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PHARM Flashcards

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1
Q

What is KD?

A

Dissociation constant, concentration at which 50% receptors bound

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2
Q

What is Emax and EC50

A

Max- Measure of efficacy, maximum response at peak
50- Measure of potency, concentration to create 50% of max response

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3
Q

How many receptors are occupied in a maximum response for full agonists and partial agonists?

A

Full- not all
Partial- all

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4
Q

How does competitive surmountable antagonists alter agonist response?

A

Efficacy unchanged, potency reduced

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5
Q

What areas and affect do a and b adrenoreceptors have?

A

a1- constricts blood vessels, dilates pupil, constricts GIT
a2- inhibit transmitter release in nerves
b1- increase rate and force of heart, renin secretion in kidney
b2- skeletal muscle contractility, dilate bronchi

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6
Q

What are the 4 areas where non-competitive inhibition can occur?

A
  1. Chemical antagonism to chemically inactive, drugs or antibodies
  2. Allosteric modulation
  3. Pathway inhibition, multiple potential targets
  4. Functional antagonism, two agonists with opposite effects e.g. Na and Ach
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7
Q

What is bioavailability?

A

Proportion of administered drug that reaches circulation e.g prodrug that is metabolizes would have low, intravenous would have high

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8
Q

What is first pass metabolism?

A

Passing through liver to reach circulation, can be metabolized and form active molecules

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9
Q

What is volume of distribution?

A

The amount of drug in body divided by the concentration in plasma

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10
Q

What are the lengths of PS and S pre-ganglionic neurons?

A

PS long close to site of action
S short, to sympathetic chain

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11
Q

What are the neurotransmitters and receptors involved in somatic, PS, sympathetic for muscle organs, sympathetic for sweat glands and sympathetic for adrenal glands?

A

Somatic- No postganglionic, ACh to nicotinic (nAChR)
PS- ACh to nAChR on postganglionic (same for all postganglionic), ACh to muscarinic (mAChR)
S, muscle/organs- ACh to nAChR on postganglionic, noradrenaline to ab adrenoreceptors
S, sweat- ACh to nAChR on postganglionic, ACh to mAChR
S adrenal- ACh to nAChR on postganglionic, Adrenaline to circulation and ab adrenoreceptors in tissue

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12
Q

What are the steps of chemical transmission?

A
  1. AP, membrane depolarisation
  2. Synthesis
  3. Storage
  4. Ca2+ dependent vesicular exocytosis
  5. Receptor activation
  6. Reuptake
  7. Degradation
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13
Q

How can catecholamine production be altered (3)?

A
  • L-DOPA, product of rate limiting stepped, increases NA/A
  • Carbidopa, DOPA decarboxylase inhibitor which turns L-DOPA to dopamine
  • VMAT inhibitor (e.g. reserpine), inhibits dopamine uptake into vesicles by VMAT where dopamine is converted to noradrenaline
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14
Q

What is the primary and secondary reuptake process?

A

Primary: NET into neuron
Secondary: OCT3 extraneuronally

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15
Q

What metabolizes noradrenaline at the nerve terminal?

A

Monoamine oxidase (MAO)

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16
Q

What drugs interfere with the reuptake process (3)?

A
  • Tricyclic Antidepressants (TCA’s) inhibit NET, prevent reuptake, longer presence in junction and increased binding
  • MAO inhibitors, noradrenaline not metabolized, more can enter vesicles
  • Indirectly-acting Sympathomimetics (IAC’s) e.g. ephedrine, similar structure to NA, uptake by NET, displace NA in vesicles, NA can exit neurons via NET and have bind in junction
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17
Q

How can acetylcholine synthesis and storage be inhibited (3)?

A
  • Hemicholinium (experimental) blocks high affinity choline transporters (rate limiting step), which will transport choline (ACh precursor) into the neuron
  • Vesamicol (experimental) blocks vesicular acetylcholine transporter from transporting ACh into the vesicle to be released into the junction
  • Botulinum Toxin, heavy chain binds irreversibly to receptors for neurons containing ACh, endocystosed, light chain cleaves SNARE proteins, SNARE complex cannot form and vesicle and membrane cannot fuse
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18
Q

What are the symptoms of Botulinum poisoning?

