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Advanced Pharmacology > Endocrine management > Flashcards

Endocrine management Flashcards

1
Q

Insulin actions

A
  • hormone that catalyzes glucose uptake
  • regulates amino acid uptake and protein synthesis
  • regulates lipid storage
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2
Q

Alpha glucosidases

A

-enzyme secreted by the intestine that breaks bond of glucosyl units, like sucrose into glucose

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3
Q

Gluconeogenesis

A
  • synthesis of glucose in the liver from lactate, amino acids, and glycerol
  • stimulated during fasting, prolonged exercise, high protein diet, and stress
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4
Q

Insulin stimulation

A

-released from beta cells, stimulated by meals, high levels of circulating glucagons and amino acids, and CNS stimulation

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5
Q

Patho of Type I DM

A
  • often caused by genetic predisposition, activated by environmental insult
  • aggressive antibodies develop against beta cells, eventually killing all beta cells
  • pancreas fails to release insulin
  • absolute/complete absence of insulin
  • body burns fat instead for fuel => ketones and acidosis
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6
Q

Patho of Type II DM

A
  • Hyperglycemia caused by peripheral tissue receptor insensitivity OR decreased beta cell production of insulin
  • circulating insulin sufficient to prevent acidosis, but inadequate to prevent hyperglycemia
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7
Q

Patho of Obese Type II DM

A
  • periph. insulin receptors not working properly d/t fat deposits =>intracellular glucose movement does not occur
  • beta cell compensate by producing more insulin (hyper insulinemia with normoglycemia for years)
  • beta cells burn out from overwork
  • body cells perceive hypoglycemia and ramp up liver gluconeogenesis
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8
Q

Non-obese type II DM

A
  • failure of beta cell to respond to insulinogenic stim-
  • low normal body weight
  • does not respond as well to typical Rx
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9
Q

MODY

A

Mature onset diabetes of the young

  • rare monogenetic disorder
  • gene mutation causes decreased beta cell response to glucose
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10
Q

Role of incretin

A
  • intestinal secretion of insulin as GLP-1 or GIP

- GLP-1 is broken down quickly by DPP4

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11
Q

Effects of GLP-1

A
  • slows gastric emptying
  • suppresses glucagon secretion
  • enhances insulin secretion
  • enhances beta cell proliferation and decreases apoptosis
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12
Q

Insulinogenic drugs

A

Sulfonylureas and meglitinides

  • stimulate insulin release by binding to beta cell receptors
  • not good very early (beta cells hyperfunctioning) or very late (beta cell burn out) in diagnosis
  • risk of hypoglycemia
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13
Q

Sulfonylureas

A
  • insulinogenic drugs for T2DM
  • highly effective if beta cells still functioning
  • Active metabolite- consider renal function (decreased excretion may cause hypoglycemia)
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14
Q

Meglitinides

A
  • insulinogenic drugs for T2DM
  • repaglinide, nateglinide
  • insulin release stimulated in glucose-sensitive manner
  • fast-acting, rapid metabolism
  • good for prandial surges (given before meals)
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15
Q

Non-insulinogenic drugs

A 
* Do not stimulate insulin release from beta cells
Metformin
Thiazolidinediones
Incretin mimetics/DPP4 inhibitors
Pramlintide
Sodium Glucose Cotransporters
Alpha glucosidase inhibitors
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16
Q

Drug of choice for Obese Type 2 DM

A

Metformin

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17
Q

Metformin

A
  • type 2 DM
  • suppresses hepatic glucogenesis
  • reduces fasting plasma insulin
  • improves insulin sensitivity
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18
Q

What patient should not take Metformin?

