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pc term 2 Flashcards

1
Q

what do NSAIDs block

A
  1. vasodilation
  2. increase vascular permeability
  3. reduce pain associated w inflam
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2
Q

side fx of NSAIDS

A 
dyspepsia, nausea, vomitting
gastric ulcer
hemorrhagic risk 
sodium and water retention, edema, htn, hyperK
pseudo allergic rxn
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3
Q

aspirin moa

A

non selective irreversible COX inhib
mostly used for its antiplatelet purposes
inhib txA2 synthesis in platelet

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4
Q

diclofenec

A

short t1/2 NSAID

drug accm in synovial fluid, gd for joint

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5
Q

non selective NSAIDs

A 
ketoprofen
piroxicam 
aspirin
naproxen 
indomethacin 
diclofenec
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6
Q

coxibs

A 
mefenamic acid
meloxicam
celecoxib
parecoxib
etoricoxib
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7
Q

unwanted fx of coxibs

A
  • renal toxicity
  • premature closure of ductus arteriosus
  • contraindicated in third trimester
  • impaired wound healing, exacerbate ulcers
  • bruising
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8
Q

NSAID safe for peds

A

paracetamol

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9
Q

coticosteroids transactivation

A

PBI:
PLA2 inhib
B2 adrenoceptor
IkB-a

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10
Q

corticosteroids transrepression

A

cytokines
chemokines
inflam enzymes
adhesion molecules

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11
Q

corticosteroid anti inflam actions

A
  • less T, B cells, monocytes, eosinophils, basophils
  • more neutrophils
  • less type 4 hypersensi
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12
Q

corticosteroids

A

methylprednisolone -> triamcinolone (strongest)
prednisone -> prednisolone
cortisone -> hydrocortisone
dexamethasone -> betamethasone

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13
Q

side fx of steroids

A 
hyperglycemia and lipidemia
hypokalemia, metab alkalosis
na H2o retention 
htn chf
prone to infections
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14
Q

commonly used inhaled corticosteroids

A

fluticasone

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15
Q

first line prophylactic tx for asthma + its MOA

A

fluticasone

  • increase macrophage effercytosis
  • increase B2 receptors on airway smooth mm
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16
Q

potent cysteinyl leukotriene receptor antagonist

A

montelukast

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17
Q

B2 agonist

A

salbutamol, salmeterol, formoterol, indacaterol

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18
Q

MOA of B2 agonist

A
  • increase cAMP, ASM bronchodilate
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19
Q

ipratropium bromide vs tiotropium bromide, which is more potent for copd

A

tiotropium bromide

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20
Q

4 classes of anti htn drugs

A

a - ace inhib
b - b blockers
c - ca channel blocker
d - diuretics

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21
Q

moa, adr of acei

A

block ang 1 -> ang 2
less water sodium retention, less peripheral vascular resistance
adr = dry cough, hypotn, hyperk
*contraindicated in pregnancy

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22
Q

nifedipine moa

A 
ca channel blocker for antihtn
block ca channel in myocytes and smooth mm cells
reduce myocardial contractility
reduce o2 req
reduce cardiac output
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23
Q

hydrochloroTHIAZIDES moa and adr

A

diuretic for antihtn
acts on dct, depends on renal prostaglandin syn
fx = pee out more stuff
adr = hypok, hyponatremia, hypouricemia

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24
Q

common antiplatelet drugs

A

aspirin

clopidogrel / prasugrel / ticagrelor

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25
Q

clopidogrel moa and adr

A
  • aspirin substitute
  • given as an oral prodrug
  • inhibits ADP induced platelet aggregation and activation
  • irreversible antag of p2y12 receptor
  • gd for prophylaxis of artherial thrombosis

adr = bleeding, dypsenea, headache, nausea, dizziness

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26
Q

anticoagulants

A

heparin

warfarin

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27
Q

heparin moa and adr

A
  • roa = iv or sq
  • binds and activate anti thrombin 3 and alpha plasma protease inhib -> cause AT3 conformation change -> enhanced interaction with clotting factors to form inactivate complexes
  • stimulates tfpi release from endo -> block coag pathways
  • safe for pregnancy, dvt, arterial thrombosis in MI

adr = narrow ti, bleeding, thrombocytopenia, osteoporosis

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28
Q

warfarin adr moa

A

moa = racemic mixture of r and s isomer, s more rapidly metab and more potent

  • roa = oral
  • vit k antag inhib coag pathways

adr = cross placenta, fetal warfarin syndrome. narrow TI. lotsa adr w other drugs
used to maintain anticoag therapy, prophy for dvt

