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All the Drugs > Endocrine Rx > Flashcards

Endocrine Rx Flashcards

1
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Lispro

A

1) Type I DM, Type II DM, gestational DM, life-threatening hyperkalemia, stress-induced hyperglycemia
2) Insulin/Bind insulin receptor (tyrosine kinase activity)
- Liver: increase glucose stored as glycogen
- Muscle: increase glycogen and protien synthesis and K+ uptake
- Fat: aids in TG storage
3) Hypoglycemia, very rarely hypersensitivy rxns
4) Rapid-acting

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2
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Aspart

A

1) Type I DM, Type II DM, gestational DM, life-threatening hyperkalemia, stress-induced hyperglycemia
2) Insulin/Bind insulin receptor (tyrosine kinase activity)
- Liver: increase glucose stored as glycogen
- Muscle: increase glycogen and protien synthesis and K+ uptake
- Fat: aids in TG storage
3) Hypoglycemia, very rarely hypersensitivy rxns
4) Rapid-acting

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3
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Glulisine

A

1) Type I DM, Type II DM, gestational DM, life-threatening hyperkalemia, stress-induced hyperglycemia
2) Insulin/Bind insulin receptor (tyrosine kinase activity)
- Liver: increase glucose stored as glycogen
- Muscle: increase glycogen and protien synthesis and K+ uptake
- Fat: aids in TG storage
3) Hypoglycemia, very rarely hypersensitivy rxns
4) Rapid-acting

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4
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Regular

A

1) Type I DM, Type II DM, gestational DM, life-threatening hyperkalemia, stress-induced hyperglycemia
2) Insulin/Bind insulin receptor (tyrosine kinase activity)
- Liver: increase glucose stored as glycogen
- Muscle: increase glycogen and protien synthesis and K+ uptake
- Fat: aids in TG storage
3) Hypoglycemia, very rarely hypersensitivy rxns
4) Short-acting

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5
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

NPH

A

1) Type I DM, Type II DM, gestational DM, life-threatening hyperkalemia, stress-induced hyperglycemia
2) Insulin/Bind insulin receptor (tyrosine kinase activity)
- Liver: increase glucose stored as glycogen
- Muscle: increase glycogen and protien synthesis and K+ uptake
- Fat: aids in TG storage
3) Hypoglycemia, very rarely hypersensitivy rxns
4) Intermediate

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6
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Glargine

A

1) Type I DM, Type II DM, gestational DM, life-threatening hyperkalemia, stress-induced hyperglycemia
2) Insulin/Bind insulin receptor (tyrosine kinase activity)
- Liver: increase glucose stored as glycogen
- Muscle: increase glycogen and protien synthesis and K+ uptake
- Fat: aids in TG storage
3) Hypoglycemia, very rarely hypersensitivy rxns
4) Long-acting

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7
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Detemir

A

1) Type I DM, Type II DM, gestational DM, life-threatening hyperkalemia, stress-induced hyperglycemia
2) Insulin/Bind insulin receptor (tyrosine kinase activity)
- Liver: increase glucose stored as glycogen
- Muscle: increase glycogen and protien synthesis and K+ uptake
- Fat: aids in TG storage
3) Hypoglycemia, very rarely hypersensitivy rxns
4) Long-acting

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8
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Metformin

A

1) First-line therapy in Type II DM, can be used in pts w/o islet function
2) Biguanide/ Exact MOA unknown –> decreases gluconeogenesis, increases glycolysis, increases peripheral glucose uptake (insulin sensitivity)
3) GI upset, lactic acidosis (most serious)
4) Contraindicated in renal failure

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9
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Tolbutamide

A

1) Type II DM –stimulate endogenous insulin release
2) Sulfonylureas (1st generation)/Close K+ channel in beta cell membrane so cell depolarizes –> triggers insulin release via Ca2+ influx
3) Disulfiram-like effects
4) Useless in Type I DM b/c requires some islet cell function

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10
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Chlorpropamide

A

1) Type II DM –stimulate endogenous insulin release
2) Sulfonylureas (1st generation)/Close K+ channel in beta cell membrane so cell depolarizes –> triggers insulin release via Ca2+ influx
3) Disulfiram-like effects
4) Useless in Type I DM b/c requires some islet cell function

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11
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Glyburide

A

1) Type II DM – stimulates endogenous insulin release
2) Sulfonylureas (2nd generation)/Close K+ channel in beta cell membrane so cell depolarizes –> triggers insulin release via Ca2+ influx
3) Hypoglycemia
4) Useless in Type I DM b/c requires some islet cell funciton

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12
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Glimepiride

A

1) Type II DM – stimulates endogenous insulin release
2) Sulfonylureas (2nd generation)/Close K+ channel in beta cell membrane so cell depolarizes –> triggers insulin release via Ca2+ influx
3) Hypoglycemia
4) Useless in Type I DM b/c requires some islet cell funciton

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13
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Glipizide

A

1) Type II DM – stimulates endogenous insulin release
2) Sulfonylureas (2nd generation)/Close K+ channel in beta cell membrane so cell depolarizes –> triggers insulin release via Ca2+ influx
3) Hypoglycemia
4) Useless in Type I DM b/c requires some islet cell funciton

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14
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Pioglitazone

A

1) Monotherapy in Type II DM or in combination therapy
2) Glitazone/Thiazolidinedione: Incraeses insulin sensitivity in peripheral tissue;, binds PPAR-gamma nuclear transcription regulator
3) Weight gain, edema, hepatoxicity, heart failure

