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1
Q

ACEi
lisinopril
ramipril

A

Limit Angiotensin-I to II by inhibiting ACE

  • vasodilation -lower perif resistance -lower afterload
  • reduction in aldosterone release - Na and H2O excretion
  • reduced ADH release -higher H2O excretion
  • bradykinin -vasodilation via NOS/NO and PGI2
*Hypotension
 dry cough
 hyperkalaemia
 renal failure
 angioedema

X renal artery stenosis, AKD, pregnancy, idiopathic angioedema

! K+ increasing drugs, NSAIDs, other antihypertensives

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2
Q

ARBs
candesartan
losartan

A

AT1 receptor blocker
No effect on bradykinin

*Hypotension
hyperkalaemia
renal failure

X renal artery stenosis, AKD, pregnancy, (CKD caution)

! K+ increasing drugs, NSAIDs

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3
Q 
CCB
Dihydropyradine class
amlodipine
nifedipine
nimodipine
A

stop contraction of smooth muscle
- selective for peripheral vasculature, little chronotropic or inotropic effects

*Ankle swelling
flushing
headaches
palpitations

X unstable angina, severe aortic stenosis

! amlodipine + simvastatin

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4
Q

CCB
Phenylalkyamines
verapamil

A

Class IV - prolongs action potential/refractory period

less peripheral vasodilation, negative inotropic and chronotropic effects

used for arrhythmia, angina (hypertension)

*Constipation
bradycardia
heart block and cardiac failure

X Poor LV function, AV nodal delay

! Beta blockers, caution with other antihypertensives and antiarrhythmics

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5
Q

CCB
Benzothiazepines
Diltiazem

A

sit between other CCB classes

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6
Q

Thiazide and thiazide like
Bendroflumethazide
indapamide

A

Inhibit Na/Cl co-transporter, in distal convoluted tubule
lower Na and H2O reabsorbtion (RAAS compensates with time)
Long term- sensitivity of vascular smooth muscle to vasoconstrictors
Good with oedema

*Hypokalaemia 
 hypernatraemia
 Hyperuricaemia - gout
 arrhythmia
 ^glucose 
 ^cholesterol and triglyceride

X Hypokalaemia, hyponatraemia, gout

! NSAIDs, K+ lowering drugs

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7
Q

Aldosterone receptor antagonist

Spironolactone

A

Potassium sparing diuretic

*Hyperkalaemia, gynaecomastia

X Hyperkalaemia, addison’s

! K+ increasing drugs, pregnancy

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8
Q

Beta adrenoceptor blockers
Labetalol
bisoprolol
metoprolol

A

Decrease sympathetic tone by blocking NAd and reducing myocardial contraction
decrease renin secretion Beta1

*Bronchospasm
 heart block
 reynauds
 lethargy
 impotence
 Mask tachycardia- sign of insulin induced hypoglycaemia

X Asthma, COPD, haemodynamic instability, hepatic failure

! non-dihydropyridines CCBs,

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9
Q

Alpha adrenoceptor blockers

Doxazosin

A

Selective antagonism of Alpha-1
reduce peripheral vasculature resistance
benign prostatic hyperplasia -Tamsulosin

*Postural hypotension
 dizziness 
 syncope
 headache
 fatigue

X postural hypotension

! in patients affected by dihydropyridine CCB -oedema

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10
Q

Loop diuretic
furosemide
bumetanide

A

inhibit N/K/2Cl co-transporter in ascending limb
decrease N K and Cl into epithelium - H2O follows
Direct dilation if capacitance veins- reduces preload

for acute pulmonary oedema, fluid overload in HF, adjunct in nephrotic syndrome

*Dehydration
 Hypotension 
 Hypokalaemia 
 hyperuricaemia 
 arrhythmia 
 tinnitus
 cholesterol and triglyceride

