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Endo Flashcards

1
Q

Type 1 DM treatment

A
  • low sugar diet

- insulin replacement

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2
Q

Type 2 DM treatment

A
  • dietary modification + exercise for weight loss
  • oral hypoglycemics
  • insulin replacement
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3
Q

Lispro

  • Class
  • MOA
  • Use
  • Toxicity
A
  • Insulin (Rapid acting)
  • MOA: binds insulin receptor (tyrosine kinase activity)
    • liver: increase glucose storage as glycogen
    • muscle: increase glycogen and protein synthesis, K+
      uptake
    • fat: aids TG storage
  • Use:
    • Type 1 DM
    • Type 2 DM
    • Gestational diabetes
    • Life threatening hyperkalemia *
    • Stress induced hyperglycemia
  • Toxicities:
    • Hypoglycemia
    • Rare hypersensitivity reaction
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4
Q

Aspart

  • Class
  • MOA
  • Use
  • Toxicity
A
  • Insulin (Rapid acting)
  • MOA: binds insulin receptor (tyrosine kinase activity)
    • liver: increase glucose storage as glycogen
    • muscle: increase glycogen and protein synthesis, K+
      uptake
    • fat: aids TG storage
  • Use:
    • Type 1 DM
    • Type 2 DM
    • Gestational diabetes
    • Life threatening hyperkalemia *
    • Stress induced hyperglycemia
  • Toxicities:
    • Hypoglycemia
    • Rare hypersensitivity reaction
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5
Q

Glulisine

  • Class
  • MOA
  • Use
  • Toxicity
A
  • Insulin (Rapid acting)
  • MOA: binds insulin receptor (tyrosine kinase activity)
    • liver: increase glucose storage as glycogen
    • muscle: increase glycogen and protein synthesis, K+
      uptake
    • fat: aids TG storage
  • Use:
    • Type 1 DM
    • Type 2 DM
    • Gestational diabetes
    • Life threatening hyperkalemia *
    • Stress induced hyperglycemia
  • Toxicities:
    • Hypoglycemia
    • Rare hypersensitivity reaction
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6
Q

Regular

  • Class
  • MOA
  • Use
  • Toxicity
A
  • Insulin (Short acting)
  • MOA: binds insulin receptor (tyrosine kinase activity)
    • liver: increase glucose storage as glycogen
    • muscle: increase glycogen and protein synthesis, K+
      uptake
    • fat: aids TG storage
  • Use:
    • Type 1 DM
    • Type 2 DM
    • Gestational diabetes
    • Life threatening hyperkalemia *
    • Stress induced hyperglycemia
  • Toxicities:
    • Hypoglycemia
    • Rare hypersensitivity reaction
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7
Q

NPH

  • Class
  • MOA
  • Use
  • Toxicity
A
  • Insulin (intermediate)
  • MOA: binds insulin receptor (tyrosine kinase activity)
    • liver: increase glucose storage as glycogen
    • muscle: increase glycogen and protein synthesis, K+
      uptake
    • fat: aids TG storage
  • Use:
    • Type 1 DM
    • Type 2 DM
    • Gestational diabetes
    • Life threatening hyperkalemia *
    • Stress induced hyperglycemia
  • Toxicities:
    • Hypoglycemia
    • Rare hypersensitivity reaction
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8
Q

Glargine

  • Class
  • MOA
  • Use
  • Toxicity
A
  • Insulin (long acting)
  • MOA: binds insulin receptor (tyrosine kinase activity)
    • liver: increase glucose storage as glycogen
    • muscle: increase glycogen and protein synthesis, K+
      uptake
    • fat: aids TG storage
  • Use:
    • Type 1 DM
    • Type 2 DM
    • Gestational diabetes
    • Life threatening hyperkalemia *
    • Stress induced hyperglycemia
  • Toxicities:
    • Hypoglycemia
    • Rare hypersensitivity reaction
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9
Q

Detemir

  • Class
  • MOA
  • Use
  • Toxicity
A
  • Insulin (long acting)
  • MOA: binds insulin receptor (tyrosine kinase activity)
    • liver: increase glucose storage as glycogen
    • muscle: increase glycogen and protein synthesis, K+
      uptake
    • fat: aids TG storage
  • Use:
    • Type 1 DM
    • Type 2 DM
    • Gestational diabetes
    • Life threatening hyperkalemia *
    • Stress induced hyperglycemia
  • Toxicities:
    • Hypoglycemia
    • Rare hypersensitivity reaction
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10
Q