A
  • decreased renal function (causes lactic acidosis)

- intolerance of adverse effects (GI intolerance)

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19
Q

Adverse effects of Metformin

A 
GI intolerance (bowel incontinence)
Lactic acidosis (from renal impairment)
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20
Q

Thiazolidinediones

A
  • Type 2 DM
  • Pioglitazone (Actose), Rosiglitazone (Avandia)
  • reduces insulin resistance and improves insulin receptor sensitivity
  • reduces glucose, insulin, and FFA
  • useful as secondary agent with Metformin or if patient not tolerating metformin
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21
Q

Safety concerns for Thiazolidinediones

A
  • hepatic toxicity
  • cardiac disease and CHF
  • Actose linked to bladder cancer
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22
Q

Incretin Mimetics

A
  • Type 2 DM
  • synthetic GLP-1
  • reduces fasting and postprandial glucose concentrations
  • stimulates insulin release and inhibits glucagon release
  • slows gastric emptying- appetite suppression and wt loss
  • Liraglutide (Victoza), Exenatide (Byetta)
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23
Q

Adverse effects of Incretin Mimetics and DPP4 inhibitors

A
  • Nausea (40% drop out rate)
  • endocrine malignancies
  • pancreatic inflammation
  • gastroparesis
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24
Q

contraindications for incretin mimetics

A
  • hx or risk of endocrine cancer

- pancreatitis

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25
Q

DPP4 inhibitors

A
  • Type 2 DM
  • blocks DPP4 enzyme from degrading GLP-1 => enhanced GLP-1
  • patient must be capable of producing own GLP-1 and have functioning beta cells
  • Sitagliptin (Januva), Saxagliptin (Onglyza), Linagliptin (Tradjenta)
26
Q

Pramlintide

A
  • Type 1 and 2 DM
  • amylin analogue
  • modulates gastric emptying, prevents post-prandial glucagon
  • produces satiety =>decreased intake and wt loss
27
Q

Adverse effects of Pramlintide

A
  • Nausea (most frequent and severe)

- can cause severe hypoglycemia

28
Q

Sodium Glucose Cotransporters

A
  • Type 2 DM
  • Canagliflozin, Dapaglifozin, Empagliflozin
  • facilitates renal exretion of sodium and glucose via renal tubules
  • acts on postprandial glucose
29
Q

Adverse effects of Sodium Glucose Cotransporters

A

d/t glucose in urine

  • urinary sx
  • genital fungal infection
30
Q

Alpha Glucosidase Inhibitors

A
  • Type 2 DM
  • prevent hydrolysis of disaccharides in gut
  • essential makes patients sucrose intolerant
  • Acarbose and miglitol
  • used as additive therapy
  • GI adverse effects
31
Q

Hypothyroidism

A
  • most common thyroid disorder
  • women > men
  • primary (Hashimotos automimmune) or secondary (to drug therapy or therapies for hyperthyroidism)
  • body systems/metabolism slows down
32
Q

Hypothyroidism treatment

A

Replacement hormones T3 or T4

  • T3 (liothyronine) - very metabolically active, so more difficult to manage
  • T4 (levothyroxine)- less metobolically active, so used more often
33
Q

Safety issue with thyroid hormone replacement

A

potential for overmedication and toxicity

34
Q

Patient education for thyroid hormone replacement

A
  • take on empty stomach- easily binds to other substances in the gut
  • will need to monitor TSH level every 8-12 wks
  • elderly may need lower dose (slow metabolism) and children may need higher dose (hypermetabolic)
35
Q

Thyrotoxicosis

A

condition of thyroid hormone excess

-d/t hyperfunctioning thyroid gland or inflammation of gland resulting in large release of hormone

36
Q

Hyperthyroidism

A

hyperfunctioning thyroid gland => excess hormone production

37
Q

Grave’s disease

A
  • most common cause of thyrotoxicosis
  • autoimmune- thyroid receptor antibodies (TRAb) develop
  • severe, will need definitive treatment
38
Q

Grave’s disease treatment

A
  • for symptoms- noncardioselective beta blocker (Propranol)
  • cure- radioactive iodine (RAI) as treatment of choice OR surgery (pregnant women)
  • can pretreat with antithyroid drugs (ATDs)- for cardiovascular disease and elderly pts
39
Q

