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Cardiology > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

MoA of ACE inhibitors (1)

A
  1. Prevent conversion of Angiotensin 1 to Angiotensin 2
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2
Q

Why do ACE inhibitors protect the kidney? (2)

A
  1. They reduce mechanical strain/wear and tear on the delicate glomeruli filtration system by
  2. Dilating the efferent arteriole (reducing intracapsular filtration pressure) - this is bc they inhibit angiotensisn which would usually “tense the angios” eg constrict these efferent arterioles
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3
Q

How do ACE inhibitors reduce blood pressure? (2)

A
  1. Reduce angiotensin 2 = reduce “tensing the angios” (vasocaonstriction) = reduction in SVR (MAP = CO x SVR)
  2. Reduce aldosterone activity as a result of inhibiting RAAS - so less sodium reabsorbed = less water retention = less circulating volume
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4
Q

S/Es of ACE inhibitors (4)

A
  1. Dry cough
  2. Angioedema
  3. Hyperkalaemia (due to less aldosterone)
  4. frist-dose hypotension
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5
Q

Contraindications/cautions with ACE inhibitor use (6)

A
  1. Preganancy or breast feeding - avoid
  2. Less effective in afro-carribean heritage
  3. Renovascular disease
  4. Aortic stenosis - can cause HypoBP
  5. Hx or FHx of angioedema
  6. Hyperkalaemia
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6
Q

Interractions of ACE inhibitors (1)

A
  1. High dose diuretics like furosemide >80mg/day

causes high risk of HypoBP

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7
Q

Monitoring required for ACE inhibitors

A
  1. U&Es before and after starting / changing dose
  2. Acceptable rise in creatinine (+30%) and potassium (up to 5.5) means continue, higher means stop
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8
Q

Indicaiton to use Adenosine (1)

A
  1. SVT
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9
Q

MoA of Adenosine (3)

A
  1. Causes transient AV block
  2. Agonist of A1 receptor in AV node reducing cAMP causing hyperpolarisation by increassing potassium outlfux
  3. Incredibly short half life of 8-10 seconds
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10
Q

S/Es of Adenosine (4)

A
  1. Chest Pain
  2. Bronchospasm
  3. Transient flushing
  4. Can enhance accessory pathway conduction - so avoid in WPW syndrome with AF/Flutter
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11
Q

Important interractions of Adenosine (2)

A
  1. Effect enhanced by Dipyridamole (antiplatelet)
  2. Effects blocked by Theophyllines
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12
Q

CI of Adenosine (1)

A
  1. Asthmatics (possible bronchospasm)
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13
Q

MoA of Amiodarone (3)

A
  1. Class 3 antiarrythmic
  2. Blocking K channels inhibiting repolarisation prolonging action potentials
  3. also blocks Na channels (class 1 effect)
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14
Q

Indicaitons for Amiodarone use (3)

A
  1. Atrial tachycardias
  2. Nodal tachycardias
  3. Ventricular tachycardias
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15
Q

Limitations of Amiodarone use (5)

A
  1. Long ass half life of 20 - 100 days
  2. Give centrally as causes thrombophlebitis
  3. Is proarrhythmic bc it lengthens QTc
  4. Interferes with drugs a lot as its a p450 inhibitor - decreases metabolism of warfarin
  5. Lots of S/Es
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16
Q

Monitoring required for amiodarone (5)

A

Prior to Tx:
1. TFT
2. LFT
3. U&E
4. CXR

Every 6 months:
5. TFT
6. LFT

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17
Q

S/Es of Amiodarone (10)

A
  1. Thyroid dysfunction - both hypo and hyper
  2. Corneal deposits
  3. Pul fibrosis / pneumonitis
  4. Liver fibrosis or hepatitis
  5. Peripheral neuropathy, myopathy
  6. Photosensitivity
  7. “slate-grey” appearance
  8. Thrombophlebitis
  9. Bradycardia
  10. Long QTc - torsades
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18
Q

MoA of ARBs (1)

A
  1. Blocks angiotensin at the AT1 receptor
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19
Q

S/Es of ARBs (2)

A
  1. Hypotension
  2. Hyperkalaemia
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20
Q

Indications for Beta Blockers (8)

A
  1. Angina
  2. Post-MI
  3. HF
  4. AFib rate control > Digoxin
  5. HTN - although reducing use
  6. Thyrotoxicosis
  7. Migraine PPx
  8. Anxiety - low dose prn
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21
Q

S/Es of Beta Blockers (5)

A
  1. Bronchospasm
  2. Cold peripheries
  3. Fatigue
  4. Sleep disturbances
  5. Erectile Dysfunction
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22
Q

CIs of Beta Blockers (4)

A
  1. Asthma
  2. Uncontrolled Heart Failure
  3. Sick SInus Syndrome
  4. CONCURRENT USE OF VERAPAMIL - SEVERE BRADY
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23
Q

MoA of Bivalirudin (1

A
  1. Reversible direct thrombin inhibitor
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24
Q

Indication for Bivalirudin (1)

