Step 1 Drugs #1

Front 1

Drugs that provide oxidative stress

Back 1

Sulfonamides
Primaquine
Isoniazid (Anti-TB)

High dose ASA
Ibuprofen
Nitrofurantoin
Dapsone
Napthalene

Hint 1

Would exacerbate G6PDH deficiency.

Front 2

Which drugs are used to shrink prolactinomas?

Back 2

DA agonists (bromocriptine, cabergoline)

Front 3

Name class, action, clinical use, and toxicity:

Lispro insulin

Back 3

Class: Insulin, rapid-acting
Action: binds insulin receptor (tyrosine kinase). Liver - increases glucose stored as glycogen; muscle - increases glycogen and ptn synthesis, potassium uptake; fat: aids TG storage

Use: DM1, DM2, gestational diabetes, life-threatening hyperkalemia and stress-induced hyperglycemia.

Toxicities:
1. hypoglycemia, rarely hypersensitivity
2. lipodystrophy (injection sites)
3. weight gain

Hint 3

rapid-acting

Front 4

Name class, action, clinical use, and toxicity:

Aspart insulin

Back 4

Class: Insulin, rapid-acting
Action: Binds insulin receptor (tyrosine kinase)
Liver: increases glycogen stores
Muscle: increases glycogen stores and ptn synthesis, potassium uptake.
Fat: Aids TG storage

Clinical use: DM1, DM2, gestational diabetes, life-threatening hyperkalemia, stress-induced hyperglycemia.

Toxicities:
1. hypoglycemia, rarely hypersensitivity
2. lipodystrophy @ injection site
3. weight gain

Hint 4

rapid-acting

Front 5

Name class, action, clinical use, and toxicity:

Glulisine insulin

Back 5

Class: Insulin, rapid-acting

Action: Binds to insulin receptor (tyrosine kinase)
Liver: increased glycogen stores
Muscle: increased glycogen and ptn synthesis, potassium uptake
Fat: Aids TG storage

Use: DM1, DM2, gestational diabetes, life-threatening hyperkalemia, stress-induced hyperglycemia

Toxicities:
1. hypoglycemia, perhaps hypersensitivity
2. lipodystrophy @ injection site
3. weight gain

Hint 5

rapid acting

Front 6

Name class, action, clinical use, and toxicity:

Regular insulin

Back 6

Class: Insulin, short-acting

Action: Binds insulin receptor (tyrosine kinase)
Liver: increases glycogen stores
Muscle: increases glycogen/ptn synthesis, potassium uptake
Fat: aids TG synthesis

Use: DM1 DM2, gestational diabetes, life threatening hyperkalemia, stress-induced hyperglycemia

Toxicity:
1. hypoglycemia, hypersensitivity (rarely)
2. lipodystrophy
3. weight gain

Hint 6

short-acting

Front 7

Name class, action, clinical use, and toxicity:

NPH insulin

Back 7

Class: insulin, intermediate acting

Action: binds insulin receptors (tyrosine kinase)
Liver: increases glycogen stores
Muscle: increases glycogen stores, ptn synthesis, potassium uptake
Fat: aids TG synthesis

Clinical use: DM1, DM2, gestational diabetes, life-threatening hyperkalemia, stress-induced hyperglycemia

Toxicity: hypoglycemia, lipodystrophy, weight gain, rarely hypersensitivity

Hint 7

intermediate acting

Front 8

Name class, action, clinical use, and toxicity:

Glargine insulin

Back 8

Class: insulin, long-acting

Action: binds insulin receptor, tyrosine kinase
Liver: increases glycogen synthesis/storage
Muscle: increases glycogen synthesis/ptn synthesis
Fat: aids TG storage

Toxicity: hypoglycemia, lipodystrophy, weight gain, rarely hypersensitivity

Hint 8

long-acting

Front 9

Name class, action, clinical use, and toxicity:

Detemir insulin

Back 9

Class: Insulin, long-acting

Action: binds insulin receptor, tyrosine kinase
Liver: increases glycogen synthesis/storage
Muscle: increased glycogen synthesis/ptn synthesis, increased potassium uptake
Fat: aids TG storage

Toxicity: hypoglycemia, lipodystrophy, weight gain, rarely hypersensitivity

Hint 9

long-acting

Front 10

Name class, action, clinical use, and toxicity:

Metformin

Back 10

Class: Biguanides

Action: unknown. BUT:
decreases gluconeogenesis
increases glycolysis
increases peripheral glucose uptake (insulin sensitivity)

Clinical Use: PO, FIRST LINE for DM2. Can be used in pts w/o islet function.

Toxicity: GI UPSET
LACTIC ACIDOSIS (most serious adverse effect) - so C/I in renal failure, C/I CT angiograms (decreases renal function)
C/I in liver failure or CHF.

