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Z MD1 Cardiac physiology > pharmacology > Flashcards

pharmacology Flashcards

1
Q

How do aquaretics reduce preload?

A

Vasopressin (ADH) receptor antagonists

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2
Q

What are the isomerases of prostaglandins?

A

prostacyclin and thromboxane A2

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2
Q

action of calcium channel blockers

A

inhibit voltage-gated L type calcium channels in myocardium and vasculature

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2
Q

adverse effects of Ca channel blockers

A

facial flushing, peripheral oedema, dizziness, bradycardia, headache, nausea

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2
Q

what causes an increased warfarin activity

A

vitamin K deficiency

hepatic disease

  • impaired synthesis of clotting factors

hypermetabolic states

drug interactions

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2
Q

what are the compensatory mechanisms the body does when taking statins

A

increase in hepatic LDL receptors –> increased clearance of LDL from the blood and therefore decreased plasma total cholesterol and LDL (and increased HDL)

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2
Q

side effects of ezetimibe

A

diarrhea headache tiredness allergic reactions severe joint or stomach pain

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2
Q

when is ezetimibe used?

A

can be used alone in statin-intolerant patients, or in combination with all other lipid-lowering agents including statins (to reduce statin dose)

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3
Q

cholinergic muscurinic antagonist effects

A

reduced salivation, lacrimation, urination and defecation reduced sweating tachycardia (dependent on how dominant the resting PNS was) bronchodilation

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3
Q

action of Monoamine oxidase in normal neuron secreting NA as its neurotransmittter

A

limits the physiological leak of NA out of the neuron

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3
Q

How is NO relaxation physiologically controlled?

A

Cyclic nucleotide phsphodiesterase converts cGMP back into GMP

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3
Q

actions of NSAIDs

A
  • anti-inflammatory - analgesia - antipyretic
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3
Q

angiotensin receptor antagonists are the what family

A

sartans

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3
Q

adverse effects of calcium channel blockers

A

oedema flushing headache bradycardia (verapamil, diltizaem) reflex tachycardia (dihydropyridines)

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3
Q

action of Na+ channel blockers

A

reduced phase 0 slope and peak of ventricular action potential

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3
Q

mechanism of vasoconstriction in haemostasis

A

collagen exposed on damaged vessel wall platelets stick to collagen and activate” –> release ADP and 5-HT –> vasoconstrictor”

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3
Q

adverse effects of heparin

A

haemorrhage thrombocytopaenia osteoporosis

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3
Q

what does streptokinase do

A
  • activates plasminogen –> plasmin
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3
Q

common adverse effects of statins

A

mild GI symptoms headache insomnia dizziness

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4
Q

Action of metoprolol

A

Beta1 blockade Decreases HR and cardiac work Inhibits renin release and its subsequent effects Protects against downregulation of B1 receptors

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4
Q

definition of thrombus

A

fibirin clot that forms in vivo

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6
Q

How is arachidonic acid released from membranes?

A

phospholipase A2 activated by increase in intracellular calcium, which cleaves glycerol from arachidonic acid

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7
Q

Types of cholinergic nicotinic receptors

A

Nm type - in skeletal muscle Nn types - in both branches of the ANS (ganglion)

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7
Q

When is bradykinin generated?

A

after plasma exudation during inflammation leading to coagulation cascade and the cleavage of inactive peptide to bradykinin

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8
Q

drugs that act as indirectly acting sympathomimetics

A

amphetamine ephedrine (psuedoephedrine) tyramine

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8
Q

What are the endothelium derived vasoactive factors?

A

Prostacyclin, NO and EDHF cause relaxation Endothelin causes contraction

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8
Q

how does mercury affect kidney function

A

1) direct toxicity and vasoconstriction - reducing flow to the glomerulus 2) binds to protein thiol groups - initiating imune response in nephron 3) reduced brush border and mitochondrial changes in the proximal tubule

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9
Q

what causes a decrease in statin levels

A

phenytoin barbituites glitazones

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10
Q

atropine

A

anti-muscarinic reduces secretions and produces bronchodilation in the lungs for certain types of bradychardia pupil dilation (for examination of the eye) ACHe-inhibitor poisoning

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10
Q

what are the stimuli that induce histamine release

A

antigen via IgE complement fragments (C3a and C5a) neuropeptides cytokines and chemokines bacterial components physical trauma