A
  1. ACS anticoagulation
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25
Q

Clopidogrel MoA (1)

A
  1. P2Y12 inhibitor stoping ADP from activating Platelets
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26
Q

Clopidogrel / P2Y12i Interactions (1)

A
  1. PPIs seem to reduce its efficacy, namely Omeprazole and Esomeprazole, Lansoprazole appears okay
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27
Q

MoA of Dagibatran (1)

A
  1. Direct thrombin inhibitor

Alternative to warfarin requiring less minitoring

28
Q

2 main indications of Dagibatran

(2 indications, 5 conditions for use in 2nd indication)

A
  1. PPx of VTE following knee replacement
  2. PPx of Storke in non-valvular AFib if patient has:
  3. Previous stroek, TIA, systemic embolism
  4. Left Vent EF<40%
  5. Symptomatic HF NYHA Class 2 or worse
  6. > 75
  7. > 65 with CAD, DM, HTN
29
Q

S/Es of Dagibatran (2)

A
  1. Major haemhorrage
  2. Unusable in creatinine clearance under 30 ml/min
30
Q

CI of Dagibatran (1)

A
  1. Mechanical Valve Replacements
31
Q

Caution/relative CI with Beta Blockers and Diabetes (3)

A
  1. Cause Insulin resistance
  2. Mask Sxs of Hypoglycaemia meaning patients get worse without knowing
  3. EVEN WORSE when combined with a THIAZIDE
32
Q

MoA of CCBs (3)

A
  1. Block voltage gated Calcium channels which
  2. relaxes smooth muscle (vessels)
  3. reduces cardiac contraction force
33
Q

MoA of Thiazides (1)

A
  1. Block sodium reabsorptuon at the beginning of the DISTAL convoluted tubtule
34
Q

S/Es of CCBs (3)

A
  1. Flushing
  2. ANkle Swelling (amlodipine bad for this)
  3. Headache
35
Q

S/Es of Thiazides (7)

A
  1. Hyponatraemia
  2. Hypokalaemia
  3. Dehydration
  4. Hyperglycaemia
  5. Gout
  6. Postural Hypotension
  7. Hypercalcaemia - meaning less calcium in urine = Useful in PPx of Kidney stones
36
Q

MoA Ivabradine (2)

A
  1. Antianginal drug which reduces heart rate
  2. Acts on I.f. (funny) ion current which is highly expressed in SAN reducing pacemaker activity
37
Q

S/Es of Ivabradine (3)

A
  1. Visual effects such as luminous phenomina
  2. Headache
  3. Brady/Heart Block
38
Q

Drugs causing prolonged QTc (10)

A
  1. Amiodarone
  2. Sotalol
  3. Class 1 antiarrhythmics
  4. TCAs
  5. SSRIs - esp. Citalopram
  6. Methadone
  7. Chloroquine
  8. Terfenadine - esp when takend with p450 inhibitor like erythromycin
  9. Haloperidol
  10. Ondansetron
39
Q

MoA of Loop Diuretics (3)

A
  1. Inhibit NKCC2 channels in thick ascending LoH
  2. Reducing absorption of NaCl
  3. They work from the luminal side of the tubule so required filtering into urine - hence patinets with shit kidneys need higher doses to be effective
40
Q

Indications of Loop Diuretics (2)

A
  1. HF both acute and chronic (but mainly acute as chornic has limited evidence of reducing mortality and its used just for Sxs contorl really)
  2. Resistant HTN - esp. in renal impairment
41
Q

S/Es of Loop Diuretics (9)

A
  1. Hypotension
  2. Hyponatraemia
  3. Hypokalaemia
  4. Hypomagnesaemia
  5. Ototoxicity
  6. Hypochloraemic acidosis
  7. Renal imparment (as directly toxic and can induce dehydration/pre-renal aki)
  8. Hyperglycaemia (less common than with thiazides)
  9. Gout
42
Q

Nicorandil MoA (2)

A
  1. Vasodilator
  2. Potassium Channel Activator vie activation of Guanylyl Cyclase increasing cGMP
43
Q

Use of Nicorandil (1)

A
  1. Angina
44
Q

Contraindications of Nicorandil (1)

A
  1. Left Ventricular Failure
45
Q

S/Es of Nicorandil (3)

A
  1. Headache
  2. Flushing
  3. SKin, mucosal and eye ulceration - GI and anal
46
Q

Use of Nicotinic Acid (3)

A
  1. Treats hyperlipidaemia
  2. Lowers cholesterol and triglycerides
  3. Raises HDL
47
Q

S/Es of Nicotinic Acid (3)

A
  1. Flusing - from prostaglandins
  2. Impaired Glucose contorl
  3. Myositis

S/Es often severe enough to limit use

48
Q

MoA of Nitrates (generally and then how they help angina) (5)

A
  1. Smooth muscle relaxants (vasodilators) through NO and cGMP modulation which drops intracellular Calcium levels (NO is potent endovascualr vasodilator)

more importantly, in angina:
2. Vasodilation of both the coronaries and the systemic venous system =