X Hypokalaemia, hyponatraemia, gout, hepatic encephalopathy

! aminoglycosides, digoxin, lithium

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11
Q

Diuretic- potassium sparing

amiloride

A

Block ENaC
decrease Na reabsorption in DCT and reduce K secretion

*Hyperkalaemia
potential arrhythmia

X Addisons, potassium suppliments

! Other K+ sparing drugs, ACEi, ARBs

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12
Q

Statin
Simvastatin
Atorvastatin

A

Simvastatin is a prodrug t1/2 = 2h
Atorvastatin first pass- active derivatives t1/2 = 24h
competative inhibition of HMG-CoA reductase - upregulation of Hepatic LDL receptors - increase clearance of LDL
improved endothelium function
stabilisation of plaque
improved haemostasis

*GI disruption
 nausea
 headache
 diffuse muscle pain
 rare- rhabdomyolysis - OAT differences and skeletal muscle ATP production
 increased liver enzymes

X renal or hepatic impairment

! CYP 3A4 important - amiodarone, diltiazem, macrolides
amlodipine

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13
Q

Fibric acid derivatives (fibrates)

fenofibrate

A

activation of nuclear transcription factor - PPA&

PPAR& regulate expression of genes that control lipoprotein metabolism- increase production of lipoprotein lipase

^triglyceride removal from lipoprotein in plasma
^fatty acid uptake in liver
^HDL
^LDL affinity to receptor

*Gall stones,
GI upset
myositis

X photosensitivity, gall bladder disease

! Warfarin - increase coag

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14
Q

Cholesterol absorbtion inhibitors

ezetimibe

A

Inhibit NPC1L1 transporter at brush border in small intestines
reduces absorption 50%
hepatic LDL receptor expression increases

prodrug- hepatic metabolism- enterohepatic circulation- limits systemic exposure
secreted by bile
Adjunct to statin

*Abdo pain
GI upset
angioedema

X hepatic failure

! mindful with static- rhabdo
ciclosporin

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15
Q

PCSK9 inhibitors

Alirocumab

A

stops LDL being recycled

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16
Q

Bisphosphonates

Alendronic acid

A

reduce bone turnover
controls osteoclast activity

*oesophagitis
Hypocalcaemia

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17
Q

biguanides

metformin

A

decrease hepatic glucose production by inhibiting gluconeogenesis
supress appetite

*GI upset- nausea, vomiting, diarrhoea

X excreted unchanged by kidneys - stop if GFR <30mL/min
alcohol intoxication

! ACEi, diuretics, NSIADs - drugs that may impair renal function
loop and thiazide diuretics - ^glucose can reduce metformin action

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18
Q

sulfonylureas

gliclazide

A

Stimulate beta cell pancreatic insulin secretion
blocking ATP-dependent K+ channels
need residual pancreatic function

*mild GI upset, hypoglycaemia (works at low [glucose])

X hepatic and renal disease, those at risk of hypo

! other hypoglycaemics, loops and thiazides ^glucose can reduce its action

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19
Q

thiazolidinediones (glitazones)
pioglitazone
rosiglitazone

A

insulin sensitisation in muscle and adipose, decrease hepatic glucose output by activation of PPAR-gamma -> gene transcription
t1/2 not related to duration of action 6-8 weeks for benefit
weight gain

*GI upset
fluid retension
fracture rist
bladder cancer

X heart failure - fluid retension

! other hypoglycaemics

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20
Q

SGLT-2 inhibitors (gliflozins)
dapagliflozin
canagliflozin

A

decrease glucose absorption from tubular filtrate
increase urinary glucose excretion
competitive reversible inhibition of SGLT-2 in pct
Modest weight loss, hypoglycaemic risk low
TIIDM as add on therapy

*UTI and genital infection
thirst
polyuria

X hypovolaemia - possible hypotension

! antihypertensive and other hypoglycaemic agents

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21
Q

DPP-4 inhibitors
Dipeptidyl peptidase-4 inhibitors (gliptins)
sitagliptin
saxagliptin

A

prevent incretin degradation- ^plasma secretin conc
glucose dependent so postprandial action
do not stimulate insulin secretion at normal blood glucose- lower hypo risk
suppress appetite