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11
Q

where does gentomycin act in the kidney

A

on the apical membrane of the proximal tubule

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13
Q

drugs of ACE inhibitor family are the what family

A

prils

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13
Q

common adverse effects of fibrates

A

nausea, dry mouth, headache, rash

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14
Q

Neostigmine/pyridostigmine

A

anti-AChE Used to reverse the effect of non-depolarising neuromuscular blockers used in the treatment of myasthenia gravis

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14
Q

clinical uses of osmotic diuretics

A

raised intracranial P intraoccular P prevention of acute renal tailure

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15
Q

hyoscine

A

anti-muscurinic used for motion sickness

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15
Q

difference between SA and ventricular Action potentials

A

SA node depolarisation is Calcium dependent Ventricular cells depolarisation is Na dependent

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16
Q

Side effects of beta-blockers

A

Hypotension and fatigue (B1 and B2) Bronchoconstriction (B2) Cold extremities (A1 reflex) Mask signs of hypoglycaemia

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18
Q

histamine is stored in and released from which cells

A

mast cells and basophils

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19
Q

Actions of bradykinin

A

vascular - releases PGs and NO to dilate arterioles and venules neural - stimulates sensory nerve endings (pain) other - contracts uterus, airways and gut. Epithelial secretion in airways and gut

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20
Q

adverse effects of ivabradine

A

brightness in the visual field due to retinal effects (have the same funny current) conduction abnormalities

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21
Q

calcium channel blocker action for angina

A

blocks Ca entry into the heart and into the vessels –> decreased HR, SV, CO, arterial dilation —> reduced demand and reduced afterload and demand

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22
Q

clinical use of spironolactone

A

in combination with loop or thiazide diuretics heart failure hyperaldosteronism

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23
Q

how do aldosterone receptor antagonists reduce preload?

A

Inhibit aldosterone action on the cortical and distual tubules of the nephron (K+ sparing - monitor for hyperkalaemia)

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24
Q

Examples of adrenoceptor agonists

A

Dobutamine Na Adrenaline

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25
Q

action of angiotensin receptor antagonists

A

block Angiotensin 1 receptor

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26
Q

what is the mechanism behind NSAIDs causing gastric ulcertation/irritation?

A

PGE2 promotes blood flow/angiogensis/mucus secretion and reduces gastric acid secretion. Therefore inhibition of PGE2 will cause increased likeliness of ulceration of the stomach

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26
Q

adverse effects of loop diuretics

A

hypokalemia metabolic alkalosis hypovolaemia hypotension

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27
Q

Receptors for bradykinin are what?

A

both GPCR (B1 and B2)

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28
Q

agonist and antagonist for b1 and b2 adrenocepgtors

A

agonist: isoprenaline antagonist: propranolol

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29
Q

adverse effects of spironolactone

A

hyperkalemia GI upset

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30
Q

Name the Ca channel blocker drugs used for angina

A

verapamil nifedipine

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31
Q

Clinical uses of agonists for cholinergic nicotinic receptors

A

Smoking cessation contraction of skeletal muscle

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31
Q

what tests are used for monitoring of warfarin

A

PT INR

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32
Q

action of sympathomimetic on B1 adrenoceptor in the heart

A

increased heart rate and force of contraction

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32
Q

what is the precursor for biologically active lipids

A

arachodonic acid

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32
Q

action of beta-adrenoceptors antagonism

A

decrease the rate and conduction of the SA and AV nodes (decreased sympathetic drive) and membrane stabilising effects in Purkinje fibres

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33
Q

5 types of antihypertensive drugs

A

Angiotensin system inhibitors beta-adrenoceptor antagonists calcium channel blockers diuretics other

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34
Q

what type of drug is aspirin?

A

NSAID

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35
Q

nitrates predominant effect is on what

A

venous vessels –> reduces preload

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37
Q

What is co-transmission?

A

when nerves release more than 1 neurotransmitter

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37
Q

structure of eicosatetraenoic acid

A

20 carbon fatty acid with 4 double bonds (first double bond is at Carbon 6) Omega 6 molecule

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37
Q

How does PNS slow SA node

A

ACh on M2 receptors - activates GPCR (inhibitory) –> decreased cAMP leading to opening of K+ channels –> slowing Na and Ca fluxes, slowed prepotential (takes longer to reach threshold (SA) and slows rate of conduction (AV))

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37
Q

mechanism of platelet activation and adhesion

A

ADP from activated platelets causes others to activate and secrete more ADP and 5-HT Thromboxane synthesised Platelets aggregate and adhere via fibrinogen bridging between GPIIb/IIIa receptors

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37
Q

where do the 4 types of diuretics act?

