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MBChB > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

When is digoxin used?

A

Rate control in AF/Atrial Flutter

Heart Failure

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2
Q

What is the MoA of digoxin?

A 
Positively inotropic (increases contractility)
Negatively chronotropic (decreased HR)
Inhibits the Na/K ATPase
Na accumulates inside the cell 
Activates the Na/Ca exchanger
Ca pumped into the cell 
Ca increases the force of contraction

Digoxin increases the vagal parasympathetic activity

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3
Q

What side effects are associated with digoxin?

A

Bradycardia
Visual disturbances (blurred/yellow vision)
Dizziness
GI disturbances

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4
Q

What are the main pharmacokinetics/pharmacodynamic principles of digoxin?

A

Narrow therapeutic window
Digoxin toxicity –> arrhythmias (life-threatening)
Long t1/2 - once daily dosing

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5
Q

When is aspirin used?

A

Secondary prevention of thrombotic events
Management of ACS
(Pain relief)

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6
Q

What is the MoA of aspirin?

A

Binds irreversibly to the cyclooxygenase (COX) enzyme
Reduces production of thromboxane –> reduces platelet aggregation and thrombus formation
Reduces endothelial prostaglandin production –> reduces nociceptive sensitisation and inflammation

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7
Q

What side effects are associated with aspirin?

A 
Gastric bleeding (1%)
Peptic ulceration 
Bronchospasm - hypersensitivity
Angiooedema
Reyes syndrome (rare)
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8
Q

What advice should be given to patients on aspirin?

A

PPI can be useful in LT uses
Avoid drug preparations that contain aspirin
Aspirin should be avoided in under 16s –> increased risk of Reyes Syndrome

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9
Q

What are the common doses of aspirin?

A

ACS: 300mg then 75mg OD

2ry prevention: 75mg OD

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10
Q

When is Clopidogrel used?

A

Secondary prevention of thrombotic events

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11
Q

What is the MoA of Clopidogrel?

A

Irreversibly blocks the ADP receptor on platelet cell membrane
Prevents formation of GPIIb/IIIa complex needed for platelet aggregation
Reduces thrombus formation

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12
Q

What side effects are associated with Clopidogrel?

A

Bleeding (GI, IC, post-surgery) in 1-10%
GI upset (dyspepsia, diarrhoea, abdo discomfort) in 1-10%
Rarely, thrombocytopenia

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13
Q

What advice needs to be given to patients on Clopidogrel?

A

Stop 7d prior to surgery

Don’t stop without consulting dr if have an arterial stent in-situ

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14
Q

Give examples of recombinant tissue plasminogen activator drugs

A

Alteplase

Tenecteplase

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15
Q

Describe the MoA of rTPA

A

Recombinant tissue plasminogen activator
Catalyse the conversion of plasminogen into plasmin
Lysis of the fibrin clot

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16
Q

What are the indications for the use of rTPA?

A

Within 4.5h of an acute ischaemic stroke
Within 12h of MI
Massive PE

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17
Q

What are the side effects associated with rTPA?

A

Bleeding

Allergic reaction/angiooedema (1%)

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18
Q

How is Alteplase administered?

A

Bolus-infusion regimen

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19
Q

How is Tenecteplase administered?

A

Single bolus

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20
Q

What pharmacodynamic interaction is associated with rTPA?

A

Interaction with anti-platelets and anti-coagulant drugs

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21
Q

Describe the MoA of unfractionated heparin

A

Enhances the activity of antithrombin III which inhibits thrombin
Also inhibits multiple other factors in the coagulation pathway
Has an anti-coagulant effect

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22
Q

What are the indications for heparin?

A

Treatment and prevention of thromboembolic events
Renal dialysis
Treatment of Acute Coronary Syndrome

23
Q

What are the side effects associated with heparin?

A

Bleeding - risk as great as 3.5%
Heparin-induced thrombocytopenia
Osteoporosis

24
Q

How is heparin administered?

A

Continuous IV infusion

SC injection

25
Q

How can the anti-coagulant effect of heparin be reversed?

A

Protamine

26
Q

How is the effect of heparin monitored?

A

aPTT

27
Q

What are the indications for Warfarin?

A

Thromboprophylaxis in AF, metallic heart valves, cardiomyopathy
Treatment of thromboembolism

28
Q

What is the MoA of Warfarin?

A

Inhibits Vit K epoxide reductase
Prevents the recycling of Vitamin K to reduced form after carboxylation of coagulation factors II, VII, IX and X
Prevents thrombus formation

29
Q

What side effects are associated with Warfarin?