*GI upset
spall pancreatitis risk

X pregnancy, history of pancreatitis

! other hypoglycaemics, drugs ^ glucose can oppose gliptins- thiazide and loops

22
Q

Glucagon-like peptide-1 (GLP-1) receptor antagonists (incretin mimetics)
exentide
liraglutide

A

increase glucose dependant synthesis of insulin from beta cells
activate GLP-1 receptor- resistant to degredation by DPP-4
subcut
promote satiety

*GI upset, decreased appetite with weight loss

X renal impairment

! other hypoglycaemic agents

23
Q

Class 1B agents
Lidocaine
mexiletine

A

lido- IV mex- orally
fast binding offset kinetics
no change in phase 0 in normal tissue (tonic block)
ADP slightly decreased (normal tissue)
increase threshold (Na+)
decrease phase 0 conduction in fast beating or ischaemic tissue
effect on ECG- normal in normal, ^QRS in abnormal

uses- acute: ventricular tachycardia
not used in atrial arrhythmias or AV junction arrhythmias

*CNS effects: dizziness, drowsiness
abdominal upset

24
Q

Class 1C

Flecainide (propafenone)

A

very slow binding offset kinetics (>10s)
substantially decreased phase 0 (Na+) in normal
decreased automaticity (increase threshold)
increased APD (K+) and increased refactory period, esp in repidly depolarising atrial tissue

ECG: ^PR ^QRS ^QT

uses: wide spectrum
used for supraventricular arrhythmias (fibrillation or flutter)
premature ventricular contactions
wolff-parkinson-white syndrome

*pro-arrhythmia and sudden death especially with chronic use and in structural heart disease
flecanide flutter
CNS and GI effects

25
Q 
Class II
propranolol
bisoprolol
metoprolol
esmolol
A

^APD anf refactory period in AV node to slow AV conduction velocity
decrease phase 4 depolarisation (catecholamine dependent)

ECG: ^PR lower HR

uses: treating sinus and catecholamine dependent tachycardia
converting re-entrant arrhythmias at AV node
protecting the ventricles from high atrial rates

*bronchospasm
hypotension

X partial AV block or acute heart failure (are used in stable heart failure)

26
Q

Class III
amiodarone
sotalol

A 
Amiodarone:
increase refractory period and ^APD (K+)
decrease phase 0 and conduction (Na+)
increase threshold 
decrease phase 4 (beta block and Ca2+ block)
decrease speed of AV conduction

ECG: ^PR ^QRS ^QT decrease HR

Uses: very wide spectrum: effective for most arrhythmias

*Pulmonary fibrosis
 hepatic injury
 increase LDL 
 thyroid disease
 photosensitivty
 optic neuritis (transient blindness)

! may need to reduce dose of digoxin and monitor warfarin more closely

Sotalol:
^APD and refractory period in atrial and ventricular tissue
slow phase 4 (beta blocker)
slow AV conduction

ECG: ^QT lower HR

uses: wide spectrum: supraventricular and ventricular tachycardia

*Proarrhythmia
fatigue
insomnia

27
Q

Class IV
verapamil
Diltiazem

A

slow conduction through AV (Ca2+)
increase refractory period in AV node
increase slope of phase 4 in SA to slow HR

ECG: ^PR increase/decrease HR depending on BP and baroreflex

uses: control ventricles during supraventricular tachycardia
convert supraventricular tachycardia (re-entry around AV)

*GI (constipation)
caution when partial AV block is present - can get asystole if Beta blocker is on board
caution with hypotension, decreased cardiac output or sick sinus- slow sinus node

28
Q

Class V

adenosine

A

rapid iv bolus

natural nucleoside binding to A1 and blocks adenylyl cyclase - reducing cAMP which activates K+ currents in AV and SA causing hyperpolarisation- stopping HR
leads to decreased Ca currents- increase refractory period in AV node
slows AV conduction

uses: convert re-entrant supraventricular arrhythmias
diagnosis of coronary artery disease (scans)

29
Q

Class V

ivabradine

A

Blocks If (funny currents) highly expressed in SA

slows SA node but doesn’t effect BP

uses: reduce inappropriate sinus tachycardia, reduce HR in heart failure and angina (avoiding BP drops)