Benefits: weight neutral, decreases LDL, decreases cholesterol a bit

Front 11

Name class, action, clinical use, and toxicity:

Tolbutamide

Back 11

Class: Sulfonylureas, First gen
Closes K+ channel in beta-cell membrane, so cell depolarizes.
Opens voltage-gated Ca2+ channels.
Calcium influx triggers release of insulin.

Insulin-secretagog.

Clinical use: Stimulate the release of endogenous insulin in DM2, requires SOME islet cell functioning. C/I in DM1.

Toxicity: Disulfuram-like fx, HYPOGLYCEMIA. (first gen). second gen hypoglycemia only.

Hint 11

like MOA of amantadine (increase DA release in cells not yet dead for PD)

Front 12

Name class, action, clinical use, and toxicity:

Chlorpropamide

Back 12

Class: Sulfonylurea, First generation

Action: Closes K+ channel on pancreatic islet beta cell.
Cell depolarizes.
Voltage-sensitive Ca2+ channels open.
Insulin is released with Ca2+ influx.

Clinical use: Stimulate release of endogenous insulin in DM2. C/I in DM1. Requires some islet cell functioning.

Toxicity: (first gen) Disulfuram-like reaction, HYPOGLYCEMIA.
(second-gen) - HYPOGLYCEMIA only.

Hint 12

Like Amantadine's MOA for PD (DA release from cells not yet dead).

Front 13

Name class, action, clinical use, and toxicity:

Glyburide

Back 13

Class: Sulfonylurea, Second generation

Action: Closes K+ channels in pancreatic islet beta cell membrane.
Cell depolarizes.
Voltage-gated Ca2+ channels open.
Calcium influx triggers insulin release.

Clinical use: Stimulate endogenous insulin release from beta cells in DM2. C/I in DM1. Requires some beta cell functioning.

Toxicity: (second gen) hypoglycemia. (first gen - disulfuram-like reaction, hypoglycemia).

Hint 13

Like Amantadine's MOA for DA release in PD.

Front 14

Name class, action, clinical use, and toxicity:

Glimepiride

Back 14

Class: Sulfonylurea, Second generation

Action: Opens K+ channels on pancreatic islet beta cell membrane.
Depolarizes cell.
Voltage-gated Ca2+ channels open.
Calcium influx triggers insulin release.

Clinical use: stimulates endogenous insulin release in DM2. Requires some islet cell functioning. C/I in DM1.

Toxicity: (second gen) - hypoglycemia. (first gen - disulfuram-like reaction, hypoglycemia).

Hint 14

MOA like amantadine for PD, same way it releases DA

Front 15

Name class, action, clinical use, and toxicity:

Glipizide

Back 15

Class: Sulfonylurea, Second gen

Action: Opens K+ channels on pancreatic islet beta cell membrane.
Depolarizes cell..
Voltage-gated Ca2+ channels open.
Influx of Ca2+ triggers insulin release.

Clinical use: Stimulates endogenous insulin release in DM2, requires some islet cell functioning. C/I in DM1.

Toxicity: (second gen) hypoglycemia. (first gen - disulfuram like reaction, hypoglycemia)

Hint 15

MOA same as amantadine for PD, releases DA

Front 16

Name class, action, clinical use, and toxicity:

Pioglitazone

Back 16

Class: TZD/glitazones (thiazolidinediones)

Action: Increases insulin sensitivity in peripheral tissue.
Binds PPAR-GAMMA nuclear transcription regulator. Regulates FA storage/glucose metabolism.
On adipose, skeletal muscle, liver.

Clinical use: MONOTHERAPY in DM2 OR combined with sulfonylureas, biguanides, or insulin.

Toxicity: weight gain, edema, hepatotoxicity (metabolized by liver), heart failure.
C/I in pts with CHF (increased fluid)
OKAY in pts with renal failure.

***Rosiglitazone increases risk of MI.

Front 17

Name class, action, clinical use, and toxicity:

Rosiglitazone

Back 17

Class: TZD/glitazones (thiazolidinediones)

Action: increases insulin sensitivity in peripheral tissues. binds PPAR-GAMMA nuclear transcription factor (regulates FA storage/glucose metabolism). On adipose, skeletal muscle, liver.

Clinical use: Used as monotherapy for DM2 or in combination with sulfonylureas, biguanides, or insulin.

Toxicity: weight gain, hepatotoxicity (metabolized by liver), edema (C/I in heart failure), and heart failure.

ROSIGLITAZONE, particularly, increases risk of MI.

OK in pts with renal failure.