Autonomous Thyrotoxicosis

A
  • single or multiple nodules on thyroid gland
  • slower disease
  • Symptoms- primarily cardiovascular, also weakness, muscle wasting, and emotional lability
40
Q

Treatment for Autonomous Thyrotoxicosis

A
  • observation if clinically euthyroid

- surgical removal of nodule if symptomatic

41
Q

TMNG

A
  • Toxic multinodular goiter
  • many nodules on thyroid gland
  • RAI treatment of choice after pretreatment with ATDs
  • requires higher dose of iodine and use low iodine diet prior to treatment
42
Q

Subacute Thyroiditis

A
  • AKA de Quervain thyroiditis
  • often virus causes inflammation =>gland dumps a bunch of hormone at once
  • s/s last 4-10 weeks and then patient returns to normal
  • self-limiting, may need propranolol for symptoms
  • no need for curative therapies or ATDs
43
Q

Beta blockers for hyperthyroidism

A
  • Propranolol and atenolol are drugs of choice
  • block CV and SNS symptoms
  • no glandular changes
44
Q

Iodides for hyperthyroidism

A
  • Lugol’s solution (and others)
  • inhibit organification and proteolysis (shut down thyroid gland function
  • inhibit peripheral deiodination of T4
  • works quickly (24 hrs), useful in toxic patients
  • also augments RAI
  • can use for several months
45
Q

Antithyroid agents

A
  • Propylthiouracil (PTU) and Methimazole (Tapazle)
  • inhibit organification, coupling, and proteolysis
  • not drugs of choice
  • side effects- agranulocytosis, rashes, dyspepsia
46
Q

Radioactive iodine (RAI)

A
  • curative treatment for hyperthyroidism
  • avoid close contact x 11 days
  • avoid pregnancy x 6 mnths
  • side effects- nausea, sore throat, edema of salivary glands
47
Q

Aldosterone

A
  • major mineralocorticoid

- reabsorption of Na in kidney => Na and H2O retention

48
Q

Cortisol

A
  • major glucocorticoid
  • utilization of fuel (fats, carbs, proteins)
  • suppression of inflammation
  • vasoconstriction
49
Q

Androgens

A
  • sex hormones

- precursors of testosterone

50
Q

What is the focus of adrenal pharmacology

A

-replacing deficient hormones

51
Q

Fludrocotrisone (Florinef)

A
  • replaces aldosterone => salt retention

- very potent- watch for s/s of na/water retention

52
Q

s/s of sodium and water retention

A

HTN, rales, edema, bounding pulse, electrolyte abn (hypernatremia, hyperkalemia)

53
Q

Hydrocortisone (Prednisone)

A
  • replaces cortisol

- concern for toxicity- HTN, hyperglycemia, lack of inflammation (poor healing)

54
Q

What group of women may benefit from hormone replacement therapy

A

Younger, perimenopausal women with no history of CVD

55
Q

What group of women may be harmed by hormone replacement therapy

A
  • Older, post-menopausal women with CVD history

- women with high risk of cancer (esp breast)

56
Q

Benefits of hormone replacement therapy

A
  • stabilizes fibrinogen
  • elevates HDL and increases LDL uptake
  • decreases cardiac workload while increasing contractility
  • reduces plasma endothelin levels
  • moderates vascular smooth muscle response to catecholamines
  • improves osteoblast/decreases osteoclastic
  • decreases vaginal dryness
  • decreases skin wrinkling
57
Q

Contraindications to H(R)T

A

breast neoplasms
liver disease
clotting abnormalities
vaginal bleeding post-menopause

58
Q

What non-hormonal agents are available for vasomotor symptoms in menopause

A

Brisdelle (paroxitine with another name)
Venlafaxine (Effexor)
-less effective than hormones

59
Q

Drug of choice for osteoporosis

A

Bisphosphonates

60
Q

Drugs used for osteoporosis

A
  • Bisphosphonates
  • SERMS- raloxifene (Evista)
  • Calcitonin

Advanced Pharmacology (9 decks)

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