*flashing lights
teratogenicity not known

30
Q

Class V

digoxin (cardiac glycosides)

A

enhances vagal activity (increases k+ currents, decreases Ca currents ^refractory period
slows AV conduction and slows HR

uses: treatment to reduse ventricular rates in atrial fib and flutter

31
Q

Class V

atropine

A

selective muscarinic antagonist

block vagal activity to speed AV conduction and increase HR

Uses: treat vagal bradycardia

32
Q

Cyclo-oxygenase inhibitor

aspirin

A

potent platelet aggregating agent thromboxane A2 (TXA2) formed from arachidonic acid by COX-1

aspirin inhibits COX-1 mediated production of TXA2 and reduces platelet aggregation- irreversible

higher doses inhibit endothelial prostacyclin (PGl2)

absorbed by passive diffusion- hepatic hydrolysis to salicylic acid

*GI irritation, GI bleeding, haemorrhage (stroke), hypersensitivity

X reye’s syndrome <16, hypersensitivity, 3rd trimester -closure of ductus arteriosus

! other antiplatelet and anticoagulants (additive/synergistic action)

33
Q

ADP receptor antagonists
Clopidogrel
prasugrel
ticagrelor

A

inhibit binding of ADP and P2Y12 receptor – inhibit activation of GPIIb/IIIa receptors -independent of COX

clopidogrel (slower onset) and prasugrel are irreversible - prodrugs with hepatic active metabolites

*Bleeding
GI upset - dyspepsia and diarrhoea
rarely thrombocytopenia

X caution in high bleed risk patients with renal and hepatic impairment

! clopidogrel requires CYPs for activation
CYP inhibitors - omeprazole, ciprofloxacin, some SSRIs
need to concider use of other PPIs with clopidigrel
ticagrelor can interact with CYP inhibitors and inducers

caution when prescribed with other antiplatelet or anticoagulant

34
Q

phosphodiesterase inhibitors

dipyridamole

A

inhibit cellular reuptake of adenosine = increased adenosine = inhibit platelet aggregation via adenosine A2 receptors
also acts as phosphodiesterase inhibitor preventing cAMP deg = inhibit expression of GPIIB/IIIa

*V+
dizziness

! antiplatelet and anticoags, adenosine

35
Q

Glycoprotein IIb/IIIa inhibitor

abciximab

A

blocks binding of fibrinogen and vWF
target final common pathway - more complete platelet aggregation

*Bleeding - dose adjust for weight

! caution with other antiplatelet and anticoags

36
Q

fibrinolytic
alteplase
streptokinase

A

convert plasminogen to plasmin

*Bleeding

! antiplatelets and anticoags

37
Q

Azathioprine

Immunosuppressant

A

anti-metabolite DNA and RNA synthesis

*bone marrow suppression
malignancy risk
risk of infection
hepatitis

38
Q

NSAIDs

A

inhibition of COX
decrease prostaglandin, prostacyclin and thromboxane synthesis
compete with arachidonic acid for hydrophobic site of COX enzymes

Analgesic:
Decrease PGE2 synthesis in dorsal horn - decrease neurotransmitter release - decrease excitability of neurones in pain relay pathway

Anti-inflammatory:
decrease in COX activity = less prostaglandin mediated increase in vasodilation so vasoconstriction and less oedema

Antipyretic:
inhibition of hypothalamic COX-2 where cytokine induced prostaglandin synthesis is elevated results in a reduction in temperature

*Dyspepsia
nausea
peptic ulcer -less mucus and bicarb ^acid, less blood flow 
bleeding
perforation
exacerbation of IBD
Renal impairment 
hypernatremia

X elderly, prolonged use, smoking, alcohol, peptic ulcer Hx, h. pylori, CKD, heart failure

! Aspirin, glucocorticoid steroid, anticoag (PPI considered) ACEi, ARBs, diuretics

