Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology > ENDOCRINE > Flashcards

ENDOCRINE Flashcards

0
Q

Levothyroxine

A

Synthetic T4–Pro hormone for T3

USES: replacement therapy for hypothyroidism

SIDE EFFECTS: tachycardia, heat intolerance, tremors, arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

Propylthiouricil

A

Anti-thyroid drug

MOA: inhibits thyroid peroxidase, inhibiting the oxidation of iodide and organification (coupling) of iodine–>inhibition of thyroid hormone synthesis. Also blocks 5’-deiodinase, which decreases peripheral conversion of T4 to T3

USES: hyperthyroidism. Used in pregnancy

SIDE EFFECTS: skin rash, agranulocytosis (can present with infection since decreased neutrophils), aplastic anemia, hepatotoxicity, vasculitis, hypoprothrombinemia, rash

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Cortisone

A

Glucocorticoid

MOA: metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-kB

USES: Addison’s disease, inflammation, immune suppression, asthma

TOXICITY: iatrogenic Cushing’s syndrome-buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes. Adrenal insufficiency when drug stopped abruptly after chronic use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Prednisone

A

Intermediate acting glucocorticoid

Converted to prednisolone in liver

Moe potent as glucocorticoid than mineralocorticoid

USES: to prevent rejection; anti-inflammatory effect is 4X more potent than cortisol

Avoid in patients with liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Triamcinolone

A

Glucocorticoid

MOA: metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-kB

USES: Addison’s disease, inflammation, immune suppression, asthma

TOXICITY: iatrogenic Cushing’s syndrome-buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes. Adrenal insufficiency when drug stopped abruptly after chronic use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Dexamethasone

A

Glucocorticoid

MOA: metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-kB

USES: Addison’s disease, inflammation, immune suppression, asthma

TOXICITY: iatrogenic Cushing’s syndrome-buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes. Adrenal insufficiency when drug stopped abruptly after chronic use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Betamethasone

A

Long acting glucocorticoid–similar to dexamethasone

Not metabolized by placenta–can be used to induce lung surfactant production in preterm fetuses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Beclomethasone

A

Glucocorticoid

MOA: metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-kB

USES: Addison’s disease, inflammation, immune suppression, asthma

TOXICITY: iatrogenic Cushing’s syndrome-buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes. Adrenal insufficiency when drug stopped abruptly after chronic use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Fludrocortisone

A

mineralocorticoid and glucocorticoid activity

MOA: metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-kB

USES: Addison’s disease, inflammation, immune suppression, asthma

TOXICITY: iatrogenic Cushing’s syndrome-buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes. Adrenal insufficiency when drug stopped abruptly after chronic use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Mifepristone

A

Progesterone receptor antagonist used as abortion pill and at higher doses an antagonist of the glucocorticoid receptor

Used for Cushing’s syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cholecalciferol

A

Vitamin D3–decreases transcription of PTH gene and increases calcium absorption

USES: osteoporosis, osteomalacia, rickets, hypoparathyroidism, secondary hypoparathyroidism (chronic kidney disease)

SIDE EFFECTS: hypercalcemia, renal calculi, hyperphosphatemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Ergocalciferol

A

Vitamin D2–decreases transcription of PTH gene and increases calcium absorption

USES: osteoporosis, osteomalacia, rickets, hypoparathyroidism, secondary hypoparathyroidism (chronic kidney disease)

SIDE EFFECTS: hypercalcemia, renal calculi, hyperphosphatemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Calcitriol

A

ACTIVE form of vitamin D–decreases transcription of PTH gene and increases calcium absorption

USES: osteoporosis, osteomalacia, rickets, hypoparathyroidism, secondary hypoparathyroidism (chronic kidney disease)

SIDE EFFECTS: hypercalcemia, renal calculi, hyperphosphatemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Cinacalcet

A

MOA: sensitized ca++ sensing receptor (CaSR) in parathyroid gland to circulating ca++ leading to decreased PTH

USES: hypercalcemia due to primary or secondary hyperparathyroidism

TOXICITY: hypocalcemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Alendronate

A

Bisphosphonate

MOA: Synthetic analog of pyrophosphate–bind to hydroxyapatite in bone and selectively localize to areas of bone turnover and inhibit resorption

USES: osteoporosis, Paget’s disease

SIDE EFFECTS: esophageal erosion, jaw osteonecrosis, acid reflux, headache, atypical femur fractures

EFFICACY: decrease incidence of vertebral AND hip fractures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Risedronate

A

Bisphosphonate

MOA: Synthetic analog of pyrophosphate–bind to hydroxyapatite in bone and selectively localize to areas of bone turnover and inhibit resorption

USES: osteoporosis, Paget’s disease

SIDE EFFECTS: esophageal erosion, jaw osteonecrosis, acid reflux, headache, atypical femur fractures

EFFICACY: decrease incidence of vertebral AND hip fractures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Ibandronate

A

Bisphosphonate

MOA: Synthetic analog of pyrophosphate–bind to hydroxyapatite in bone and selectively localize to areas of bone turnover and inhibit resorption