A

Facial weakness, difficulty swallowing, limb paralysis, anti-SLUD (salivation, lacrimation, urination, defecation) dry mouth, dry eyes, urinary retention, constipation

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19
Q

What drugs interfere with cholinergic metabolism at neuromuscular junction (3)?

A
  • Anticholinesterases prevent acetylcholinesterases from metabolizing ACh into choline
  • d-Tubocurarine, competitive reversible antagonist of nAChR postjunction, allows skeletal m. relaxation during surgery
  • Suxamethonium, nAChR agonist, causes prolonged depolarization, muscle relaxes as it cannot undergo repolarization
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20
Q

What is Myasthenia Gravis and how is it treated?

A

Muscle weakness caused by auto-antibodies degrading nAChRs meaning ACh is degraded before getting a big enough response. Eye movement, swallowing, facial expression first effected then limbs.

Neostigme is a reversible anti-cholinesterase specific for neuromuscular junction. Prevents ACh metabolism, bigger response.

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21
Q

Muscarinic Effects, SLUDGE, DUMBBELS

A

Salivation, Lacrimation, Urination, Diarrhea, GIT upset, Emesis (vomiting)

Diarrhea/Diaphoresis (sweating), Urination, Miosis (pupil contracted), Bradycardia/Bronchospasm, Emesis/excitation, Lacrimation/Lethargy, Salivation

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22
Q

Where are M2 and M3 receptors found?

A

M2- heart
M3- glandular smooth muscle

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23
Q

What are N1 and N2 receptors?

A

N1- neuromuscular junction
N2- autonomic ganglia

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24
Q

What are high nicotinic and muscarinic agonists?

A

Nicotinic- Acetylcholine, Carbachol, Nicotine
Muscarinic- Acetylcholine, Methacholine, Bethanechol, Muscarine

