Questions Flashcards
Low dose aspirin is an effective anti-coagulant that can reduce the risk of heart attacks and stroke
when administered chronically.
a) Describe its main pharmacological mechanism of action to prevent heart attacks. [3 marks]
b) Why is aspirin a relatively safe and effective medicine when used chronically as an anticoagulant? [3 marks]
A) Low-dose aspirin irreversibly inhibits the enzyme cyclooxygenase-1 (COX-1) in platelets, which decreases the synthesis of thromboxane A2, a molecule that promotes platelet aggregation and vasoconstriction. This action reduces the formation of blood clots in arteries, lowering the risk of heart attacks.
B) Aspirin is relatively safe and effective at low doses because it specifically targets platelet function, reducing clot formation without affecting the coagulation cascade. Additionally, the effects of aspirin are long-lasting due to the irreversible inhibition of COX-1 in platelets, which do not have nuclei and therefore cannot resynthesize the enzyme.
Draw a diagram showing the main processes involved in neurotransmission by noradrenaline.
For a diagram: Include the synthesis of noradrenaline from tyrosine, its storage in vesicles, release into the synaptic cleft upon stimulation, binding to adrenergic receptors (α and β receptors) on the postsynaptic membrane, and reuptake or breakdown by enzymes like monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT).
List TWO (2) common side effects observed when indirect sympathomimetic drugs are administered.
Common side effects include hypertension and tachycardia.
Cocaine is one of the many examples of a natural compound which has pharmacological effects in
human beings. It is somewhat unique, however, in that it has multiple targets in the central nervous
system as well as in the periphery, so routes of administration can be crucial.
a) Using a diagram for control and treated cases, what is the mechanism of action of cocaine within
the brain? [3 marks]
b) What is the origin of heroin and what is its mechanism of action in the brain? How can its use
lead to dependence? [3 marks] c) Why is the combination of heroin and cocaine avoided, even by addicts? [2 marks]
d) Cocaine was, perhaps, the original dental anaesthetic and it also reduced blood loss from
infected or injured areas in the mouth and throat.
What are the TWO (2) mechanisms of action involved to achieve these outcomes? [4 marks]
A) Platelet Activation:
Trigger: Injury exposes collagen and von Willebrand factor (vWF) in the blood vessel.
Adhesion: Platelets adhere to the injury site and are activated, releasing ADP and thromboxane A₂ (TXA₂).
Amplification: Released ADP binds to P2Y12 receptors on other platelets, activating them and recruiting more platelets.
Platelet Aggregation:
Fibrinogen Binding: Activated platelets express GPIIb/IIIa receptors, which bind fibrinogen, linking platelets together to form a clot.
Drug Interference:
P2Y12 Inhibitors (e.g., Clopidogrel): Block ADP from binding to P2Y12 receptors, preventing platelet activation and recruitment.
GPIIb/IIIa Inhibitors (e.g., Abciximab): Block the GPIIb/IIIa receptors, preventing fibrinogen binding and platelet aggregation.
B) Heroin is derived from morphine and acts as an opioid receptor agonist in the brain, particularly at mu-opioid receptors. Its use leads to dependence due to the release of dopamine in reward pathways, reinforcing drug-taking behavior.
C) The combination, known as a “speedball,” is avoided due to the opposing effects of heroin (depressant) and cocaine (stimulant), increasing the risk of severe cardiovascular effects like arrhythmias and death.
D) Local Anesthetic Mechanism: Cocaine blocks sodium channels on nerve cell membranes, preventing the initiation and transmission of nerve impulses. This leads to a localized loss of sensation by inhibiting the depolarization necessary for action potentials, thus numbing the area and providing anesthesia.
Vasoconstriction Mechanism: Cocaine causes vasoconstriction by stimulating the sympathetic nervous system and blocking the reuptake of norepinephrine at adrenergic nerve terminals. This leads to prolonged norepinephrine action, resulting in the narrowing of blood vessels, which reduces blood flow and minimizes bleeding in the affected area.
