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First Aid Drugs > Endocrine > Flashcards

Endocrine Flashcards

1
Q

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Pramlinitide

A

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

19
Q

Exenatide

A

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

20
Q

Liraglutide

A

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

21
Q

Linagliptin

A

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

22
Q

Saxagliptin

A

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

23
Q

Sitagliptin

A

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

24
Q

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

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

Levothyroxine

A

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

27
Q

Triiodothyronine

A

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

28
Q

GH

A

1)GH deficiency, Turner’s Syndrome

29
Q

Somatostatin (octretodie)

A

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

30
Q

Oxytocin

A

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

31
Q

ADH (Desmopressin)

A

1)Central DI

32
Q

Demeclocycline

A

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

33
Q

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

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

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

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

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

First Aid Drugs (17 decks)

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