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Step One > Pharm endocrine > Flashcards

Pharm endocrine Flashcards

1
Q

What are the treatment strategies for type 1 DM ?Type 2? Gestational?

A

Low carb diet, insulin

dietary modification and exercise for weight loss
oral agents
non insulin injectables
insulin replacement

dietary modifications
Exercise
insuling replacement if modificaitons fails

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2
Q

What type of drugs are aspart, glulisine, and lispro? Action? Clinical use? Toxicities?

A

Insulin, rapid acting

Bind insulin receptor (tyrosine kinase)
Live: incr. glucose stored as glycogen
Muscle: incr. glycogen, protein synth, incr. K+ uptake
Fat: Incr. TG storage

Type I DM, Type 2 DM, GDM (postprandial)

Hypoglycemia
Rare HSR

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3
Q

What type of drugs are regular insulin? Action? Clinical use? Toxicities?

A

Insulin, short acting

Bind insulin receptor (tyrosine kinase)
Live: incr. glucose stored as glycogen
Muscle: incr. glycogen, protein synth, incr. K+ uptake
Fat: Incr. TG storage

Type I DM, type 2 DM, GDM, DKA (IV), hyperkalemia , stress hyperglycemia

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4
Q

What type of drugs are NPH? Action? Clinical use? Toxicities?

A

Insulin, intermediate

Bind insulin receptor (tyrosine kinase)
Live: incr. glucose stored as glycogen
Muscle: incr. glycogen, protein synth, incr. K+ uptake
Fat: Incr. TG storage

Type I DM, type 2 DM, GDM

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5
Q

What type of drugs are Detemir, glargine? Action? Clinical use? Toxicities?

A

Insulin, long acting

Bind insulin receptor (tyrosine kinase)
Live: incr. glucose stored as glycogen
Muscle: incr. glycogen, protein synth, incr. K+ uptake
Fat: Incr. TG storage

type I DM, type 2 DM, GDM (basal glucose control)

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6
Q

What type of drugs are metformin? Action? Clinical use? Toxicities? CI?

A

Biguanide-oral hypoglycemic

Exact mechanism unknown
Decr. glucoeneogenesis
Incr. glycolysis
Incr. periph. glucose uptake (incr. insulin sensitivity)

Oral: First line therapy in type 2 DM, causes modest weight loss
Can be used in patients w/o islet function

Lactic acidosis (CI in renal insufficiency)

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7
Q

What type of drugs are chlorpropamide, tolbutamide? Action? Clinical use? Toxicities?

A

First generation Sulfonylurea (oral hypoglycemic)

Close K+ channel in b cell membrane
Cell depolarizes
Insulin release via incr. Ca influx

Stimulate release of endogenous insulin in type 2 DM
Useless in type I DM (no islet function)

Risk of hypoglycemia incr. in renal failure
Disulfiram like effects

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8
Q

What type of drugs are glimepiride, glipizide, glyburide? Action? Clinical use? Toxicities?

A

Second generation Sulfonylurea (oral hypoglycemic)

Close K+ channel in b cell membrane
Cell depolarizes
Insulin release via incr. Ca influx

Stimulate release of endogenous insulin in type 2 DM
Useless in type I DM (no islet function)

Risk of hypoglycemia incr. in renal failure
Hypoglycemia

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9
Q

What type of drugs are Pioglitazone, rosiglitazone? Action? Clinical use? Toxicities?

A

Glitazones/thiazolidiediones

Incr. insulin sensitivity in peripheral tissue
Binds to PPARgamma nuclear transcription regulator

Monotherapy in type 2 DM or combined with other agents

Weight gain
edema
hepatotoxicity
HF
Incr. risk of fractures
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10
Q

What type of drugs are Pioglitazone, rosiglitazone? Action? Clinical use? Toxicities?

A

Glitazones/thiazolidiediones

Incr. insulin sensitivity in peripheral tissue
Binds to PPARgamma nuclear transcription regulator

Monotherapy in type 2 DM or combined with other agents

Weight gain
edema
hepatotoxicity
HF
Incr. risk of fractures
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11
Q

What type of drugs are Exenatide, liraglutide? Action? Clinical use? Toxicities?

A

GLP-1 analogs

Incr. insulin
Decr. glucagon release

Type 2 DM

Nausea, vomiting, pancreatitis

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12
Q

What type of drugs are linagliptin, saxagliptin, sitagliptin? Action? Clinical use? Toxicities?

A

DPP-4 Inhibitors

Incr. insulin
decr. glucagon

Type 2 DM

Mild urinary or resp infections

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13
Q

What type of drugs are pramlintide? Action? Clinical use? Toxicities?

A

Amylin analog

decr. gastric emptying
decr. glucagon

Type I DM
Type II DM

Hypoglycemia, nausea, diarrhea

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14
Q

What type of drugs are canagliflozin? Action? Clinical use? Toxicities?

A

SGLT-2 inhibitors

Block reabsorption of glucose in PCT

Type 2 DM

Glucosuria
UTIs
Vaginal yeast infections

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15
Q

What type of drugs are acarbose, miglitol? Action? Clinical use? Toxicities?

A

Alpha glucosidase inhibitors

Inhibit intestinal brush border alpha glucosidases
Delayed carb hydrolysis and glucose absorption
Decr. postprandial hyperglycemia

Monotherapy in type 2 DM or in combo therapy

GI disturbances

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16
Q

What type of drugs are acarbose, miglitol? Action? Clinical use? Toxicities?

