Module written assignment

There are 4 activities in is assignment. 3 of them have schedules and the final activity question has two parts,

use a diagram to explain the first part and you will see the second part.

gather up the solutions in the same method and attitude as I wrote it. Additionally, he will put some references for me from these:

1. Australia medicine handbook.
2. Catalyst database.
3. Stocklys drug interaction.
4. And just do a random search for receptors copy the reference online.

write in symbols, instead, just write using normal letters.Try to draw the diagram and explain it.

Activity 1
Foreachof the body systemslisteddescribe the consequence of activation of the parasympathetic and sympatheticnervous systems,thendescribe aclinical symptom or condition that as a paramedic you may observe in someone with a highly activatedPARASYMPATHETIC nervous system. (6 marks)
Body System Parasympathetic Activation Sympathetic Activation Clinical Symptom / Condition
e.g.Heart – Rate Decreased heart rate Increased heart rate Bradycardia
Heart – Force of Contraction Decrease contraction Increased muscle contraction Heart Failure
Pupil Miosis Mydriasis Catarax
Lungs Deep Breathing Shallow breathing Respiratory depression
Stomach Increased acid secretion and increased Motility Decreased acid secretion and low motility Diarrhoea
Activity 2
For each drug,identify ONE paramedic indication,then in the subsequent columns listthe molecular target, target tissue, type of interaction (i.e. agonist / antagonist / allosteric modulator / inhibitor) and briefly explain how the interaction of the drugwith the molecular targetaccounts forthe observed therapeutic effect for theparamedic indication identified in the first column.(24 marks)
Drug Paramedic Indication Molecular Target Target Tissue Type of interaction Mechanism of Therapeutic Effect
e.g. Salbutamol Acute asthma ß2-adrenoreceptor Lungs Agonist Activation of ß2 adrenoceptors in the lung causes relaxation of the bronchiole smooth muscle, bronchodilation and increased airflow.
Adrenaline Cardiac Arrest ß1 receptors Heart Agonist Increases cardiac output by binding to ß1 receptorsFentanyl Severe Pain µ-opioid
Spinal Cord Agonist Fentanyl binds µ-opioid G-protein-coupled receptors, which inhibit pain neurotransmitter release by decreasing intracellular Ca2+ levels
Ondansetron Vomitting 5 HT3 Terminnal of the Vagus nerve Antagonist Stimulation of 5-HT3 receptors causes transmission of sensory signals to the vomiting centre via vagal afferent fibres to induce vomiting. Ondansetroncompetitively binds to 5-HT3 receptors and blocks vomiting mediated by serotonin release
Midazolam Sedative-hypnotic GABAA CNS agonists Midazolam reportedly interferes with reuptake of GABA, thereby causing accumulation of GABA. The mechanism of action is not fully understood but it acts the same way as the benzodiazepines work by potentiating the inhibitory effects of GABA throughout the CNS
Ipratropium Acute Asthma Muscuranic Receptors Lungs Antagonist The bronchodilation produced by ipratropium is primarily a local, site-specific effect rather than a systemic effect. Ipratropium appears to produce bronchodilation by competitive inhibition of cholinergic receptors on bronchial smooth muscle. This effect antagonises the action of acetylcholine at its membrane-bound receptor site and thereby blocks the bronchoconstrictor action of vagal efferent impulses
Adenosine Arrythmia A1 receptor
Heart Antagonist Slows impulse formation in the sinoatrial (SA) node, slows conduction time through the atrioventricular (AV) node, and can interrupt re-entry pathways through the AV node. Adenosine depresses left ventricular function, but because of its short half-life, the effect is transient, allowing use in patients with existing poor left ventricular function. The action is mediated Via the A1 receptor, inhibiting adenylyl cyclase, reducing cAMP and so causing cell hyperpolarization by increasing outward K+ flux. It also causes endothelial-dependent relaxation of smooth muscle as is found inside the artery wall
Naloxone Opiate Overdose µ-opioid
CNS Antagonist It is thought that naloxone acts as a competitive antagonist at mu-, kappa- and sigma-opioid receptors within the central nervous system (CNS). Antagonism of opioid actions may precipitate withdrawal symptoms in patients who are physically dependent on opioids. Naloxone prevents or reverses the effects of opioids,
Aspirin Pain/Fever Cyclooxygenase
hypothalamus Nonselective Aspirin has analgesic, antipyretic, anti-inflammatory and antiplatelet actions. It is a nonselective NSAID, preventing synthesis of prostaglandins by noncompetitively inhibiting both forms of cyclo-oxygenase (COX), COX-1 and COX-2.
Activity 3
In pharmacodynamics, a drug can be thought of as ‘selective’ when it shows preference for interaction with one molecular target, even though it may be faced with many molecular targets to choose from. Indeed, salbutamol can act as an agonist at all ß adrenergic receptors, but at therapeutic doses it ‘selects’ the ß2 adrenergic receptor subtype in preference to others.
Considering the drugs used in your clinical practice as a paramedic:
• In the first column, list FOUR receptors from different classes,thenin the second column, list their endogenous agonist(s).(2 marks)
• In the third column give an example of ONE drug that is a clinically relevant SELECTIVE agonist OR antagonist for each of the receptors.(2 marks)
Receptor Endogenous agonist Selective drug agonist or antagonist
M1 Receptor Acetylcholine Atropine as M1 Receptor
?1 Receptors Epinephrine Atenelol as a ?1 Receptors antagonist
µ-opioid receptors Enkephalins
Nalexone as a µ-opioid Antagonist
5 HT3 Receptor Seretonin Quipazine as a agonist

Activity 4
Antagonists at receptors for neurotransmitters or hormones are often used clinically.
• Use a diagram to explain how ß-adrenoceptors antagonists produce clinically useful effects. (2 marks)

 

• Considering the actions of ß-adrenoceptorsthroughout the body, would it be the most appropriate treat uncomplicated hypertension in 68yo patient with moderate asthma and renal impairment with atenolol, metoprolol or propranolol? Briefly explainthe reasons for your decision. (4 marks)

According to the heart foundation, 1st line treatment of uncomplicated hypertension is usually ACE inhibitor such as ramipril- this has better cardiovascular pretction and higher rate of primary prevention of further complication. However, from the available options of beta blocker; atenolol is contraindicated due the renal elimination so not recommended in renal impairment. Propanlol is a non-selective blocker (beta1 and Beta 2) hence contraindicated with asthmatics. Therefore, metoprolol is the most appropriate as it is eliminated via hepatic metabolism and beta 1 selective.
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