Endocrine Pharmacology

Front 1

Insulin, rapid acting agents

Back 1

Lispro,Aspart,Glulisine

Front 2

Mechanism of action of Lispro, Aspart, Glulisine

Back 2

Binds insulin receptor (tyrosine kinase activity) rapidly, no LAG.

Liver: Increases glucose stored as glycogen.

Muscle: Increases glycogen, protein synthesis; K+ uptake.

Fat: Increases TG storage.

Front 3

Clinical Use of Lispro, Aspart, Glulisine?

Back 3

Type 1 DM, type 2 DM, GDM (postprandial glucose control).

Front 4

Risk/Concerns with using Lispro, Aspart, Glulisine?

Back 4

Hypoglycemia,lipodystrophy, rare hypersensitivity reactions.

Front 5

Clinical use of Insulin, short acting Regular?

Back 5

Type 1 DM, type 2 DM,GDM, DKA (IV),hyperkalemia (+ glucose),stress hyperglycemia.

Front 6

Clinical use of Insulin, intermediate acting NPH?

Back 6

Type 1 DM, type 2 DM, GDM.

Front 7

Insulin, long acting agents?

Back 7

Detemir, glargine

Front 8

Clinical use of Insulin, long acting Detemir,glargine?

Back 8

Type 1 DM, type 2 DM, GDM (basal glucose control).

Front 9

Biguanide?

Back 9

Metformin

Front 10

Mechanism of Action of Metformin?

Back 10

Exact mechanism unknown.

Decreases gluconeogenesis

Increases glycolysis

Increases peripheral glucose uptake(Increases insulin sensitivity).

Front 11

Clinical use of Metformin?

Back 11

Oral. First-line therapy in type 2 DM, causes modest weight loss.

Can be used in patients without islet function.

Front 12

Risk/Concerns Metformin?

Back 12

GI upset; most serious adverse effect is lactic acidosis (thus contraindicated in renal insufficiency).

Front 13

Name the first generation sulfonylureas

Back 13

chlorpropamide,tolbutamide

Front 14

Name the second generation sulfonylureas?

Back 14

glimepiride, glipizide, glyburide

Front 15

Mechanism of Action of Sulfonylureas?

Back 15

Close K+ channel in β-cell membrane cell depolarizes insulin release via increased Ca2+influx.

Front 16

Clinical use of Sulfonylureas?

Back 16

Stimulate release of endogenous insulin in type2 DM. Require some islet function, so useless in type1 DM.

Front 17

Risk/Concerns of Sulfonylureas?

Back 17

Risk of hypoglycemia in renal failure, weight gain. First generation: disulfiram-like effects.

Second generation:hypoglycemia.

Front 18

Glitazones/thiazolidinediones?

Back 18

Pioglitazone,rosiglitazone

Front 19

Mechanism of Action of Pioglitazone,rosiglitazone?

Back 19

Increases insulin sensitivity in peripheral tissue. Binds to PPAR-γ nuclear transcription regulator.

Front 20

Clinical use of Pioglitazone, rosiglitazone?

Back 20

Used as monotherapy in type2 DM or combined with above agents. Safe to use in renal impairment.

Front 21

Risk/Concerns with Glitazones/thiazolidinediones Pioglitazone,rosiglitazone?

Back 21

Weight gain, edema. Hepatotoxicity, HF, risk of fractures.

Front 22

Which drugs belong to the Meglitinides?

Back 22

Nateglinide,repaglinide

Front 23

Mechanism of Action of Meglitinides Nateglinide,repaglinide?

Back 23

Stimulate postprandial insulin release by binding to K+ channels on β-cell membranes (site differs from sulfonylureas).

Front 24

Clinical use of Meglitinides Nateglinide, repaglinide?

Back 24

Used as mono therapy in type 2 DM or combined with metformin.

Front 25

Risk/Concerns with Meglitinides Nateglinide, repaglinide?

Back 25

Hypoglycemia ( risk withrenal failure), weight gain.

Front 26

GLP-1 analogs?

Back 26

Exenatide, liraglutide (sc injection)

Front 27

Mechanism of Action of GLP-1 analogs: Exenatide,liraglutide (sc injection)?

Back 27

Increases glucose-dependent insulin release

Decreases glucagon release

Decreases gastricemptying

Increases satiety.

Front 28

Clinical use of GLP-1 analogs: Exenatide, liraglutide (sc injection)?

Back 28

Type 2 DM

Front 29

Risk/Concerns GLP-1 analogs: Exenatide, liraglutide (sc injection)?

Back 29

Nausea, vomiting, pancreatitis; modest weight loss.

Front 30

DPP-4 inhibitors?

Back 30

Linagliptin, saxagliptin, sitagliptin

Front 31

Mechanism of action of DPP-4 Inhibitors: Linagliptin, saxagliptin, sitagliptin?

Back 31

Inhibits DPP-4 enzyme that deactivates GLP-1, thereby

Increases glucose-dependent insulin release,

Decreases glucagon release, Decreases gastric emptying, Increases satiety.

Front 32

Clinical use of DPP-4 inhibitors?

Back 32

Type 2 DM

Front 33

Risk/Concerns DPP-4 inhibitors?

Back 33

Mild urinary or respiratory infections; weight neutral.

Front 34

Mechanism of action of Amylin analogs: Pramlintide(sc injection)?

Back 34

Decrease gastric emptying

Decrease glucagon.

Front 35

Clinical use of Amylin analogs: Pramlintide (sc injection)?

Back 35

Type 1 DM, type 2 DM.

Front 36

Risk/Concerns Pramlintide (sc injection)?

Back 36

Hypoglycemia (in setting of mistimed prandialinsulin), nausea.

