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pharm Flashcards

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1
Q

histamine triple response

A

red - vasodilation
wheal - increase permeabilty
flare - spreading response through sensory neurons

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2
Q

how does histamine cause acid secretion

A

acts on H2 R on parietal cell, to increase cAMP

activates K/H pum p

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3
Q

biosynthesis of bradykinin

A

prekallikrein converted to kallikrein by factor XII

kallikrein converts HMW kinninogen to bradykinin

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4
Q

C1 esterases

A

kallikreins

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5
Q

hereditary angioedema

A

deficiency in CI esterase inhibitor - use B2 R ant

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6
Q

activation and effects of NO

A

ach/bradykinin/sheer stress - causes increase Ca
Ca activates nitric oxide synthase
converts arginine to NO
NO activates guanylate cyclase to increase cGMP and cause relaxation

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7
Q

what regulates vascular tone

A

basal release of NO

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8
Q

symp or parasymp has greater influence on HR at rest

A

parasymp

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9
Q

symp action on heart

A

act on B1, increase cAMP, opens Ca channels - decrease time to reach potential, increase rate of firing, increase conduction time

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10
Q

3 mechanisms underlying dysrhythmias

A
  1. altered pulse formation - abnormal AP generation
  2. altered pulse conduction - conduction block, re-entry
  3. triggered activity - early or late afterdepolarisations:
    - early - abberant Na or Ca channel opening
    - late - Ca overload - excitation on completion of repolarisation
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11
Q

4 Classes of antidysrhythmics

A
  1. Na channel blockers - 1a, b,c
  2. B blockers
  3. K channel blockers
  4. Ca channel blockers
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12
Q

class 1 a b c antidysrhythmics

A

Na channel blockers
1a - quinidine - moderate block, prolong repolarisation, increase ERP
1b - lignocaine - mild block, shorten repolarisation, decrease ERP
1c - flecainide - big block, same repolarisation, same ERP

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13
Q

amiodarone

A

K channel blocker, also other ones

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14
Q

antihypertensives

A

a - angiotensin system inhibitors - Ace inhibitors, AngiR ants
b - B antagonists
c - L-type Ca blockers
d - diuretics

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15
Q

olols

A

B blockers

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16
Q

sartans

A

angI R ant

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17
Q

prils

A

ACE inhibitors

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18
Q

digoxin mehcanism of action

A

inhibits Na/K atpase, increase Na intracellular, decreases Ca extrusion - builds up in SR, increase Ca release with each AP

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19
Q

dobutamine

A

B agonist

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20
Q

heparin

A

enhances antithrombin 3 activity - inactivates factor Xa and thrombin

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21
Q

monitoring of heparin with

A

APTT

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22
Q

warfarin

A

inhibits vit K reductase - inhibits reduction of vit K, therefore inhibits gamma carboxylation in blood coagulation factors