4 [Total Q4: 12 marks]
a) Complete the table below to indicate:
(i) what EACH of the following drugs / hormones is primarily used for, or used to treat in female
and male reproductive health; and
(ii) the principal intracellular mechanism of action of the drug / hormone. [7 marks]
b) Complete the following paragraph by filling in the blanks. [5 marks]
The female menstrual cycle is largely controlled by the ________________ that releases the hormone
_____________________ into the anterior pituitary. The anterior pituitary then releases the
gonadotrophins ___________________ and ___________________ which act on the ovaries to
regulate release of the hormones oestrogen and ____________________. This whole process is
dominantly controlled via a _____________________ feedback process that acts at the level of the
_________________ and pituitary. In the absence of the hormones ___________________ and
________________, however, ___________________ feedback dominates.
A) in picture
B) The female menstrual cycle is largely controlled by the hypothalamus that releases the hormone gonadotropin-releasing hormone (GnRH) into the anterior pituitary. The anterior pituitary then releases the gonadotrophins follicle-stimulating hormone (FSH) and luteinizing hormone (LH), which act on the ovaries to regulate the release of the hormones oestrogen and progesterone. This whole process is dominantly controlled via a negative feedback process that acts at the level of the hypothalamus and pituitary. In the absence of the hormones oestrogen and progesterone, however, positive feedback dominates.
Four clowns are suffering from various ailments, as shown in the first row of the table. They meet
and decide that it would be funny to exchange the medications they were prescribed and take high
amounts of the following drugs:
a histamine H2 receptor antagonist (ranitidine)
a non-selective β-adrenoceptor antagonist (propranolol)
a use-dependent sodium channel blocker (carbamazepine)
an opioid receptor agonist (morphine)
adrenaline
a muscarinic acetylcholine receptor agonist (pilocarpine)
Complete the answers in the table on the next page:
a) Which medication(s) is/are EACH person taking for their disorders? (Row 2) [3 marks]
b) What are the mechanisms of action for the medication? (Row 3) [3 marks].
After exchanging their medications, they suffer from the drug-induced symptoms shown in Row 4.
c) Which drugs were taken by each patient and why? (Row 5) [6 marks]
Row 2: Drugs patients are supposed to take.
Epilepsy: Carbamazepine
Ulcer, severe pain: Ranitidine
Asthma: Adrenaline
Hypertension, dry mouth: Propranolol
Row 3: Mechanisms of action of the drugs.
Carbamazepine: Sodium channel blocker; stabilizes hyperexcitable neural membranes.
Ranitidine: H2 receptor antagonist; reduces stomach acid secretion.
Adrenaline: β-adrenergic agonist; bronchodilation for asthma.
Propranolol: Non-selective β-blocker; reduces blood pressure by decreasing heart rate.
Row 5: Drugs taken by mistake and reasons why.
Epilepsy patient: Took morphine by mistake, causing CNS depression and miosis due to opioid receptor activation.
Ulcer patient: Took pilocarpine by mistake, leading to increased salivation and GI effects due to muscarinic stimulation.
Asthma patient: Took propranolol by mistake, triggering bronchoconstriction due to β-blockade.
Hypertension patient: Took adrenaline by mistake, causing increased blood pressure due to vasoconstriction and β-adrenergic stimulation.
Briefly describe the molecular events that occur between activation and aggregation of platelets.
List TWO (2) drug classes other than aspirin that can interfere with this process and describe
their mechanisms of action. [6 marks]
Platelet activation begins with exposure to collagen and release of thromboxane A₂ (TXA₂).
TXA₂ and ADP from platelets attract additional platelets.
Aggregation occurs via the binding of fibrinogen to GPIIb/IIIa receptors.
Antiplatelet drugs: Thienopyridines block ADP receptors, preventing aggregation.
GPIIb/IIIa inhibitors: These drugs (e.g., abciximab) prevent fibrinogen cross-linking of platelets.
Mechanism: These drugs interrupt ADP pathways or block fibrinogen binding, reducing aggregation.