  1. Wider lumen and reduced stenosis of coronary arteries
  2. Reduced venous returnt o R heart = less for the Left to pump = reduced cardiac oxygen demand
  3. In short, they increase supply and reduce demand
49
Q

S/Es of Nitrates (4)

A
  1. Hypotension
  2. Tachycardia
  3. Headaches
  4. Flushing
50
Q

MoA of Fondaparinux and administration route (2)

A
  1. Activates antithrombin 3, which inhibits Coag factor Xa.
  2. Subcutaneous administraiton
51
Q

MoA of Statins (1)

A
  1. Inhibit HMG-CoA Reductase - the rate-limiting enzyme in hepatic cholesterol synthesis - reducing rate of cholesterol production
52
Q

S/Es of Statins (3)

A
  1. Myopathy - myalgia, myositis, rhabdo, and ASx raised CK. More common with Atorva and Simva
  2. Liver Impairment - Check LFTs at baseline, 3 months, then every 12 months. Stop if AST/ALTs x3 baseline consitently
  3. May increase risk of brain bleed in previous Stroke patients - avoid.
53
Q

CI of Statins (2)

A
  1. Macrolide use (erythro, clarithro) - stop statins till course complete -increases myopathy risk
  2. Pregnancy
54
Q

Who gets a Statin? (6)

A
  1. QRISK >10%
  2. Established CVD / TIA / Stroke
  3. If Type 2 DM - treat like everyone else and QRISK them

Give if Type 1 AND:
4. Dx >10 yrs ago

  1. > 40 y/o
  2. Existing nephropathy
55
Q

Dose of Statins for Primary vs Secondary CVD prevention (2)

A
  1. Primary - Atorva 20mg - increase if not reduced non-HDL >40%
  2. Secondary - Atorva 80mg
56
Q

CI of Adenosine (1)

A
  1. Asthmatics

in SVT use Verapamil instead

57
Q

Rare adverse effects of Thiazides (4)

A
  1. Pancreatitis
  2. Thrombocytopaenia
  3. Agranulocytosis
  4. Photosensitvity rash
58
Q

MoA of Thrombolytic Drugs (alteplase, streptokinase, tenecteplase)

A
  1. Activate Plasminogen into Plasmin = Clot Buster
59
Q

Indicaitons for Thrombolytic Drugs (3)

A
  1. MI where PCI is > 120 minutes away

WITH STRICT CRITERIA:
2. Acute Ischaeic Stroke

  1. PE
60
Q

CI to Thrombolysis (8)

A

To do with Blood:

  1. Active Bleeding
  2. Recent haemorrhage, trauma or surgery
  3. Coagulation or bleeding disorders

To do with the Noggin

  1. Intracranial Neoplasm
  2. Stroke in last 3 months
  3. Recent Head Injury

To do with CVS:

  1. Aortic Disseciton
  2. Severe HTN
61
Q

MoA of Warfarin (2)

A
  1. Inhibits epoxide reductase preventing reduction of Vit K
  2. Reducing synthesis of Factor 10,9,7,2, (1972), Protein C&S
62
Q

Indicaitons for Warfarin (2)

A
  1. Mechanical Heart Valves - INR depends on type, Mitral = higher INR than Aortic
  2. Second Line after DOACs

VTE - INR = 2.5, 3.5 if reccurrent
AFib - INR 2.5

63
Q

Factors increasing Warfarin effect (5)

A
  1. Liver Disease
  2. P450 inhibitors - amiodarone, ciprofloxacin
  3. Cranberry juice
  4. Drugs which displace warfatin from albumin - NSAIDS
  5. Platelet inhibitors - NSAIDS, P2Y12s
64
Q

S/Es of Warfarin (4)

A
  1. Haemorrhage - obvs
  2. Teratogenic! but can be used in breastfeeding
  3. Skin necrosis - this is due to Protein C being used up and is why u usually bridge with heparin to avoid this
  4. Purple toes - hahah that sucks mate
65
Q

Interacitons of Warfarin that INCREASE INR (7)

A
  1. Antiepileptics
  2. Barbiturates
  3. Rifampicin
  4. St Johns Wort
  5. Chronic Alcohol
  6. Griseofulvin
  7. Smoking
66
Q

Interracitons with Warfarin that DECREASE INR (8)

A
  1. ABxs - Ciprofloxacin, macrolides
  2. Isoniazid
  3. Cometidine, Omeprazole
  4. Amiodarone
  5. Allopurinol
  6. Imidazoles - ketocunazole, fluconazole
  7. Sodium Valproate
  8. Acute Alcohol
67
Q

MoA of Digoxin (4)

A
  1. Blocks cardiac myoctye Na/K pumps so Na cant escape and is instead pumped out by the Ca2/Na channels, swapping Na for calcium
  2. Intracellular ca increases which increases cardiac contractility
  3. Increased parasympathetic stimulation also causes reuded SAN firing rate
  4. good for HF and AFib at the same time

Cardiology (8 decks)

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