A

Bleeding (Increased risk with increasing INR)
Warfarin necrosis
Osteoporosis

30
Q

What are the key PD/PK principles of Warfarin?

A

Multiple interactions with other drugs/foods
Requires regular monitoring of INR and dose adjustment (requires compliance)
Can be reversed with Vit K

31
Q

Give an example of a direct thrombin inhibitor

A

Dabigatran

32
Q

What is the MoA of Dabigatran?

A

Direct thrombin inhibitor
Inhibits conversion of fibrinogen into fibrin
Prevents thrombus formation

33
Q

What are the indications for Dabigatran?

A

Venous thrombus prophylaxis post surgery

Thromboprophylaxis in non-valvular AF

34
Q

What are the side-effects associated with Dabigatran?

A

Bleeding

Dyspepsia

35
Q

What are the key PD/PK principles of Dabigatran?

A

Rapid onset
Not metabolised by cytochrome p450 so no drug/food interactions
No monitoring required
No antidote available

36
Q

What is the MoA of Rivaroxaban?

A

Inhibits the conversion of prothrombin into thrombin
Reduces the concentration of thrombin in the blood
Inhibits the formation of fibrin clots

37
Q

What are the indications for Rivaroxaban?

A

Venous thromboembolism prophylaxis (post-surgery)
Thromboprophylaxis in non-valvular AF
Treatment of venous thromboembolism

38
Q

What side effects are associated with RIvaroxaban?

A

Bleeding

Nausea

39
Q

What are the key PD/PK principles of Rivaroxaban?

A

Metabolised by cyrochrome p450
No antidote
No therapeutic monitoring required

40
Q

What is the MoA of metformin?

A

Suppresses gluconeogenesis
Reduces amount of glucose absorbed in the gut
Increases uptake of glucose into skeletal muscle

41
Q

What side effects are associated with metformin

A

Dose related GI upset

Lactic acidosis

42
Q

What is the MoA of sulphonylureas (glipizide, gliclazide)?

A

Binds to the SU receptor on the surface of beta cells
Blocks K ATPase –> cell depolarises
L-type Ca channels open –> influx of Ca into cell
Exocytosis of insulin

43
Q

What side effects are associated with sulphonylureas (glipizide, gliclazide)?

A 
Prolonged severe hypoglycaemia
Bone marrow toxicity
Skin rashes
GI upset
Increased appetite --> weight gain
44
Q

What is the MoA of meglitinides (Repaglitinide, nateglitinide)?

A

Binds to SU receptor on B cell will less potency compared to sulphonylureas (lower risk of hypoglycaemia)

45
Q

What is the MoA of thiozolidinediones (Pioglitazone?)

A

Binds to PPAR-gamma receptor (present in adipose tissue, liver and muscle)
Increases lipogenesis
Increases uptake of fatty acid and glucose

46
Q

What side effects are associated with thiozolidinediones (Pioglitazone)?

A

Fluid retention (worsens heart failure)
Increased risk of fracture
Increased risk of bladder cancer
Weight gain

47
Q

What is the MoA of alpha-glucosidase inhibitors (acarbose)?

A

Delays carbohydrate absorption

48
Q

What side effects are associated with alpha-glucosidase inhibitor (acarbose)?

A

Flatulence
Loose stools/diarrhoea
Abdominal bloating
Abdominal pain

(useful in obese patients)

49
Q

What is the MoA of incretin mimics (exenatide, liraglutide)?

A

Increases insulin secretion
Decreases glucagon secretion
Slows gastric emptying

50
Q

What side effects are associated with incretin mimics (exenatide, liraglutide)?

A

Hypoglycaemia
Range of GI effects
Pancreatitis

51
Q

What is the MoA of -gliptans?

A

Competitively inhibit DDP4
Increase GLP-1 in circulation
Increase insulin secretion
Reduce glucagon secretion

52
Q

What side effects are associated with -gliptans?

A

GI
Liver disease
Worsening of pancreatitis, heart failure

53
Q

What is the MoA of SGLT-2 inhibitors (-flozin)?

A

Inhibit SGLT2 channel in PCT
Reduce amount of glucose reabsorbed from filtrate
More glucose lost in urine

54
Q

What side effects are associated with SGLT-2 inhibitors (-flozin)?

A

Hypoglycaemia
UTI
Genital candidiasis

MBChB (14 decks)

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