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Pathophysiology > Endocrine Disorders > Flashcards

Endocrine Disorders Flashcards

1
Q

Which hormones do the anterior pituitary release?

A

ACTH, TSH, FSH, LH, and GH

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2
Q

Which hormones do the posterior pituitary release?

A

Oxytocin, ADH

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3
Q

What is ACTH?

A

Released by anterior pituitary, triggers adrenal glands to release cortisol in response to stressors

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4
Q

What is the function of growth hormone?

A

Also called somatotropin, stimulates growth/cellular reproduction/cell regeneration

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5
Q

What often results in hypo/hyperfunction of the anterior pituitary glands?

A

Tumors

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6
Q

What disease is result of the posterior pituitary hyperfunction?

A

Syndrome of inappropriate antidiuretic hormone secretion (SIADH)

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7
Q

What prompts the posterior pituitary to release ADH?

A

Osmoreceptors in the hypothalamus–monitor blood solute levels

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8
Q

What clinical consequence results as a result of SIADH?

A

Hyponatremia–too much water being reabsorbed, osmolarity of extracellular fluid decreases

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9
Q

What disease is a result of posterior pituitary HYPOfunction?

A

Diabetes insipidus

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10
Q

What are key clinical manifestations of diabetes insipidus?

A

Polydipsia (frequent drinking), polyuria, hypotonic urine production and hyperosmotic extracellular fluid

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11
Q

What are the two forms of diabetes insipidus?

A

Neurogenic form (lesions of the hypothalamus or pituitary gland interfere with ADH synthesis transporter) or nephrogenic form (inadequate response to ADH in kidney)

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12
Q

What is the cellular composition of the thyroid?

A

Follicular cells and parafollicular cells (C cells)

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13
Q

What is the role of follicular cells and parafollicular cells?

A

Follicular cells secrete iodine CONTAINING thyroid hormone, parafollicular cells secrete calcitonin

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14
Q

What are the two thyroid hormones?

A

T3 (10%) and T4 (90%)

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15
Q

What is calcitonin?

A

Hormone involved in calcium/phosphate homestasis, works opposite of PTH and works to decrease calcium levels in the blood

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16
Q

What are the functions of thyroid hormone?

A

Hormones derived from amino acid TYROSINE (with some iodine added)–circulate bound to plasma proteins, work on target cells to alter expression of genes related to metabolism. Have effect on growth, maturation of tissue, cell metabolism, heat production and oxygen consumption.

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17
Q

What is the feedback loop for thyroid hormone?

A

Hypothalamus secretes TRH (thyrotropin releasing hormone), stimulates anterior pituitary to release TSH, TSH stimulates thyroid gland follicular cells to produce thyroid hormones

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18
Q

What is Hasimoto’s disease?

A

Also called chronic lymphocytic thyroiditis. Autoimmune destruction of thyroid gland due to infiltration of autoreactive B and T cells, damages follicular cells

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19
Q

What can result in hypothyroidism?

A

Hashimoto’s, iodine deficiency, congenital hypothyroidism

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20
Q

What are some of the clinical manifestations of hypothyroidism?

A

Decreased metabolism–weight gain, difficulty generating body heat, lethargy, goiter, myexedma*

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21
Q

What causes goiter?

A

Decrease in thyroid hormone results in increased TSH which stimulates thyroid tissue to proliferate in attempt to increase thyroid hormone production

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22
Q

What is myxedema?

A

Alteration in composition of dermis. Severely advanced hypothyroidism, can result in myxedema coma (in response to infection) which can be fatal. Body’s attempt to compensate for lack of thyroid hormone. Results in puffiness, coarse/sparse hair, periorbital edema, etc.

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23
Q

What is Grave’s disease?

A

Autoimmune disease that stimulates the thyroid gland. T cells become sensitized to thyroid antigens and stimulate B cells to produce IgG antibodies that bind to TSH receptors= thyroid stimulating immunoglobulins

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24
Q

What is the result of thyroid stimulating immunoglobulins in Graves?