Metformin

  • Class
  • MOA
  • Use
  • Toxicity
A
  • Biguanide
  • MOA: exact mechanism is unknown
    • decreases gluconeogenesis
    • increase glycolysis
    • increase peripheral glucose uptake (insulin sensitivity)
  • Use: oral
    • first line type 2 DM
    • used in patients without islet function
  • Toxicities:
    • GI upset
    • lactic acidosis
      • most serious adverse effect
      • contraindicated in renal failure
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11
Q

Tolbutamide

  • Class
  • MOA
  • Use
  • Toxicity
A
  • Sulfonylureas (first generation)
  • MOA: close K+ channel in B cell membrane c
    • Cell depolarizes
    • Triggers insulin release via increase Ca++ influx
  • Use: stimulate release of endogenous insulin
    • Type 2 DM
    • Require islet function –> useless in DM1
  • Toxicities:
    • Disulfiramine like effects (antabuse)
      • headache, drowsiness…
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12
Q

Chlorpropamide

  • Class
  • MOA
  • Use
  • Toxicity
A
  • Sulfonylureas (first generation)
  • MOA: close K+ channel in B cell membrane c
    • Cell depolarizes
    • Triggers insulin release via increase Ca++ influx
  • Use: stimulate release of endogenous insulin
    • Type 2 DM
    • Require islet function –> useless in DM1
  • Toxicities:
    • Disulfiramine like effects (antabuse)
      • headache, drowsiness…
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13
Q

Glyburide

  • Class
  • MOA
  • Use
  • Toxicity
A
  • Sulfonylureas (second generation)
  • MOA: close K+ channel in B cell membrane c
    • Cell depolarizes
    • Triggers insulin release via increase Ca++ influx
  • Use: stimulate release of endogenous insulin
    • Type 2 DM
    • Require islet function –> useless in DM1
  • Toxicities:
    • Hypoglycemia
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14
Q

Glimepiride

  • Class
  • MOA
  • Use
  • Toxicity
A
  • Sulfonylureas (second generation)
  • MOA: close K+ channel in B cell membrane c
    • Cell depolarizes
    • Triggers insulin release via increase Ca++ influx
  • Use: stimulate release of endogenous insulin
    • Type 2 DM
    • Require islet function –> useless in DM1
  • Toxicities:
    • Hypoglycemia
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15
Q

Glipizide

  • Class
  • MOA
  • Use
  • Toxicity
A
  • Sulfonylureas (second generation)
  • MOA: close K+ channel in B cell membrane c
    • Cell depolarizes
    • Triggers insulin release via increase Ca++ influx
  • Use: stimulate release of endogenous insulin
    • Type 2 DM
    • Require islet function –> useless in DM1
  • Toxicities:
    • Hypoglycemia
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16
Q

Pioglitazone

  • Class
  • MOA
  • Use
  • Toxicity
A
  • Glitazones/ Thiazolidinediones
  • MOA: increase insulin sensitivity in peripheral tissue
    • binds PPAR-gamma nuclear transcription factor
    • genes regulate FA storage and glucose metabolism
    • increase adiponectin
    • increases glut 4 expression on adipocyte membranes
  • Use: monotherapy in 2DM
    • can be combined
  • Toxicity:
    • weight gain
    • edema - exacerbate heart failure
    • hepatotoxicity*
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17
Q

Rosiglitazone

  • Class
  • MOA
  • Use
  • Toxicity
A
  • Glitazones/ Thiazolidinediones
  • MOA: increase insulin sensitivity in peripheral tissue
    • binds PPAR-gamma nuclear transcription factor
    • genes regulate FA storage and glucose metabolism
    • increase adiponectin
    • increase glut 4 expression on adipocyte membranes
  • Use: monotherapy in 2DM
    • can be combined
  • Toxicity:
    • weight gain
    • edema - exacerbate heart failure
    • hepatotoxicity*
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18
Q

Acarbose

  • Class
  • MOA
  • Use
  • Toxicity
A
  • Alpha- glucosidase inhibitors
  • MOA: inhibit intestinal brush boarder alpha-glucosidases
    • delayed sugar hydrolysis and glucose absorption
    • decrease postprandial hyperglycemia
  • Use: monotherapy in type 2 DM
    • or in combo with above agents
  • Toxicities: GI disturbance
19
Q

Miglitol

  • Class
  • MOA
  • Use
  • Toxicity
A
  • Alpha- glucosidase inhibitors
  • MOA: inhibit intestinal brush boarder alpha-glucosidases
    • delayed sugar hydrolysis and glucose absorption
    • decrease postprandial hyperglycemia
  • Use: monotherapy in type 2 DM
    • or in combo with above agents
  • Toxicities: GI disturbance
20
Q

