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Pharmacodynamics > Specific mechanism of action > Flashcards

Specific mechanism of action Flashcards

1
Q

what is the MOA of opioid ant/agonists

A

cell membrane receptor sites

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2
Q

what is the MOA of corticosteroids

A

nuclear receptors

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3
Q

what is the MOA of diuretics

A

transport mechanisms

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4
Q

what is the MOA of calcium channel blockers

A

ion channels

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5
Q

what is the MOA of cyclo-oxygenase COX inhibitors

A

enzyme inhibitors

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6
Q

what receptor does morphine stimulate

A

all receptors especially the (mu) ‘mew’ receptor

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7
Q

Why does morphine have multiple side effects

A

Due to the multiple opioid receptors across the body - brain, spinal cord, GI tract, skin, eyes, medulla (resp, vomiting, cough).

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8
Q

Opioid agonsits

A

Analgesia, cough suppression, sedation, constipation, N/V, resp depression
Stimulation of opioid receptors results in the pattern of pain signals reaching the cortex being modified so they are not interpreted as being painful
Multiple examples each varies in selectivity, potency, duration of action, metabolism

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9
Q

Opioid antagonists

A

Competitive antagonists
Reversal of opioid overdose esp in resp depression
e.g. naloxone, naltrexone

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10
Q

Glucocoticoid

A

Metabolic, anti-inflammatory and immunosuppressant effects
Used in skin conditions, autoimmune conditions, allergic reactions
e.g. hydrocortisone, prednisone, beclomethasone

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11
Q

MOA of glucocorticoids

A

Enter cell + bind to glucocorticoid receptors
Complex undergoes binding with tissue factors that allow attaching to genes
Binding either induces or suppresses messenger RNAs involved in inflammatory mediators (suppressed) or anti-inflammatory proteins (induced)

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12
Q

Mineralocorticoid

A

Maintain blood volume, retains sodium and water, excretes hydrogen and potassium
e.g. aldosterone

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13
Q

Diuretics MOA

A

Promote excretion of sodium through blocking Na transports

Water is also excreted to maintain osmotic balance

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14
Q

Diuretics uses

A

Increase urine output in oedematous states
Reduces high BP
Correct electrolyte imbalances

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15
Q

Diuretics uses

A

Increase urine output in oedematous states
Reduces high BP
Correct electrolyte imbalances

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16
Q

Classes of diuretics

A 
Loop diuretics (e.g., furosemide, bumetanide)
Thiazide diuretics (e.g., bendrofluazide, hydrochlorthiazide)
Potassium sparing diuretics (e.g., amiloride)
Aldosterone antagonists (e.g., spironolactone)
17
Q

Adverse effects with loop diuretics

A

dehydration esp elderly
Major hypokalaemia
High doses required in renal failue

18
Q

Adverse effect with thiazides

A

Hypokalaemia

Increase glucose and uric acid

19
Q

Adverse effects with potassium-sparing diuretics

A

hyperkalaemia

20
Q

Adverse effects in spironolactone

A

hyperkalaemia

breast enlargement in males

21
Q

MOA calcium channel blockers

A

Smooth muscle cells in the heart (myocardium), blood vessels and other internal organs require influx of extracellular calcium to stimulate release of internal calcium stores and cause smooth muscle contraction
The calcium enters the smooth muscle cells through specialized voltage-dependent calcium channels (called L-channels
These voltage-dependent calcium channels in smooth muscle cells can be partially blocked by CCBs
This causes smooth muscle relaxation in blood vessels and myocardial cells leading to vasodilation and reduced cardiac contractility

22
Q

CCB’s

A

Used in HTN and angina
e.g. felodipine, amplodopine, verapamil, diltiazem
Vasodilation

23
Q

What is the COX enzyme

A

cyclo-oxygenase enzyme - catalyses conversion of arachidonic acid in cell membranes resulting in a cascade of reactions to produce prostaglandins and thromboxanes

24
Q

Effect of TXA2 - thromboxane

A

platelet aggregation and vasoconstriction

25
Q

Effect of PGI2 prostacyclin

A 
platelet inhibition 
vasodilation
renal homeostasis
pain
inflammation
26
Q

effect of PGE2 prostaglandin

A 
GI cytoprotection
fever
renal homeostasis
pain
inflammation
27
Q

How does COX inhibitors create renal and GI side effects

A

PGE2 - protective to stomach mucosa
PGI2 - protective to kidney
Inhibiting / decreasing these can lead to gastric ulcers and renal impairment

28
Q

COX-1 enzyme

A

Mediates cytoprotective prostaglandins

29
Q

COX-2 enzyme

A

mediates inflammatory prostaglandins

30
Q

COX-2 inhibitors

A

Inhibit production of pro-inflammatory PGs
Reduced GI effects
e.g. celecoxib, parecoxib

30
Q

COX-2 inhibitors

A

Inhibit production of pro-inflammatory PGs
Reduced GI effects
e.g. celecoxib, parecoxib

31
Q

Why do COX-2 inhibitors increased CVD risk

A

Increased risk of CVD/events due to reduction in PGI2 (platelet inhibition) allowing higher proportion of TXA2 (platelet aggregation)

32
Q

What is the triple whammy?

A

Commonly known to induce kidney failure

Duiretics, ACE inhibitors, NSAIDS

Pharmacodynamics (9 decks)

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