A

Alpha glucosidase inhibitors

Inhibit intestinal brush border alpha glucosidases
Delayed carb hydrolysis and glucose absorption
Decr. postprandial hyperglycemia

Monotherapy in type 2 DM or in combo therapy

GI disturbances

17
Q

What is the mechanism of propylthiouracil? Clinical use? Toxicity?

A

Block thyroid peroxidase, inhibiting oxicaiton of iodide and the organification of iodine (inhibit thyroid hormone synth)

Blocks 5’ deiodinase (periph conversion to T3)

Hyperthyroidism

Skin rash, agranulocytosis, aplastic anemia, hepatotoxicity

18
Q

What is the mechanism of methimazole? Clinical use? Toxicity?

A

Block thyroid peroxidase, inhibiting oxicaiton of iodide and the organification of iodine (inhibit thyroid hormone synth)

Hyperthyroidism

Skin rash, agranulocytosis, aplastic anemia, teratogen (aplasia cutis)

19
Q

What is the mechanism of methimazole? Clinical use? Toxicity?

A

Block thyroid peroxidase, inhibiting oxicaiton of iodide and the organification of iodine (inhibit thyroid hormone synth)

Hyperthyroidism

Skin rash, agranulocytosis, aplastic anemia, teratogen (aplasia cutis)

20
Q

What is the mechanism of Levothyroxine (T4) and triiodothyronine (T3)?

A

Thyroid hormone replacement

Hypothyroidism, myxedema
Off label=weight loss

Tachycardia, heat intolerance, tremors, arrhythmias

21
Q

What is the mechanism of Levothyroxine (T4) and triiodothyronine (T3)? Clinical use? Toxicity?

A

Thyroid hormone replacement

Hypothyroidism, myxedema
Off label=weight loss

Tachycardia, heat intolerance, tremors, arrhythmias

22
Q

What is the clinical use of:

Conivaptan/tolvaptan:
Desmopressin acetate:
GH:
Oxytocin:
Octreotide:
A

Conivaptan/tolvaptan: ADH antag (V2 receptor), SIADH
Desmopressin acetate: Central DI
GH: GH defic, Turners
Oxytocin: Stimulate labor, uterine contractions, milk let down; controls uterine hemorrhage
Octreotide: acromegaly, carcinoid syndrome, gastrinoma, glucagonoma, esophageal varices

23
Q

What is the clinical use of:

Conivaptan/tolvaptan:
Desmopressin acetate:
GH:
Oxytocin:
Octreotide:
A

Conivaptan/tolvaptan: ADH antag (V2 receptor), SIADH
Desmopressin acetate: Central DI
GH: GH defic, Turners
Oxytocin: Stimulate labor, uterine contractions, milk let down; controls uterine hemorrhage
Octreotide: acromegaly, carcinoid syndrome, gastrinoma, glucagonoma, esophageal varices

24
Q

What is the mechanism of demeclocycline? Clinical use? Toxicity?

A

ADH antagonist (member of tetracycline family)

SIADH

Nephrogenic DI, photosensitivy, abnormalities of bone and teeth

25
Q

What type of drug are beclomethasone, dexamethasone, fludrocortisone (1), hydrocortisone, methylprednisolone, prednisone, triamcinolone? Mechanism of action? Of 1? Clinical use? Toxicity?

A

Glucocorticoid

Metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements, inhibition of phospholipase A2, and inhibition of transcription factors such as NF-kappa B

Addisons, inflammation, immunosuppression, asthma

Iatrogenic Cushings
Adrenocortical atrophy
peptic ulcers
steroid diabetes
steroid psychosis
Adrenal insufficiency when stopped suddenly after chronic use
26
Q

What type of drug are beclomethasone, dexamethasone, fludrocortisone (1), hydrocortisone, methylprednisolone, prednisone, triamcinolone? Mechanism of action? Of 1? Clinical use? Toxicity?

A

Glucocorticoid

Metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements, inhibition of phospholipase A2, and inhibition of transcription factors such as NF-kappa B
1=mineralocorticoid and glucocorticoid

Addisons, inflammation, immunosuppression, asthma

Iatrogenic Cushings
Adrenocortical atrophy
peptic ulcers
steroid diabetes
steroid psychosis
Adrenal insufficiency when stopped suddenly after chronic use
27
Q

What type of drug are beclomethasone, dexamethasone, fludrocortisone (1), hydrocortisone, methylprednisolone, prednisone, triamcinolone? Mechanism of action? Of 1? Clinical use? Toxicity?

A

Glucocorticoid

Metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements, inhibition of phospholipase A2, and inhibition of transcription factors such as NF-kappa B
1=mineralocorticoid and glucocorticoid

Addisons, inflammation, immunosuppression, asthma

Iatrogenic Cushings
Adrenocortical atrophy
peptic ulcers
steroid diabetes
steroid psychosis
Adrenal insufficiency when stopped suddenly after chronic use
28
Q

What is the mechanism of cinacalcet? Clinical use? Toxicity?

A

Sensitizes Ca sensing receptor in parathyroid gland to circulating Ca leading to decr. PTH

Hypercalcemia due to primary or secondary hyperparathyroidism

Hypocalcemia.

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