A

Binding of autoantibodies to follicular cells results in stimulation and synthesis of thyroid hormone independent of TSH. Negative feedback intact, overrun by immunological stimulation.

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25
Q

Why do goiters occur in hyperthyroidism?

A

Immunological stimulation of thyroid gland, results in hyperproliferation of follicular tissue. With more follicular tissue, causes more thyroid hormone to be released.

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26
Q

What are the types of goiter in hyperthyroidism?

A

Single nodule or multiple nodules (toxic multinodular goiter) on thyroid gland

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27
Q

What are some clinical manifestations of hyperthyroidism?

A

Increased metabolic rate, increased heat production, weight loss, goiter, exophthalmos (bulging of eyes), pretibial myexedema, can result in thyroid storm in severe cases

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28
Q

Why does exophthalmos occur in hyperthyroidism?

A

Immune system attacks muscles and fatty tissue behind the eye and results in inflammation

29
Q

What occurs in thyroid storm?

A

Fast and irregular heartbeat, high fever, diarrhea, agitation

30
Q

What are adrenal glands?

A

Encapsulated pyramid shaped glands that sit on top of the kidney

31
Q

What are the two portions of the adrenal glands?

A

Outer cortex and inner medulla

32
Q

What are the cells of the adrenal cortex called and what are their function?

A

Crofermann cells, secrete and store epinephrine and norepinephrine

33
Q

What are the zones of the adrenal cortex?

A

Zona glomerulosa (outermost layer), zona fasciculata (middle layer), zona reticularis (inner layer)

34
Q

What hormones does the zona glomerulosa produce?

A

Primarily produces mineralocorticoids (aldosterone)

35
Q

Which hormones does the zona fasciculata produce?

A

Glucocorticoids such as cortisol, cortisone, and corticosterone

36
Q

Which hormones does the zona reticularis secrete?

A

Sex hormones such as androgens and estrogens with small amount glucocorticoids

37
Q

What is the cortisol feedback loop?

A

Hypothalamus releases CRH in response to stressor, causes ACTH to be released by the anterior pituitary, ACTH binds to receptors in the zona fasciulata and causes release of cortisol

38
Q

What are the effects of cortisol?

A

Immunosuppressant and counterregulatory hormone, reduces the effects of insulin. Promotes catabolism in skeletal muscle cells, promotes gluconeogenesis, enhances bone resorption (to enhance calcium in blood for muscle contraction) *Fight or flight!

39
Q

What disease is a result of the hyperfunctioning of the adrenal glands?

A

Cushing syndrome

40
Q

What is the PRIMARY cause of Cushing syndrome?

A

Tumors within the adrenal cortex that result in excessive secretion of cortisol

41
Q

What are some SECONDARY causes of Cushing syndrome?

A

Tumors of the anterior pituitary, small cell carcinomas in the lung–enhance production of ACTH or CRH. Also from exogenous corticosteroids used as treatment for other conditions

42
Q

What are some of the clinical manifestations of Cushing syndrome?

A

Weight gain (especially in face, trunk, upper back–central obesity, moon face, buffalo hump from increase in adipose tissue secondary to cortisol), glucose intolerance, muscle wasting/thinning of limbs, osteoporosis, purple striae/bruising (loss of collagen and weakening of integumentary system), hypertension (increased sensitivity to catecholamines, vasoconstriction), suppression of immune system

43
Q

What disease is the result of hypoproduction of the adrenal glands?

A

Addison’s disease–causes high ACTH and low cortisol

44
Q

What is the cause of Addison’s disease?

A

Autoimmune destruction of adrenal cortex

45
Q

What are some clinical manifestations of Addison’s disease?

A

Muscle weakness, fatigue secondary to hypoglycemia, weight loss, hypotension, may lose secondary sex characteristics

46
Q

What are the Islet of Langerhans?

A

Group of cells in the pancreas. Alpha cells (glucagon), beta cells (insulin), and delta cells (somatostatin and gastrin)

47
Q

What is gastrin?

