Brainscape's Knowledge GenomeTM

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


See full index

Top 200 > Exam 4 pcol > Flashcards

Exam 4 pcol Flashcards

1
Q

Pitavastatin

livalo

A

Statin -HMG co Reductase inhibitor
Lowers LDL
Lowers triglycerides
Increases HDL

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

Atorvastatin

lipitor

A

Statin- HMG coa Reductase inhibitor
Lowers LDL
Lowers triglycerides
Increase HDL
Is metabolize by CYP 3A4
High intensity dose is 40-80mg
Moderate intensity dose is 10-20mg

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

Rosuvastatin

Crestor

A

HMG coa reductase inhibitor
Lowers LDL
Lowers triglycerides
Increases HDL
If use for high intensity the dose is 20-40mg
If use for moderate intensity the dose is 5-10mg

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

Pravastatin

Pravachol

A

HMG-Coa Reductase inhibitor
Lowers LDL
Increases HDL
Use for moderate intensity and the dose is 40-80mg

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

Simvastatin

zocor

A

HMG Coa Reductase inhibitor
It will lower LDL
Lower Triglycerides
Increases HDL
Use for moderate intensity dose is 20-40mg

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

Lovastatin

Mevacor

A

HMG Coa Reductase inhibitor
It will decrease LDL
Increase HDL
For moderate dose is 40mg

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

Ezetimibe

A

Cholesterol absorption inhibitor it will inhibit NPC1L1

Zetie

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

Vitamin B3 Nicotinic Acid (Niacin )

Has Pyridine ring is absober by active transport
A

Lowers LDL lower triglycerides increases HDL

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

Gemfibrozil

is lipophilic and is acidic has strong plasma protein binding bioavailability is high Phenoxy butyric acid
A

Lowers LDL lowers triglycerides
activated PPAR

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

Fenofibrate

phenyl isubutyric is lipophilic and is well absorb has high bioavailability
A

Activates PPAR Lowers triglycerides lowers LDL

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

Cholestyramine

Questran

A

Bile acid sequestran it will inhibit the reabsorption of bile acid
Lowers LDL but AE can increase triglycerides so cannot give to pt that triglyceride levels are >300
Will bind to other drugs and decrease the absorption of other drugs
It causes constipation and bloating–> Acts locally in the GIT because of the quaternary ammonium slat is not absorb
It will inhibit the absorption of fat soluble vitamins Vitamin D,E,A,K
The compensatory mechanism of the body is to increase LDL receptors so decreases LDL in the blood because LDL will be taken in to the liver and is needed so is brokendown need cholesterol in order to form billie acid
Another compensatory mechanism of the body is to increase HMG Reductase –> So need to co-administer a statin

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

Colestipol

Colestid

A

Is a bile acid sequestran
It will react with the lipophilic backbone of bile acid and will prevent the reabsorption of the bilie acid to the liver because it will form non absorbable complex and acts locally om the GIT
The liver will sense the decrease in the bilie acid and as a compensatory mechanism it will increase LDL receptors so more LDL is taken from the blood so lowers the LDL
It will also cause increase in production of HMG coa reductaser so need to co-administer a statin

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

Colesevalem

A

bilie acid sequestran

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

Acetazolamide

Diamox

the liver hates the sulfonamide group so it has high bioavailability but give locally for glaucoma
A

Carbonic anhydrase inhibitor

Works in the proximal tubule

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

Methazolamide

Is lipophilic and acidic the liver hates the sulfonamide group so bioavailability is high
A

Carbonic anhydrase inhibitor

Works in the proximal tubule

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

Dorzolamide

A

Carbonic anhydrase inhibitor

works in the proximal tubule

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

Chlorothiazide

C 6 has Cl electron withdrawing C-7 Sulfonamide Is lipophilic acidic has protein binding The liver hates the sulfonamide so it goes to the kidney but is least potent so dose is 500mg -2g PO QD because short duration of action
A

Thiazide diuretic

works in the proximal distal tubule

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

Hydrochlorothiazide

6-Cl electron withdrawing 7-Sulfonamide group The double bond is saturated so is more potent Dose is 50-100mg QD
A

Thiazide diuretic

works in the proximal distal tubule

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

Metolazone

has a methyl at C2 Has Sulfonamide group at 6 Is lipophilic and is acidic has protein binding It is more resistant and quinethazone because of the tolune substituent It is more potent so dose is 0.5mg -5mg QD
A

Thiazide like diuretic
quinazoline derivative

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

Chlorthalidone

Longer acting 10x more potent dose is 15-50mg has monosubstituted unfused ring
A

Thiazide like diuretics
Phathalamide derivative

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

Indapamide

It is more potent is only given twice weekly 1.25-5mg Is lipophilic and acidic it bind to plasma proteins
A