A

loop diuretics - ascending limb of loop of henle

thiazide diuretics - distal tubule

K+ sparing diuretics - collect duct

osomotic diuretics - mainly proximal tubule

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38
Q

What metabolises arachidonic acid? And what are the outcomes?

A
  • COX-1 (constitutive) –> physiological prostaglandins - COX-2 (inducible by inflammatory stimuli) –> pathophysiological PG overproduction - lipoxygenase (expressed in mast cells and basophils) –> products associated with inflammation
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40
Q

action of resins?

A

they bind bile acid - preventing gut absorption –> up to 10 fold increase in bile excreted. This increases the demand for cholesterol for bile acid synthesis causing upregulation of hepatic LDL receptors and removal of LDL from the plasma

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41
Q

Ca2+ channel blockade

A

reduce rate and conduction in SA and AV nodes (reduces slope of pre-potential)

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41
Q

why are statins contraindicated in pregnancy?

A

cholesterol is needed for the normal synthesis of fetal myelination

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42
Q

What are the receptors for NA, and what are there structures?

A

alpha-adrenoceptors (GPCR) beta-adrenoceptors (GPCR)

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42
Q

action of angiotensin converting enzyme inhibitors

A

block the conversion of Ang 1 to Ang 2 Prevent bradykinin breakdown

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43
Q

definition of venous thrombus

A

fibrin + platelets + RBCs usually associated with blood stasis breaks off leading to embolus lodging in lungs or brain

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43
Q

precaution for fibrates

A

causes mild elevation of serum aminotransferase –> liver toxicity

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45
Q

rationale for drugs used in angina…

A

they try to either increase oxygen supply (dilate coronary arteries, reduce HR) or decreased oxygen demand (reduce HR, SV, preload, afterload)

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46
Q

onset and duration of triamterene and amiloride

A

tiamterene: onset - 2hours, duration 12-16hrs amilordie: onset: slow, duration 24 hours

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48
Q

which tests are used for the monitoring of a patient on heparin

A

APTT - time for clot formation in citrated plasma after addition of Ca, contact activator and phospholipid

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49
Q

action of heparin

A

enhances the activity of antithrombin III (inactivates Xa and thrombin) Inhibits factors 2, 9, 10, 11, 12

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51
Q

action of beta-blockers in the treatment of angina

A

blocks the effects of the SNS on cardiac B1 adrenoceptors –> decrease contractility, HR and SV –> increased diastole and therefore increased coronary perfusion

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52
Q

action of monoamine oxidase inhibitors

A

enhanced leak of NA out of the pre-synaptic neuron and into the synaptic cleft –> enhance NA action

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54
Q

max effect time and duration of action of thiazide diuretics

A

max effect at 4-6 hours duration 8-12 hours

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56
Q

what is a longer acting nitrate

A

isosorbide dinitrate

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57
Q

furosemide is what kind of drug

A

Diuretic

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58
Q

what are the main drug interactions of warfarin

A
  • aspirin
  • NSAIDs - competition for plasma protein binding
  • alcohol - competition for cytochrome p450 pathway
  • cimetidine - competition for cytochrome p450 pathway
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59
Q

What are the receptors for ACh, and what are there structures?

A

Nicotinic - ligand gated ion channel Muscurinic - GPCR

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59
Q

negative aspect of streptokinase

A

used IV antigenic - so single use only

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60
Q

How does SNS increase SA node

A

NA on B1-adrenoceptors –> activates GPCR (stimulatory) –> increases cAMP leading to opening of Ca channels –> increases slope of pre-potential and therefore increased firing rate and more rapid conduction

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60
Q

How do phosphodiesterase inhibitors work?

A

Increase the cAMP in the cell by inhibiting conversion to AMP This increases PKA and Ca influx

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62
Q

action of sympathomimetic on B2 adrenoceptor in the lungs

A

relaxation of bronchial smooth muscle

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62
Q

agonist to b2 adrenoceptor in the lungs

A

salbutamol

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64
Q

4 types of drugs used to treat angina

A

1) nitrates - affect preload 2) Ca channel blockers - affect afterload and myocardium 3) beta-adrenergic antagonists - affect myocardium to reduce HR and SV 4) ivabradine - affect myocardium - reduce HR only

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65
Q

action of beta-adrenoceptor antagonists

A

act on beta-1 receptors and reduce CO (by reducing HR and contractility) and reduce renin release (by reducing blood volume and TPR)

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67
Q

how is bradykinin degraded?

