module 4 drugs Flashcards
1
Q
pramlinitide
A
- amylin analog
- delays gastric emptying
- lets T2D reduce their insulin dose
2
Q
octreotide
A
- somatostatin analog
- used to treat hyperglycemia or insulin-secreting tumors
- will decrease amount of insulin released
3
Q
glibenclamide, glipizide, glimiperide
A
-secretagogue: sulfonylureas
- inhibit the K-ATP channels on beta cells in pancreas, depolarizing the cell, Ca2+ comes in, causing release of insulin
- cause hypoglycemia
4
Q
Repaglinide, Nateglinide
A
-secretagogue: Meglinitides
- structurally different than sulfonylureas, but they also bind and inhibit K-ATP channels, causing insulin release
- rapidly absorbed and cleared, requires multiple daily doses, but also lower risk for hypoglycemia
5
Q
exenatide, liraglutide
A
-secretagogue: GLP-1 receptor agonists (incretin mimetic)
- they act like the gut hormones and potentiate glucose-dependent secretion of insulin
- side effect: acute pancreatitis
6
Q
Gliptins
A
-secretagogue: DPP-4 inhibitors (incretin mimetics)
- inhibit DPP4 which breaks down the incretins
- potentiate glucose-dependent secretion of insulin by potentiating endogenous incretins
- possible pre-cancerous changes in the pancreas?
7
Q
Metformin
A
Sensitizer: Biguanide
- lowers blood glucose by decreasing hepatic glucose output and sensitizing peripheral tissues to insulin.
- increases glucose uptake and utilization in skeletal muscle
- does not cause hypoglycemia because insulin secretion is not altered
8
Q
Pioglitazone, Rosiglitazone
A
-Sensitizers: the glitazones (aka TZDs)
- bind to nuclear receptors and alter transcription of genes that enhance function of insulin receptors and signaling (like Glut-4)
- slow onset (1-2 months)
- used in combination w sulfonylureas, metformin, or insulin
9
Q
Acarbose, Miglitol
A
- alpha glucosidase inhibitors
- MOA: inhibit the alpha-glucosidase enzymes that line the brush border of the s.i., interfering with the hydrolysis of carbohydrates and delaying absorption of glucose
- only lower AIC by 0.5%-1.0%
- drug taken w each meal to lower post-prandial glucose concentrations
10
Q
Canagliflozin, Dapagliflozin
A
-Sodium glucose co-transporter 2 (SGLT-2) inhibitors
- SGLT2 is a membrane protein in kidney that transports glucose from proximal tubule into tubular epithelial cells
- SGLT2 inhibitors decrease renal glucose reabsorption and increase urinary glucose excretion
- weight loss drug
11
Q
pramlinitide
A
- amylin analog
- delays gastric emptying
- lets T2D reduce their insulin dose
12
Q
colesevelam
A
a bile-acid sequestrant used to lower LDL cholesterol
13
Q
Bromocriptine
A
DA agonist
- modestly effective at decreasing blood glucose levels in T2DM
- safer cardiovasvular profile
14
Q
Orlistat
A
- pancreatic and gastric lipase inhibitor that decreases fat absorption
- SI: flatulance with discharge, oily spotting, fecal urgency
- ~ 3 kg loss
15
Q
Lorcaserin
A
- 5-HT- 2C agonist
- works on the POMC neurons –> they release alpha MSH, signals to satiety center = more full
- SI: cardiac valvulopathy, serotonin syndrome
- ~ 3 kg loss
16
Q
Liraglutide
A
insulin secretagogue… GLP1 agonist
- decreases gastric emptying
loss: 5.8 kg
17
Q
Benzphetamine, Diethylpropion, Phentermine, Phendimetrazine, QYSMIA
A
sympathomimetic amines
- reduce appetite by eliciting norepinephrine release, and by modulating other catecholamine systems
18
Q
off label treatments
A
antidepressants, antiepileptics, antihyperglycemics
19
Q
Zonisamide
A
antiepileptic drug
3.3 kg loss
zonisamide + olanzapine prevented weight gain normally seen with olanzapine
20
Q
anti-hyperglycemics
A
exenatide- GLP1 agonist. stimulates glucose dependent insulin secretion. ~ 4 kg weight loss seen.