There are several mechanisms of action for antiepileptic drugs.
a) Explain the antiepileptic mechanisms of antiepileptic drugs acting at:
i. voltage-gated sodium channels [1 mark]
ii. voltage-gated calcium channels [1 mark]
b) Name the drug classes for phenobarbital and diazepam. [2 marks]
How do they act to suppress seizures? [1 mark]
c) What is ONE (1) other mechanism of action of antiepileptic treatments? [1 mark]
a) Voltage-gated sodium channels: Drugs prolong the inactivated state, reducing repetitive firing (e.g., phenytoin).
a) Voltage-gated calcium channels: Blocking T-type channels reduces neurotransmitter release, helpful in absence seizures (e.g., ethosuximide).
b) Phenobarbital: Barbiturate that enhances GABA activity, suppressing neuronal excitability.
b) Diazepam: Benzodiazepine that also enhances GABA, reducing seizure risk.
c) Other mechanism: GABAergic inhibition is increased by drugs like vigabatrin, preventing seizures.
Provide the words that would fill in the blanks in the following scenario by using the table provided
below to give your 1-2 word answer for each numbered blank.
A 24-year old man is found unconscious in a public park and is brought to a trauma centre. There are
no signs of injury and blood sugar is normal. He has needle track marks on his arms and is noted to
have small pupils and slow, shallow respiration. The doctor on duty thinks that the patient may have
injected __(1)__, and administers naloxone immediately. She remembers back to her pharmacology
course, in which she learned that the __(2)__ is the specific part of the brain that is involved in drug
dependence. She also remembers that users can develop __(3)__ to drug use, which drives them to
obtain greater doses of drugs more often to achieve their ‘high’. The specific subtype of receptors
involved in addiction is __(4)__ , as mice which have these receptors ‘knocked out’ do not display
addictive behaviour.
The duty doctor sees the patient a bit later, after the naloxone has had some effect, and she discusses
treatment options with him. While naloxone provides temporary relief due to its short __(5)__, she
recommends him to consider long-term treatment from a clinic near his home which runs a monitoring
__(6)__ program, in which he can check in daily for his medication. This treatment does not prevent
__(7)__, but can certainly alleviate some of the __(8)__ symptoms that he will experience once he
stops using the drug.
Afterwards, she goes to her office to have a much needed cup of coffee, reflecting on how caffeine
antagonises __(9)__ receptors, hopefully disrupting sleep patterns. Later in the evening at the trauma
centre, she will likely see patients who consume excess levels of alcohol. Alcohol acts as an allosteric
modulator of the __(10)__ receptors, leading to depressed brain function and judgement. Of the
enzymes involved in alcohol metabolism, one is also used by methanol (__(11)__). Ironically, the
treatment of infrequent methanol poisoning is to simply administer __(12)__, as it has a greater
affinity for this enzyme than methanol.
(1) Opioid: Based on symptoms of small pupils and shallow breathing.
(2) Nucleus accumbens: Brain area involved in drug dependence.
(3) Tolerance: Drives users to increase dosage.
(4) μ-opioid receptors: Linked to addictive behaviors.
(5) Half-life: Describes naloxone’s temporary relief.
(6) Maintenance: Monitoring program for addiction management.
(7) Cravings: Persistent even with treatment.
(8) Withdrawal: Symptoms that occur on drug cessation.
(9) Adenosine: Caffeine’s antagonistic target.
(10) GABA receptors: Alcohol’s depressive effect on brain.
(11) Alcohol dehydrogenase: Shared enzyme with methanol.
(12) Ethanol: Competes with methanol for metabolism.
A 20-year old man is having surgery to remove two impacted wisdom teeth under general anaesthesia.
He is healthy, has no known allergies and is taking no medication.
On the day of the surgery, he is given a benzodiazepine and fentanyl (an opioid), followed by
intravenous injection of propofol, with maintenance using isoflurane.
