Pharmacology Flashcards
(66 cards)
1
Q
First pass metabolism
A
Drugs that are swallowed are carried from the gut to the liver by portal circulation, where they undergo variable metabolism by the liver before reaching systemic circulation. Concentration is greatly reduced before the drug reaches systemic circulation
2
Q
Anti-cholesterol drugs (4)
A
Statins, PCSK9 inhibitors, fibrates, ezetimibe
3
Q
Statins:
- What do they do?
- Examples
- What are they used in?
- Side effects
A
- Blocks HMG coenzyme reductase
- Simvastatin, atorvastatin, fluvastatin, pravastatin, rosuvastatin
- Hypercholesterolaemia, diabetes, angina, MI, TIA/stroke
- Renal failure, myalgia, myopathy
4
Q
PCSK9 inhibtors:
- What do they do?
- Examples
- What are they used to treat and why?
- How are they administered?
A
- Increase number of LDL receptors for LDL to bind to leading to less LDL in the bloodstream and decreased cholesterol
- Evolucumab, alirocumab
- Used to treat FH because they are stronger
- Administered subcutaneously
5
Q
Fibrates:
- Example
- When are they used?
- Side effects
A
- Bezafibrate
- As an alternative to statins - when patients don’t tolerate statins. Also used in hypertriglyceridaemia and low HDL cholesterol
- Nausea, stomach upset, inflammation of liver
6
Q
Familial hypercholesterolaemia
A
Inherited condition where there is a naturally occurring high level of cholesterol
7
Q
Anti-hypertensive drugs (7)
A
Beta-blockers, diuretics, calcium antagonists, ACE inhibitors, angiotensin receptor blockers, alpha blockers, mineralocorticoid antagonists
8
Q
Diuretics:
- Mechanism
- 2 types and examples
- Side effects
A
- Blocks sodium reabsorption in kidneys
- Thiazide diuretics (e.g. bendrofluozide), loop diuretics (e.g. furosemide, not used in hypertension)
- Hypokalaemia, hyperglycaemia, increased uric acid (gout), impotence
9
Q
Beta blockers:
- 2 types
- Side effects
A
- Cardioselective and non-selective
- Worsen asthma, tiredness, cold peripheries
10
Q
Cardioselective beta blockers:
- What do they block?
- Examples
- What are they generally used in?
A
- Only beta-1 receptors
- Atenolol, bisoprolol
- Angina, acute coronary syndrome, MI, hypertension and heart failure
11
Q
Non-selective beta blockers:
- What do they block?
- Examples
- When are they used?
A
- Beta-1 and beta-2 receptors
- Propanolol, carvedilol
- Thyrotoxicosis, migraines
12
Q
Calcium antagonists:
- What do they do?
- 2 types
- They shouldn’t be given in combination with which drug?
A
- Act on AV node to slow heart rate
- Rate limiting calcium antagonists, dihydropyridines
- Beta blockers
13
Q
Rate limiting calcium antagonists:
- Examples
- When are they used?
A
- Verapamil, diltiazem
- Hypertension, angina, supraventricular arrhythmias
14
Q
Dihydropyridines:
- Example
- What are they used in?
- Common side effect
A
- Amlodipine
- Hypertension and angina
- Ankle oedema
15
Q
ACE inhibitors:
- How do they work?
- Example
- When are they used?
- When should they not be used?
- Side effects
A
- Stop angiotensin I converting to angiotensin II
- Lisinopril
- Used in hypertension and heart failure
- Never use in pregnancy
- Dry cough, renal dysfunction, angioneurotic oedema
16
Q
Angiotensin receptor blockers:
- How do they work?
- Example
- When are they used?
- When should they not be used?
- Side effects
A
- Block angiotensin II receptors
- Losartan
- Hypertension and heart failure, often when ACE inhibitors can’t be used
- Never use in pregnancy
- Renal dysfunction
17
Q
Alpha blockers:
- What do they do?
- Example
- What can it be used to treat?
