Past paper learning Flashcards
Causes of hypothyroidism
Autoimmune
Post surgery or drugs such as amiodarone
Autoimmune hypothyroidism and antibody involved
Hashimotos
Anti thyroperoxidase
Phases of addisonian crisis
Vomiting and diarrorhoea
Decreased consciousness and collapse
Cardiac arrest
Clinical features addisonian crisis
Hyponatraemia
Hyperkalaemia
Hypoglycaemia
Why are there no anti-aggregatory effects in other NSAIDS to aspirin
They inhibit COX 2
Aspirin binds covalently irreversibly
Why isnt paracetamol a NSAID
Has no anti-inflammatory effects
Paracetamol OD
- Paracetamol forms the electrophile NAPQI, which is removed by glutathione conjugation, which is inactive.
- Paracetamol overdose – too much NAPQI, therefore binding to -SH groups on hepatocyte enzymes, leading to enzyme failure and thus liver failure
3 ways beta blockers reduce BP
- Decrease CO – by decrease HR and contractility
- Decrease renin release therefore less angiotensin II formed, therefore less vasoconstriction via AT1 receptor
- Block presynaptic B1 therefore decreasing NA release from presynaptic neurone
How do pre junctional beta adrenoceptors lead to reduced TPR
Vasodilation at andrenoceptors in peripheral vasculature
In angina how do beta blockers reduce myocardial oxygen demand
Decrease heart rate and contractility
Decrease venous return therefore decrease preload – due to less venous constriction
Less TPR therefore causing decreased afterload
How and where do cholinomimetics control glaucoma
At the short ciliary ganglion to cause pupil constriction therefore increased drainage – increased angle between the cornea and iris
How do beta antagonists control glaucoma
on ciliary bodies to decrease carbonic anhydrase activity therefore decrease aqueous humour production
How are anticholinesterases a problem at NMJ
Cause increase Ach which leads to depolarising block, causing the muscle to be unable to contract
2 drugs with a low therapeutic windown
Warfarin
Phenylbarbitol
Difference in where parkinson drugs act
i) Carbidopa – Peripheral – acts on DOPA decarboxylase
ii) Entacapone – COMT inhibitor. Acts centrally and peripherally
iii) Domperidone – Dopamine receptor antagonist – more central
iv) Bromocriptine – Ergot derivative Dopamine D2 receptor antagonist - central
How does selegiline cause hallucinations
Affects mesolimbic pathway
How does chlorpromazine cause breast enlargement
Hyperprolactinaemia due to decreased activity of the tuberoinfundibular pathway therefore less inihibtion of prolactorophs to release prolactin
Enzyme responsible for various metabolism rates of Isonizad
Acetyl transferase
Why does do peoples metabolism of fat vary
Polymorphism in acetyl transferase
Liver damage
How to prevent overdose of oral anti-anticoagulant
- Give fresh frozen plasma/cryoprecipitate to increase factor concentration
- Stop taking the drug
- Supplement vit K, especially if warfarin
D2 antagonist extre-pyramidal side effects
Jerky movements
Torticollis
Problems with azothioprine metabolism
- Xanthine oxidase normally metabolises azathioprine into 6-TU which is inactive
- If treating gout with allopurinol, this blocks xanthine oxidase activity, causing the azathioprine to be metabolised into 6-MeMP (cause hepatotoxicity) and 6-thioguanine (cause myelosuppression)
What do excipients do
• Increase the chemical and physical stability of the drug, thus increasing the acceptability for the patient
d) How do anticholinesterases lead to respiratory depression? Explain in terms of its effects on the CNS, the lungs, and voluntary muscles
- CNS: increase levels of Ach in synapses, thus increase the activity of parasympathetic outflow – increased impact of post-ganglionic transmission. Also caused increased sweating and increase secretions. The increased secretions would result in the size of the lumen decreasing leading to less air reaching the lungs
- Lungs – binds to M3 receptors to cause bronchial smooth muscle to constrict. This would lead to less air traveling through the lungs, with less air reaching the bloodstream, thus causing respiratory depression
- Voluntary muscle – cause contraction and possibly resulting in a depolarising block, causing decreased activity. This would decrease respiratory muscle activity causing less air to reach the lungs