Front 18

Name class, action, clinical use, and toxicity:

Acarbose

Back 18

Class: alpha-glucosidase inhibitors

Action: Inhibit intestinal brush border alpha glucosidases (convert disaccharides --> glucose).
Delayed sugar hydrolysis and glucose absorption --> decreased postprandial hyperglycemia.

Clinical use: monotherapy for DM2 or in combination with sulfonylureas, biguanides, insulin, or glitazones.

Toxicity: GI disturbances (flatulence, diarrhea, abd pain, cramping.
C/I in Crohn's disease. C/I in pts with cirrhosis or elevated creatinine.

Hint 18

Not used much in US

Front 19

Name class, action, clinical use, and toxicity:

Miglitol

Back 19

Class: alpha-glucosidase inhibitor

Action: inhibits intestinal brush border alpha glucosidases (convert disaccharides to glucose).
Delayed sugar hydrolysis means less glucose uptake, which means less postprandial hyperglycemia.

Clinical use: Monotherapy for DM2, or in combination with insulin, biguanides, sulfonylureas, or TZD.

Toxicity: GI disturbances (flatulence, abd pain, diarrhea, cramping).

C/I in Crohns, cirrhosis or elevated creatinine.

Hint 19

Not used much in US

Front 20

Name class, action, clinical use, and toxicity:

Pramlintide

Back 20

Class: Amylin analogs

Action: decreases glucagon

Clinical use: DM1, DM2

Toxicity: hypoglycemia, Nausea, Diarrhea

Front 21

Name class, action, clinical use, and toxicity:

Exenatide

Back 21

Class: GLP-1 analogs

Action: increases insulin, decreased glucagon release
GLP-1 is secreted in response to CHO, ptn, and lipid in the gut. It's degraded instantly after the glucose levels drop. Anti-hyperglycemia incretin.

Clinical use: DM2

Toxicity: nausea, vomiting, PANCREATITIS

Front 22

Name class, action, clinical use, and toxicity:

Liraglutide

Back 22

Class: GLP-1 analogs

Action: Decreases glucagon, increases insulin
GLP-1 is secreted in response to CHO, ptn, and lipid. Degraded instantly after flucose levels are no longer elevated. Anti-hyperglycemia.

Clinical use: DM2

Toxicity: N/V, Pancreatitis

Front 23

Name class, action, clinical use, and toxicity:

Linagliptin

Back 23

Class: DPP-4 inhibitors

Action: increases insulin, decreases glucagon release (DPP-4 degrades incretins like GLP-1).

Clinical use: DM2

Toxicity: Mild urinary or respiratory infections

Front 24

Name class, action, clinical use, and toxicity:

Saxagliptin

Back 24

Class: DPP-4 inhibitors

Action: increases insulin, decreases glucagon.
DPP-4 degrades incretins like GLP-1

Clinical use: DM2

Toxicity: Mild urinary or respiratory infections

Front 25

Name the MOA of ASA related to clotting:

Back 25

Irreversibly inhibits COX, which prevents synthesis of TXA2. TXA2 is necessary for decreasing blood flow in vessels where the platelet plug formation has begun. It is released by platelets after they've bound GPIIb/IIIa and fibrinogen, and is released from its alpha granules.

Front 26

Name the MOA of ticlopidine and clopidogrel related to clotting:

Back 26

Both inhibit ADP-induced expression of GpIIb/IIIa by irreversibly blocking the ADP receptor on the platelet cell surface.

ADP is released from platelets' dense granules (along with Ca2+) to activate platelet cells.This is the signal needed to release GpIIb/IIIa inorder to bind more platelets.

Front 27

Name the MOA of abciximab:

Back 27

Inhibits GpIb/IIIa receptor directly, preventing interaction with fibrinogen, thus preventing linkage of platelets.

Front 28

Name the MOA of Warfarin, and its clinical use:

Back 28

Warfarin inhibits epoxide reductase. This is an enzyme required to reduce Vitamin K, thus acting as cofactor to make mature factors 2, 7,9,10, 11, and 12. This prevents clotting.

Front 29

Name the MOA of heparin, and its clinical use:

Back 29

Activates antithrombin, which inhibits factor II. This prevents factor II from maturing and activating fibrinogen to become fibrin monomers and aggregate.

Front 30

What is the clinical indication for cromolyn sodium?

Back 30

Asthma prophylaxis. It prevents mast cell degranulation.

Front 31

How do you reverse heparin OD?

Back 31

rapid reversal by protamine sulfate (positively charged molecule that binds negatively-charged heparin.

Front 32

How do you reverse warfarin OD?

Back 32

reversal by Vitam K administration.

Rapid reversal by fresh frozen plasma administration.

Front 33

What is HIT (heparin-induced thrombocytopenia) and how to you remedy it?