Front 37

Sodium-glucoseco-transporter 2(SGLT-2) inhibitors?

Back 37

Canagliozin, dapagliozin, empagliozin

Front 38

Mechanism of action of Sodium-glucose co-transporter 2 (SGLT-2) inhibitors?

Back 38

Block reabsorption of glucose in PCT.

Front 39

Clinical use of Sodium-glucose co-transporter 2 (SGLT-2) inhibitors?

Back 39

Type 2 DM

Front 40

Risk/Concerns Sodium-glucose co-transporter 2 (SGLT-2) inhibitors?

Back 40

Glucosuria, UTIs,vaginal yeast infections,hyperkalemia, dehydration (orthostatic hypotension).

Front 41

α-glucosidaseinhibitors?

Back 41

Acarbose,miglitol

Front 42

Mechanism of action α-glucosidase inhibitors?

Back 42

Inhibit intestinal brush-border α-glucosidases. Delayed carbohydrate hydrolysis and glucose absorption > decrease postprandial hyperglycemia.

Front 43

Clinical use of α-glucosidase inhibitors?

Back 43

Type 2 DM

Front 44

Risk/Concerns α-glucosidase inhibitors?

Back 44

GI disturbances

Front 45

Thionamides?

Back 45

Propylthiouracil (PTU), methimazole.

Front 46

Mechanism of action of Propylthiouracil (PTU), methimazole?

Back 46

Block thyroid peroxidase, inhibiting the oxidation of iodide and the organi cation (coupling) ofiodine > inhibition of thyroid hormone synthesis. Propylthiouracil also blocks 5′-deiodinase > decrease peripheral conversion of T4 to T3.

Front 47

Clinical use of Propylthiouracil (PTU), methimazole?

Back 47

Hyperthyroidism. PTU blocks Peripheral conversion and is used in Pregnancy.

Front 48

Adverse effects of Propylthiouracil (PTU), methimazole?

Back 48

Skin rash, agranulocytosis (rare), aplastic anemia, hepatotoxicity. Methimazole is a possible teratogen (can cause aplasia cutis).

Front 49

Mechanism of Action of Levothyroxine (T4), triiodothyronine (T3)?

Back 49

Thyroid hormone replacement.

Front 50

Clinical use of Levothyroxine (T4), triiodothyronine (T3)?

Back 50

Hypothyroidism, myxedema. Used off-label as weight loss supplements.

Front 51

ADVERSE EFFECTS of Levothyroxine (T4), triiodothyronine (T3)?

Back 51

Tachycardia, heat intolerance, tremors, arrhythmias.

Front 52

Hypothalamic/pituitary drugs?

Back 52

ADH antagonists(conivaptan,tolvaptan)

Desmopressin acetate

GH

Oxytocin

Somatostatin(octreotide)

Front 53

Clinical use of ADH antagonists (conivaptan, tolvaptan)?

Back 53

SIADH, block action of ADH at V2-receptor.

Front 54

Clinical use Desmopressin acetate?

Back 54

Central (not nephrogenic) DI

Front 55

Clinical use of GH?

Back 55

GH deficiency, Turner syndrome.

Front 56

Clinical use of Oxytocin?

Back 56

Stimulates labor, uterine contractions, milk let-down; controls uterine hemorrhage.

Front 57

Clinical use of Somatostatin(octreotide)?

Back 57

Acromegaly, carcinoid syndrome, gastrinoma, glucagonoma, esophageal varices.

Front 58

Mechanism of Action Demeclocycline?

Back 58

ADH antagonist (member of tetracycline family).

Front 59

Clinical use of Demeclocycline?

Back 59

SIADH

Front 60

ADVERSE EFFECTS of Demeclocycline?

Back 60

Nephrogenic DI, photosensitivity, abnormalities of bone and teeth.

Front 61

Name the Glucocorticoids?

Back 61

Beclomethasone, dexamethasone, hydrocortisone, methylprednisolone, prednisone, triamcinolone.

Front 62

Mechanism of Action of Glucocorticoids?

Back 62

Metabolic, catabolic, anti-in ammatory, and immunosuppressive effects mediated by interactionswith glucocorticoid response elements, inhibition of phospholipase A2, and inhibition oftranscription factors such as NF-κB.

Front 63

Clinical use of Glucocorticoids?

Back 63

Adrenal insuficiency, in ammation, immunosuppression, asthma.

Front 64

ADVERSE EFFECTS of glucocorticoids?

Back 64

Iatrogenic Cushing syndrome (hypertension, weight gain, moon facies, truncal obesity,buffalo hump, thinning of skin, striae, acne, osteoporosis, hyperglycemia, amenorrhea,immunosuppression), adrenocortical atrophy, peptic ulcers, steroid diabetes, steroid psychosis,cataracts. Adrenal insuficiency when drug stopped abruptly after chronic use.

Front 65

Mechanism of action of Fludrocortisone?

Back 65

Synthetic analog of aldosterone with little glucocorticoid effects.

Front 66

Clinical use of Fludrocortisone?

Back 66

Mineralocorticoid replacement in 1° adrenal insuficiency.

Front 67

Adverse effects of Fludrocortisone?

Back 67

Similar to glucocorticoids; also edema, exacerbation of heart failure, hyperpigmentation.

Front 68

Mechanism of action of Cinacalcet?

Back 68

Sensitizes Ca2+-sensing receptor (CaSR) in parathyroid gland to circulating Ca2+ > decreases PTH.

Front 69

Clinical use of Cinacalcet?

Back 69

1° or 2° hyperparathyroidism.

Front 70

ADVERSE EFFECTS of Cinacalcet?

Back 70

Hypocalcemia