Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiac Drugs > Extra / PK > Flashcards

Extra / PK Flashcards

1
Q

Metoprolol / propranolol are both what, what does that mean

A

Lipophilic so pass the blood brain barrier leading to CNS effects

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

Metoprolol / propranolol bioavailability

A

25-50% - extensive FPP

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

Atenolol - low what, means what. Half life

A

Low lipid solubility - can’t pass bbb, no cns effects. P
Longer half-life, excreted unchanged

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

Carvedilol has what and does not cause what

A

Has an improved lipid profile and does not cause reflex tachycardia

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

Alpha 1 blockers: good what, undergoes what, highly what, less what

A

Good oral absorption, good bioavailability, undergoes hepatic metabolism, highly protein bound. Less reflex tachycardia and LDL/HDL profile than other drugs

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

Alpha 2 agonist effect

A

Has an additive effect with other hypertensives

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

ACE inhibitors: absorption and bioavailability

A

Good oral absorption, bioavailability of 60%

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

Cilazapril metabolised

A

To active drug cilazaprat 1st pass

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

Hepatic and renal impairment and cilazapril

A

Hepatic impairment affects cilazaprat formation and renal impairment reduces clearance

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

Angiotensin receptor blockers

A

Oral admission and rapidly converted to active form by esterases

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

Angiotensin receptor blockers bioavailability

A

Relatively low <50%

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

Angiotensin receptor blockers elimination

A

Mostly hepatic elimination

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

Statins route of admission and metabolism

A

Given orally. Metabolised in liver releases active plasma compounds

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

Statins plasma peak

A

In 1-4hrs after oral dosing

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

Statins bioavailability

A

Poor

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

Statins protein bound?

A

Highly protein bound

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

Statins - elimination of metabolites

A

Metabolites eliminated after extensive first pass hepatic metabolism

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

Statins source of drug interactions

A

Fibrates and erythromycin

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

Fibrates - 2 other LDL lowering drugs

A

Monoclonal PCSK9 inhibitors (alirocumab), cholesterol uptake inhibitors (ezetimibe)

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

Low dose aspirin metabolism

A

Rapidly metabolised in liver to inactive salicylate

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

Clopidogrel and aspirin

A

Acts in synergy with aspirin

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

Clopidogrel - 1 other anti-platelet drug

A

Dipyridamole

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

Monoclonal PSC9 inhibitors (alirocumab)

A

Prevents hepatic LDL receptor destruction

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

Cholesterol uptake inhibitors (ezetimibe)

A

Prevents dietary and biliary cholesterol absorption in gut causing LDL receptor upregulation

25
Q

Dipyridamole

A

Platelet phosphate inhibitor, blocks ADP mediated platelet activation

26
Q

Enoxaparin duration and bioavailability

A

Longer duration and increased bioavailability compared to UF heparin

27
Q

Enoxaparin delivery

A

Subcutaneous

28
Q

Warfarin route of admission and pk

A

Oral - 24-48hrs to take effect

29
Q

Warfarin bridging therapy

A

Bridging therapy with cleans or heparin first cos slow onset and decreased protein C and S initially

30
Q

Warfarin monitoring

A

Monitored using INR - aim for between 2 and 2.5

31
Q

Alteplase (Fibrinolytics) dosage

A

Strictly controlled

32
Q

Alteplase (Fibrinolytics)metabolims

A

Metabolised by liver to amino acids

33
Q

Alteplase (fibrinolytics) half life

A

72 mins

34
Q

Tenecteplase (fibrinolytics)

A

Longer half life compared to alteplase, increased fibrin specificity and resistance to PAI-1 inactivication

35
Q

Amlodipine, absorption, onset,

A

Well absorbed orally, slow onset of action

36
Q

Amlodipine metabolism and excretion

A

Hepatically metabolised and excreted as inactive metabolites in urine

37
Q

Amlodipine affected by what interactions

A

CYP3A4

38
Q

Verapamil absorption

A

Well absorbed orally

39
Q

Verapamil metabolism

A

Rapid metabolism by 1st pass CYP3A4 metabolism

40
Q

Verapamil doesn’t affect what

A

No bronchoconstriction or affect lipid profiles like beta blocker

41
Q

Diltiazem absorption

A

Well absorbed orally

42
Q

Diltiazem metabolism

A

Rapid metabolism by 1st pass CYP3A4 metabolism

43
Q

Diltiazem doesn’t affect what

A

No bronchoconstriction or affect lipid profiles like beta blocker

44
Q

GTN

A

100% first pass metabolism, so given sublingual. Fast acting

45
Q

Isosorbide (nitrates and nitrodilators) mononitrate

A

Oral, 100% bioavailable, longer half life

46
Q

Isosorbide dinitrate (nitrates)

A

Metabolised to mononitrate with extended half life

47
Q

Osmotic diuretics

A

Pharmamologically inert but osmotically active. IV administration

48
Q

Loop diuretics, oral route, absorption, max effect, lasts

A

Rapidly absorbed, max effect 1-2hrs, lasts 4-6

49
Q

Loop diuretics, IV route, onset, max effect, lasts

A

Onset 1-2 mins, max effect 30mins, lasts 2hrs

50
Q

Loop diuretics, bound to what, secretion

A

Bound to plasma proteins. Actively secreted into proximal tubules by OATs

51
Q

Thiazide diuretics absorption and elimitation

A

Variable absorption and elimination (mostly renal or metabolised

52
Q

Thiazide diuretic OATs

A

Everest into PT by OATs intersects by competing for OATs - urid acid, probenecid. Cheap and effective

53
Q

Potassium sparing diuretics, oral delivery - absorption, 1st pass metabolism, bound to, excretion

A

70% absorbed in GI tract, extensive 1st pass hepatic metabolism, bound to plasma proteins. Excreted in urine

54
Q

Sodium channel antagonist acts is what wa

A

In a use depended way - binds most strongly in open and inactive states

55
Q

Potassium channel antagonist gradual what needed

A

Gradual oral loading needed

56
Q

Potassium channel antagonist, elimination half life

A

Long elimination half life, so may accumulate when on repeated dosiny

57
Q

Potassium channel antagonist damage to veins

A

Damages veins undiluted in IV

58
Q

Digoxin therapeutic index, drug interactions

A

Narrow therapeutic index, lots of drug interactions - CCB, NSAIDS, amiodarone, BB, diuretics

Cardiac Drugs (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions