade de pointes (polymorphic VT) further depolarisations can happen during repolarisation period sotalol, methadone, clarithromycin
28
Drugs causing hyperkalaemia
ACE inhibitors ARBs spiro and eplerenone amiloride/triamterene trimethoprim (acts like amiloride at ENaC) heparin - suppresses aldosterone synthesis propranolol - beta blockers reduce cellular K+ uptake
29
Drugs worsening asthma
non selective beta blockers (act on beta 2 - bronchodilation) e.g. propronolol, timolol, sotalol, pindolol, labetalol altered arachidonic acid metabolism e.g. NSAIDs or aspirin block cyclooxygenase leading to reduced prostaglandin synthesis, arachidonic acid diverted to leukotriene pathway
30
Benzodiazepines
sedative and anticonvulsant, anxiolytic diazepam: long half, lipid soluble chlordiazepoxide, alcohol withdrawal midazolam - IV, buccal lorazepam GABAa receptors - chloride channels, act as main inhibitory neurotransmitter in brain benzos facilitate and enhance GABAa binding most depend on CYP450 for elimination
31
Lithium
used in bipolar disorder narrow therapeutic index toxicity in sodium depletion, confusion, tremor ataxia treated in similar way to Na in body
32
tricyclic antidepressants
amitriptyline, nortriptyline mod-severe depression neuropathic pain inhibit neuronal reuptake of 5HT and noradrenaline increasing availability for neurotransmission also block muscarinic, histamine, a-adrenergic and dopamine receptors dangerous in OD - anticholinergic effects, cardiac conduction abnormalities, respiratory depression, convulsions, metabolic acidosis
33
SSRIs
fluoxetine, sertraline, citalopram mod-sev depression, panic disorder, obsessive compulsive disorder inhibit neuronal reuptake of 5-HT common adverse effects: GI, appetite, hyponatraemia if used with other serotonergic drugs - serotonin syndrome autonomic hyperactivity, altered mental state, neuromusclar excitation
34
Antihistamines - nausea
cyclizine promethazine H1 receptor antagonists
35
Vomiting centre
medulla receives input from: - chemoreceptor trigger zone - solitary tract nucleus - vestibular system - higher neurological centres dopamine 2 receptors are main receptor in CTZ histamine and acetylcholine muscarinic receptors predominate in vomiting centre and vestibular system
36
metoclopromide/domperidone
dopamine D2 receptor antagonists acts on D2 receptors in CTZ dopamine also neurotransmitter in gut - promotes relaxation of stomach and lower oesophageal sphincter dopamine antagonists -> prokinetic diarrhoea common side effect extrapyramidal syndromes avoid in PD - domperidone safe as doesn't cross BBB
37
Antipsychotics 1st gen
phenothiazines - chlorpromazine sedating, hypotension, anticholinergic and extrapyramidal effects, neuroleptic malignant syndrome (high temp, rhabdo) butyrophenones - haloperidol, not sedating, calming effect, also used as antiemetic in palliative care block post synaptic dopamine D2 receptors
38
Antipsychotics 2nd gen
quetiapine, olanzapine better side effect profile than 1st gen block post synaptic dopamine D2 receptors
39
paracetamol
mechanism poorly understood weak inhibitor of cyclooxygenase (COX 2 specific) in brain COX inhibition increases pain threshold weak antiinflammatory - actions inhibited by peroxides metabolised in liver by CYP450 to toxic metabolite NAPQI which is conjugated with glutathione - pathway saturated in overdose, NAPQI hepatotoxic
40
opiates
morphine - naturally occuring oxycodone - synthetic activation of opioid u receptors in CNS - G protein coupled receptors medulla - blunt response to hypoxia and hypercapnia codeine and dihydrocodeine both weak opiates, activated in liver by CYP2D6 to morphine and dihydromorphine tramadol synthetic opioid, also has serotonergic and adrenergic effects
41
Carbemazepine
antiepileptic focal and grand mal epilepsy, trigeminal neuralgia inhibits neuronal Na channels, stablising resting membrane potentials and reduces neuronal excitability enzyme inducer ataxia, dizziness, drowsiness
42
Phenytoin
second line in status epilepticus narrow therapeutic index
43
anti epileptic hypersensitivity syndrome
often within 2 months of starting anti epileptic, common in carbemazepine and lamotrigine severe skin reactions e.g. SJS or TEN, fever, lymphadenopathy mortality 10%
44
sodium valproate
inhibitor of sodium neuronal channels, stabilising resting potential and reducing neuronal excitibility also increases availability of GABA teratogenic in 1st trimester
45
Penicillins mechanism of action
inhibit enzymes responsible for cross linking peptido-glycans in bacterial cell wall weakens cell wall -> influx of water, causing swelling, lysis and cell death contain beta lactam ring
46
Pen V (methylphenoxypenicillin)
