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Clin Path > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

endocrine system

A

a system of organs; that by the way of hormones, coordinate and influence other body systems in order to maintain homeostasis

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2
Q

hormones

A

chemical messengers that influence activity of target cells
produced by ductless glands
travel via the bloodstream

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3
Q

neurohormones

A

produced by specialized neurons

stored in bulb like terminals; released into capillaries and travel to target organs

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4
Q

ADH (antidiuretic hormone; vasopressin)

A 
conserve water (water retention by the kidneys)
constricts arterioles (raises blood pressure)
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5
Q

oxytocin

A 
stimulates uterine contraction durin labor
milk ejection (nursing)
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6
Q

posterior pituitary gland (neurohypophysis)

A

neural tissue; stores hormones produced by hypothalamus; releases upon neural stimulation from hypothalamus

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7
Q

anterior pituitary (adenohypophysis)

A

endocrine gland; produces hormones; connected to hypothalamus by portal vessels
regulated by releasing and inhibiting hormones from the hypothalamus and by feedback from t.organ

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8
Q

growth hormone (GH)

A

promotes linear growth of bones, muscle mass, and organ size, decreases fat mass, increases blood glucose

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9
Q

Adrenocorticotropic hormone (ACTH)

A

stimulates production and secretion of hormones from adrenal cortex:
cortisol and aldosterone: adrenal lecture
androgens: libido, secondary sex characteristics in females

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10
Q

Prolactin

A

stimulates breast development, milk production and release, inhibits ovulation

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11
Q

thyroid-stimulating hormone (TSH)

A

stimulates production and secretion of thyroid hormones (t3/t4) by thyroid gland

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12
Q

follicle-stimulating hormone (FSH)

A

Females: stimulates follicle development and estrogen production by ovaries
Males: stimulates sperm maturation in testes

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13
Q

Luteinizing hormone (LH)

A

Females: stimulates ovulation and formation of corpus luteum. Stimulates estrogen and progesterone production by ovaries
Males: Stimulates testosterone production in testes; important for development of sperm and male secondary sex characteristics

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14
Q

hyposecretion of hormones

A

agenesis, atrophy, destruction

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15
Q

hypersecretion of hormones

A

secreting tumor, hyperplasia

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16
Q

primary endocrine disorder

A

defects within the hormone-secreting target gland

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17
Q

secondary endocrine disorder

A

abnormal hypothalamic-pituitary secretion

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18
Q

hypopituitarism (hyposecretion of ant. pituitary hormones)

A

hyposecretion of pituitary hormones

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19
Q

hypopituitarism cause

A

pituitary adenoma (most common cause in adults); nonsecreting pituitary tumor; destroys functioning pituitary tissue; (others)

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20
Q

hypopituitarism clinical consequences

A

hypogonadism-due to low FSH and LH (most common); premenopausal females: menstrual disorders, oligomenorrhea, amenorrhea, decreased libido, infertility, breast shrinkage;
males: loss of sexual function, loss of secondary sex characteristics (decrease in muscles mass and facial and body hair), infertility

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21
Q

hypopituitarism clinical consequence 2

A 
Growth hormone (GH) deficiency
-children-short stature (decrease growth in long bones)
-adults: (abnormal body composition-increased fat, decreased muscle mass)
Thyroid-stimulating hormone (TSH) deficiency (hypothyroidism)
Adrenocorticotropic hormone (ACTH) deficiency (adrenal insufficiency)
Prolactin deficiency (failure of milk production)
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22
Q

panhypopituitarism

A

loss of all anterior pituitary hormones

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23
Q

hypersecretion of Ant. pituitary hormones cause

A

hypersecreting pituitary adenoma; each tumor secretes a specific pituitary hormone

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24
Q

hypersecretion of ant pituitary hormones consequences

A

increased ACTH:Cushing’s syndrome
increased TSH: hyperthyroidism
increased Prolactin (prolactinoma)
increased growth hormone: gigantism; acromegaly

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25
Q

acromegaly

A

coarse facial features, cardiovascular complications, musculoskeletal problems

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26
Q

increases glycogen formation

A

decrease blood glucose conc

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27
Q

decreases glycogenolysis

A

decrease blood glucose conc

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28
Q

increases glucose uptake into cells

A

decrease blood glucose conc

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29
Q

decreases gluconeogenesis

A

decreases blood glucose conc

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30
Q

increases protein synthesis (anabolic)

A

decrease blood amino acid conc

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31
Q

increases fat deposition

A

decrease blood fatty acid conc

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32
Q

decreases lipolysis

A

decrease blood ketoacid conc

33
Q

increases K+ uptake into cells

A

decrease blood K+ conc

34
Q

pancreatic somatostatin

A

inhibits the release of insulin and glucagon; modulates the response of these hormones to the ingestion of food

35
Q

amylin

A

decreased in insulin-dependent diabetics; decreases postprandial blood glucose

36
Q

incretins

A

released by si in response to food: GLP-1; increases insulin secretion; delays gastric emptying and decreases food intake

37
Q

Counterregulatory hormones: hypoglycemia

A

glucagon, growth hormone, cortisol, and catecholamines (epinephrine)

38
Q

pathogenesis of Type 1 diabetes

A

insulin dependent: genetic factors, environmental factors, autoimmunity (insulitis early and fibrosis late)