Answer a) and b) based on this information.
a) Briefly describe the rationale for use of EACH of these FOUR (4) medications. [4 marks]
b) The anaesthetist is also using nitrous oxide, in combination with the isoflurane.
What is the medical benefit of using these drugs together? [2 marks]
a) Atropine vs. β-adrenoceptor antagonist
Acetylcholine addition: Atropine will block response; β-blocker will not.
Noradrenaline addition: β-blocker will show a reduction in contraction.
b) Muscarine vs. acetylcholinesterase inhibitor
Acetylcholine test: Prolonged effect in acetylcholinesterase inhibitor presence.
Antagonist addition: Muscarine effects blocked by atropine.
c) Eye effects identification
Mydriasis, inability to read: Atropine.
Mydriasis, normal accommodation: Adrenaline.
Miosis, far objects blurred: Muscarine.
No change: Water.
d) Distinguishing Miosis Effects on Skeletal Muscle
Acetylcholinesterase inhibitor will increase skeletal muscle contraction.
Muscarine has no direct effect on skeletal muscle contraction.
A 20-year old man is having surgery to remove two impacted wisdom teeth under general anaesthesia.
He is healthy, has no known allergies and is taking no medication.
On the day of the surgery, he is given a benzodiazepine and fentanyl (an opioid), followed by
intravenous injection of propofol, with maintenance using isoflurane.
Answer a) and b) based on this information.
a) Briefly describe the rationale for use of EACH of these FOUR (4) medications. [4 marks]
b) The anaesthetist is also using nitrous oxide, in combination with the isoflurane.
What is the medical benefit of using these drugs together? [2 marks]
A)
Benzodiazepine: Helps calm the patient and reduce anxiety before surgery.
Fentanyl (Opioid): Provides strong pain relief during the surgery.
Propofol: Puts the patient to sleep quickly so the surgery can start.
Isoflurane: Keeps the patient asleep and comfortable throughout the surgery.
B) The combination of nitrous oxide with isoflurane provides a synergistic effect that enhances anesthesia while allowing for lower doses of isoflurane. This reduces the potential side effects associated with high-dose isoflurane alone, and nitrous oxide’s rapid onset and offset properties aid in a quicker recovery post-surgery, offering a balanced anesthetic profile.
a)
i. What are EACH of the drugs, levonorgestrel and mifepristone, mainly used for? [2 marks]
ii. What are the key pharmacological mechanisms of action that differentiate these TWO (2)
uses? [1 mark]
b) Why should oestrogen never be given without a progestin to women with a uterus? [1 mark]
a)
i. Levonorgestrel is mainly used as an emergency contraceptive to prevent pregnancy after unprotected intercourse.
Mifepristone is primarily used to terminate an early pregnancy, often in combination with a prostaglandin.
ii. The key difference in pharmacological mechanisms is that levonorgestrel works by inhibiting ovulation, while mifepristone blocks progesterone receptors, disrupting the uterine lining and making it inhospitable for pregnancy maintenance.
b) Oestrogen should never be given alone to women with a uterus because it can lead to the thickening of the endometrial lining, increasing the risk of endometrial cancer. Progestin is added to counteract this effect by opposing endometrial proliferation.
Provide the words that would fill in the blanks in the following scenario by using the table provided
below to give your 1-2 word answer for each numbered blank.
During the ______(1)______ phase of the menstrual cycle, low plasma concentrations of oestrogen
stimulate ______(2)______ release from the _____(3)______ via _______(4)_______ feedback.