Pramlintide

  • Class
  • MOA
  • Use
  • Toxicity
A
  • Amylin analogs
  • MOA: decrease glucagon
  • Use: type 1 + 2 DM
  • Toxicity:
    • Hypoglycemia
    • Nausea
    • Diarrhea
21
Q

Exenatide

  • Class
  • MOA
  • Use
  • Toxicity
A
  • GLP-1 Analog (GI hormones released after meals)
  • MOA:
    • increase insulin
    • decrease glucagon release
  • Use:
    • Type 2 DM
  • Toxicities:
    • Nausea
    • Vomiting
    • Pancreatitis
22
Q

Liraglutide

  • Class
  • MOA
  • Use
  • Toxicity
A
  • GLP-1 Analog (GI hormones released after meals)
  • MOA:
    • increase insulin
    • decrease glucagon release
  • Use:
    • Type 2 DM
  • Toxicities:
    • Nausea
    • Vomiting
    • Pancreatitis
23
Q

Linagliptin

  • Class
  • MOA
  • Use
  • Toxicity
A
  • DDP- inhibitors ( DPP-4 degrades GLP-1)
  • MOA:
    • increase insulin
    • decrease glucagon release
  • Use:
    • Type 2 DM
  • Toxicity
    • Mild urinary infection
    • Mild respiratory infections
24
Q