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29
Q

warfarin antidote

A

vit k

30
Q

heparin antidote

A

protamine sulfate

31
Q

rapid acting insulin + duration

A

lispro
aspart
glulisine

2-5h

32
Q

short acting insulin + duration

A

humulin r
actrapid

6-8h

33
Q

intermediate acting insulin + duration

A

NPH

12-20h
peak = 4-8h -> highest hypoglycemia risk

34
Q

long acting insulin + duration

A

glargine
detemir
24h

35
Q

insulins that cannot be mixed

A

glargine and detemir cannot mix w other stuff

glulisine can only mix w NPH

36
Q

factors to increase insulin absoprtion

A
  • abdomen
  • inject into mm layer
  • smaller vol
  • exercising the mm before before being injected
  • massage / heat
37
Q

metformin moa + adr

A

[insulin sensitiser]

  • decrease hepatic glucose pdtn, increase density of insulin receptors
  • no fx on insulin secretion
  • improve glucose tolerance, decrease basal and postprandial plasma glucose

adr = git issues. need to be taken w meal. b12 malabsorption. bad for renal and liver. lactic acidosis

FIRST LINE THERAPY FOR DM2

38
Q

thiazoldinediones (TZD) [prioglitazone, rosiglitazone] moa + adr

A

[insulin sensitiser]

  • increase insulin dependent glucose disposal
  • decrease insulin resistance in periphery and liver wo increasing insulin pdtn

adr = risk of bone fracture

39
Q

repaglinide moa + adr

A

[insulin secretagogues]
- administer just before meal to control post prandial gluc lvl
- induce pancreatic b cells to secrete insulin
only for DM2
- insulin is released in a gluc dependent manner

40
Q

acarbose moa + adr

A

[alpha glucosidase inhib]

  • must take w food
  • slow down glucose rise after a meal
  • glucose bypass small intestine and hang out in colon = gastric distention and flatulence

adr = bad for git, renal, hepatic probs

41
Q

linagliptin moa + adr

A

[incretin based therapy]
- prolongs action of endogenous incretins which stimulates beta cells to increase glucose stimulated insulin release and suppress alpha cells glucagon release

adr = git probs. relatively low risk

42
Q

exenatide / liraglutide moa + adr

A

[incretin based therapy]
roa = sq
- initiate rapid release of endogenous insulin + suppress glucagon release + delay gastric emptying + decrease appetite
- glucose dependent insulin release

adr = git, caution w pancreatitis. safe drug.

43
Q

empagliflozin
canagliflozin
dapagliflozin

A

sglt2 inhib
- prevent reabs of glucose

adr = uti, genital infection, diabetic ketoacidosis

44
Q

amide LA

A 
lidocaine (medium t)
mepivacaine 
bupivacaine (long t)
etidocaine 
prilocaine
45
Q

ester LA

A

cocaine
procaine (short t)
chloroprocaine
tetracaine

46
Q

msot cardiotoxic LA

A

bupivacaine

47
Q

moa of LA

A

LA = weak bases but manufactured as neutral uncharge form for rapid penetration of lipid membranes
becomes charged form = become active
LA are sodium channel blockers, bind to intracellular end of Na channels, cause voltage and t dependent blockage, reduce depol, prolong repol
LA less fxtive when injected to acidic tissue e.g. infected

48
Q

offset of LA action determined by what

A

absorption and distribution

49
Q

factors affecting systemic absorption of LA

A 
dosage 
site of injection - more vascularised = absorbed quicker 
tissue binding affinity of drug 
local blood flow
use of vasocon 
drug properties
50
Q

ester vs amide LA metab

A

esters - rapidly hydrolysed into inactive metabolites
amide - metab in liver by cyp450
Renal excretion

51
Q

what kind of nerves easier to block by LA

A

small fibre diameter e.g. pain fibres
unmyelinated
(because these fibres can only propagate e impulses over short distance so easier to block)