A

cleave by kininase I and kininase II (AGE)

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68
Q

major ACh removal is by

A

degredation –> AChE

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69
Q

action of leukotrienes

A

bronchoconstrictor vasoactive –> leaky vessels and tissue oedema

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70
Q

problem with taking nitrates over time

A

desensitization can occur

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71
Q

examples of anti muscurinic drugs

A

atropine hyoscine ipratropium

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71
Q

how do indirectly acting sympathomimetics work with noradrenaline

A

They get taken up by the uptake 1 receptor and go to the NA vesicles and kick out NA. This NA then goes out into the cleft via the reverse action of uptake 1 –> increased NA affects

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73
Q

synthesis of Noradrenaline

A

tyrosine converted to L-DOPA (tyrosine hydroxylase) L-DOPA converted to dopamine (DOPA decarboxylase) Dopamine converted to NA within vesicle (dopamine B-hydroxylase)

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75
Q

action of thromboxane A2 and where is it produced?

A

produced by platelets to increase platelet activation and vasoconstriction pro-thrombotic - promotes CAD

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76
Q

clinical uses of antagonists for cholinergic nicotinic receptors

A

pre-surgical skeletal muscle relaxants (non-depolarising) Ganglion blockers

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78
Q

Treatment of myasthenia gravis at early stages

A

Give the patient more ligand to compensate for the lack of receptors

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79
Q

how does the action of angiotensin receptor antagonists decrease BP?

A

reduces vasoconstriction reduces aldosterone (decreased water retention) reduced cardiac hypertropy reduced sympathetic activity

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80
Q

clinical use for loop diuretics

A

salt and water overload hypertension

81
Q

What are the types of prostaglandins?

A

PGE, PGF, PGD

82
Q

action of ivabradine

A

treatment for angina specific and selective inhibition of the funny current in the sinus node –> decreases HR –> reducing oxygen demand and increasing oxygen supply

83
Q

definition of clot

A

fibrin clot that forms in static blood in vitro

85
Q

adverse effects of nifedipine

A

flushing, headache, oedema, hypotension, reflex tachycardia

86
Q

action of alpha 1 adrenoceptor

A

vasoconstriction in the blood vessels

87
Q

drugs that block the metaboilsm of NA

A

Monoamine oxidase inhibitors

88
Q

How is NO generated?

A

ACh/Bradykinin and mechanical shear stress on the endothelium causes an increase in Ca in the wall and the activation of nitric oxide synthase and the production of NO from arginine

89
Q

common adverse effects of resins?

A

abdominal discomfort bloating constipation flatulence

90
Q

what are two bile acid sequestrants/resins

A

cholestyramine colestipol

91
Q

action of PGE2

A
  • relaxes vascular smooth muscle –> decreases BP - hyperalgesic - pyrogenic - angiogenic
92
Q

How can drugs influence the production of NO?

A

Block the synthesis! analogue of arginine

93
Q

Why do cardiac glycosides have a narrow margin of safety?

A

They affect all excitable tissues: gut, CNS, cardiac

94
Q

agonist and antagonist to a1 adrenoceptors

A

agonist: phenylephrine (nasal decongestant) antagonist: prazosin (hypertension)

95
Q

distal consequence of loop diuretics

A

increases the osmotic P in the distal tubule –> reducing water reabsorption in distal tubule

96
Q

Variabilities within anti-AChE drugs?

A

They have: Variable selectivity (between NMJ and postganglionic parasympathetic junctions) Variable CNS access Variable duration of action

96
Q

adverse effects of beta-adrenoceptor antagonists

A

cold extremities fatigue dreams/insomnia bronchoconstriction

97
Q

mechanism of diuretics

A

increase Na and water excretion from kidney lowering blood volume and blood pressure

98
Q

angiotensin system inhibitors are contraindicated in who?

A

pregnant women bilateral renal stenosis angioneurotic oedema

100
Q

rare but serious adverse effects of statins

A

myopathy rhabdomyolysis renal failure liver failure

101
Q

how does the action of ACE inhibitors decrease BP

A

no Ang 2 –> vasodilation, reduced aldosterone production (preventing water rentention) and reduce cardiac hypertropy

103
Q

mechanism of action of gentomycin toxicity on the kiney

A

bins to phsopholipids and effects calcium levels –> effects mitochondria –> cell damage –> apoptosis

104
Q

adverse effects of nitrates

A

1) effects on other SM –> gut and airways 2) postural hypotension 3) venous pooling 4) headache and flushing due to cerebral, head and neck arterial dilation 5) reflex tachycardia

105
Q

What is the unstable intermediate of arachidonic acid to prostaglandins?

A

cyclic-endoperoxide

107
Q

Bradykinin is a local peptide mediator involved in what?

