How do NSAIDS have an analgesic effect?
Decreased prostaglandin synthesis (e.g. bradykinin)
How do NSAIDS have an anti-inflammatory effect?
Decrease in prostaglandin E2 and prostacyclin (PGI2)
- Via COX2 inhibition
How do NSAIDS have an anti-pyretic effect?
Prevent IL-1 releasing prostaglandins in the CNS
Normally these prostaglandins elevate the hypothalamic temp set point
Name 4 SE’s of alpha-adrenoreceptor antagonists?
Dizziness, postural hypotension, dry mouth, depression
Furosemide (I,M,SE)
I: Diuretic (AntihyperT + oedema)
M: Blocks Na/K/2Cl reabsorbtion in ascending loop of Henle
SE: Dehydration, electrolyte imbalance, meta alkalosis
Which types of diuretic are best used in patients with:
a) Impaired renal function
b) Preserved renal function
a) Loop (Furosemide, butnetanide, torasemide)
b) Thiazide (Chlorthalidone, bendrofulamethiazide, indapamide)
Name two potassium sparing diuretics?
Amiloride and Eplerenone
Bendrofluamethiazide (I,M,SE)
X-thiazide
I: Thiazide diuretic (HyperT and odema)
M: Blocks Na/Cl symporter in DCT (increased Na secretion)
SE: Hypokalaemia, postural hypotension, gout
Asprin (I,M,SE)
I: Antiplatlet, antipyrexic, antiinflam, analgesic
M: Blocks thromboxane A2, cox-1 (irreversable) and cox-2
SE: GI ulcers, bleeds
Name 4 NSAIDS and 3 NSAID SE’s
Ibuprofen, naproxen, diclofenac, asprin
SE: GI ulcers, bleeds, impaired clotting, affects renal blood flow
Against which type of bacteria would penicillin be most effective, what is it’s MoA?
Gram +ve
Inhibits peptidoglycan so bacteria can’t make a cell wall
Name 3 side effects of steroids?
Inhibtion of bone formation, decreased Ca absorbtion and decreased wound healing
Prazosin (I,M,SE)
I: Anti-hypertensive + for BPH
M: Alpha1-adrenoceptor antagonist
SE: Dizziness, postural hyperT,
Doxazosin (I,M,SE)
I: Anti-hypertensive + for BPH
M: Alpha1-adrenoceptor antagonist
SE: Dizziness, postural hyperT,
Atropine (I,M)
I: Depress PNS (Bradycardia, Pupil dilation, hyperhidrosis)
M: Muscarinic acetylcholine receptor antagonist
Loperamide (I, M)
I: Control and relief of diarrhea (Gastroenteritis + IBD)
M: Acts on opoid receptors to slow peristalsis (but does not cross brain so no analgesic)
Ipatropium (I,M)
I: Bronchodilator
M: Blocks acetylcholine receptor action (blocks muscarinic receptors)
= Bronchodilation and less mucus secretion
Omeprazole (I,M,SE)
I: Ulcers, reflux, heartburn etc
M: PPI (inhibits gastric acid secretion by inhibiting H+/K= ATPase enzyme on parietal cells
SE: Stomach pain, gas
Cimetidine (I,M,SE)
I: Ulcers, reflux, indigestion, heartburn
M: Histamine H2 receptor competitive antagonist- On basolateral parietal cell, reducing stim to secrete gastric acid
SE: Tiredness, gynecomastia
Gaviscon (I,M,SE)
OTC
I: Heartburn and GERD
M:Uses aluminum hydroxide and magnesium carbonate as antacids
SE: Constipation or diarrhea
Pepto-bismol (I,M,SE)
OTC
I: Heartburn, indigestion, nausea, diarrhea
M: Contains bismuth subsalicylate (it’s antacid and bactericidal)
SE: Black tongue/ stools
Pancreatin (contents)
Enzyme mixed from porcine/bovince pancreas
Contains amylase, lipase and a protease (trypsin)
SE: Diarrhea, skin rash, nausea, stomach pain
Which opposing side effects are seen in aluminium and magnesium hydroxides?
AlOH: Constipation
MgOH: Diarrhea
Fluorouracil (5-FU) - I,M
I: Chemotherapy treatmennt
M: Masquerades as a pyrimidine, stopping the cell getting through S phase of cell division so blocks conversion of cytosine and stops incorporation of thymidine into the DNA strand
Leucovorin (I,M)
I: Antidote to folic acid antagonist chemotherapy (i.e methotrexate)
M: Is a folic acid derivative so provides the needed folate
It also enhances the effect of fluorouracil
Peginterferon alfa-2a (I,M)
I: Chemotherapy treatment
M: Bind to interferon receptors which upregulate MHC proteins on the cell surface allowing them to be targeted by CD8+ cells
Methotrexate (I,M)
I: Chemotherapy agent
M: Inhibits folic acid reductase (so inhibits DNA synthesis)
Name 7 side effects of methotrexate chemo:
Low blood counts, mouth sores, N+V, poor appetite, kidney toxicity, skin rash, diarrhoea, hair loss
Propylthiouracil (I, M, SE)
I: Hyperthyroidism (incl graves)
M: (central) Inhibits thyroperoxidase enzyme (iodide to iodine) and (peripheral) inhibits 5’ diodinase (converts T4 to T3)
SE: Skin rash/ hair loss/ itch
Rare: Agranulocytosis/ liver failure
What is carbimazole and how does it act?