This hormone then stimulates the recruitment of many _____(5)_______ follicles. Only the dominant
oestrogen secreting one develops into the _______(6)__________ that contains the ovum to be
released. The secondary and mature follicles produce and release ________(7)________. The high
plasma concentrations of this hormone stimulates the release of _______(8)________ via
_______(9)_______ feedback. The component of the combined oral contraceptive pill that inhibits
this part of the menstrual cycle is ______(10)________. High plasma concentrations of this
exogenous hormone inhibit the secretion of ______(11)_________, and to a lesser extent
_______(12)________ via _______(13)________ feedback. As a result, ________(14)________ and
______(15)________ are inhibited, preventing conception. The surge in this hormone then stimulates
the follicle to rupture and release the ovum. What remains of the follicle is called the
_______(16)_________.
- follicular
- gonadotropin-releasing hormone (GnRH)
- hypothalamus
- negative
- primary
- Graafian follicle
- oestrogen
- luteinizing hormone (LH)
- positive
- progestin
- follicle-stimulating hormone (FSH)
- luteinizing hormone (LH)
- negative
- ovulation
- follicle maturation
- corpus luteum
Chronic exposure to certain organochlorine pesticide residues have been linked to disorders of the
nervous system. Traces of some neurotoxic pesticides have recently been detected in groundwater
systems of regional farming communities.
Risk assessment studies for the primary pesticide toxicant have determined that it has an animal
NOAEL (No Observed Adverse Effect Level) of 2.5 mg/kg/day. The oral reference dose for the
toxicant was found to be 0.008 mg/kg/day. Human exposure to the toxicant is through drinking water
ingestion.
Assume that a 70 kg human consumes 2 litres of drinking water per day and the concentration of the
toxicant in drinking water is 0.875 µg (micrograms) per litre.
Calculate the Margin of Exposure (MOE) for the toxicant and describe the risk level implied by the
MOE for residents. [5 marks]
To calculate the Margin of Exposure (MOE), we use the following formula:
MOE = NOAEL / Exposure
Step 1: Calculate human daily exposure to the toxicant.
Human weight = 70 kg
Daily water consumption = 2 liters
Toxicant concentration in water = 0.875 µg/L
Daily exposure in µg:
2L/day x 0.875ug/L = 1.75 ug/day
Convert µg to mg:
1.75µg=0.00175mg
Daily exposure per kg body weight:
0.00175mg / 70kg = 0.000025 mg/kg/day
Step 2: Calculate the MOE.
Given:
Animal NOAEL = 2.5 mg/kg/day
Human exposure = 0.000025 mg/kg/day
MOE = 2.5 / 0.000025 = 100000
Step 3: Describe the risk level.
An MOE of 100,000 is very high, indicating a low risk level for residents. Typically, an MOE above 100 is considered acceptable and low-risk, so 100,000 suggests minimal risk of adverse effects from the toxicant at current exposure levels.
List FOUR (4) objectives of toxicology risk assessments. [4 marks]
Identify potential hazards: Determine whether a substance (chemical, drug, environmental toxin) has the potential to cause harm to humans, animals, or the environment.
Assess dose-response relationships: Establish the relationship between the dose of a toxicant and the severity or frequency of adverse effects, aiding in setting safe exposure levels.
Evaluate exposure levels: Quantify the extent of human or environmental exposure to the toxicant under typical conditions, including routes, frequency, and duration of exposure.
Characterize risk: Integrate hazard, dose-response, and exposure data to estimate the likelihood and severity of adverse health effects in specific populations or ecosystems.
According to the ICH guidelines, what are the THREE (3) main types of studies that are
required for Development Toxicity Testing (ICH 4.1)? [3 marks]
Fertility and Early Embryonic Development Studies: These studies assess the potential effects of a substance on reproductive performance, fertility, and early embryonic development from conception to implantation.
Embryo-Fetal Development Studies: This type of study evaluates potential adverse effects of a substance on fetal development, including structural abnormalities, growth, and survival, typically from implantation to the end of organogenesis.
Pre- and Postnatal Development Studies: These studies examine the impact of a substance on the development and health of offspring from late pregnancy through birth and lactation, covering growth, functional development, and reproductive performance.
What are the key features of physiological antagonists? [2 marks]
Physiological antagonists produce opposing effects by activating different receptors or pathways, rather than competing for the same receptor as the agonist. They counterbalance the initial effect through independent mechanisms, helping restore physiological balance without directly blocking the agonist’s receptor. This approach can effectively neutralize effects while maintaining receptor functionality.
a) Name a competitive antagonist of acetylcholine in the rat ileum. [0.5 mark]
b) Which receptor does acetylcholine and the competitive antagonist act on in the rat ileum?