- Side effect
A
- Block alpha adrenoreceptors causing vasodilatation
- Doxazosin
- Hypertension and prostatic hypertrophy
- Postural hypotension
18
Q
Mineralcorticoid Antagonists:
- What do they do?
- Examples
- When are they used?
- Side effects
A
- Block aldosterone receptors
- Spironolactone, eplerenone
- Used in heart failure and resistant hypertension
- Gynaecomastia, hyperkalaemia, renal impairment
19
Q
Anti-anginal drugs (6)
A
Nitrates, nicorandil, calcium antagonists, beta blocker, ivabradine, metabolic modulator
20
Q
Nitrates:
- What do they act as?
- Administration
- Example
- What are they used in?
- Side effects
A
- Venodilators
- Sublingually either as GTN spray or GTN tablet
- Isosorbide mononitrate
- Used in angina and heart failure
- Headache, syncope, nausea
21
Q
Nicorandil:
- What is it?
- Side effects
A
- K ATP channel opener
- Headache, mouth ulcers
22
Q
Ivabradine:
- What does it do?
- When does it work/not work
- Side effects
A
- Slows heart rate by acting on funny current
- Works in the SA node and only works in sinus rhythm, doesn’t work in atrial fibrillation
- Altered visual disturbances
23
Q
Metabolic modulator:
- Example
- What does it do?
- Side effects
A
- Ranolazine
- Decreases calcium load on heart
- Dry mouth, pre-syncope, nausea
24
Q
Drugs used in plaque rupture and MI (4)
A
Anti-thrombotics, anti-platelets, anti-coagulants, fibrinolytics
25
Anti-platelet drugs:
- Examples
- What do they do?
- What are they used to treat?
- Side effects
- Aspirin, clopidogrel, ticagrelor, prasugrel
- Prevent new thrombosis
- Angina, acute MI, patients at high risk of TIA/stroke
- Haemorrhage, peptic ulcer leading to haemorrhage, aspirin sensitivity leading to asthma
26
Anticoagulants:
- Examples
- What do they do?
- What are they used to treat?
- Side effects
- What are they reversed by?
- Heparin (IV only), warfarin (oral use only), rivaroxaban, dabigatran
- Block clotting factors (2, 7, 9, 10)
- DVT, PE, NSTEMI, atrial fibrillation
- Haemorrhage
- Vitamin K
27
Fibrinolytic drugs:
- Examples
- What do they do?
- What are they used to treat?
- Side effects
- When should they be avoided?
- Steptokinase and tissue plasminogen activator
- Dissolve a formed clot
- STEMI, select cases of PE, select cases of CVA
- Serious risk of haemorrhage
- Recent haemorrhage, trauma, bleeding tendencies, severe diabetic retinopathy, peptic ulcer
28
Atrial fibrillation:
- Drugs to control rate
- Drugs to chemically cardiovert
- Beta blockers, digoxin, rate limiting calcium channel blockers
- Amiodarone
29
Drugs used in the treatment of heart failure (7)
ACE inhibitors, ARBs, Beta-blockers, mineral corticosteroid antagonists, neprilysin inhibitors, diuretics, digoxin
30
Digoxin I:
- What does it do?
- What is it good in?
- Why is it bad in excess?
- Blocks AV conduction, produces a degree of AV conduction delay
- Good in atrial fibrillation
- Heart rate falls too much giving bradycardia and heart block
31
Why is digoxin II bad?
Increases ventricular irritability producing ventricular arrhythmias and has a very narrow therapeutic index
32
Signs and symptoms of digoxin toxicity
Nausea and vomiting, yellow vision, bradycardia, heart block, ventricular arrhythmias
33
Neprilysin inhibitors:
- Example
- What does it do?