39
Q

secondary causes of diabetes

A

endocrine diseases, diseases of the exocrine pancreas, drug-induced, viral infections, impaired fasting glucose (IFG), impaired glucose tolerance (IGT)

40
Q

metabolic derangements of type 1 diabetes

A

polyphagia, polydipsia, polyuria

41
Q

pathogenesis of type 2 diabetes

A

non-insulin dependent: genetic factors, obesity, beta cell defect, alpha cell defect; less ketone prone (amyloid late)

42
Q

ketoacidosis

A

due to severe insulin deficiency; marked hyperglycemia and glycosuria, increase in lipolysis & ketoacids; acidosis

43
Q

Nonketotic hyperosmolar state

A

mild insulin deficiency; gradual onset, severe hyperglycemia and hyperosmolality, no ketosis or metabolic acidosis, higher mortality

44
Q

hypoglycemia

A

epinephrine related symptoms (sweating, shakiness, palpitations, headache)…. CNS related symptoms (altered mental status, stupor, coma, seizures, permanent brain damage, death)

45
Q

microvascular complications of diabetes

A

retinopathy, nephropathy, neuropathy

46
Q

macrovascular complications of diabetes

A

heart, brain, peripheral vasculature

47
Q

zona glomerulosa

A

secretes mineralocorticoids; end product is aldosterone

48
Q

zona fasciculata

A

secretes glucocorticoids; end product is cortisol

49
Q

zona reticularis

A

secrets androgens; DHEA and androstenedione

50
Q

ACTH dependent (increased ACTH)

A

pituitary adenoma and solid tumors (oat cell carcinoma of lung)

51
Q

ACTH independent (decrease ACTH)

A

adrenal adenoma & carcinoma (atrophy), and exogenous glucocorticoid administration

52
Q

primary adrenal insufficiency

A

ACTH levels are high (to compensate for low cortisol); Addison’s disease, infection, infiltrative

53
Q

secondary adrenal insufficiency

A

ACTH levels are low due to exogenous corticosteroid administration

54
Q

loss of glucocorticoids

A

hypoglycemia

55
Q

loss of mineralocorticoids

A

hypovolemia, hypotension, hyponatremia, hyperkalemia

56
Q

loss of adrenal androgens

A

decreased axillary and pubic hair in women; menstrual irregularities

57
Q

increased ACTH levels (primary adrenal insufficiency)

A

hyperpigmentation (addison’s disease)

58
Q

aldosterone functions

A

retention of sodium by the kidney, enhanced exretion of potassium by the kidney, enhanced excretion of hydrogen ion by the kidney

59
Q

primary aldosteronism (conn’s syndrome)

A

aldosterone producing adenoma or hyperplasia; increase BP and decrease serum (K+), metabolic alkalosis, no edema;

high plasma aldosterone, low plasma renin

60
Q

secondary aldosteronism

A

hypovalemia, CHF, nephrotic synd, cirrhosis (high plasma renin)

61
Q

congenital adrenal hyperplasia

A

21 hydroxylase deficiency-most common; excess androgen secretion; decreased cortisol and aldosterone secretion (masculinization);

high ACTH due to low cortisol levels

62
Q

adrenal medulla disorder: pheochromocytoma

A

increase catecholamines = increase BP (10% rule)

63
Q

T3 and T4

A

T3 is more potent
T3 and T4= bound to plasma proteins (TBG)
Only free fractions are biologically active; alterations of binding protein levels affect total T4 and T3 but not free T4 and T3

64
Q

Actions of thyroid hormones

A

Growth, CNS development, Cardiovascular, metabolism

65
Q

TSH measurement

A

used to determine thyroid gland function

66
Q

Hyperthyroidism

A

increase in T4 and gland fxn

67
Q

Thyrotoxicosis

A

increase in T4 from any source

68
Q

Primary hyperthyroidism

A

graves disease, goiter, adenoma or cancer

69
Q

secondary hyperthyroidism

A

tsh-secreting tumor, ectopic T4 (ovarian tumor)

70
Q

primary hypothyroidism

A

congenital, hashimoto’s thyroiditis, iodine deficiency, thyroidectomy

71
Q

secondary hypothyroidism

A

hypopituitarism (decrease TSH); hypothalamic lesion (decrease TRH)

72
Q

Grave’s disease

A

thyroid stimulating immunoglobulin binds to gland and mimics TSH (exopthalmos, pretibial myxedema) most common in young women

73
Q

Hashimoto’s thyroiditis

A

autoimmune t-cell mediated gland injury; most common cause in USA, painless goiter

74
Q

hyperthyroidism symp

A

anxious, tremor, tachycardia, heat intolerance, diarrhea, weight loss

75
Q

hypothyroidism symp

A

sluggish, tired, bradycardia, cold intolerance, constipation, weight gain

76
Q

thyroid fxn tests-hyperthyroidism

A

increase RAI, decrease in TSH

77
Q

thyroid fxn tests-hypothyroidism

A

decrease RAI

78
Q

thyroid neoplasm-adenomas

A

benign, painless; most nonfunctioning (cold) some functioning (hot)

79
Q

thyroid neoplasm-carcinomas

A

most nonfunctioning (cold); frequency: papillary>follicular>medullary (aggressiveness: medullary>follicular>papillary)

Clin Path (3 decks)

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