[0.5 mark]
c) Name ONE (1) medicinal use of the competitive antagonist. [1 mark]
a) A competitive antagonist of acetylcholine in the rat ileum is atropine.
b) Acetylcholine and the competitive antagonist act on muscarinic receptors in the rat ileum.
c) One medicinal use of atropine is to reduce salivation and respiratory secretions during surgery.
A patient ingested high amounts of atropine and is referred to the Poison Centre.
a) Which drug class does atropine belong to? [1 mark]
b) List THREE (3) TYPICAL autonomic symptoms that you expect to observe at the heart, the
gastrointestinal tract and the eyes. [3 marks]
c) What is the antidote to atropine, and how does it act? Also name the drug class of the antidote.
[2 marks]
a) Atropine belongs to the drug class of antimuscarinic (or anticholinergic) agents and is a reversible competitive antagonist at muscarinic acetylcholine receptors.
b) Three typical autonomic symptoms due to atropine’s antimuscarinic effects:
Heart: Tachycardia (increased heart rate)
Gastrointestinal tract: Decreased motility, leading to constipation
Eyes: Mydriasis (pupil dilation) and difficulty focusing on near objects (cycloplegia)
c) The antidote to atropine is physostigmine. It acts by inhibiting acetylcholinesterase, which increases acetylcholine levels to counteract the effects of atropine. Physostigmine belongs to the cholinesterase inhibitor drug class.
Therapeutic Communities (TCs) are a common form of long-term residential treatment for substance
use disorders (SUDs). Residential treatment for SUDs started in the 1950s out of the self-help
recovery movement, which included groups like Alcoholics Anonymous. While originally designed
as a mutual self-help and drug-free alternative to medically oriented strategies used to address
addiction, they have adapted over time to address the treatment needs of different populations
(homeless individuals and those with psychiatric disorders) making use of professional staff with
substance abuse counselling or mental health training, some of whom themselves are in recovery.
TCs are now found in over 65 countries around the world.
a) What are the key features of the brain’s reward circuit? [3 marks]
b) Residents addicted to prescription opioids or heroin would experience very challenging
withdrawal symptoms if they suddenly stopped use without support.
What are TWO (2) possible opioid withdrawal symptoms? [2 marks]
c) How is the brain’s reward circuit affected by the presence of opioids or heroin used chronically?
[3 marks]d) Name a medication that might be used in pharmacological management of opioid withdrawal
and state if the drug is an agonist or antagonist on its target receptors. [2 marks]e) Why might living in a facility like Therapeutic Communities play a key role in breaking the
cycle of drug dependence and addiction? [2 marks]
a)
Involves the mesolimbic pathway, primarily the nucleus accumbens.
Dopamine release in response to rewarding stimuli.
Reinforces behaviors, leading to addiction when overstimulated.
b)
Nausea and vomiting.
Muscle aches and cramps.
c)
Decreased dopamine receptor sensitivity.
Reduced natural dopamine release, leading to dependence.
Need for higher doses to achieve the same reward sensation.
d)
Example: Methadone.
Receptor action: Agonist on opioid receptors.
e)
Provide structured, drug-free environment for recovery.
Support through counseling and peer interaction, helping to break dependence cycles.
a) Identify and list the labelled items 1-8 in the figure below to explain the intercellular and
intracellular mechanisms that stimulate erections. [4 marks]
b) In Australia, erectile dysfunction medications typically act via one of two specific pathways.
Name ONE (1) drug that acts on EACH of these two pathways and the primary ‘target’ for
EACH drug. [2 marks]
a)
1. Nitric oxide (NO) production in endothelial cells.
2. Guanylate cyclase activation by NO.
3. Cyclic GMP (cGMP) production.
4. Calcium channels (Ca2+ influx).
5. G-protein activation.
6. Adenylate cyclase production of cAMP.
7. Influx of Ca2+ through N-type Ca2+ channels.
8. Potassium channels (K+ efflux).
b)
Sildenafil: Targets phosphodiesterase-5 (PDE5) to increase cGMP levels.