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23
Q

monitor warfarin with

A

PT and INR

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24
Q

3 drugs affecting platelet activation/adhesion

A

ADP R ant
aspirin
GPIIb/IIIa R ant

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25
fibrinolytic drugs
streptokinase | alteplase - hrtPA - clot selective, not antigenic
26
loop diuretics mech of action
block Na/K/Cl carrier in thick ascending limb
27
thiazide diuretics mech
inhibit Na/Cl in distal tubule
28
side effects of thiazide
K loss, increase uric acid
29
loop diuretics side effect
K loss, H loss - metabolic alkalosis
30
K Sparing diuretics mech
spironolactone - ald R ant - block Na channels and decreased Na/K pump synthesis amiloride - Na luminal channel blocker
31
3 drugs that can damage kidney
mercury - toxicity and vasoconstriction gentamicin - alters Ca metabolism cisplatin - forms ROs
32
statins mech
HMG-CoA reductase inhibitors - decrease cholesterole synth so increase LDL R on liver and increase LDL uptake and increase HDL
33
bile acid sequestrants
prevent absorption cholesterol, increase excretion, increase demand for chol for bile acid syntheiss, increase LDL R adn removal of LDL
34
Ezetimibe
inhibits sterol transporter in intestine - only as adjacent to statin
35
treatment for hypertriglyceridaemia
fibrates - increase LPL so decrease TAGs in plasma
36
nicotinic acid
hypercholesterolaemia treatment - all statin things plus decreases atherogenic lipoprotein a - but poor tolerance
37
4 treatments for stable angina
1. nitrates - No release 2. Ca channel blockers - decrease afterload, HR, SV 2. B blockers 3. ivabradine
38
unstable angina treatment
as for stable plus aspirin
39
process of mast cell degranulation
FcR clustering - tyrosine K activity - PLC - Dag (PKC) and IP3 (Ca mobilisation) - degranulation
40
where cys-LT released from
eosins, masts, macs
41
cys-LT physiological role or path
only path
42
endogenous mast cell inhibitors
PGE2, Adrenaline, cortisol
43
disodium chromoglycate
causes annexin-1 releaes - inhibits cys-LT production
44
omalizumab
binds IgE
45
montelukast
cys-LT R ant for aspirin or exercise induced asthma
46
asthma airway hyperresponsiveness
airways constrict too easily and too much
47
SABA mech of action
B2 ag - Gs - PKA - activates SERCA, blocks Ip3 - both decrease Ca intracellular - decrease contraction
48
treatment of bronchoconstriction in COPD
anti-musc
49
actions of glucocorticoids in asthma
- decrease activity, recruitment, survival of eosins and Th2 - decrease mast cell activation and cytokine production - decrease prolif, cyt and collagen production of smooth muscle adn fibroblasts
50
indication for inhaled GCS
if B2 ag needed more than 3 times a week
51
cell infiltration in COPD
neuts, CD8, lots of macs
52
Triple wammy
ace inhibitor - dilate efferent arteriole diuretic - decrease volume NSAID - vasoconstrict afferent arteriole
53
methotrexate
blocks human dihydrofolate reductase - anticancer, immunosuppressant
54
amphotericin
stops ergosterol synthesis - antifungal
55
paclitaxel
bind polymerised tubulin - prevents dissassembly therefore mitosis - anti cancer
56
short term infusion useful for what drugs
low TI
57
problem with low bioavailability
patient variability will have higher consequences
58
problem with slowly distributing drug
peak conc will be higher than expected based on Vd as in beginning its distributing in smaller compartment as hasnt reached fat or muscle yet
59
newborns deficinet in what metabolism enzymes
phase II
60
elderly deficient in what metabolism enzymes
phase I - CYT
61
what is pharmacokinetic drug drug interaction
drug a effects conc of drug b at receptor
62
what is pharmacodynamic drug drug interaction
drug a effects actions of drug b without altering conc at R
63
esomeprazole
PPI - H/K atpase - PUD
64
ranitadine
H2R ant - PUD
65
sodium bicarb
antacids
66
hyoscine butylbromide
musc R ant - smasmolytic
67
misoprostol
PGE2 anaolgue
68
promethazine
H1R ant - antiemetic - motion sick
69
hyoscine hydrobromide
M R ant - anti-emetic
70
metoclopramide
D2R ant (also blocks 5HT3 and 4 )- anti-emetic
71
prochlorperazine
D2R ant - less sedative - anti-emetic, extrapyramidal side effects
72
ondansetron
5HT3 R ant - antiemetic - no extrapyramidal side effects
73
aprepitant
NK1R ant - anti-emetic
74
4 laxatives
bulking agents faecal softeners and lubricants - docusate magnesium sulphate - osmotic laxative senna - stimulant
75
antidiarrhoeals
loperamide - opioid mebeverine - anti-spasmolytic hyoscine butylbromide - anti-spasmolytic
76
treatment for gas
simethicone - defoaming agent activated charcol carminatives - peppermint, dil
77
two types of dose dependent side effects
on target and off target
78
what problem with terfenadine and grapefruit
terfenadine usually 0% bioavailable and converted to active metabolite grapefruit competitively binds to CYP3A4 - terf becomes bioavailable and inhibits K channels - fatal ventricular arrhythmias
79
2 metabolism pathways of paracetamol
1. conjugated to suphate or glucoronide metabolite | 2. oxidised by CYP450 into intermediate metabolite and glutathione conjugates into non-toxic product
80
why does paracetamol toxicity occur
glutathione overwhelmed, ROS produced
81
epiphyses fusing in upper limb
``` cats make rob laugh capitulum - 1 med epicondyle - 5 radial head - 5 lat epicondyle, trochlea, olecranon- 10 ```

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