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Created by Elizabeth Then
about 8 years ago
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| Question | Answer |
| HCL secretion | secreted by parietal cells in the stomach |
| Drugs which reduce acid | antacids H2 receptor antagonists Proton pump inhibitors |
| Antacids | alkali to neutralise effect of acid good for short term management of minor symptoms not useful for ulcer healing |
| Antacids adverse effects | constipation, diarrhoea |
| H2 receptor antagonists mechanism of action | Block H2 receptor, 90% reduction in HCL secretion, e.g. ranitidine |
| H2 receptor antagonist adverse effects | very few, and well tolerated |
| Proton pump inhibitors mechanism of action | blocks acid secretion via proton pump e.g. omeprazole, pantoprazole |
| Proton pump inhibitor adverse effects | inhibit P450, drug interactions, long term: increase risk of pneumonia and osteoporosis, B12 malabsorption |
| HCL secretion stimulated by | Gastrin, histamine, acetylcholine |
| Gastrin mechanism of action | acts on receptors to cause release of histamine and parietal cell influx of Ca to increase HCL |
| Ach mechanism of action | acts on muscarinic receptors and parietal cells to increase HCL secretion |
| Histamine mechanism of action | acts on H2 receptors on parietal cells to increase HCL secretion |
| Vomiting nausea CTZ | Chemoreceptor trigger zone, vomiting centre, outside blood-brain barrier |
| Drugs used to treat vomiting and nausea: D2 receptor antagonist (dopamine) Mechanism of action: | acts in CTZ to prevent vomiting reflex, peripherally increase gut motility e.g. metoclopramide |
| D2 receptor antagonist adverse effects | blocks CNS receptors, fatigue, motor restlessness |
| Drugs used to treat nausea and vomiting: Histamine (H1) antagonists mechanism of action: | blocks H1 receptors in vomiting centre e.g. promethazine |
| H1 receptor antagonist adverse effects | Blocks CNS receptors, fatigue, dry mouth, constipation |
| Drugs used to treat vomiting and nausea: 5HT3 antagonists Mechanism of action: | particularly effective for prevention and treatment of post-operative and chemotherapy induced vomiting. e.g. ondansetron, tropisetron |
| 5HT3 antagonists adverse effects | constipation, diarrhea, headache |
| Drugs that target the GIT | Gastric secretion: HCL and pepsinogen secretion Vomiting (nausea): in response to ingestion of toxic substances, unwanted side effects |
| Local anaesthesia | reversible loss of sensation in a localised area |
| General anesthesia | loss of sensation and loss and consciousness |
| Local anaesthesia desirable properties: | sufficient duration of action low systemic toxicity at effective concentrations quick onset reversible |
| LA mechanism of action: | blocks NA channels, halts nerve action potentials, small fibres first, large fibres last. reverse order for recovery. |
| 2 types of LA properties | ester: cocaine, procaine, short duration of action Amide: lignocaine, bupivacaine, long duration of action ester= reactive metabolite= allergy and hypersensitivity |
| Administration of LA routes | topical, infiltration, nerve block, spinal, epidural, different onset and duration of action |
| LA duration of action | increase with vasoconstrictor (e.g. adrenaline), increase due to contact with nerve, decrease rate of absorption |
| LA adverse effects | cardiovascular, hypersensitivity, CNS (seizures/coma), treat acute toxicity by giving respiratory assistance, drugs to control seizures (diazepam) drugs to control hypotension (adrenaline) |
| General anaesthetics desirable properties: | analgesia amnesia loss of consciousness inhibition of sensory and autonomic reflexes |
| GA desirable properties | use combination of drugs to achieve balanced anaesthesia |
| 4 stages of anaesthesia | 1. analgesia= conscious but not drowsy, without amnesia 2. delirium= amnesic, irregular respiration 3. surgical anaesthesia = re-establishment of regular breathing 4. medullary paralysis = severe depression of medulla, require circulatory and respiratory support |
| GA mechanism of action | nerve block, increase inhibitory and excitatory neurotransmitters |
| Inhalational GA agents mechanism of action | PK uptake and distribution from lungs to blood to CNS: depends on solubility, conc in inspired air, ventilation rate, and pulmonary blood flow |
| Types of inhalational agents GA | Gaseous: nitrous oxide volatile liquid: halothane, enflurane, isoflurane |
| GA: inhalation agents: solubility indicators | lipid solubility: determines potency aqueous solubility: determines rate of induction and recovery |
| Inhalation agents | provide controlled anaesthesia |
| Nitrous oxide advantages/disadvantages | advantages: non-flammable, rapid induction, no muscle relaxant activity disadvantages: low potency, no surgical anaesthesia, can cause decrease in RBC |
| Halothane advantages and disadvantages | moderately potent disadvantages: little analgesia and muscle relaxation, resp depression, hypotension, hypoxemia |
| Enflurane advantages and disadvantages | fast induction and recovery Disadvantages: may cause seizures, potential renal toxicity |
| Intravenous (IV) agents GA: | induce anaesthesia, hypnosis, analgesia, muscle relaxation, control of autonomic reflexes |
| IV agents GA: advantages/disadvantages | advantages: rapid onset, short duration, no resp irritation Disadvantages: inability controlling depth, severe resp and cardiovascular depression |
| Other agents GA used in combination muscarinic receptor antagonist: mechanism of action: | limit bronchial and salivary secretion e.g. atropine |
| Other agents: neuromuscular blockers mechanism of action | prevent reflex movement and paralysis of skeletal muscles e.g.suxamethonium |
| Other agents: anxiolytics mechanism of action | decrease anxiety e.g. diazepam |
| Other agents: opioids mechanism of action | analgesia, sedation e.g. morphine |
| Other agents antipsychotics mechanism of action | decrease vomiting, cause sedation e.g. droperidol |
| GA overall goal | balanced anaesthesia induction (IV) maintenance (inhalation) muscle relaxation analgesia |
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