Back 33

HIT is the development of IgG antibodies against heparin bound to platelet factor 4 (PF4). Ab-Heparin-PF4 complex activates platelets --> thrombosis (hypercoagulable) and thrombocytopenia.

Rx: Stop heparin
Start different anticoagulant (e.g. direct thrombin inhibitor, like lepirudin, bivalirudin (deriv of hirudin) or dabagitran (newer). These are given IV.
Also start warfarin for long-term therapy outpatient (po admin).

Front 34

What is the MOA of enoxaparin and dalteparin for clotting?

Back 34

These are LMWH (low molecular weight heparins) which act more on factor 10a than thrombin, have longer 1/2 lives (2-4x longer), and better bioavailability. They can be admin subQ and without lab monitoring (like PTT for heparin) because the dose is weight dependant. Not easily reversible.

Front 35

What is the MOA of lepirudin, bivalirudin, and desirudin for clotting?

Back 35

These are derivatives of hirudin, the anticoagulant used by leeches. They directly inhibit thrombin. Used as alternative to treating HIT in pts treated with heparin.

Front 36

What is the MOA of argatroban and dabigatran?

Back 36

Inhibit thrombin directly, but are noit derivatives of hirudin like lepirudin, bivalirudin, and desirudin. Don't need INR monitoring.

Front 37

What is the reversal agent for the thrombolytics (such as streptokinase, urokinase, alteplase (tPA), reteplase (rPA), and tenecteplase (TNK-tPA)?

Back 37

Aminocaproic acid. Inhibits fibrinolysis.

Front 38

What is the MOA of tPA, streptokinase, rPA, or TNK-tPA?

Back 38

Directly or indirectly facilitate the conversion of plaminogen to plasin, which cleaves thrombin and fibrin clots. Increased PTT and PT, no change in platelet counts.

Front 39

Which drug is used to inhibit topoisomerase in prokaryotes?

Back 39

Fluoroquinolones.

Etoposide is the eurkaryotic equivalent.

Front 40

Which drug is used to inhibit topoisomerase in eukaryotes?

Back 40

Etoposide.

Fluoroquinolones are the prokaryotic equivalent.

Front 41

What is the MOA of etoposide and fluoroquinolones?

Back 41

Inhibitis eukaryotic and prokaryotic topoisomerase ENZ respectively.

Front 42

Action and clinical applications of Bethanechol?

Back 42

Action: Direct cholinomimetic agonist.
Activates bowel and bladder smooth muscle, resistant to AChE.

Clinical use: Postoperative ileus, neurogenic ileus, and urinary retention.

Hint 42

Bethany, call me maybe, if you want to activate your bowels and bladder.

Front 43

Action and clinical applications of carbachol?

Back 43

Action: Direct cholinomimetic agonist.
Carbon copy of Ach.

Clinical use: Glaucoma, pupillary contraction, relief of intraocular pressure.

Front 44

Action and clinical application of Policarpine?

Back 44

Action: Direct cholinomimetic agonist.
Contracts ciliary muscle of eye (open agnle glaucoma) pupillary sphincter (closed angle glaucoma);
resistant to AchE.

Hint 44

You cry, drool, and sweat on your "pillow"

Front 45

Action and clinical application of methacholine?

Back 45

Direct cholinomimetic agonist.

Stimulates muscarinic receptors in airway when inhaled.

Challenge test for diagnosis of asthma. QUICK.

Front 46

Action and clinical application of Neostigmine?

Back 46

Action: Indirect cholinomimetic agonist (Ach esterase) --> more activation of muscarinic receptors.

Increases endogenous Ach.

Use: postoperative and neurogenic ileus, urinary retention, myasthenia gravis, reversal of neuromuscular junction blockade (postoperative).

Hint 46

Neo CNS = No CNS penetration.

Front 47

Action and clinical application of pyridostigmine?

Back 47

Use: Indirect cholinomimetic agonist (Achesterase)

Increases endogenous Ach, increases strength.

Use: Myasthenia gravis (long acting), DN penetrate CNS.

Hint 47

PyRIDostiGMine gets RID of Myasthenia Gravis.

Front 48

Action and clinical use for Edrophonium?

Back 48

Indirect cholinomimetic agonist (Achesterase).

Increases endogenous Ach.

Use: Dx myasthenia gravis (Tinsulin test) - very short acting.

Hint 48

Tinsulin test

Front 49

Action and use for Donepezil?

Back 49

Action: Achesterase (indirect choline agonist) - increases endogenous Ach.

Use: Alzheimer's disease - decreases cerebral production of ChAT, decreases Ach synthesis and impaired cortical cholinergic function.
Use meds to increased choline.

Front 50

Treatments for Alzheimer's disease (x3)?

Back 50

Donepezil
Galantamine
Rivastigmine