A

pain and inflammation

108
Q

What type of drug is digoxin?

A

Cardiac glycoside

109
Q

PNS control of heart rate involves

A

ACh acting on muscarinic receptors on SA and AV nodes –> slows HR most dominant at rest

110
Q

how does botulinum toxin act

A

cleaves the snare protein that allows the vesicles of ACh to bind to the presynaptic neuron to exocytose their contents. Therefore stops exocytosis of ACh into the synaptic cleft

111
Q

bad points about walfarin

A
  • haemorrhage - reversed by Vit K - diet dependent - delayed onset of action - very labile
112
Q

major adverse effect of NSAIDs

A

gastric irritation/ulceration

114
Q

mechanism of action of spironolactone

A

acts as an aldosterone R antagonist - decreases activation of Na channels in the Collecting duct - decreases the stimulation of Na pump synthesis this reduces osmotic P and therefore reduces water reabsorption

115
Q

3 isoforms of nitric oxide synthase

A

nNOS (nerves, epithelial cells) iNOS (inducible - macrophages, smooth muscle) eNOS (endothelial cells)

116
Q

agonist and antagonist to b1 adrenoceptors in the heart

A

agonist: dobutamine antagonist: atenolol

118
Q

what is an example of an aldosterone receptor antagonist

A

spirolactone

120
Q

What causes myasthenia gravis?

A

Autoimmune response to the post-synaptic cleft causing decreased surface area and degredation of the architecture of post-synaptic cleft and loss of nicotinic receptors on the muscles. With degredation of ACh by AChE in the background –> unable to create contraction –> weakness in the muscles

121
Q

mechanism of action of triamterene and amiloride

A

blocks the luminal Na channels in the collecting duct - inhibiting Na reabsorption and K secretion

122
Q

alpha 1 and 2 adrenoceptor antagonist drug

A

phentolamine

124
Q

What is “The Triple Response”?

A

The actions of histamine: Reddening - due to vasodilatation at initiating site Wheal - due to increased vascular permeability (localised oedema response) Flare - spreading response through the sensory fibres

126
Q

common adverse effects of niacin

A

vasodilation, flushing, hypotension nausea, vomiting

127
Q

definition of coagulation

A

formation of a fibrin clot in a blood vessel

128
Q

H2 receptor antagonist were originally used for what?

A

treatment of peptic ulcers

129
Q

beta-adrenoceptor antagonists are the what family

A

olols

131
Q

How do venodilators reduce preload

A

Increase venous dilation - blood reservoir –> less going back to he heart

133
Q

3 broad causes of heart failure

A

Decreased contracility Pressure overload (increased afterload) Volume overload (increased preload)

134
Q

difference in action between regular heparin and low molecular weight heparin

A
  • low MW heparin has less effect on thrombin - longer elimination half life - can be used for self administration
135
Q

what two changes in body metabolism can statins cause? (other than decreased cholesterol synthesis)

A

mild elevation of serum aminotransferase –> liver toxicity minor increases in creatine kinase –> can lead to muscle pain and tenderness

136
Q

definition of haemostasis

A

arrest of blood loss from damaged vessels

137
Q

Where is 5-lipoxygenase found

A

restricted in distribution to inflammatory cells

138
Q

What are the two main dietary poly unsaturated fatty acids?

A

linoleic acid arachidonic acid

139
Q

SNS control of heart rate involves

A

NA (and adrenaline) acting on beta-adrenoceptors on SA node, conducting tissue and myocardial cells –> increases HR and contracility

141
Q

fibrinolytic drugs

A

streptokinase alteplase

142
Q

how is fibrin synthesised

A

formed from fibrinogen (which is activated itself by thrombin)

143
Q

when is niacin used?

A

not widely used except in combination with other lipid lowering drugs

144
Q

5 types of drugs to reduce preload

A

venodilators Diuretics Aldosterone receptor antagonists Aquaretics Beta-adrenoceptor antagonist

145
Q

types of angina

A

stable - CP on exertion or with stress (not affected at rest) variant - coronary vasospasm at rest unstable - angina at rest and with effort

146
Q

what does clopidigrel do

A

ADP receptor antagonists prevents binding of ADP to its receptor on platelets –> preventing platelet activation

148
Q

How do beta-adrenoceptors help in heart failure?