39
Q

selective COX-2 inhibitors
celecoxib
etoricoxib

A

inhibits COX-2 more than COX-1
less GI ADR
does not share antiplatelet action but inhibits PGl2 - potentially leading to unopposed aggregatory effects

X increased risk of MI

40
Q

paracetamol

A

COX-2 selective inhibition in CNS (spinal cord)

NAPQI
highly reactive metabolite- some analgesic effect suggested
harmless at therapeutic doses- conjugation with glutathione
-hepatic glutathione is limited
NAPQI highly neucleophilic - oxidising key metabolic enzymes - causing cell death- neurosis and apoptosis

41
Q

N-Acetylcystine

A

glutathione thiol replacement - gets in hepatocyte

42
Q

ICS
beclometasone
budesonide
fluticasone

A

activate cytoplasmic receptors, activated receptor then passes in to nucleus to modify transcription
reduces mucosal inflammation, widens airways, reduces mucus
reduces symptoms, exacerbations and prevents death

*can cause a local immunosuppressive action - candidiasis, hoarse voice

X Pneumonia risk in COPD at high doses

! Few if taken correctly

43
Q

SABA

LABA

A

relaxes smooth muscle
prevention of bronchoconstriction prior to exercise

*Adrenergic- fight or flight effects
 Tachycardia 
 palpitations
 anxiety and tremor 
 ^glycogenolysis (liver) ^renin (kidney) 
 SVT

X LABA should only be prescribed along ICS, CVD

! beta blockers may reduse effects of B2 agonists

44
Q

LTRA
leukotriene receptor antagonist
montelukast

A

Block CysLT1 at CYSLTR1 that are released by mast cells/eosinophils

*headache
GI upset
dry mouth
hyperactivity

X used as add on in specific circumstances

! nothing major

45
Q

LAMA
long acting muscarinic antagonist
tiotropium

A

block vagally mediated contraction of airway smooth muscle

*Infrequent- anticholinergic effects- dry mouth, urinary retension, dry eyes

X generally ok

46
Q

adenosine receptor antagonist

theophylline

A

decrease bronchoconstriction

X narrow theraputic index - arrhythmia

! CYP450 inhibitors - increase conc

47
Q

opioids

A

opioid receptor agonist
Morphine:
metabolism = morphine + glucuronic acid = M6G+M3G

*resp depression
 emesis 
 decreased GI motility ^sphincter tone
 cardiovascular
 miosis
 histamine release -asthma caution

Fentanyl:
metabolism = CYP3A4
less histamine release

*resp depression
constipation
vomiting

Codine:
codine -> morphine via CYP2D6
CYP2D6 inhibited by fluoxetine
mild analgesia, cough depressant

*constipation
resp depression - worse in children

48
Q

alginates and antacids

gaviscon

A

buffering in stomach
increase stomach content viscosity and reduce reflux

*Magnesium salts can cause diarrhoea and aluminium salts cause constipation

X Na and K containing preparations caution in renal failure
hyperglycaemia in DM

! can reduce absorbtion of many drugs - separate doses
increases aspirin excretion

49
Q

PPI
Lansoprazole
Omeprazole

A

irreversibly inhibit H/K ATPase in gastric parietal cells
final stage in pathway- very significant reduction in acid secretion

*GI disturbance - abdo pain, constipation diarrhoea
Headache, dizziness
Drowsiness/confusion

X mask symptoms of gastro-oesophageal cancer
osteoporosis

! omeprazole CYP inhibitor - reduced clopidogrel action
PPIs can increase effects of warfarin and phenytoin - monitor

50
Q

H2 receptor antagonists

ranitidine

A

inhibition of H2 receptors
only partial reduction because of other pathways

  • generally ok, diarrhoea, headache

X mask symptoms of gastro-oesophageal cancer, renal impairment

! few

ranitidine - possible carcinogen

51
Q

Aminosalicylates

Mesalazine

A

used for ulcerative colitis
release of 5-aminosalsylic acid - reduce inflamation

*GI disturbance - nausia, dyspepsia
leukopenia

X aspirin sensitivity

! enteric coated tablets may break down quicker in presence of PPI

CPT (2 decks)

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