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pharmacology osce


Thiazide diuretics - inhibits Na/Cl transporter in the distal convulted tubule(kidney) - less Na/Cl resorption = less water reabsorption - reduces Blood pressure SE: Potassium loss - use with angiotensin receptor blockers
Calcium channel blockers - antihypertensive - VERAPAMIL - By acting on vascular smooth muscle, they reduce contraction of the arteries and cause an increase in arterial diameter, a phenomenon called vasodilation - have no effects on HR so used on angina patients
Angiotensin 2 receptor blockers - SARTANs ( avapro ) -Antihypertensive - blocks the ang2 receptor, blocking ang2 from binding - ang2 is a vasoconstricter therefore blocking causes vessel dilation -SE: hyperkalemia: use with a thiazide diuretic
Beta blockers -LOLs -antihypertensive - bind to beta cell receptors, stop epinephrine from binding (adrenaline) Blocking epinephrine decreases heart contracts + force - therefore reduces blood pressure. SE: erectile dysfunction, insomnia / nightmares
Protein pump inhibitor -ZOLES -reflux medication - reduces stomach acid production - inhibits the hydrogen/potassium ATP enzyme - proton pump is at the terminal stage of stomach acid production SE: increase risk of fractures as it has vitamin b-12 problems > neurop aetiol
Warfarin -anticoagulant - inhibits vitamin k reductase, vit k is an activator of coagulating factors SE: hemorrhage, tissue necrosis, GI effects
GABA analogue -Anti-convulsant / nerve pain (LYRICA) - re balances neurotransmitters by: reducing substance P + glutamate levels and restores the release of noreipinephrine ( neurotransmitter ) SE: loss of balance ( falls risk), blurred vision
methotrexate - immunosuppresent -ra / cancer - inhibits tetrahydrolate which is necessary to create DNA SE: infection risks
Antibiotics -bacterial infections - the 3 x inhibits + 2 modifications SE: gut floral effects > nutrition / resistance to ABs
Salbutamol Asthma / b2- agonist - BRONCHODILATOR - stimulates cells to bronchodilate + decreases mast cell degrenulation SE: anxiety / muscle cramps / headache
Colchicine Anti-gout agent / acute attacks - doesn't lower uric acid however works to block inflammation caused by urc acids (12-24hrs) - quite toxic , dont use with liver problems - aspirin can worsen gout
Allopurinol Anti-gout agent / long term use - inhibits xanthine oxidase which is responcible for uric acid production - itchiness / rash
Statins -DISLIPEDEMIA / used for High cholestrol - Statins are similar structure to HMG-COA reductase, competitively bind for binding site. - Stops the production of mevlonate which is key in the production of cholestrol SE: myalgia>rhabdomyolysis>kidney fai
Aspirin -Anti-platelet - weak inhibitor of platelet aggregation - indirect thromboxane inhibitor + inhibits the platelet cox-1 enzyme SE: excess bleeding
acetaminophen -Analgesic PARACETAMOL - mechanism isn't understood / selectively inhibits the COX enzyme in the brain SE: dark urine / coloured stools /nausea
Opiate CODENE analgesic / pain releif - binds to piod receptors in the brain which are necessary for pain transmission - respiratory depretion / sedation / vomitting
ace inhibitors -antihypertensive PRILs - inhibits the angiotensin converting enzyme. ang1>2 ( vasoconstrictor) - vasodilation > r educed sat / water retention - SE cough / headache / back pain
biguanside - metformine - 1st line of treatment t2dm - requires insulin - increases insulin sensitivity - decreaes hepatic glucose prod / GI absorption of glucose / LDL - No risk of weight gain / hypoglycaemia SE: gi effects
sulphonylureus T2DM - GLICAZIDE - stimulates beta cells to release insulin - binds to solfonylurea receptors on pacreatic beta cells, the binding causes closure of potassium channels > depolorisation > creation of insulin -SE weight gain / risk of hypoglycaemia
NSAIDs - analgesic - inhibits cox-1 /2 which are involved in inflammation -SE: GI ulcers / bleeding - use acetimnophen (paracetemol) where possible, less side effects
Humira TNF alpha antagonist used for arthritis
corticosteroids -prendnisolone / cortisone -Bonds to glucocorticoid receptor incide cell nucleus, which then inhibits transcription on inflammatory genes.
Created by: lolcasaaaa22