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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
Q

Sitagliptin

  • 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
26
Q

Propylthiouracil

  • MOA
  • Effect
  • Use
  • Toxicity
A
  • 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
Q

Methimazole

  • MOA
  • Effect
  • Use
  • Toxicity
A
  • 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
Q

Levothyroxine

  • MOA
  • Use
  • Toxicity
A
  • MOA: thyroxine replacement
  • Use: hypothyroidism
    • myxedema
  • Toxicity:
    • tachycardia
    • heat intolerance
    • tremors
    • arrhythmias
29
Q

Triiodothyronine

  • MOA
  • Use
  • Toxicity
A
  • MOA: thyroxine replacement
  • Use: hypothyroidism
    • myxedema
  • Toxicity:
    • tachycardia
    • heat intolerance
    • tremors
    • arrhythmias
30
Q

GH

- Use

A
  • Hypothalamic/ pituitary drugs
  • Use:
    • GH deficiency
    • Turner syndrome
31
Q

Somatostatin (octreotide)

- Use

A
  • Hypothalamic/ pituitary drugs
    • GH inhibitor
  • Use:
    • acromegaly
    • carcinoid
    • gastrinoma
    • glucagonoma
    • esophageal varices
32
Q

Oxytocin

- Use

A
  • Hypothalamic/ pituitary drugs
  • Use:
    • stimulate labor
    • uterine contractions
    • milk let down
    • controls uterine hemorrhage
33
Q

ADH (desmopressin)

- Use

A
  • Hypothalamic/ pituitary drugs
  • Use:
    • pituitary
    • Central Diabetes insipidis

– also increases vWF release + factor 8 release from endothelial cells —> hemophilia A

34
Q

Demeclocycline

  • MOA
  • Use
  • Toxicity
A
  • MOA: ADH antagonist
    • member of tetracycline family
  • Use: SIADH
  • Toxicity:
    • Nephrogenic Diabetes insipidis
    • Photosensitivity
    • Abnormalities of bone and teeth
35
Q

Hydrocortisone

  • Class
  • MOA
  • Use
  • Toxicity
  • CBC
A
  • 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
Q

Prednisone

  • Class
  • MOA
  • Use
  • Toxicity
  • CBC
A
  • 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
Q

Triamcinolone

  • Class
  • MOA
  • Use
  • Toxicity
  • CBC
A
  • 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
Q

Dexamethasone

  • Class
  • MOA
  • Use
  • Toxicity
  • CBC
A
  • 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
Q

Beclamethasone

  • Class
  • MOA
  • Use
  • Toxicity
  • CBC
A
  • 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
Q

Nephrogenic Diabetes Insipidus Treatment

A
  • 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
Q

Phenoxybenzamine

  • Class
  • MOA
  • Use
  • Toxicity
A

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
Q

Phentolamine

  • Class
  • MOA
  • Use
A

Non selective alpha block

  • MOA: block alpha receptors
  • Use: give to patients on MAO inhibitors who eat tyramine containing food (HTN crisis)
43
Q

Beta blocker

- thyrotoxicosis

A
  • decrease effect of sympathetic adrenergic impulses reaching target organs
  • decrease in rate of conversion of T4 –> T3

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