USES: osteoporosis, Paget’s disease

SIDE EFFECTS: esophageal erosion, jaw osteonecrosis, acid reflux, headache, atypical femur fractures

EFFICACY: decrease incidence of vertebral AND hip fractures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Pamidronate

A

Bisphosphonate–IV only

MOA: Synthetic analog of pyrophosphate–bind to hydroxyapatite in bone and selectively localize to areas of bone turnover and inhibit resorption

USES: Paget’s disease, hypercalcemia of malignancy

SIDE EFFECTS: esophageal erosion, jaw osteonecrosis, acid reflux, headache, atypical femur fractures

EFFICACY: decrease incidence of vertebral AND hip fractures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Zoledronic acid

A

Bisphosphonate-IV only

MOA: Synthetic analog of pyrophosphate–bind to hydroxyapatite in bone and selectively localize to areas of bone turnover and inhibit resorption

USES: Paget’s disease, hypercalcemia of malignancy

SIDE EFFECTS: esophageal erosion, jaw osteonecrosis, acid reflux, headache, atypical femur fractures

EFFICACY: decrease incidence of vertebral AND hip fractures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Raloxifene

A

Selective estrogen receptor modulator–acts at estrogen receptor selectively in bone (does not increase risk for breast or uterine cancer)

USES: osteoporosis

SIDE EFFECTS: hot flashes, venous thromboembolism

EFFICACY: decreases vertebral but NOT hip fractures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Calcitonin nasal spray

A

MOA: binds to and activates the calcitonin receptor on osteoclasts and decreases resorptive activity

USES: post menopausal osteoporosis treatment NOT prevention

SIDE EFFECTS: rhinitis, nasal symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Calcitonin injection

A

MOA: binds to and activates the calcitonin receptor on osteoclasts and decreases resorptive activity

USES: post menopausal osteoporosis treatment NOT prevention, Paget’s disease,

SIDE EFFECTS: nausea, flushing, diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Denosumab

A

Humanize monoclonal antibody to RANKL–prevents bone resorption

USES: osteoporosis

SIDE EFFECTS: hypocalcemia, infections, dermatitis, eczema, rash, jaw osteonecrosis, musculoskeletal pain

23
Q

PTH in pulses

A

Briefly stimulates osteoclasts, increases blood calcium, decreases blood phosphorus, and activates 1,25-vitamin D–> results in brief period of bone turnover followed by osteoblast recruitment of the BFUs

24
Q

PTH analogs

A

Blocks osteoblasts from undergoing apoptosis–cerastes trabecular connections, increases cortex thickness, makes bones stronger

USES: good for osteoporosis

25
Q

Regular insulin

A

Rapid-acting to be administered 30-45 minutes prior to meals; Duration of action 3-6h (increases with increasing doses)

USES: DM1/2, GDM, DKA (IV), hyperkalemia (+ glucose), stress hyperglycemia

26
Q

NPH

A

Intermediate-acting insulin analog

USES: DM1, DM2, GDM

27
Q

Glargine

A

Long acting insulin

USES: DM1/2, GDM

28
Q

Detemir

A

Long acting insulin

USES: DM1/2, GDM

29
Q

Pramlinitide

A

Amylin analog

MOA: decreases emptying and glucagon

USES: type 1/2 diabetes

TOXICITY: hypoglycemia, nausea, diarrhea

30
Q

Metformin

A

Biguanide diabetes drug

MOA: exact mechanism unknown–increases insulin sensitivity, decreases gluconeogenesis, increases glycolysis, increases peripheral glucose uptake

USES: drug of choice for T2DM. Can be used with patients without islet function

TOXICITY: GI upset; most serious adverse effect is lactic acidosis via anaerobic glycolysis (thus contraindicated in renal failure)

31
Q

Rosiglitazone

A

Glitazone/Thiazolidinedione

MOA: increases insulin sensitivity in peripheral tissues–binds PPARgamma nuclear transcription regulator and enhances glucose uptake into fat and muscle

USES: mono therapy in T2DM or combined

SIDE EFFECTS: edema, weight gain, CHF, hepatotoxicity. Takes days-weeks to see effects

32
Q

Pioglitazone

A

Glitazone/Thiazolidinedione

MOA: increases insulin sensitivity in peripheral tissues–binds PPARgamma nuclear transcription regulator and enhances glucose uptake into fat and muscle

USES: mono therapy in T2DM or combined

SIDE EFFECTS: edema, weight gain, CHF, hepatotoxicity. Takes days-weeks to see effects

33
Q

Acarbose

A

Alpha glucosidase inhibitor

MOA: inhibit intestinal brush border alpha glucosidase–>delayed sugar hydrolysis and glucose absorption–>decreases postprandial hyperglycemia

USES: Monotherapy in T2DM or in combination

TOXICITY: GI disturbances

34
Q

Miglitol

A

Alpha glucosidase inhibitor

MOA: inhibit intestinal brush border alpha glucosidase–>delayed sugar hydrolysis and glucose absorption–>decreases postprandial hyperglycemia