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25
What is atropine?
Muscarinic antagonist, stops secretions (DUMBBELS) during surgery
26
What are some modifiable and non-modifiable risk factors for CVD?
Non-mod- age, sex, ethnicity, family history Mod- diet, exercise, substance abuse
27
Function of CVD?
DR MED Distribute hormones, essential substances, heat Remove metabolic by-products Mediate inflammatory factors
28
What factors affect cardiac output?
Stroke volume, volume ejected per beat Heart rate
29
How do adrenergic and cholinergic receptors affect heart rate?
ACh -> M2, decrease Adrenaline/Noradrenaline -> B1, increase
30
What is preload and how does it influence stroke volume?
Load placed on muscle before contraction, greater muscle length -> greater force of contraction
31
What is contractility and how do adrenergic and cholinergic receptors affect it?
Strength of contraction, A/NA -> B1
32
What factors affect stroke volume?
Contractility, preload and afterload (resistance to outflow from left ventricle)
33
How does B1 activation affect preload?
B1 activation causes renin release which increases blood volume and thus preload
34
What is the ABCD?
ACE inhibitors Beta blockers Calcium Antagonists Diuretics
35
What is the action of beta blockers?
Inhibit activation of cardiac B1 receptors, decrease cardiac output Inhibit activation of renal B1 receptors, decrease renin secretion, H2O retention and thus preload
36
What are some AE's of beta blockers
Reduced exercise capacity, muscle fatigue, bronchoconstriction
36
What is the action of diuretics?
Increase secretion of Na+, water follows resulting in decreased blood volume and pressure
37
What is the action of thiazide diuretics?
Inhibits Na-Cl cotransporter to increase Na+ excretion
38
What are some AE's of thiazide diuretics?
Hypokalemia (decreased blood K+), uric acid retention, impaired glucose tolerance.
39
What is the results of angiotensin II (3)?
- Cardiovascular remodelling (hypertrophy and vascular redistribution of mass) - Vasoconstriction, increasing TPR and blood pressure - Aldosterone secretion, increase Na+/H2O retention, increase BP
40
What is the action of ACE inhibitors?
Inhibit ACE, the enzyme that converts Angiotensin I to Angiotensin II, decreases BP. Also decreases BP as ACE breaks down bradykinin into inactive metabolites, a build up of bradykinin causes vasodilation and decreased BP
41
How are AT1R antagonists different to ACE inhibitors?
AT1R antagonists prevent binding of angiotensin II at At1R receptors that normally cause vasodilation and aldosterone secretion. It also prevents the dry cough that can occur due to bradykinin build up during ACE inhibition.
42
What are some RAAS inhibitor AEs
1st dose hypotension (excessive BP fall), hyperkalemia (aldosterone also secretes K+ into urine) and acute renal failure
43
What is the action of Calcium Channel Blockers?
No Ca2+ enters the cell, no smooth muscle contraction, increased BP
44
What are the three classes of CCBs and effective sites of action?
Dihydropyridines e.g. nifedipine Benzothiazepines e.g. diltiazem Phenylakylamines e.g.verapamil Arterial smooth m. Nifedipine >> Verapamil > Diltiazem Myocardium/non-conducting tissue Verapamil > Diltiazem >> Nifedipine
45
What are AEs for each class and general AEs?
Nifedipine- reflex tachycardia, palpitations, nausea, headaches Diltiazem- bradycardia, AV block Verapamil- " " General- Reflex tachycardia, flushing, headache
46
What are the steps before pharamacotherapy for regulation of serum lipids?
Establish fasting blood lipid profile Cardiovascular risk Treat secondary cause of dyslipidaemia Manage modifiable risk factors
47
What is the action of statins?
Resembles HMG-CoA, precursor for HMG-CoA reductase (rate limiting step), decreases cholesterol synthesis
48
What are the AEs of statins?
mild GI symptoms, headache, insomnia, dizziness
49
What is the action of bile sequestrants/resins?
Bind negatively charged bile acids, inhibit reabsorption, excretion
50
What are the AEs of bile sequestrants/resins?
Abdominal discomfort, bloating, constipation, flatulence
51
What is the action of ezetimibe?
Binds to NPC1L1 transporter preventing cholesterol absorption and lowering LDL
52
What are the AEs of ezetimibe?
Diarrhea, headache, tiredness, stomach pain
53
What is the action of nicotinic acid/niacin?
Lowers secretion of VLDL from liver, lowers LDL and triglycerides, increases HDL
54
What are the AEs of nicotinic acid/niacin?
Flushing, nausea,
55
What is the action of PCSK9 monoclonal antibodies (e.g.evolovumab)?
Prevent PCSK9 from binding to LDL bound receptors and initiating endocytosis
56
What are the AEs of PCSK9 monoclonal antibodies (e.g.evolovumab)?
Headache, nausea, diarrhea
57
What are the drugs for treatment of hypercholesterolaemia?
SPENB Statins, PCSK 9 inhibitors, Ezetimibe, Niacin, Bile acid resins
58
What is the action of fibrates?
Alter the gene expression, increase lipolysis, moderate decrease in triglycerides, moderate increase in HDL
59
What do fish oils do?
Omega 3 fatty acids, decreases VLDL and therefore circulating trigylcerides
60
What are the four classes and an example of heart rate drugs?
Na+ channel block, Lignocaine B-adrenoreceptor antagonism, Propranolol K+ channel block, Amiodarone Ca2+ channel block, Verapamil
61
What is the action and AEs of Na+ channel blockers?
Slow phase 0 of ventricular action potential, decrease excitability and conduction of heart Light headedness, muscular twitching, lip/tongue numbness
62
What is the action and AEs of K+ channel blockers?
Prolongs ventricular action potential, slowing of phase 3 repolarization Skin discoloration, hypothyroidism
63
What is the action and AEs of Ca+ channel blockers?
Inhibit calcium influx that contributes to increased contractility and rate Oedema, flushing, headache
64
What is the action of Digoxin?
Inhibit Na/K ATPase, Ca2+ remains in sarcoplasmic reticulum, increased contractility, slows rates
65
What unclassified agents increase rate?
Atropine, adenosine
66
What is the action of nitrates NO in angina and an example?
Relaxation of vessels, decrease preload Glyceryl trinitrate, 1st pass metabolism
67
What are AEs of nitrates?
Headache, flushing, reflex tachycardia
68
What are AEs of beta blockers?
Fatigue, bradycardia, bronchoconstriction
69
What is the action of Ivabradine?
Inhibition of inward Na-K current in sinus node, decreases diastolic depolarization, pure heart rate reduction
70
What are the AEs of Ivabradine?
Bradycardia, blurred vision
71

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