Pharm Revision Flashcards
How does the SS and PS regulate HR
SS increase cAMP which increases opening of iF and iCa to inc depolarisation
PS dec cAMP which inc opening of iK to prolong repolarisation
How do beta 1 receptors regulate contractility
inc cAMP which inc pKA to promote contraction by decreased calcium going into the SR so more is available for contraction
What is the class of drug that verapamil comes under
Phenylalkylamines
What is the other class of rate slowing calcium antagonists (not verapamil)
Benzothiazepines such as Diltiazem
What is the problem with dihydropyridines for dec contractility
No effect on the heard but profound vasodilation can cause reflex tachycardia
How does vasodilation and venodilation affect preload and afterload
vasodilation dec afterload
venodilation dec preload
5 key beta blocker side effects
Bronchoconstriction
Cold extremities + worsening of peripheral artery disease
Dec heaptic gluconeogenesis and glycogenolysis DIABETICS
Bradycardia (heart block)
Worsening of cardiac failure (reduction in CO)
Side effects of both type of calcium blockers
Verapamil = bradycardia and AV block. Constipation Dihydro = ankle oedema, headache flushing, palpitations due to reflex tachy
Adenosine MOA and USE
stimulates alpha 1 in SAN and AVN to reduce cAMP and dec chronotropy and dromotopy
stimulates alpha 2 in vasc smooth muscle to inc cAMPt to relax
SVT’s short lived
Verapamil MOA and USE for anti arrhythmic
Depress SA atuoomaticity and AV
reduce ventricular responsivess to atrial arrhythmias
SVT and AF
Amiodarone moa use adverse
SVT and VT
multiple ion block
accumulates and can cause skin rash, hypo/hyper thyroidism, pulmonary fibrosis
effect of digoxin bc of blocking the pump
USE
Adverse effects
inc intracellular ca
positive ionotropic effect
vagal stimulation causes inc refractory period and reduced rate of conduction through AV node
AF and Flutter
Dysrhythmias and hypokalaemia can lower toxicity
M1 Receptors
neural tissue
M3 receptors
exocrine and smooth muscle
ACh enzyme to make
choline acetyl transferase
Dopamine to noradrenaline
Dopamine beta hydroxylase
COMT stands for
catechol-O-methyl trasnferase
SS vs PS response key words
coordinated and divergent
discrete and localised
why do effects of cannabis last so long
storage in adipocytes
Dronabinol
delta 9 thc = chemo NV
nabilone
delta 9 thc = chemo NV
sativex
delta 9 thc and cannabidiol = symptom improved for spasticity due to MS
rimonabant
CB1 antagonists = anti-obesity but depression and suicide
effect of enterohepatic recycling on measuring intoxication
11 OH THC is more potent and recycles so delta 9 thc is a bad indicator
what is anterior cingulate cortex function
performance monitoring and behavioural adjustment
part of brain for munchies
lateral hypothalamus
endogenous cannibinoid
anandamide
appetite neurones for pharm
Melanin concentrating hormone neurones
orexin
cannabis and hunger neurones
inhibits GABA on MCH so inc in MCH and orexin production so inc hunger
cannabis and psychomotor performance
depresses cerebral cortex
cannabis and CV system
TRPV1 receptor to cause calcium influx-> tachycardia
cannabis vasodilation
conjunctivae
cannabis memory loss
inhibits production of brain derived neurotrophic factor in hippocampus
cannabis levels in the brain
rise v quickly but fall v quickly bc brain is highly perfused
how much smoked cannabis reaches bloodstream
30%
define alkaloid
any class of nitrogenous compound of plant origin that has profound physiological actions on humans
THC =
tetrahydrocannabinol
what type of receptors is CB
g protein i = negative with AC
four types of cocaine
crack = precipitated with alkaline solution
cocain paste = plant mushed up
freebase= dissolve crack in a non-polar solvent
cocaine hcl = therapeutic
what is the cocaine plant name
erythroxylum coca
cocaine CVS risks (3 actions)
vasoconstriction
platelets
atherosclerosis
cocaine and seizures
vasoconstriction in brain arteries leading to inc in temp
why is nicotine in a cigarette so effective
melts the tar to make droplets
alkaloids dissolve in droplets
easily absorbed
why is nicotine not absorbed in the mouth
cigarette smoke is acidic and pKa of mouth is alkaline so ioniside
nicotine euphoria
nachr causes sodium influx so inc firing rate
nicotine and CVS
inc SS
vasoconstriction coronary arterioles
atherosclerosis
inc thromboxane A2
nicotine and parkinson’s and alzheimers
inc cyp450 which remove neurotoxins which contribute to onset of parkinson’s
diminishes some of the proteins
caffeine and euphoria
adenosine antagonist so removed inhib effect on dopamine and D1 receptor function
nicotine metabolism
CYP2A6 in liver
produces cotinine
excreted in urine
cocaine pKA
weak base so less absorbed in stomach
cocaine half life
20-90 mins
cocaine metabolism
liver = inactive ecgonine methyl ester and benzoylecgonine plasma = plasma cholinesterases
how to work out how much alcohol in g/100ml
ABV% x 0.78
how much alcohol is metabolises
90%
acetaldehyde metabolism
aldehyde dehydrogenase -> acetic acid
chronic alcohol and ataxia
cerebellar cortex degeneration
Alcohol receptor targets in CNS
Allopregnelone -> enhances GABA
dec NMDA
reduces Ca2+ influx so less exocytosis
why alcohol and cutaneous vasodilation
less calcium influx and more prostaglandins
acetaldehyde
alcohol and reward pathways
less dopamine bc inc gaba and reduces nmda
brain targets of alcohol
hypothaalmus RAS hippocampus cerebellum basal ganglia= time