Saxagliptin

  • Class
  • MOA
  • Use
  • Toxicity
A
  • DDP- inhibitors ( DPP-4 degrades GLP-1)
  • MOA:
    • increase insulin
    • decrease glucagon release
  • Use:
    • Type 2 DM
  • Toxicity
    • Mild urinary infection
    • Mild respiratory infections
25
Sitagliptin - Class - MOA - Use - Toxicity
- DDP- inhibitors ( DPP-4 degrades GLP-1) - MOA: - increase insulin - decrease glucagon release - Use: - Type 2 DM - Toxicity - Mild urinary infection - Mild respiratory infections
26
Propylthiouracil - MOA - Effect - Use - Toxicity
- MOA: block peroxidase (TPO) - inhibit organification of iodine - inhibit coupling of thyroid hormone synthesis - blocks 5- Deiodinase - Effect: - Decrease thyroid hormone - decrease peripheral conversion T4 --> T3 - Use: - Hyperthyroidism - Toxicity: - skin rash - agranulocytosis (Rare) -- presents as fever and sore throat, must do WBC count and determine differential - aplastic anemia - hepatotoxicity (propylthiouracil)
27
Methimazole - MOA - Effect - Use - Toxicity
- MOA: block peroxidase (TPO) - inhibit organification of iodine - inhibit coupling of thyroid hormone synthesis - Effect: - Decrease thyroid hormone - Use: - Hyperthyroidism - Toxicity: - skin rash - agranulocytosis (Rare) -- presents as fever and sore throat, must do WBC count and determine differential - aplastic anemia - Teratogen
28
Levothyroxine - MOA - Use - Toxicity
- MOA: thyroxine replacement - Use: hypothyroidism - myxedema - Toxicity: - tachycardia - heat intolerance - tremors - arrhythmias
29
Triiodothyronine - MOA - Use - Toxicity
- MOA: thyroxine replacement - Use: hypothyroidism - myxedema - Toxicity: - tachycardia - heat intolerance - tremors - arrhythmias
30
GH | - Use
- Hypothalamic/ pituitary drugs - Use: - GH deficiency - Turner syndrome
31
Somatostatin (octreotide) | - Use
- Hypothalamic/ pituitary drugs - GH inhibitor - Use: - acromegaly - carcinoid - gastrinoma - glucagonoma - esophageal varices
32
Oxytocin | - Use
- Hypothalamic/ pituitary drugs - Use: - stimulate labor - uterine contractions - milk let down - controls uterine hemorrhage
33
ADH (desmopressin) | - Use
- Hypothalamic/ pituitary drugs - Use: - pituitary - Central Diabetes insipidis -- also increases vWF release + factor 8 release from endothelial cells ---> hemophilia A
34
Demeclocycline - MOA - Use - Toxicity
- MOA: ADH antagonist - member of tetracycline family - Use: SIADH - Toxicity: - Nephrogenic Diabetes insipidis - Photosensitivity - Abnormalities of bone and teeth
35
Hydrocortisone - Class - MOA - Use - Toxicity - CBC
- Glucocorticoids - MOA: - Inhibit COX 2 --> inhibit phospholipase A2 - decrease production of leukotrienes - decease prostaglandins - Use: - Addison disease - inflammation - imune suppression - asthma - Toxicity: - Iatrogenic Cushing syndrome - buffalo hump - moon facies - truncal obesity - muscle wasting - thin skin - easy bruising - osteoporosis - adrenocortical atrophy - peptic ulcers - diabetes (chronic) - adrenal insufficiency when stopping drug abruptly after chronic use - CBC: -- decreased lymphocytes, monocytes, basophils, eosinophils -- increased neutrophils: demargination of those attached to vessel wall
36
Prednisone - Class - MOA - Use - Toxicity - CBC
- Glucocorticoids - MOA: - Inhibit COX 2 --> inhibit phospholipase A2 - decrease production of leukotrienes - decease prostaglandins - Use: - Addison disease - inflammation - imune suppression - asthma - Toxicity: - Iatrogenic Cushing syndrome - buffalo hump - moon facies - truncal obesity - muscle wasting - thin skin - easy bruising - osteoporosis - adrenocortical atrophy - peptic ulcers - diabetes (chronic) - adrenal insufficiency when stopping drug abruptly after chronic use - CBC -- decreased monocytes, lymphocytes, basophils, eosinophils -- increased neutrophils: demargination of those attached to vessel wall
37
Triamcinolone - Class - MOA - Use - Toxicity - CBC
- Glucocorticoids - MOA: - Inhibit COX 2 --> inhibit phospholipase A2 - decrease production of leukotrienes - decease prostaglandins - Use: - Addison disease - inflammation - imune suppression - asthma - Toxicity: - Iatrogenic Cushing syndrome - buffalo hump - moon facies - truncal obesity - muscle wasting - thin skin - easy bruising - osteoporosis - adrenocortical atrophy - peptic ulcers - diabetes (chronic) - adrenal insufficiency when stopping drug abruptly after chronic use - CBC -- decrease in monocytes, lymphocytes, basophils, eosinophils -- increase in neutrophils: demargination of those attached to vessel wall
38
Dexamethasone - Class - MOA - Use - Toxicity - CBC
- Glucocorticoids - MOA: - Inhibit COX 2 --> inhibit phospholipase A2 - decrease production of leukotrienes - decease prostaglandins - bind nuclear receptor in cytoplasm and move to nucleus - Use: - Addison disease - inflammation - imune suppression - asthma - promote differentiation of surfactant producing cells - Toxicity: - Iatrogenic Cushing syndrome - buffalo hump - moon facies - truncal obesity - muscle wasting - thin skin - easy bruising - osteoporosis - adrenocortical atrophy - peptic ulcers - diabetes (chronic) - adrenal insufficiency when stopping drug abruptly after chronic use - CBC -- decreased monocytes, lymphocytes, basophils, eosinophils -- increased neutrophils: Demargination of those attached to vessel wall
39
Beclamethasone - Class - MOA - Use - Toxicity - CBC
- Glucocorticoids - MOA: - Inhibit COX 2 --> inhibit phospholipase A2 - decrease production of leukotrienes - decease prostaglandins - Use: - Addison disease - inflammation - imune suppression - asthma - Toxicity: - Iatrogenic Cushing syndrome - buffalo hump - moon facies - truncal obesity - muscle wasting - thin skin - easy bruising ` - osteoporosis - adrenocortical atrophy - peptic ulcers - diabetes (chronic) - adrenal insufficiency when stopping drug abruptly after chronic use - CBC -- decrease monocytes, lymphocytes, basophils, eosinophils -- increased neutrophils: demargination of those attached to vessel wall
40
Nephrogenic Diabetes Insipidus Treatment
- Hydrochlorathiazide (Na/Cl inhibited in distal tubule) - Amiloride (K+ sparing diuretic, inhibit Na+ channel) - -> decrease Na+ reabsorption in distal tubule thereby increasing H20 loss --> hypovolemia --> body responds by increasing Na+ and H20 reabsorption in proximal nephron - Indomethacin (NSAID) - -> works for acquired nephrogenic diabetes insipidus - -> prostaglandins inhibit action of ADH in kidney
41
Phenoxybenzamine - Class - MOA - Use - Toxicity
Non selective alpha blocker - MOA: irreversibly alkylates alpha receptors - - long acting, 1/2 life is 24 hr - Use: prior to removal of pheochromocytoma - - prevent excess catecholamines from causing severe HTN - Toxicity: - - orthostatic hypotension - - reflex tachycardia
42
Phentolamine - Class - MOA - Use
Non selective alpha block - MOA: block alpha receptors - Use: give to patients on MAO inhibitors who eat tyramine containing food (HTN crisis)
43
Beta blocker | - thyrotoxicosis
- decrease effect of sympathetic adrenergic impulses reaching target organs - decrease in rate of conversion of T4 --> T3

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