A

Released in the pancreas, serves to stimulate release of gastric acid (break down food in stomach)

48
Q

What initiates the release of insulin?

A

Flooding of glucose into the beta cells

49
Q

What are the target cells of insulin?

A

Skeletal cells, cardiac muscle, liver, adipose tissue

50
Q

What occurs in muscle and adipose tissue in response to insulin?

A

Insulin binds to tyrosine receptor on the surface of the plasma membrane, leads to autophosphorylation of insulin receptor substrate one (IRS1)–causes movement of glucotransporter 4 to cell membrane and allows for glucose to enter cells

51
Q

What causes T1DM?

A

Primary Beta cell defect/failure, absolute deficiency due to atrophy or loss of beta cells secondary to auto-immune mediated destruction. Autoantigens form on the beta cells and the cellular and humoral mediated immunity are activated and attack

52
Q

What are the two types of T1DM?

A

Type 1A= autoimmune, type 1B= non-autoimmune

53
Q

What occurs in T2DM?

A

Insulin resistance with inadequate insulin secretion. Tissues no longer sensitive/responsive to insulin which results in higher glucose levels in blood and decreased uptake/storage

54
Q

What is the role of adipose tissue in T2DM?

A

Serves as active endocrine tissue, secretes adipokines (TNF-a, leptin, adiponectin), contributes to pro-inflammatory state

55
Q

What are some of the pathogenic characteristics of T2DM?

A

Risk factors can contribute to insulin signaling/response, resistance forms in peripheral tissues, beta cells start to lose capacity, inflammatory state contributes to decreased beta cell function by damaging pancreas. Eventually, insulin response no longer able to keep up with demand

56
Q

What role does the liver have in diabetes?

A

Main storage area of glucose, stores it as glycogen when glucose in excess. In fasted state, glucagon stimulates liver to initiate gluconeogenesis. In T2DM, liver does not respond to insulin and doesn’t understand there’s excess glucose (initiates gluconeogenesis anyways)

57
Q

What are three major mechanisms that contribute to tissue damage secondary to hyperglycemia?

A

Oxidative stress, glycation, polyol pathway

58
Q

What is the process of glycation?

A

Enzymes add glucose to proteins= glycosylation, when excess more of this occurs and accumulates which results in advanced glycation end products (AGE)

59
Q

What occurs in the polyol pathway?

A

Glucose converted to fructose through enzymatic reactions and enzymes for this pathway found in tissues that are insulin independent (nerves, retina, glomerulus, vasculature, vessels), results in oxidative stress, glucose floods into these cells and is coverted to soribitol (a polyol) and then fructose. Sorbitol causes changes in osmotic pressure which results in swelling and complications

60
Q

What are insulin independent tissues?

A

These cells have glucose transporters at their cell surface, always take in glucose when it’s high

61
Q

What is the most common complication of diabetes?

A

Neuropathies

62
Q

What areas are more subject to microvascular disease in diabetes?

A

Small capillaries in retina and kidney

63
Q

What contributes to the pathophysiology of macrovascular disease in diabetes?

A

Glycation and AGE accumulation increase the athlerosclerotic process and contribute to CAD, stroke, peripheral artery disease. Hyperglycemia can result in endothelial dysfunction and formation of fibrous plaques and lesions

64
Q

What hormones work to maintain calcium homeostasis?

A

Calcitonin and parathyroid hormone

65
Q

What glands releases parathyroid hormone and calcitonin?

A

PTH= parathyroid gland, thyroid= calcitonin

66
Q

What does PTH result in?

A

Stimulates bone resorption and increase circulating blood calcium, tells kidney to absorb more, activates Vitamin D

67
Q

What are the clinical manifestations of hyperparathyrodism?

A

Osteoporosis, high levels of calcium= kidney stones, hypercalcemia, moans + groans/confusion (nerves cannot effectively fire due to increased calcium)

68
Q

What causes the microvascular complications of clients with DM?

A

The capillary basement membranes thicken and there is endothelial cell hyperplasia

69
Q
A

Pathophysiology (12 decks)

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