USES: Monotherapy in T2DM or in combination

TOXICITY: GI disturbances

35
Q

Exenatide

A

GLP-1 receptor agonist

MOA: slows gastric emptying, stimulates glucose-induced insulin secretion, and suppresses glucagon release

USES: T2DM

SIDE EFFECTS: nausea, vomiting, pancreatitis

36
Q

Liraglutide

A

GLP-1 receptor agonist

MOA: slows gastric emptying, stimulates glucose-induced insulin secretion, and suppresses glucagon release

USES: T2DM

SIDE EFFECTS: nausea, vomiting, pancreatitis

37
Q

Somatostatin

A

USES: acromegaly, carcinoid, gastronomy, glucagonoma, esophageal varices

38
Q

Oxytocin

A

USES: stimulates labor, uterine contractions, milk let-down; controls uterine hemorrhage

39
Q

ADH

A

USES: pituitary (central, not nephrogenic) DI

40
Q

Demeclocycline

A

MOA: ADH antagonist (member of the tetracycline family)

USES: SIADH

TOXICITY: nephrogenic DI, photosensitivity, abnormalities of bone and teeth

41
Q

Canagliflozin

A

Sodium-glucose co transporter (SGLT2) inhibitor

42
Q

Hydrocortisone

A

Glucocorticoid

MOA: metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-kB

USES: Addison’s disease, inflammation, immune suppression, asthma

TOXICITY: iatrogenic Cushing’s syndrome-buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes. Adrenal insufficiency when drug stopped abruptly after chronic use

43
Q

Growth hormone

A

USES: GH deficiency, turners syndrome

44
Q

Triiodothyronine

A

MOA: thyroxine replacement

USES: hypothyroidism, myxedema

TOXICITY: tachycardia, heat intolerance, tremors, arrhythmia

45
Q

Sitagliptin

A

DPP-4 inhibitor

MOA: increases insulin, decreases glucagon release

USES: T2DM

TOXICITY: mild urinary or respiratory infections

46
Q

Saxagliptin

A

DPP-4 inhibitor

MOA: increases insulin, decreases glucagon release

USES: T2DM

TOXICITY: mild urinary or respiratory infections

47
Q

Linagliptin

A

DPP-4 inhibitor

MOA: increases insulin, decreases glucagon release

USES: T2DM

TOXICITY: mild urinary or respiratory infections

48
Q

Glipizide

A

Second generation Sulfonylurea

MOA: closes K+ channel in B cell membrane, so cell depolarizes–>triggering of insulin release via increased calcium influx

USES: stimulate release of endogenous insulin on type 2 DM. Require some islet function, so useless in T1DM

TOXICITY: risk of hypoglycemia increased in renal failure. First generation: disulfiram-like effects. Second generation: hypoglycemia

49
Q

Glimepiride

A

Second generation Sulfonylurea

MOA: closes K+ channel in B cell membrane, so cell depolarizes–>triggering of insulin release via increased calcium influx

USES: stimulate release of endogenous insulin on type 2 DM. Require some islet function, so useless in T1DM

TOXICITY: risk of hypoglycemia increased in renal failure. First generation: disulfiram-like effects. Second generation: hypoglycemia

50
Q

Glyburide

A

Second generation Sulfonylurea

MOA: closes K+ channel in B cell membrane, so cell depolarizes–>triggering of insulin release via increased calcium influx

USES: stimulate release of endogenous insulin on type 2 DM. Require some islet function, so useless in T1DM

TOXICITY: risk of hypoglycemia increased in renal failure. First generation: disulfiram-like effects. Second generation: hypoglycemia

51
Q

Chlorpropamide

A

First generation Sulfonylurea

MOA: closes K+ channel in B cell membrane, so cell depolarizes–>triggering of insulin release via increased calcium influx

USES: stimulate release of endogenous insulin on type 2 DM. Require some islet function, so useless in T1DM

TOXICITY: risk of hypoglycemia increased in renal failure. First generation: disulfiram-like effects. Second generation: hypoglycemia

52
Q

Tolbutamide

A

First generation Sulfonylurea

MOA: closes K+ channel in B cell membrane, so cell depolarizes–>triggering of insulin release via increased calcium influx

USES: stimulate release of endogenous insulin on type 2 DM. Require some islet function, so useless in T1DM

TOXICITY: risk of hypoglycemia increased in renal failure. First generation: disulfiram-like effects. Second generation: hypoglycemia

53
Q

Methimazole

A

Anti-thyroid drug

MOA: thyroid peroxidase inhibitor–prevents incorporation of iodide ion onto tyrosyl residues of thyroglobulin, resulting in decreased production of T3/T4

USES: hyperthyroidism (action takes time due to large stores of thyroid hormone that must be exhausted)

SIDE EFFECTS: agranulocytosis, hepatotoxicity, vasculitis, hypoprothrombinemia, rash, associated with birth defects

54
Q

Tesamorelin

A

GHRH analog used to treat HIV-associated lipodystrophy

55
Q

Octreotide

A

Somatostatin analog used to treat GH excess.

56
Q

Pegvisomant

A

Growth hormone receptor antagonist used to treat GH excess

Pharmacology (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions