Deck 2

Question 1

1. Q. Where are muscarinic and nicotinic receptors found?

Answer 1

A. Muscarinic acetylcholine receptors are found on all cardiac muscle, smooth muscle and gland cells. –parasympathetic (they can be excitatory or inhibitory)
B. Gq coupled – M1, M3, M5 (Ca2+), Gi/o = M2, M4 (K+)
C. Nicotinic receptors are found on all autonomic nervous system post ganglionic neurons, in the adrenal medulla and at all neuromuscular junctions of skeletal muscle (excitatory when Ach binds). Some CNS pathways.

Question 2

1. Q. Where are acetylecholine, epinephrine and norepinephrine used?

Answer 2

A. Parasympathetic – neurotransmitter is Ach
B. Sympathetic - epinephrine and norepinephrine at the effector (Ach can be found at interneurons)
C. Somatic (conscious) neurotransmitter is Ach

Question 3

1. Q. What are cholinergic agonists?

Answer 3

A. Cholinergic agents produce or alter the release of Ach
B. They can mimic Ach = producing parasympathetic effects
C. Prevent release of Ach – botox (by degrading vesicle proteins)
D. Bind to acetylcholinesterase so Ach cannot be broken down into acetate and choline = build-up of Ach in synaptic cleft
E. Indirect – sarin gas forms strong bonds with acetylcholinesterase

Question 4

1. Q. What side effects occur due to overstimulation of cholinergic agents?

Answer 4

A. DUMBELS (diarrhoea, urination, miosis/muscle weakness/bronchorrhea, bradycardia, emesis, lacrimation, salivation/sweating)

Question 5

1. Q. Name the major difference between noradrenaline and adrenaline?

Answer 5

A. Noradrenaline is considered a neurotransmitter while adrenaline is considered a hormone

Question 6

1. Q. What does each class of adrenoceptor do? Alpha 1/2 and beta 1,2,3

Answer 6

A. Alpha-1; vasoconstriction (vasodilation) also bladder contraction
B. Alpha-2; self-inhibition (reuptake on presynaptic cleft), also acts on the pancreas decreasing insulin
A. Beta-1; most clinically important -heart. Increased force, rate and contraction of heart. Also affects the kidney increasing renin and therefore blood pressure.
B. Beta-2; vasodilation/(vasoconstriction), bronchodilation, also GI decreased motility
C. Beta-3 increased lipolysis, also bladder relaxation

Question 7

1. Q. Is adrenaline a direct-acting (selective) agonist or an indirect-acting (non-selective) agonist? Which adrenoceptors does it target and what are the effects?

Answer 7

A.	Adrenaline is a non-selective agonist
It targets:
B.	alpha-1 = vasoconstriction 
C.	beta-1 = positive inotropic effects (increased strength of cardiac contraction)
D.	beta-2 = bronchodilation

Question 8

1. Q. Define pain? What is the difference between nociceptive and neuropathic pain?

Answer 8

A. An unpleasant, sensory and emotional experience associated with actual or potential tissue damage.
B. Nociceptive: inflammatory
C. Neuropathic: nerve related pain

Question 9

1. Q. Name two differences between A-delta fibres and C fibres

Answer 9

A. A delta fibres – fast, myelinated - carry cold, pressure and some pain signals
B. C afferent fibres – slow, unmyelinated (sudden, sharp prick)
C. A class – thickly myelinated, fast (burning or aching)

Question 10

1. Q. Explain the Rawlin-Thompson/ABCDE system of adverse effects

Answer 10

A. Augmented; commonest, predictable, dose related, self-limiting (manage by lowering dose)
B. Bizarre; unrelated and not expected from known pharmacological action, unpredictable – hypersensitivity etc (manage by withdrawing drug immediately)
C. Chronic; occurs after long therapy, may not be immediately obvious with new medicines
D. Delayed; also occurs after a long period of time after treatment, eg neoplasia
E. End of use; relatively long term (days/weeks), withdrawal reactions

Question 11

1. Q. What are the four main types of hypersensitivity?

Answer 11

A. Type 1 – acute anaphylaxis
B. Type 2 – igG-mediated cytotoxicity
C. Type 3 – Immune-complex deposition
D. Type 4 – T-cell mediated

Question 12

1. Q. Name two features of anaphylaxis?

Answer 12

A. Exposure to drug, immediate onset, rash blotches, swelling of lips and face, hypotension (anaphylactic shock), cardiac arrest
B. Release of histamine, thromboxanes, prostaglandins, TMF and other acute inflammatory mediators

Question 13

1. Q. Name three ways to manage an adverse drug reaction?

Answer 13

A. Continue the drug and manage the ADR by other means, reduce the dose, stop the drug

Question 14

1. Q. Describe a situation in which adverse drug reactions should be reported

Answer 14

A. All suspected ADRs for new medications, all ADRs in children, all serious reactions (fatal, life threatening, disabling, incapacitating, or which result in or prolong hospitalisation).

Question 15

1. Q, Name two risk factors that may increase drug interactions a) Patient related b) Drug related

Answer 15

A. Patient related; polypharmacy, old age, genetics, hepatic disease, renal disease
B. Drug related; narrow therapeutic index, steep dose/response curve, saturable metabolism

Question 16

1. Q. What is the concept of homeopathy?

Answer 16

A. “like to treat like”, (modern day medicine is based on allopathy – the treatment of opposites)

Question 17

1. Q. Name two naturally occurring opioids

Answer 17

A. Morphine and codeine (from the opium poppy)

Question 18

1. Q. What is the difference between; a) tolerance b) dependence

Answer 18

A. Tolerance is the down regulation of receptors with prolonged use; this means that higher doses are needed in order to achieve the same effect
B. Dependence is the physical and psychological craving for euphoria

Question 19

1. Q. What is action mechanism of opioids?

Answer 19

A. Opioid receptors are coupled with inhibitory G-proteins and their activation has a number of actions;
B. Closing of voltage sensitive calcium channels
C. Stimulation of potassium efflux leading to hyperpolarisation and reduced cyclic adenosine monophosphate (cAMP) production
D. Overall reduction in neuronal cell excitability – reduced transmission of nociceptive impulses
E. = Inhibition of pain transmitter release at spinal cord and midbrain and modulation of pain perception in higher centres – changes the emotional perception of pain
F. Sustained activation leads to tolerance and addiction

Question 20

1. Q. What side effects are associated with opioids?

Answer 20

A. Respiratory depression; sedation, nausea, vomiting, constipation, itching, immune suppression (dependence and addiction)

Question 21

1. Who is at a higher risk of respiratory depression due to morphine?

Answer 21

A. Morphine (converted to morphine 6 glucuronide in the body) is renally excreted this means that patients with renal failure have a higher risk of respiratory depression

Question 22

1. Codeine is a prodrug; what does this mean?

Answer 22

A. This means that it must be metabolised by cytochrome CYP2D6 within the body to produce any effect

Question 23

1. What is bioavailability? What is the oral bioavailability of morphine?

Answer 23

A. Bioavailability is the proportion of a drug or other substance which enters the circulation when introduced into the body to have an active effect
B. Oral morphine is subject to first pass metabolism by the liver
C. This means that 50% of oral morphine is metabolised before the drug reaches the systemic circulation (so only half the dose must be given parenterally- s/c, IM, IV etc)
D. First-pass metabolism is when the concentration of a drug is reduced before it reaches the systemic circulation.