A

bring back operating point on cardiac function curve to more linear part of the curve Despite blockade - stroke volume increases

149
Q

action of ezetimibe

A

specifically inhibits cholesterol absorption in the intestine by binding to a sterol transporter (does not affect absorption of bile acids or fat soluble vitamins)

150
Q

mechanism of action of statins

A

competitive inhibitor of HMG-CoA reductase this decreases the synthesis of mevalonic acid and therefore cholesterol synthesis

152
Q

how does grapefruit juice interact with statins

A

they use a common metabolic pathway

153
Q

3 mechanisms that can cause kidney toxicity

A

reactive oxygen species causing cell damage

interference with calcium metabolism protein

interference with enzyme binding

155
Q

when are adrenoceptor agonists used for heart failure?

A

Used for short term support for acute heart failure and cardiogenic shock

156
Q

uses for botulinum toxin

A

Bo-Tox - cosmetic Over active sweat glands overactive blink response

157
Q

physiological roles of NO

A

flow-dependentvasodilatation inhibits platelet adhesion and aggregation neurotransmitter

158
Q

what are some modifiable risk factors to try and change to try treat dyslipidaemia

A

stop smoking, avoid alcohol, weight reduction, increase exercise, modify diet (reduce saturated fat, plant sterol esters, mediterranean diet, fish oils)

159
Q

Role of Vitamin K in haemostasis

A

essential for formation of clotting factors 2, 7, 9, and 10 reduced vitamin K is a cofactor in carboxylation of glutamate (which is required of the blood factors after synthesis)

160
Q

Examples of anti-AChE drugs?

A

Edrophonium Neostigmine/Pyridostigmine Donepezil

161
Q

adverse effects of angiotensin receptor antagonists

A

hyperkalemia headache dizziness

161
Q

when look at a serum profile of a patients lipids…. What is the most important variable to look at?

A

total cholesterol/HDL

162
Q

action of PGD2

A

bronchoconstrictor (act locally only)

163
Q

ipratropium

A

anti-muscurinic used for COPD

165
Q

2 major neurotransmitters of the PNS

A

ACh Noradrenaline

166
Q

What do diuretics (in general) do?

A

increase Na and water excretion by reducing the Na and Cl reabsorption in the nephron

167
Q

what does niacin cause

A

decreased secretion of VLDL particles from the liver –> reduces LDL and TG and increases HDL potentially lowers atherogenic lipoprotein a

169
Q

symptoms of arrhythmia

A

SOB fainting fatigue chest pain

170
Q

How do diuretics reduce preload

A

Act on the loop of Henle to decrease Na and Water reabsorption –> increase urine output –> decrease blood volume

171
Q

onset and half life of spironolactone

A

slow onset short half life of 10 mins, but metabolite longer half life of 16 hours

172
Q

examples of fibrates

A

gemfibrozil fenofibrate

174
Q

action of prostacyclin and where is it produced?

A

reduces platelet activation and vasodilation. Produced by endothelial cells. non-thrombotic - protects against CAD

175
Q

when are fibrates used?

A

generally used as adjunct to dietary changes for high TGs, mixed hyperlipidaemia and second line therapy for hypercholesterolaemia

176
Q

Major sites for pharmacological manipulaion

A

transmission of action potential synthesis of neurotransmitter storage of NT Release of NT Action of post-syn receptor Degredation in the cleft reuptake in pre syn membrane action on pre-syn receptor metabolism of NT in pre-syn terminal

177
Q

adverse effects of amiodarone

A

blocks Na and CA and beta-adrenoceptors as well reversible photosensitisation, skin discolouration and hypothyroidism pulmonary fibrosis with long term use

178
Q

action of K+ channel blockade

A

delay phase 3 of ventricular action potential and prolong APD

179
Q

Tensilon test

A

Test for myasthenia gravis Gives short duration anti-AChE –> prevent breakdown of ACh in the cleft and therefore more time for the ACh to work in the cleft –> contraction

179
Q

adverse effects of thiazide diuretics

A

hypokalaemia increased plasma uric acid - gout

180
Q

How does dobutamine work

A

Selective B1 adrenoceptor - increases contractility and HR

181
Q

How does digoxin relieve symptoms of heart failure?

A

inhibits the Na/K ATPase Increases I/C Na and therefore reduces Ca extrusion through Na/Ca cotransporter This increases the Ca in SR and therefore increases Ca release with each AP Increased Ca - increased contractility of heart

182
Q

Benefits of having pre and post ganglionic neurons compared to one long neuron

A

allows amplification of downstream signalling and integration of signalling

183
Q

3 classes of H1 receptor antagonists

A

sedative, non-sedative, newer non-sedative

184
Q

action of PGF2a

A

bronchochonstrictor (act locally only)

185
Q

What type of receptors are histamine receptors

A

GPCR

185
Q

definition of arterial thrombus

A

platelets plus WBCs in a fibrin mesh usually associated with vessel wall damage. Breaks off leading to BV obstruction

186
Q

what are the effects of antineoplastics on the kidney?