Alprostadil: Acts on prostaglandin E1 receptors to increase cAMP.
25 Explain, using dot points, how tamoxifen works to inhibit the growth of breast cancer cells.
[6 marks]
- Tamoxifen is a selective estrogen receptor modulator (SERM).
- It competitively inhibits estrogen binding to receptors on breast cancer cells.
- This blocks estrogen’s proliferative effect on these cells.
- Reduces cancer cell division and tumor growth.
- Acts as an estrogen antagonist in breast tissue.
- Can act as an agonist in other tissues (e.g., bone), reducing side effects.
26 Describe FOUR (4) mechanisms by which two toxicants can interact and the functional
outcomes of each interaction. [4 marks]
Additive effect: Combined toxicant effect equals the sum of individual effects.
Synergistic effect: Combined effect is greater than the sum of individual effects.
Antagonistic effect: One toxicant reduces the effect of another.
Potentiation: One non-toxicant increases the toxicity of another toxicant.
27 List any FOUR (4) of Wilson’s general principles of teratology. [4 marks]
Susceptibility depends on the developmental stage at exposure.
Teratogenicity is dose-dependent.
Genotype of the fetus affects susceptibility.
Teratogens cause specific malformations in target organs.
28 Describe the TWO (2) main dose-response patterns of teratogenesis and how EACH of these
relates to teratogen severity. [4 marks]
Threshold response: Effect occurs only above a certain dose; high dose equals more severe defects.
No-threshold response: Any dose can cause defects, severity increases with dose.
Aspirin is one of the world’s most frequently used drugs. It is used as an analgesic, but also in more
recent times, as a treatment for heart disease.
a) Describe the mechanism by which aspirin can prevent heart attacks. [3 marks]
b) Why is aspirin a relatively safe and effective medicine when used chronically as an anticoagulant? [3 marks]
a)
Aspirin irreversibly inhibits cyclooxygenase-1 (COX-1) in platelets.
This action blocks thromboxane A₂ synthesis, reducing platelet aggregation.
Reduced platelet aggregation prevents thrombus formation in arteries, lowering heart attack risk.
b)
Low-dose aspirin affects platelets without significant effects on prostacyclin in endothelial cells.
Its effects are irreversible due to lack of platelet nucleus, which limits clotting for platelet lifespan (7-10 days).
Low dosing minimizes gastrointestinal side effects and bleeding risks.
Antiepileptic and anti-dysrhythmic drugs can have different mechanisms of actions. Two different
mechanisms of actions pertaining to voltage-gated ion channels are shared between these drugs.
a) Briefly explain the two different mechanisms shared by antiepileptic and anti-dysrhythmic
drugs in the brain and heart, respectively. Include their effects on neurons and cells of the
heart (pacemaker cells and myocytes). [4 marks]
b) Name and briefly explain the mechanism of action of anti-epileptic drugs that act
allosterically on receptors found mostly on brain neurons. Name a common side effect of
these drugs. [2 marks]
a)
Sodium Channel Blockade: Both antiepileptic and anti-dysrhythmic drugs block voltage-gated sodium channels, reducing the rapid influx of sodium ions. In neurons, this helps prevent seizures by limiting abnormal firing, and in cardiac cells, it stabilizes the heart’s rhythm by slowing conduction.
Calcium Channel Blockade: These drugs also block voltage-gated calcium channels, decreasing excitatory neurotransmitter release in the brain to control seizures. In the heart, calcium channel blockade slows the heart rate and reduces contractility, aiding in dysrhythmia management.
b)
Benzodiazepines act as allosteric modulators on GABA(A) receptors, enhancing the inhibitory effect of GABA.
Common side effect: Sedation due to increased inhibitory action in the CNS.