It’s a pro-drug
Converted to methimazole
Methimazole (I,M,SE)
And its pro-drug carbimazole
I: Hyperthyroidism
M: Inhibits thyroperoxidase (Iodide to iodine)
SE: Skin rash/ itch/ hair loss
Rare: Agranulocytosis
Propanolol (I.M,SE)
I: Antihypertensive/ Angina/ Thyrotoxicosis
M: Bind to B1-adrenoreceptors in the heart, inhibiting sympathetic action (reduce rate/ force)
SE: Fatigue/ cold hands and feet/ disturbed sleep
Name a drug which primary acts on the heart which can be used to treat thyrotoxicosis:
Propanolol
Reduces tachycardia symptoms but also:
Inhibits 5’-monodeiodinase which converts T4 to T3
(So also lowers active T3 levels)
Levothyroxine (I, M, SE)
I: Hypothyroidism
M: Levothyroxine acts like the endogenous thyroid hormone thyroxine (T4)
SE: Many but rare
What are common SE’s of NSAIDS?
Gastric irritation, skin rashes, lowers renal blood flow, prolonged bleeding, and increased risk of thrombotic events (MI/Stroke)
What is the MOA of NSAIDS?
Inhibition of arachidonic acid oxidation by COX enzymes
Most antacids are salts of magnesium or aluminium. Which SE’s relating to motility are caused by each of these?
Magnesium hydroxides: Diarrhoea
Aluminum hydroxides: Constipation
A single dose of omeprazole will affect gastric acid for roughly how long?
2-3 days as it accumulates in the canaliculi and inhibits H+/K+ ATPase irreversibly
What are alginates used for?
Alginates are added to help protect the lining of the gullet (oesophagus) from stomach acid. Alginates include sodium alginate and alginic acid.
When is radioactive iodine used?
Thyroid is the only part of the body to uptake large amounts of Iodide (apart from the kidneys). Sodium Iodide (I131) can be used to target the cells of the thyroid gland and reduce it’s size without severely affecting other organs.
Metformin (I,M,SE)
I: T2DM (lowers blood glucose)
M: Activates AMP-activated protein kinase (AMPK), a liver and muscle enzyme. AMPK causes GLUT-4 translocation to the cell membrane
SE: Lactic acidosis
Sitagliptin (I, M, SE)
and all X-gliptin
I: T2DM (increase insulin secretion)
M: Inhibits DPP-4 enzyme which degrades incretins such as GLP-1
SE: Hypoglycemia in OD
Exenatide (I,M)
and all X-tide
I: T2DM (increase insulin secretion)
M: Acts as functional analog of GLP-1 so increases insulin levels
Dapagliflozin (I,M, SE)
and all X-gliflozin
I: T2DM
M: Inhibits SGLT2 so blocks Na/glu cotransporter re-absorption in prox tubule
SE: UTI risk
Gliclazide (I,M,SE)
and all X-azide/ X-amide
I: T2DM
M: Binds to ATP dependent K+ channel on pancreatic Bcells to inhibit depolarization and thus insulin granule secretion
SE: Hypoglycaemia/ weight gain
Alfa-interferon (I, M, SE)
I: Anti-viral (hep C, leukaemia)
M: Interferon alpha binds to T1 interferon receptors which upregulates MHC1 proteins so increased likelihood of immune destruction
SE: Flu like symptx/ fatigue
Mannitol (I, M)
I: Hypertension/ oedema
M: Increases osmolarity of filtrate in kidney, preventing water re-absorption, sucks fluid from tissue as raises blood osmolarity
Spironolactone (I,M)
I: Low renin hypertension and hypokalaemia
M: Antagonises aldosterone so increases water/ Na+secretion and decreases K+ secretion
Bevacizumab, ranbizumab (I, M)
I: Inhibits VEGF-A (treat cancers)
M: Binds with VEGF to prevent interaction with it’s receptors, prevents growth of new BV’s
How can thiazide diuretics cause gout?
Cause increased urea retension and therefore increased levels of uric acid (can lead to gout)
What is cholestyramine used for?
Binding bile salts to prevent reabsorption in terminal ileum
Used for itching in obstructive jaundice