pc term 2 Flashcards
1
Q
what do NSAIDs block
A
- vasodilation
- increase vascular permeability
- reduce pain associated w inflam
2
Q
side fx of NSAIDS
A
dyspepsia, nausea, vomitting gastric ulcer hemorrhagic risk sodium and water retention, edema, htn, hyperK pseudo allergic rxn
3
Q
aspirin moa
A
non selective irreversible COX inhib
mostly used for its antiplatelet purposes
inhib txA2 synthesis in platelet
4
Q
diclofenec
A
short t1/2 NSAID
drug accm in synovial fluid, gd for joint
5
Q
non selective NSAIDs
A
ketoprofen piroxicam aspirin naproxen indomethacin diclofenec
6
Q
coxibs
A
mefenamic acid meloxicam celecoxib parecoxib etoricoxib
7
Q
unwanted fx of coxibs
A
- renal toxicity
- premature closure of ductus arteriosus
- contraindicated in third trimester
- impaired wound healing, exacerbate ulcers
- bruising
8
Q
NSAID safe for peds
A
paracetamol
9
Q
coticosteroids transactivation
A
PBI:
PLA2 inhib
B2 adrenoceptor
IkB-a
10
Q
corticosteroids transrepression
A
cytokines
chemokines
inflam enzymes
adhesion molecules
11
Q
corticosteroid anti inflam actions
A
- less T, B cells, monocytes, eosinophils, basophils
- more neutrophils
- less type 4 hypersensi
12
Q
corticosteroids
A
methylprednisolone -> triamcinolone (strongest)
prednisone -> prednisolone
cortisone -> hydrocortisone
dexamethasone -> betamethasone
13
Q
side fx of steroids
A
hyperglycemia and lipidemia hypokalemia, metab alkalosis na H2o retention htn chf prone to infections
14
Q
commonly used inhaled corticosteroids
A
fluticasone
15
Q
first line prophylactic tx for asthma + its MOA
A
fluticasone
- increase macrophage effercytosis
- increase B2 receptors on airway smooth mm
16
Q
potent cysteinyl leukotriene receptor antagonist
A
montelukast
17
Q
B2 agonist
A
salbutamol, salmeterol, formoterol, indacaterol
18
Q
MOA of B2 agonist
A
- increase cAMP, ASM bronchodilate
19
Q
ipratropium bromide vs tiotropium bromide, which is more potent for copd
A
tiotropium bromide
20
Q
4 classes of anti htn drugs
A
a - ace inhib
b - b blockers
c - ca channel blocker
d - diuretics
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
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
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
24
Q
common antiplatelet drugs
A
aspirin
clopidogrel / prasugrel / ticagrelor
25
clopidogrel moa and adr
- 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
26
anticoagulants
heparin
| warfarin
27
heparin moa and adr
- 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
28
warfarin adr moa
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
29
warfarin antidote
vit k
30
heparin antidote
protamine sulfate
31
rapid acting insulin + duration
lispro
aspart
glulisine
2-5h
32
short acting insulin + duration
humulin r
actrapid
6-8h
33
intermediate acting insulin + duration
NPH
12-20h
peak = 4-8h -> highest hypoglycemia risk
34
long acting insulin + duration
glargine
detemir
24h
35
insulins that cannot be mixed
glargine and detemir cannot mix w other stuff
| glulisine can only mix w NPH
36
factors to increase insulin absoprtion
- abdomen
- inject into mm layer
- smaller vol
- exercising the mm before before being injected
- massage / heat
37
metformin moa + adr
[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
thiazoldinediones (TZD) [prioglitazone, rosiglitazone] moa + adr
[insulin sensitiser]
- increase insulin dependent glucose disposal
- decrease insulin resistance in periphery and liver wo increasing insulin pdtn
adr = risk of bone fracture
39
repaglinide moa + adr
[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
acarbose moa + adr
[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
linagliptin moa + adr
[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
exenatide / liraglutide moa + adr
[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
empagliflozin
canagliflozin
dapagliflozin
sglt2 inhib
- prevent reabs of glucose
adr = uti, genital infection, diabetic ketoacidosis
44
amide LA
```
lidocaine (medium t)
mepivacaine
bupivacaine (long t)
etidocaine
prilocaine
```
45
ester LA
cocaine
procaine (short t)
chloroprocaine
tetracaine
46
msot cardiotoxic LA
bupivacaine
47
moa of LA
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
offset of LA action determined by what
absorption and distribution
49
factors affecting systemic absorption of LA
```
dosage
site of injection - more vascularised = absorbed quicker
tissue binding affinity of drug
local blood flow
use of vasocon
drug properties
```
50
ester vs amide LA metab
esters - rapidly hydrolysed into inactive metabolites
amide - metab in liver by cyp450
Renal excretion
51
what kind of nerves easier to block by LA
small fibre diameter e.g. pain fibres
unmyelinated
(because these fibres can only propagate e impulses over short distance so easier to block)
52
how to prolong LA fx
- increase dose
- use vasoconstrictor like epinephrine
- add sodium bicarb so that it is a basic envt
- use an LA w rapid skin penetration
53
adr of LA
- 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
what to do when pt sensi to ester LA
dont use amide
| change to ester
55
outcomes of GA
```
unconsciousness
amnesia
analgesia
relax smooth mm
loss of autonomic ns reflexes
```
56
how GA go to brain
GA from alveolar air to blood -> travel to brain and other tissue -> brain reach therapeutic brain conc
57
factors affecting therapeutic brain conc
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
factors affecting metab and excretion of GA
- more insoluble in blood = eliminate faster
- duration of exposure - long = slower to eliminate
- excretion is mainly through lungs so affected by ventilation
59
fx of GA on brain
decreases cerebral vascular resistance - increase cerebral blood flow
*not gd for ppl w raised icp
60
methoxyflurane adr
methoxyflurane (GA) releases fluoride during metab, not gd for renal dysfn
61
inhaled GA
N2O, cyclopropane
- analgesic agent for labour pain
- lacks potency
62
IV GA
thiopental
bzd
propofol
ketamine
63
thiopental moa + adr
| barbiturates
- 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
bzd moa + adr
- 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
propofol moa + adr
- 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
ketamine moa + adr
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
adr of diazepam
- dose related drowsiness
- diminished motor skills
- long rxn time
- anterograde amnesia
- decrease bp...
- dependency
- irritability, hallucination etc.
68
seizures vs epilepsy
```
seizures = abnormal discharge in a group of neurons in brain
epilepsy = chronic disorder characteristed by recurrent seizures
```
69
phenobarbitone
[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
phenytoin
[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
carbamazepine
[antiepileptic]
- similar to phenytoin
- cyp450 inducer
adr = diplopia, nystagmus, GI upset, drowsiness, folate vit D deficiency, antidiuretic
72
valproate
[anti epileptic]
- increase GABA by preventing its breakdown
increase k conductance by hyperpolarising membrane potential
