Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Cardiac Drugs > Extra / PK > Flashcards

Extra / PK Flashcards

(58 cards)

Start Studying
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)

Study These Flashcards
A

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

25
Dipyridamole
Platelet phosphate inhibitor, blocks ADP mediated platelet activation
26
Enoxaparin duration and bioavailability
Longer duration and increased bioavailability compared to UF heparin
27
Enoxaparin delivery
Subcutaneous
28
Warfarin route of admission and pk
Oral - 24-48hrs to take effect
29
Warfarin bridging therapy
Bridging therapy with cleans or heparin first cos slow onset and decreased protein C and S initially
30
Warfarin monitoring
Monitored using INR - aim for between 2 and 2.5
31
Alteplase (Fibrinolytics) dosage
Strictly controlled
32
Alteplase (Fibrinolytics)metabolims
Metabolised by liver to amino acids
33
Alteplase (fibrinolytics) half life
72 mins
34
Tenecteplase (fibrinolytics)
Longer half life compared to alteplase, increased fibrin specificity and resistance to PAI-1 inactivication
35
Amlodipine, absorption, onset,
Well absorbed orally, slow onset of action
36
Amlodipine metabolism and excretion
Hepatically metabolised and excreted as inactive metabolites in urine
37
Amlodipine affected by what interactions
CYP3A4
38
Verapamil absorption
Well absorbed orally
39
Verapamil metabolism
Rapid metabolism by 1st pass CYP3A4 metabolism
40
Verapamil doesn’t affect what
No bronchoconstriction or affect lipid profiles like beta blocker
41
Diltiazem absorption
Well absorbed orally
42
Diltiazem metabolism
Rapid metabolism by 1st pass CYP3A4 metabolism
43
Diltiazem doesn’t affect what
No bronchoconstriction or affect lipid profiles like beta blocker
44
GTN
100% first pass metabolism, so given sublingual. Fast acting
45
Isosorbide (nitrates and nitrodilators) mononitrate
Oral, 100% bioavailable, longer half life
46
Isosorbide dinitrate (nitrates)
Metabolised to mononitrate with extended half life
47
Osmotic diuretics
Pharmamologically inert but osmotically active. IV administration
48
Loop diuretics, oral route, absorption, max effect, lasts
Rapidly absorbed, max effect 1-2hrs, lasts 4-6
49
Loop diuretics, IV route, onset, max effect, lasts
Onset 1-2 mins, max effect 30mins, lasts 2hrs
50
Loop diuretics, bound to what, secretion
Bound to plasma proteins. Actively secreted into proximal tubules by OATs
51
Thiazide diuretics absorption and elimitation
Variable absorption and elimination (mostly renal or metabolised
52
Thiazide diuretic OATs
Everest into PT by OATs intersects by competing for OATs - urid acid, probenecid. Cheap and effective
53
Potassium sparing diuretics, oral delivery - absorption, 1st pass metabolism, bound to, excretion
70% absorbed in GI tract, extensive 1st pass hepatic metabolism, bound to plasma proteins. Excreted in urine
54
Sodium channel antagonist acts is what wa
In a use depended way - binds most strongly in open and inactive states
55
Potassium channel antagonist gradual what needed
Gradual oral loading needed
56
Potassium channel antagonist, elimination half life
Long elimination half life, so may accumulate when on repeated dosiny
57
Potassium channel antagonist damage to veins
Damages veins undiluted in IV
58
Digoxin therapeutic index, drug interactions
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.
© 2025 Bold Learning Solutions. Terms and Conditions