Brainscape's Knowledge GenomeTM

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


See full index

FCRAP > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Causes of a reverse hysteresis loop

A

Secondary messengers
Prodrug–>Active metabolite
Redistribution phase

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

amantadine

A

NMDA receptor antagonist
used in dyskinesias in PD
fatigue in MS

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

rivaroxaban

A

Xa inhibitor
Cmax 4 hours; good oral bioavailability
irreversible
inhibits both extrinsic and intrinsic pathways

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

what is the interaction between verapamil and digoxin

A

raised digoxin levels due to non competitive inhibition of p glycoprotein in renal tubules leading to decreased renal secretion. biliary clearance is also reduced.
also display synergism in their effects on heart rate

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

which antibiotics inhibit cell wall synthesis

A

beta lactams, glycopeptides, cyclosporin

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

which antibiotics inhibit protein synthesis

A

aminoglycosides, tetracyclines
chloramphenicol, clindamycin, macrolides, fusidic acid, linezolid aicd
mupirocin

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

which antibiotics inhibit nucleic acid synthesis or activity

A

folic acid: trimethoprim, sulphonamides
DNA gyrase; fluoroquinolones
RNA polymerase: rifampicin
DNA: nitrofurantoin, metronidazole

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

GWAS

A

looks at entire genome of a population to find SNPs a/w traits
huge likelihood of random associations - need to do bonferoni correction to control for this
hardy weinberg equilibrium aims to eliminate selection bias (alleles should be equal between all individuals)

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

bioavailability

A

F = AUC oral / AUC IV

AUC o / dose o) / (AUC iv / dose iv

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

hepatic extraction ratio

A

HER = 1 - bioavailability

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

Volume of distribution

A

Vod = dose / concentration

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

loading dose for desired concentration

A

loading dose = Vod x concentration steady state

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

clearance

A

Cl = amount of body fluid cleared of substance per unit time
Cl = L / h
does not depend on concentration

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

zero order kinetics

A

a set amount of drug is eliminated per unit time

slow plug away at sobering up from a big night regardless of how drunk you were

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

first order kinetics

A

a set proportion of drug is eliminated per unit time
increased elimination with increased concentration

(c/w clearance which does not depend on concentration)

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

albumin

A

binds acid drugs; other acids will compete for binding

eg: salicylic acid, warfarin, penicillins, sulphonamides

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

alpha1 acid glycoprotein

A

binds basic drugs

eg: propranolol, quinidine, impramine, lignocaine

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

dialysis

A

does not affect highly protein bound drugs

or drugs with high VoD (as they are not in the blood)

19
Q

adjusting dose for renal impairment

A

(1-fu) + (fu x % renal fx remaining)

% renal fx = CrCl/1.5

20
Q

maintenance dose

A

maintenance dose or infusion rate = clearance x steady state drug concentration

21
Q

half life

A

t1/2 = 0.7 X Vd/Cl

22
Q

VoD

A

VoD = dose / peak plasma concentration

assume peak plasma concentration occurs 1 hour post IV infusion

23
Q

how do you increase excretion of an acid drug

A

alkalinise the urine

eg: salicylate overdose

24
Q

EC50

A

concentration of drug to give half maximal response

Emax is maximal effect (obtained when all receptors are occupied by the drug)

25
Q

therapeutic index

A

TI = adverse effect EC50/ therapeutic effect EC50

26
Q

tachyphylaxis

A

need greater concentration for same effect ie: down regulation of receptors eg: cocaine

27
Q

antagonists

A

competitive: need increased concentration to achieve effect as competing for the same receptors (curve moves right)
non competitive: irreversible binding to receptor so will decrease maximum effect (curve moves down)

28
Q

lithium

A

SEs: hypothyroid, hyperparathyroid, reduced renal tubular fx
toxicity: acute - GI - N, V, D
chronic - neurological - ataxia, tremor, confusion
increased QTc
toxicity worsened by hypovolaemic states as Li is treated like Na+ in the kidney
Rx with IVT, very dialysable
short half life

29
Q

raloxifene

A

SERM; used for osteoporosis
CI if hx of DVT / PE
increases stroke risk if RFxs
increases hot flashes

30
Q

digoxin

A

toxicity:
visual change - esp colour
confusion
nausea, vomiting, abdominal pain

31
Q

carbamazepine

A

Stevens Johnson Syndrome esp if HLA B1502

32
Q

cetuximab

A

EGFR inhibitor
k ras wild type (does not work with k ras mutant)
CRC, adeno lung, SCC head and neck

33
Q

dabigatran

A

direct thrombin inhibitor
prodrug
indications: DVT prophylaxis post ortho surgery
DVT treatment, non valvular AF
CI: pregnancy, CrCl < 30
interactions: rifampicin, verapamil, amiodarone, ketoconazole, quinidine, tacrolimus, cyclosporin, clarithromycin
monitor TCT; evidece for increased MI
150mg BD increased GI bleed
less ICH than warfarin
prothrombinex if life threatening bleeding

34
Q

CYP2D6

A 
poor metabolisers 10% cauc
ineffective codeine (prodrug)
systemic timolol
toxic perhexiline
cannot metabolise propranolol, quinidine
avoid inhibitors (SSRIs) when on tamoxifen as tamoxifen is metabolised to active form by 2D6
substrates: tramadol
35
Q

CYP2C9

A

poor metabolisers 1-3%

1mg warfarin

36
Q

CYP2C19

A

poor metabolisers 20% asians

reduced clearance omeprazole

37
Q

acetylation

A

slow: procainamide, hydralazine –> SLE

isoniazid –> peripheral neuropathy is slow; hepatitis if fast

38
Q

p glycoprotein substrates

A 
terfenadine, fexofenadine
digoxin
daunorubicin, doxorubicin, etoposide, paclitaxel, vinblastine, vincristine
colchicine
ritonavir
ciclosporin
ivermectin, loperamide
aldosterone, hydrocortisone, dexamethasone, progesterone ,estrogen
39
Q

potency

A 
potency ED50 (point of x axis where half way)
efficacy is Emax (height)
40
Q

erlotinib

A

TKI for lung, pancreatic CA - CYP1A1 metabolism - induced by smoking; need higher doses

41
Q

CYP3A4

A

substrates tramadol, docetaxel, etoposide, irinotecan, imatinib, vincristine, aprepitant, pred

inhibitors: aprepitant, ketoconazole, ciprofloxacin, clarithromycin, ritonavir, verapamil, quinidine
inducers: phenobarbitone, phenytoin, rifampicin

42
Q

avoid in pregnancy

A 
mycophenolate - both mum and dad
leflunomide - washout prior to conception
methotrexate
sirolimus / everolimus
efavirenz
43
Q

renal maintenance

A

induction: cyclophosphamide
maintenance: aza for ANCAs; MMF for SLE

44
Q

tamsulosin

A

1a alpha blocker

FCRAP (19 decks)

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