metformin- biguanide. modest but sustained weight loss
pramlinitide- weight loss bc delays gastric emptying
SGLT2 inhibitors- pee out the glucose
21
Q
Statins
A
- specific, reversible, Hmg-CoA reductase inhibitors
- prevent synthesis of cholesterol
- increase expression of LDL receptors, increasing uptake of LDL
- longer acting : Atoravastatin, Rosuvastatin
22
Q
ciprofibrate, gemfibrozil, etc
A
Fibrates (fibric acid derivatives)
- influence transcription of genes beneficial to prevent atherosclerosis
- fibrates bind PPAR alpha –> activated PPAR/RXR complex –> PPAR response elements =
- decrease VLDL, decrease TG, decrease inflammation
- increase LDL size, increase HDL synthesis, increase reverse cholesterol transport
23
Q
Colestyramine, colestipol, colesevelam
A
bile acid sequestrants (resins)
- bind to bile acids with cholesterol and cholesterol gets excreted
- decreased LDL levels
24
Q
Ezetimibe
A
(fancier version of a resin)
- impairs dietary and biliary cholesterol absorption at brush border without affecting fat-soluble vitamins)
- reducing the pool of cholesterol absorbed from diet –> less cholesterol available to the liver
- upregulate LDL receptor, so LDL levels in the blood decrease
25
Vytorin
ezetimibe/ simvastatin
| dual inhibitory effect
26
nicotinic acid
Niacin (vitamin)
- used in gram quantities
- converts itself to nicotinamide, which inhibits hepatic VLDL secretion = reducing LDLs and TGs
27
Fish oil derivatives
long chain omega 3 fatty acids (PUFA) (second line therapy)
- inhibition of HSL and VLDL secretion
- increase LPL activity, decrease TGs
28
Alirocumab, Evolocumab
- PCSK9 inhibitors
| prevent degradation of LDL receptors
29
anti-platelets
- COX inhibitors
- PDE inhibitors
- ADP inhibitors
- GpIIa-IIIb antagonists
- thrombin receptor antagonists
30
aspirin
- COX inhibitor
- aspirin inhibits the synthesis of prostaglandins, inhibiting the platelet granule release reaction- interfering with normal platelet aggregation
- used to prevent thrombosis
- used in low/ intermittent doses
- NSAIDs covalently acetylate a serine residue on COX enzyme near the active site --> blocking effects of TxA2
31
Dipydramole
- PDE inhibitor
| - blocks the reuptake of adenosine... increases cAMP... decreasing platelet aggregability
32
"The Grels" ... Clopidogrel, prasugrel, ticagrelor, annnnd (Ticlopidine)
P2Y-12 ADP receptor inhibitors
- P2Y receptors are Gi coupled --> decrease cAMP
- we want to antagonize them bc we want to increase cAMP to decrease platelet aggregability
- another why: ADP receptors mediate platelet shape change and expression of functional GpIIb-IIIa... we dont want that
33
Abciximab, eptifibatide, tirofiban
GpIIb-IIIa antagonists
| - stops the crosslinking of platelets... they prevent fibrinogen binding to the GpIIb-III1 receptor
34
Voraxapar
thrombin receptor antagonist (PAR1 selective)
| - inhibits thrombin's ability to excise the N-terminus thats silencing platelet aggregation
35
Warfarin
- warfarin inhibits epoxide reductase, preventing vitamin K from being in its reduced, active form.
- vitamin K is required for 4 coagulation factors: II, VIII, IX, and X, as well as proteins C and protein S
- oral drug, 100% bioavailable, 36 hr half life
36
drugs that diminish warfarin's anticoagulant effect
- colestyramine
- vitamin K (reduced, active form)
- barbiturates, carbamazapine, phenytoin, rifampin
- these drugs would decrease the INR
37
drugs that enhance warfarin's anticoagulant effect
- antifungals
- antibiotics
- ethanol
- steroids, testosterone
- chloral hydrate
- amiadarone
- clopidogrel
- these drugs would increase the INR
38
Heparins
- lets the anti-thrombin III reaction happen (speeds it up by 1000x)
- highly negative charge- making it a sticky molecule
39
unfractionated heparins
- can bind simultaneously to thrombin and anti-thrombin III, inactivating both thrombin and Factor Xa by anti-thrombin III
- monitoring with aPTT: activated partial thromboplastin time (tests the intrinsic & common pathways)
40
low molecular weight heparins
can inactivate Factor Xa
is ehhhh at inactivating thrombin
- the parns/ parins
41
rivaroxaban, apixaban, edoxaban
- direct factor 10 inhibitors
42
direct thrombin inhibitors
- derived from medicinal leech protein hirudin
43
tissue plasminogen activator
- t-PA is a serine protease produced by intact endothelial cells, therefore not antigenic
- t-PA binds to thrombus/ clot with high affinity, undergoes conformational change making it a plasminogen activator, causing fibrinolysis
