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
Alcohol leading to hepatitis
During metabolism it produces oxygen free radicals, which damage mitochondria and result in inflammation
How does GABA work
GABA receptor protein on the GABA-A receptor, which causes benzodiazepine and GABA receptor proteins to be linked by the GABA modulin protein, causing opening of the chloride channel
Benzodiazpeine used today
Diazepam
Uses of diazepam
• Used to treat Status Epilepticus
• Anxiolytic
Anti convulsant
How do you reverse the effects of benzodiazepines
Competitive receptor
Drugs interacting with benzodiazepines
Barbiturates
Alcohol
Man comes in with bacterial infection after MI
ECG
Sepsis screening
what is a rebound reaction
A condition where the pathology returns after removal of treatment, to a worse degree than before treatment. E.g. clonidine and hypertension
Who is in charge of yellow card scheme
MHRA (Medical Healthcare Products Regulatory Agency)
Best anti-hypertensive drug used for diabetics
ACE inhibitors
Clopidogrel MOA
P2Y12 receptor antagonist, which are found on platelet surface. Prevents ADP binding, thus preventing platelet activation and aggregation
Why is GTN given sublingually
Increase systemic absorption
Why are Benzodiazepines better than barbiturates
Larger window of safety
Less potent withdrawal effect
Mild effect on REM sleep
Doesn’t induce liver microsomal enzyme
MOA flumezanil
Competitive benzodiazepine receptor protein antagonist so prevent benzodiazepine from bind and having a subsequent effect
Drugs with anxiolytic effects
TCA SSRI Antipsychotics Antiepileptic Propranolol (symptom treatment)
4 routes of administration and their speed of action
- Smoke – absorbed through the mucosal membrane of the nose. Relatively fast speed of onset, but would still slightly longer to have an effect on the brain as it needs to pass through the mucosal layer and then through the venous system before it can enter the arterial system to reach the brain
- Orally – absorbed through the GI tract. Very slow onset as absorption would take a while, and there would be hepatic first pass metabolism which would decrease the concentration available to have an effect and thus it would take longer for an effect to occur
- IV – injected straight into the venous system. Speed of onset would be very fast, but not the fastest to reach the brain, as it would need to pass through the venous system, and then enter the arterial system before it reaches the brain
- Inhaled – via the alveoli of the lungs. Causes fastest onset of action for most drugs as it returns directly to the heart via the pulmonary vein before entering the systemic arterial circulation in order to reach the brain and have an effect
Reason for long half life of cannabis
- Cannabinoids are stores in poorly vascularised tissue and fat, and thus the cannabinoids would not easily be removed from the tissue, leading to the cannabis having a long half-life
- Cannabis is excreted mainly in the bile. However, in the GI tract it may be reabsorbed and thus this would allow it to re-enter circulation, thus prolonging its clearance from the body. This is known as enterohepatic cycling
What to consider before administering antiepileptics
- Type of seizure which they are having – is it partial or general and subtype of these categories
- Other medication which they may be on which may interact with the medication
- Duration and frequency of the seizures
MOA phenytoin
Phenytoin (not a drug which we have covered) acts on the VGSC to either inactivate them or to keep them in the inactive phase for longer
How does phenytoin influence aspirin, warfarin and amiodarone concentration
- Amiodarone – increased risk of peripheral neuropathy and increased levels of phenytoin. Decrease levels of amiodarone as there would be increased metabolism
- Aspirin – may displace phenytoin from plasma protein binding and thus increase levels of phenytoin
- Warfarin – Phenytoin increases levels of isozyme of p450 and thus this would lead to increased metabolism of phenytoin
What is cavulanic acid
Beta lactamase inhibitor
If patient is allergic to penicillin what 2 other drugs cant be given
Cephalasorins
Carbapenems
Effect of physostigmine on cholinoceptor agonist
Physostigmine: Curve would shift left and possibly down. The curve would shift left as physostigmine is a reversible anticholinesterase. As a result, by blocking acetylcholinesterase, it would cause less methacholine to be broken down, leading to a smaller concentration having a greater effect, causing the curve to shift to the left. However, the peak of the curve may be lower and by the muscarinic receptor constantly being opened, it would lead to a depolarising block forming, therefore leading to no more tissue response, and as a result, the maximum tissue response being lower
Effect of atropine on cholinoceptor agonist
Curve would shift to the right but remain at the same height. Atropine is a muscarinic receptor antagonist. This would mean that it would compete with the methacholine for the muscarinic receptor, causing the curve to shift to the right. However, by increasing the concentration of methacholine, it would outcompete the atropine for the binding site of the muscarinic receptor. As a result, the maximum tissue response would be reached but a greater concentration of methacholine would be required
Why would brain receive more General Anaesthetic than adipose tissue
Brain recieves much more CO
Why is heroin a stronger analgesiac than morphine
Heroin (Diacetylmorphine) – has 2 added acetyl groups, replacing the hydroxyl groups. As a result, it is more lipophilic leading to it entering the brain more. As a result, it would have a greater action within the brain due to more accumulating within the brain, thus leading to a stronger analgesic effect
When does GnRH release begin
8
3 stages to birth
- Dilation Phase – cervix undergoes effacement and widening with fundally dominant contractions of the myometrium
- Expulsion Phase – birth of the child
- Placental phase – where placenta is delivered within 30min of the expulsion
Where do contractions begin and end
Fundally dominant, starting from the fundus and ending at the cervix