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15
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Rosiglitazone

A

1) Monotherapy in Type II DM or in combination therapy
2) Glitazone/Thiazolidinedione: Incraeses insulin sensitivity in peripheral tissue;, binds PPAR-gamma nuclear transcription regulator
3) Weight gain, edema, hepatoxicity, heart failure

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16
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Acarbose

A

1) Monotherapy in Type II DM, or in combination therapy
2) Alpha-glucosidase Inhibitor/ Inhibits intestinal brush-border alpha-glucosidases –> get delayed sugar hydrolysis and glucose absorption
- decreases postprandial hyperglycemia
3) GI disturbances

17
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Miglitol

A

1) Monotherapy in Type II DM, or in combination therapy
2) Alpha-glucosidase Inhibitor/ Inhibits intestinal brush-border alpha-glucosidases –> get delayed sugar hydrolysis and glucose absorption
- decreases postprandial hyperglycemia
3) GI disturbances

18
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Pramlinitide

A

1) Type I and II DM
2) Amylin Analog/ Decreases glucagon
3) Hypoglycemia, nausea, diarrhea

19
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Exenatide

A

1) Type II DM
2) GLP-1 Analog/ Increase insulin and decrease glucagon release
3) Nausea, vomiting, pancreatitis

20
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Liraglutide

A

1) Type II DM
2) GLP-1 Analog/ Increase insulin and decrease glucagon release
3) Nausea, vomiting, pancreatitis

21
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Linagliptin

A

1) Type II DM
2) DPP-4 Inhibitors/ Increase insulin and decrease glucagon release
3) Mild urinary or respiratory infections

22
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Saxagliptin

A

1) Type II DM
2) DPP-4 Inhibitors/ Increase insulin and decrease glucagon release
3) Mild urinary or respiratory infections

23
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Sitagliptin

A

1) Type II DM
2) DPP-4 Inhibitors/ Increase insulin and decrease glucagon release
3) Mild urinary or respiratory infections

24
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Propylthiouracil

A

1) Hyperthyroidism
2) Block peroxidase inhibiting organificatoin of iodide anda coupling of thyroid hormone synthesis
- also blocks 5’-deiodinase –> decreases peripheral conversion of T4 to T5
3) Skin rash, agranulocytosis (rare), aplastic anemia, hepatotoxicity

25
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Methimazole

A

1) Hyperthyroidism
2) Block peroxidase inhibiting organificatoin of iodide anda coupling of thyroid hormone synthesis
3) Skin rash, agranulocytosis (rare), aplastic anemia
4) Possible teratogen

26
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Levothyroxine

A

1) Hypothyroidism, myxedema
2) THyroxine replacement
3) Tachycardia, heat intolerance, tremors, arrhythmias

27
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Triiodothyronine

A

1) Hypothyroidism, myxedema
2) THyroxine replacement
3) Tachycardia, heat intolerance, tremors, arrhythmias

28
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

GH

A

1)GH deficiency, Turner’s Syndrome

29
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Somatostatin (octretodie)

A

1)Acromegaly, carcinoid, gastrinoma, glucagonoma, espohageal varices

30
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Oxytocin

A

1)Stimulate labor, uterine contractions, milk let-down, controls uterine hemorrhage

31
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

ADH (Desmopressin)

A

1)Central DI

32
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Demeclocycline

A

1) SIADH
2) Tetracycline/ ADH antagonist
3) Nephrogenic DI, photosensitivity, abnormalities of bone and teeth

33
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Hydrocortisone

A

1) Addison’s Disease, inflammation, immune suppression, asthma
2) Glucocorticoid/Decrease production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and COX-2 expression
3) Iatrogenic Cushing’s –> buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, bruise easily, osteoporosis, adrenocortical atrophy, peptic ulcers, DM (if chronic)
4) Can see adrenal insufficiency when drug is stopped abruptly after chronic use

34
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Prednisone

A

1) Addison’s Disease, inflammation, immune suppression, asthma
2) Glucocorticoid/Decrease production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and COX-2 expression
3) Iatrogenic Cushing’s –> buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, bruise easily, osteoporosis, adrenocortical atrophy, peptic ulcers, DM (if chronic)
4) Can see adrenal insufficiency when drug is stopped abruptly after chronic use

35
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Triamcinolone

A

1) Addison’s Disease, inflammation, immune suppression, asthma
2) Glucocorticoid/Decrease production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and COX-2 expression
3) Iatrogenic Cushing’s –> buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, bruise easily, osteoporosis, adrenocortical atrophy, peptic ulcers, DM (if chronic)
4) Can see adrenal insufficiency when drug is stopped abruptly after chronic use

36
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Dexamethasone

A

1) Addison’s Disease, inflammation, immune suppression, asthma
2) Glucocorticoid/Decrease production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and COX-2 expression
3) Iatrogenic Cushing’s –> buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, bruise easily, osteoporosis, adrenocortical atrophy, peptic ulcers, DM (if chronic)
4) Can see adrenal insufficiency when drug is stopped abruptly after chronic use

37
Q

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Beclomethasone

A

1) Addison’s Disease, inflammation, immune suppression, asthma
2) Glucocorticoid/Decrease production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and COX-2 expression
3) Iatrogenic Cushing’s –> buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, bruise easily, osteoporosis, adrenocortical atrophy, peptic ulcers, DM (if chronic)
4) Can see adrenal insufficiency when drug is stopped abruptly after chronic use

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