52
Q

how to prolong LA fx

A
  • increase dose
  • use vasoconstrictor like epinephrine
  • add sodium bicarb so that it is a basic envt
  • use an LA w rapid skin penetration
53
Q

adr of LA

A
  • direct neurotoxicity due to high conc in close proximity to spinal cord / nerve trunks
  • systemic toxicity from rapid absorption or accidental OD
  • cns fx of sleepiness, light headed
  • cvs fx of decrease myocardial contractility…
  • prilocaine metab cause methemoglobinema
  • allergic rxn to metabolites esp for esters
54
Q

what to do when pt sensi to ester LA

A

dont use amide

change to ester

55
Q

outcomes of GA

A 
unconsciousness
amnesia 
analgesia
relax smooth mm
loss of autonomic ns reflexes
56
Q

how GA go to brain

A

GA from alveolar air to blood -> travel to brain and other tissue -> brain reach therapeutic brain conc

57
Q

factors affecting therapeutic brain conc

A

solubility of GA (low solubilty = rapid onset)
con of GA - higher conc = higher rate of tf
rate and depth of pulm ventilation - more ventilation = higher rate of tf

58
Q

factors affecting metab and excretion of GA

A
  • more insoluble in blood = eliminate faster
  • duration of exposure - long = slower to eliminate
  • excretion is mainly through lungs so affected by ventilation
59
Q

fx of GA on brain

A

decreases cerebral vascular resistance - increase cerebral blood flow
*not gd for ppl w raised icp

60
Q

methoxyflurane adr

A

methoxyflurane (GA) releases fluoride during metab, not gd for renal dysfn

61
Q

inhaled GA

A

N2O, cyclopropane

  • analgesic agent for labour pain
  • lacks potency
62
Q

IV GA

A

thiopental
bzd
propofol
ketamine

63
Q

thiopental moa + adr

barbiturates

A
  • rapid onset and short acting IV GA
  • gd for induction bc crosses BBB quickly
  • high lipid solubility = distribute out to mm and fat
  • potent respi depressent bc decrease arterial bp, stroke vol, cardiac output
  • gd for ppl w raised icp
64
Q

bzd moa + adr

A
  • IV GA, hypnotic for antianxiety
  • increase freq of GABA gated cl channel oppening
  • e.g. diazepam, lorazepam, midazolam
  • gd for sedative and amnesia properties
  • need high dose to achieve deep sedation
65
Q

propofol moa + adr

A
  • most commonly used IV gA bc of rapid onset and rapid recovery
  • potentiates GABA a recepor activity, slow down channel closing time
  • rapidly abs by liver and excreted by kidney

adr = decrease bp and potent respi depressant

66
Q

ketamine moa + adr

A

the only Iv GA that has analgesic and anaesthetic properties

  • highly lipophillic, rapidly distributed to brain metab by liver, excreted by kidney and bile
  • inhibs reuptake of norepinephrine, stimulate symp ns
  • increase cerebral flow and icp

adr = post op disorientation, illusions

67
Q

adr of diazepam

A
  • dose related drowsiness
  • diminished motor skills
  • long rxn time
  • anterograde amnesia
  • decrease bp…
  • dependency
  • irritability, hallucination etc.
68
Q

seizures vs epilepsy

A 
seizures = abnormal discharge in a group of neurons in brain 
epilepsy = chronic disorder characteristed by recurrent seizures
69
Q

phenobarbitone

A

[antiepileptic]

  • @ low dose: binds to GABA increase frequency of channel opening induced by GABA
  • @ high dose: independent of GABA, prolonged channel opening (may lead to death)

adr = diplopia, sedation, drowsiness, depression, loss concentration

70
Q

phenytoin

A

[antiepileptic]
decrease membrane excitability by altering Na and Ca conductance during action potential
stops channels from being activated and creating an AP
slows down how fast and how well Na channels work
stop nerons from sending repeated msgs

adr = gum hypertrophy, convulsions

71
Q

carbamazepine

A

[antiepileptic]

  • similar to phenytoin
  • cyp450 inducer

adr = diplopia, nystagmus, GI upset, drowsiness, folate vit D deficiency, antidiuretic

72
Q

valproate

A

[anti epileptic]
- increase GABA by preventing its breakdown
increase k conductance by hyperpolarising membrane potential

pc (3 decks)

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