Thiazides like diuretics
Indoline derivative

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

Mannitol

A

Osmotic diuretic it draws H2O and Na+ out

23
Q

Furosemide

Dose is 80mg in two dived doses is short acting because can be conjugated in phase 2 metabolism (amino acid structure Carboxylic + amine) but has high bioavailability
A

Loop diuretic “high ceiling”

Works in the ascending loop of henly

24
Q

Ethacrynic acid

Dose is 50-100mg Short acting because can be conjugated in phase 2 metabolism
A

Loop diuretics

25
Q

Bumetanide

dose is 0.5-1mg IV, IM or PO Short acting--> Phase 2 conjugation High bioavailability
A

Loop diuretic

26
Q

Torsemide

A

Loop diuretic

27
Q

Spironolactone

can be metabolize by esterase hydrolysis so it will decrease the bioavailability becase it will go throw hepatic metabolism
A

Aldosterone endocrine antagonist - medchem
For pcol is non selective aldosterone antagonist

28
Q

Eplerenone

A

selective aldosterone antagonist

29
Q

Finerenone

A

Selective aldosterone antagonist

30
Q

Vasopressin

A

V1 And V2 agonist

Antidiuretic hormone

31
Q

Desmopressin

DDAVP

A

Selective V2 agonist

32
Q

Conivaptan

also known as aquaretic

A

Non selective V1 and V2 antagonist

Treat SIADH

33
Q

Tolvaptan

A

Selective V2 antagonist

Treat SIADH

34
Q

Oxytocin

A

Oxytocin receptor ligand agonist

35
Q

Atosiban

A

VOTRA
Vassopresin and Oxytocin Receptor antagonist

36
Q

Colchine

A

Inhibit WBC migration and phagocytosis to the uric acid crystals so reduce the inflammation

dose for accute is 1.2mg then 0.6mg BID
Dose for prophylactic is 0.6mg B

37
Q

Allopurinol

A

Xanthine oxidase inhibitor

For hyperurecemia dose is 100mg QD first then 300mg then 600mg
CrCl 90-6

38
Q

Febuxostat

dose initially is 40mg QD
If after 2 weeks goal is not achieve –> Dose

A

Xanthine oxidase inhibitor

Uloric

39
Q

Probenecid

initial dose is 250mg BID for 7 days then 500mg BID then if needed 2g di

A

uricosuric agent
Inhibit URAT-1 in the proximal tubule so no uric acid reabsorbtion

40
Q

Lesinurad

Zurampic

A

uricosidic agent
Inhibit URAT-1 in the proximal tubule

41
Q

Pegloticase

dose is 8mg every 2 weeks IV

A

Is a enzyme Uricase and breaks down uric acid to allantoin that is more easy excreted

42
Q

Dobutamine

A

B1 agonist inotropic drug for treatment of HF
-Initially there is a decrease in CO and SV and the heart is enlarge so is harder to contract and pump the blood

43
Q

Dopamine

A

D1 agonist in cardiac myocyte
Treat acute heart failure that initially has decrease in CO and in SV and the heart is enlarge so is harder for the heart to contract and pump the blood

44
Q

Glucagon

A

release from the pancreas it is link to gS and will bind to the cardiac myocyte and increase CO and Sv and increase contractility
-Treat acute heart failure because initially there is a decrease in CO and in SV and the heart is enlarge and is harder for the heart to pump blood

45
Q

Milrinone

A

PDE 3 inhibitor

46
Q

Inamrinone

A

PDE 3 inhibitor

47
Q

Adenosine

A

It binds to A1 receptors in the SA node and the AV node
The A1 receptors are couple to Gi –> Decrease in Adenylate Cyclase –> Decrease CAMP. It will also directly open K+ Channels so it causes hyperpolarization
Gi M2 M4 in the SA node and AV node
-Decrease HR –> Decreases SA node firing
-Decreases AV nodal conduction–> Treat atrial arrythmia
-But adenosine is taken up by the RBC and very little get to the site of action –>so is only given to terminate the arrythmia given for IV for Acute

AE:
-Assystole–> The patient feels the heart suddenly stops

48
Q

Procainamide

A

1a class Na+ channel blocker

49
Q

Disopyramide

A

Class 1a Na+ channel blockers

50
Q

Lidocaine

A

Class 1B Na+ Channel blockers

51
Q

Mexilitene

A

Class 1b Na+ channel blocker

52
Q

Flecainide

A

Class 1C Na+ Channelo blocker

slow dissociation

53
Q

Propafenone

A

Class 1c Na+ Channel blocker

Slow dissociation

Top 200 (16 decks)

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