- Side effects
- Salcubitril valsartan
- ARB and endopeptidase inhibitor
- Hypotension, renal impairment, hyperkalaemia, angioneurotic oedema
34
Haemostasis
Arrest of blood loss from a damaged vessel
35
Sequence of events in haemostasis
- Vascular wall damage exposing collagen and tissue factor
- Primary haemostasis - forms a soft plug
- Activation of blood clotting (coagulation) and the formation of a stable clot by fibrin enmeshing platelets – forms a solid clot
36
Events in primary haemostasis to form a soft plug
Local vasoconstriction
Platelet adhesion, activation and aggregation of fibrinogen
Platelets are held together loosely by fibrinogen forming a soft plug
37
How is a soft plug converted into a solid clot
- Inactive factor X is converted by tenase to the active factor Xa by IXa and VIIIa
- Inactive factor II (prothrombin) is converted by prothrombinase (Xa and Va) to the active factor IIa (thrombin)
- Thrombin converts fibrinogen to fibrin which forms a solid clot
38
Thrombosis
A haematological plug in the absence of bleeding
39
Arterial thrombus:
- Describe colour and structure
- If it detaches where does the embolus usually lodge?
- Treatment
- White thrombus: mainly platelets held together in a fibrin mesh
- Embolus usually lodges in an artery in the brain or other organ
- Treated with antiplatelets
40
Venous thrombus:
- Describe colour and structure
- If it detaches where does the embolus usually lodge?
- Treatment
- Red thrombus: white head, jelly-like red tail, fibrin rich
- Embolus usually lodges in the lungs
- Treated with anticoagulants
41
What does warfarin block?
A modification of factors X and II (prothrombin) essential for their function
42
What does rivaroxaban inhibit?
Directly inhibits factor Xa (prothrombinase)
43
What do heparin, LMWHs and fondaparinux inactivate?
Factor Xa (prothrombinase) via antithrombin III
44
What does dabigatran inhibit?
Directly inhibits factor IIa (thrombin)
45
Another thing that heparin inactivates
Factor IIa (thrombin) via antirhombin III
46
Role of vitamin K reductase
Allows vitamin K to go from epoxide, to quinone and then hydroquinone
47
Which drug blocks vitamin K reductase?
Warfarin
48
Important side effect of anticoagulants
Significant risk of haemorrhage
49
What factors does warfarin render inactive?
Factors II, VII, IX, X
50
Administration of warfarin
Orally
51
Is the onset of warfarin slow or fast?
Slow (2-3 days), whilst inactive factors replace active gamma-carboxylated factors that are slowly cleared from the plasma
52
Half-life of warfarin
About 40 hours
53
Therapeutic index for warfarin
Very low therapeutic index
54
Treatment of warfarin overdose
Administration of vitamin K1 as phytomenanadione
55
Factors that can increase the risk of haemorrhage whilst on warfarin
Liver disease (decreased clotting factors), high metabolic rate (increased removal of clotting factors), drug interactions
56
Drug interactions that can increase the risk of haemorrhage with warfarin
Agents that inhibit hepatic metabolism of warfarin by CYP2C9, drugs that inhibit platelet function, drugs that inhibit reduction, or decreased availability of, vitamin K
57
Factors that can increase the risk of thrombus with warfarin
Physiological state (e.g. pregnancy, hypothyroidism), vitamin K consumption, drug interactions
58
Role of antithrombin III
Inhibitor of coagulation by neutralising the enzymatic activity of thrombin
59
What is heparin?
Heparin is a naturally occurring sulphated glycosaminoglycan of variable molecular size
60
Examples of low molecular weight heparins
Enoxaparin and dalteparin
61
Administration of heparin and LMWHs
Heparin - IV (immediate onset) or SC (delayed onset by 1 hour)
LMWHs - SC
62
What is required to determine optimum dosage of heparin?
In vitro clotting test
63
Elimination of heparin vs LMWHs
Heparin - zero order
| LMWHs - first order, excreted by kidneys
64
What inactivates heparin
Sulfate - given as IV
65
Adverse effects of heparin and LMWHs
Haemorrhage, osteoporosis, hypoaldosteronism, hypersensitivity reactions
66
When are orally active inhibitors used to prevent thrombosis?
In patients undergoing hip and knee replacements