A

causes proteinuira, increased blood urea and electotrolyte imbalance –> focal necrosis

187
Q

adverse effects of verapamil

A

flushing, headache, oedema bradycardia, AV block

189
Q

How do anti-AChE work?

A

it blocks the degradation of ACh in the synaptic cleft and therefore leads to enhancement and longeivity in the synaptic cleft

190
Q

beta-adrenoceptor antagonists contraindicated in who?

A

asthma diabetes AV block

192
Q

what does abciximab do

A

it is a GPIIb/IIIa receptor antagonist - monocolonal antibody –> stops platelet aggregation by blocking the binding of fibrinogen to the receptor

194
Q

Movement and action of NO

A

NO diffuses out of the endothelial cells very rapidly and into the smooth muscle cells. In the smooth muscle, NO activates Guanylate cyclase and causing the convertion of GTP into cGMP causing relaxation

195
Q

how do calcium channel blockers decrease BP?

A

reduce cardiac/vascular contractility

196
Q

what is hereditary angioedema?

A

C1esterase inhibitor deficiency –> no braking system on the production of bradykinin causing vasodilation and angioedema

198
Q

adverse effects of beta-adrenoceptor antagonists?

A

bradycardia, reduced exercise capacity, hypotension, AV conduction block, broncoconstriction, hypoglycaemia

199
Q

risk factors for hypertension

A

smoking, diet, weight stress

201
Q

size of pre and post ganglionic fibres in PNS and SNS

A

PNS tend to have longer pre-ganglionic fibres compared to post SNS tend to have longer post ganglionic fibres compared to pre

202
Q

action of 5-lipoxygenase?

A

Converts arachidonic acid into leukotrienes

203
Q

mechanism of action of osmotic diuretics

A

decrease the passive reabsorption of water, with only a small decrease in Na reabsorption

204
Q

What is arachidonic acid metabolised to?

A

eicosanoid - biologically active metabolites of arachidonic acid

205
Q

principle mechanisms underlying dysrhythmia

A

altered impulse formation altered impulse conduction triggered activity

206
Q

How does aspirin work?

A
  • it is an irreversible COX inhibitor –> reduced thromboxane synthesis –> decreased platelet aggregation and decreased vasoconstriction
207
Q

absorption and duration of action of loop diuretics

A

well absorbed - onset less than 1 hour plasma protein bound - duration 3-6 hours

208
Q

definition of thromboembolus

A

a blockage in a BV caused by a dislodged thrombus

209
Q

Neurotransmitters used in PNS, SNS,somatic and ganglionic transmission

A

Somatic uses ACh PNS uses ACh SNS uses NA (except for ACh in sweat glands and adrenals) Ganglionic transmission uses ACh

210
Q

indications for resins?

A

hypercholesterolaemia mixed hyperlipidaemia

211
Q

3 types of drugs that can act on kindeys

A

1) diuretics 2) drugs that alter pH of urine 3) drugs that alter secretion of organic molecules

212
Q

types of dyslipidaemia

A

hypercholesterolaemia hypertriglyceridaemia mixed hyperlipidaemia

213
Q

adverse effects of adrenoceptor agonists during heart failure

A

Increases the oxygen demand of the heart muscle Increases risk of arrythmias

214
Q

action of walfarin

A

inhibits reduction of vitamin K, thereby inhibiting gamma carboxylation of glutamate in factors 2, 7, 9 and 10

216
Q

what causes a decrease in warfarin activity

A
  • pregnancy - drug interactions
217
Q

action of fibrates

A

agonists at nuclear receptors –> regulate gene expression –> increase synthesis of lipoprotein lipase (LPL) –> breaks down TGs into free FA moderate increase in HDL variable effects on LDL

218
Q

4 major classes of antidysrhythmics

A

Na+ channel block B-adrenoceptor antagonism K+ channel blockade Ca2+ channel blockade

219
Q

What is an example of a drug that prevents ACh action?

A

Botulinum toxin

220
Q

what causes an increase in statin levels

A

grapefruit juice antibiotics, antifungals, fibrates

221
Q

drugs that affect reuptake of NA in the synaptic cleft

A

cocaine tricyclic anti-depressants

222
Q

4 types of diuretics?