S viridans S pyogenes cell wall disruption, modest oral absorption as acid-labile bacteriocidal bio availability 60%
47
Penicillin G (benzylpenicillin)
S viridans S pyogenes IV
48
amoxicillin
synthetic penicillin bioavailability 95% rash in infectious mononucleosis (EBV) extended spectrum, covers some gram -ve, resistence in S pneumoniae and H influenzae
49
co-amoxiclav
beta-lactamase inhibited by clavulanic acid broad spectrum gram +ve and -ve cover tazocin (piperacillin/tazobactam) IV only, greater spectrum
50
cephalosporins
cell wall disruption mechanism similar to penicillins cross sensitivity in pen allergy 10% in 1st gen 4 generations associated with c diff
51
sulphonamides
anti folate allergic reactions in HIV 60%, SJS co trim strep, staph, e coli and h infl
52
trimethoprim
UTIs particularly e coli anti folate, well absorbed orally sulphonamide for pneumocystis
53
macrolides
erythromycin, clarithromycin (more gram +ve than ery) mycoplasma, atypical pneumonia, pertussis bind to ribosomes and inhibit protein synthesis inhibit CYP450 enzymes so increase levels of other drugs prolong QTc
54
Clindamycin
anaerobes, gram +ve binds ribosomes and inhibits protein synthesis 90% bioavailability good tissue penetration, useful for osteomyelitis strongly associated with c diff
55
tetracyclines
malaria, rickettsia, chlamydia, lymes disease binds to ribosomes and inhibits protein synthesis teratogenic photosensitising
56
aminoglycosides
gram -ve cover some resistance in pseudomonas, can transmit resistance via plasmids gentamicin protein synthesis inhibition, not absorbed orally ototoxic and renal toxicity
57
glycopeptides
vancomycin and teicoplanin gram +ve and c diff (oral) disrupts cell wall synthesis MRSA
58
nitrofurantoin
gram -ve good for e coli no activity for proteus or pseudomonas damages bacterial DNA 25% oral dose concentrated in urine
59
quinolones
broad spectrum cover inc gram -ve levofloxacin, moxifloxacin, ciprofloxacin disrupt DNA biggest cause of c diff internationally tendon rupture good oral absorption
60
metronidazole
anaerobes and protozoa c diff and h pylori well absorbed orally
61
chloramphenicol
broad spectrum disrupts protein synthesis causes aplastic anaemia eye drops penetrates BBB well
62
fusidic acid
disrupts protein synthesis good anti staph, resistance develops rapidly
63
antimalarials
quinine: first line in falciparum (+doxy), SEs nausea, tinnitus and vertigo chloroquine: first line in vivax, ovale and malariae malarone (proguanil and atovaquone) alt first line for falciparum
64
sulphonylureas
gliclazide stimulates release of insulin by pancreas risk of prolonged hypoglycaemia
65
biguanides
metformin reduces gluconeogenesis, increases peripheral utilisation of glucose lactic acidosis
66
NaCl 0.9% fluids
Na 154 Cl 154 pH 5
67
dextrose 4%/saline 0.18%
Na 30 Cl 30 dextrose 40g pH 4
68
Hartmann's
Na 131 K 5 Ca 2 Cl 111 lactact 29 pH 6.5
69
Bicarbonate 8.4%
Na 1000 HCO3 1000 pH 8
70
albumin 4.5%
Na <160 K <2 Cl 136 albumin 40-50g pH 7.4
71
NSAIDs
inhibit COX1 and COX2 -> reducing prostaglandin production COX 2 most valuable, anti-inflam and analgesic, COX 1inhibition predisposes to peptic ulcers (prostaglandin protection in stomach) ibuprofen and naproxen most COX2 selective SEs: peptic ulcer disease, HF, aggravation of asthma, interstitial nephritis increased thrombotic risk in COX 2 selective agents
72
Gout
indomethacin colchicine
73
Thiopental sodium
induction agent smooth induction, rapid recovery due to tissue redistribution cardiorespiratory suppression, large doses cause prolonged sedation
74
etomidate
rapid recovery, less hypotension suppresses adrenal function, best avoided in sepsis
75
propofol
sedation and anaesthesia loss of airway, hypotension, bradycardia rapid recovery
76
ketamine
dissociative anaesthetic good maintenance of airway and BP bronchodilation - good in asthma increases salivation-> laryngospasm distressing emergence
77
nitrous oxide
usually with 50/50 O2 good analgesic
78
non depolarising neuromuscular blocking agents
atracurium, rocuronium non depolarising antagonises acetylcholine receptors slower onset than suxamethonium
79
depolarising agents
suxamethonium valuable for intubation rapid onset and recovery paralysis preceded by painful muscle fasculations - anaesthetic agent first avoid in FHx malignant hyperthermia, hyperkalaemia, recent major trauma or burns
80
local anaesthetics
lidocaine 3mg/kg max dose, duration 20mins lidocaine with adrenaline 7mg/kg max dose, duration 90mins bupivicaine 240-480mins, 2.5mg/kg prilocaine 20mins, 7mg/kg
81
MRCEM primary
flashcards
Decks in class (6)
# Cards
Brainscape helps you reach your goals faster, through stronger study habits.
© 2026 Bold Learning Solutions. Terms and Conditions