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10 Cards in this Set
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What is alendronate, how does it work and what are its SE and uses |
Biphosphonate/antiresorptive agent
Analogues of endogenous pyrophosphate, they are concentrated in bone (bind to calcium) and are incorporated into mineralized hydroxyapatite matrix → ingested into osteoclasts when they try to resorb bone tissue They then inhibit an enzyme in the cholesterol synthesis pathway, and therefore damage osteoclasts (in particular establishment of a proper cell membrane and cytoskeleton), and thus encourage osteoclast apoptosis, thus inhibiting bone digestion and slowing bone loss.
SE: Rare osteonecrosis of jaw, rare atypical fractures. Can cause upper GI irritation (stomach pain)/ulceration – Thus take 30 min before food on anempty stomach, with water only, swallow tablet whole, take separately from other meds, remain upright for 30 min – 1 hour after dose. Newer preparations IV can minimize GIT effects, however have serious renal effects
Used in Paget's disease or those with previous fractures (when taken for 3-4 years)
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why is hormone replacement therapy used in osteoporosis and what are its SE |
Oestrogen inhibits bone loss: Stimulates osteoclast apoptosis- ↑OPG to act as decoy receptor for RANKL and thus to ↓osteoclastic differentiation and thus ↑BMD
Good for postmenopausal women.
SIDE EFFECTS OF HRT: ↑risk of cancers (i.e. breast cancer if oestrogen dependent), ↑risk of adverse CVS events (stoke, CHD, VTE).
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What is denosumab, what is it used for, how does it work |
A monoclonal antibody that mimics OPG and inhibitsRANKL, thus ↓osteoclastic differentiation that is induced by osteoblasts. Osteoporosis |
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What is calcitriol, how does it work and SE |
A naturally occurring hormone ↑Calcium and PhosphateGIT absorption, ↑Ca mobilization from bone to a small degree, small effect to↑Ca/P reabsorption in kidney. SE: monitor for riskof hypercalcaemia → bones, moans, stones, abdo groans, polyuria – bemindful of these risks especially if pt is on calcium supplements. |
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What is metformin, how does it work and what are its SE |
Insulin sensitiser MOA: acts on liver to cause decrease ininsulin resistance - ↓hepaticglucose output, ↑peripheral/muscle/fat glucose uptake.↓LDL, ↓TAG SE: No weight gain (weightloss), unlikelyto cause hypoglycaemia. GIT (diarrhoea, dyspepsia, nausea),kidney disease (risk of lactic acidosis – malaise, myalgia)/ heart failure, metallic taste.↑risk of lactic acidosis if undergoing radiograph with iodinated contrast |
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What is Gliclazide, how does it work and what are its SE |
Secretagogues (sulphonylurea 2nd gen) Inhibit ATP sensitive K channels inbeta cells → cell depolarization → calcium influx → insulin exocytosis.Less GIT effects, no BP/LDL effects,inexpensive. SE: Weight gain. Hypoglycaemia (mild episodes in 2-4% ofpatients/year). Dont use with short-acting secretagogue - similar MOA and exacerbated SE |
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What is repaglinide, how does it work and what are its SE |
Nonsulfonylureainsulin secretagogues: Same MOA, cause more rapid insulin secretion,have a greater effect on postprandial glucose. SE: Weight gain, hypoglycaemia. |
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What are Acarbose, miglitol, how do they work and what are SE |
α-glucosidase Saccharides that act as competitive inhibitors of enzymes that digest carbohydrates (a-glucosidase in brushborder of small intestine). Thus, they reduce the rate of digestion of carbohydrates → less glucose absorbed.↓TAG, no effect on cholesterol.
SE: Symptoms of lactose intolerance due to breakdown by bacteria in LI - flatulence, bloating (not used so much due to these). No weight gain.Expensive.
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What is Pioglitazone, how does it work and what are its SE |
Insulin sensitiser:
Activate PPAR-gamma (peroxisome proliferator-activated receptor-gamma), a nuclear receptor in adipose tissue, which stimulates lipid/glucose uptake and lipogenesis in fat/muscle/liver cells, thus lowering serum glucose – better glucose utilization and uptake in liver/muscle/ peripheral tissues. Also decreases glucose withdrawal from liver↑HDL.
SE: Weight gain. Lower risk of hypoglycaemia. ↑risk of HF/cardiac events by virtue of ↑fluid retention and ↑ oedema, aneamia, hepatotoxicity, bone fractures. Expensive.
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What are Gliptins, how do they work and what are SE |
Incretins are released by the intestine as endogenous insulin secretagogues (GLP-1, GIP) released to ↑insulin release, ↓glucagon release. Both are rapidly inactivated by DPP-4 (dipeptidylpeptidase-4). Gliptins - These drugs bind to, and inhibit, DPP-4 to increase plasma concentrations of GLP-1 by preventing it’s degradation. Exanetide – GLP-1 synthetic analogue (secretagogue). Requires parenteral administration. Derived from saliva of gila monster
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