A

loop diuretics thiazide duiretics osmotic diuretics postassium sparing diuretics

223
Q

mechanism of action of thiazide diuretics

A

inhibit the Na/Cl cotransporter in the distal convuluted tubule –> decreasing the osmotic P and therefore reducing water reabsorption

224
Q

indications for taking statins

A

hypercholesterolaemia mixed hyperlipidaemia

225
Q

What is the action of aspirin?

A

increases the ratio of prostacylcin to thromboxane promoting non-thrombotic actions

227
Q

Clinical use of agonists for cholinergic muscurinic receptors

A

pilocarpine–> used for reducing intraoccular pressure in glaucoma

228
Q

cardiac blood supply depends on

A

oxygen demand (cardiac workload - preload, afterload, HR and SV) oxygen supply (coronary artery blood flow)

229
Q

how is arachidonic acid stored?

A

stored in the esterified form (joined with glycerol) in membrane phospholipids of the plasma membrane and nuclear membrane

231
Q

where is cholesterol derived from

A

diet (in animal fats, eggs) –> absorbed by intestine do novo synthesis (liver) - adequate for needs

232
Q

loop diuretics - mechanism of action

A

the Na/K/Cl carrier in the ascending limb of the loop of henle –> decreases the hypertonicity in the interstitium, decreasing osmotic P and therefore reduces water reabsorption

233
Q

What is the front line therapy for heart failure

A

ACE inhibitors Reduce effects of angiotensin II –> decrease blood volume Slows the progression of cardiac hypertrophy

234
Q

rare adverse effects of resins?

A

increased TGs faecal impaction decreased absorption of fat soluble vitamins steatthorea

235
Q

Donepezil

A

anti-AChE enters the CNS well - able to pass the BBB Used in the treatment of Alzheimer’s disease

236
Q

action of nitrates in angina

A

drug undergoes transformation once absorbed –> releases NO –> stimulates guanylate cyclase in vascular smooth muscle –> converts GTP to cGMP –> activates myosin light chain –> vascular relaxation

237
Q

major NA removal is by

A

uptake Uptake 1 in pre-synaptic cleft (high uptake) Uptake 2 is extranueronal (low affinity)

238
Q

what is considered chronically high BP

A

> 140/90

239
Q

synthesis of ACh

A

Choline + ACoA —> ACh (with CoA)

240
Q

Why does ACh act as a vasodilator in vivo but a vasoconstrictor in vitro?

A

ACh induces endothelium of blood vessels to release EDRF/NO causing vasodilation in vivo

241
Q

what are the effects of gentomycin kidney toxicity

A

proteinuria

decreased GFR

altered concentrating ability

242
Q

Icatibant

A

selective bradykinin 2 antagonist used in the treatment of hereditary angioedema

243
Q

drugs for anticoagulation

A

walfarin

heaprain

direct and indirect Xa inhibitors

direct thrombin inhibitors

245
Q

Why is the long term use of B-adrenoceptor agonists bad in general?

A

Chronic stimulation of beta-adrenoceptors results in downregulation of B1-adrenoceptor expression and impaired B1-adrenoceptor coupling Leads to decreased sensitivity to B1 adrenoceptor agonist or sympathetic drive

246
Q

when is 5-lipoxygenase activated?

A

activated by an increase in intracellular calcium by inflammatory stimuli

247
Q

4 drugs for reducing afterload in heart failure

A

Arterial vasodilators ACE inhibitors Angiotensin 1 antagonist Beta-adrenoceptor antagonist

248
Q

definition of thrombosis

A

pathological formation of a haemostatic plug in a blood vessel in the absence of blood loss

249
Q

where do antineoplastics act in the kidney

A

acts in the distal tubule and collecting duct

250
Q

anti-platelet drugs

A

thromboxane A2 inhibitor - aspirin

ADP R antagonists - clopidigrel

glycoprotein IIb/IIIa R antagonist - abciximab

251
Q

Action of carvidelol

A

B1 and A1 blockade Vasodilation –> reduces afterload Decreases HR and cardiac work Inhibits renin release and its subsequent effects Protects against downregulation of B1 receptors

252
Q

Which drugs act like B1 adrenoceptor agonist but does not effect he receptor?

A

Phosphodiesterase inhibitors

253
Q

What does histamine act on?

A

H1, H2, H3 and H4 receptors

254
Q

Cholinergic muscurinic agonist effects

A

Salivation, lacrimation, urination, defecation Sweating Slowing of heart bronchoconstriction vasodilation

255
Q

adverse effects of all ACE inhibitors

A

first-dose hypertension drug cough loss of taste hyperkalaemia acute renal failure itching, rash, angio-oedema foetal malformations

Z MD1 Cardiac physiology (13 decks)

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