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Physiology > Endocrine > Flashcards

Endocrine Flashcards

1
Q

types of hormones

A

-amino acids -> peptides
-cholesterol -> steroids
-tyrosine -> amines

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2
Q

Amines

A

-T3 and T4
-norepinephrine and epinephrine
-dopamine

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3
Q

steroids

A

-cortisol (glucocorticoid)
-aldosterone
-DHEA and androstenedione
-testosterone
-estradiol
-progesterone
-estriol
-1,25-dihydroxycholecalciferol

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4
Q

hypothalamic-pituitary relationships

A

-hypothalamus -> posterior pituitary -> ADH (to kidney) or oxytocin (to mammary glands)
-hypothalamus -> hypothalamic hormone via hypophysial portal vessel -> anterior pituitary -> anterior pituitary hormone released -> target organ

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5
Q

anterior pituitary

A

-hypothalamic hormone stimulates -> anterior pituitary hormone
-GnRH -> FSH/LH -> gonads
-CRH -> ACTH -> adrenal cortex
-TRH -> TSH -> thyroid
-TRH+dopamine -> prolactin -> mammary
-GHRH + somatostatin -> GH -> liver (and all of body)
-dopamine is the only amine -> everything else is peptide

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6
Q

up and down regulation

A

-dose-response relationship- dependent on concentration of hormone
-regulation:
-change in # of receptors
-change in affinity of receptors
-ex. chronic high T3 -> decrease TRH affinity of receptors
-ex. chronic high progesterone -> down regulates its own receptors in uterus AS WELL as estrogens receptors
-ex. prolactin -> increase # receptors in breast
-ex. GH -> increase # receptors in muscle and liver
-ex. estrogen increase # of its receptors in uterus AND LH receptors in ovaries

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7
Q

posititive feedback

A

-follicular phase in menstruation- estrogen -> anterior pituitary -> GnRH -> FSH/LH -> FSH/LH stimulate more estrogen -> ovulation
-child birth -> dilation of cervix -> oxytocin release from posterior pituitary -> uterine contraction -> dilation of cervix -> repeat

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8
Q

growth hormone

A

-GHRH + somatostatin -> GH -> somatomedins
-FUNCTION- insulin resistance, increase protein/organ growth, increase linear growth
-STIMUALTE- decreased glucose, decrease free fatty acid, fasting, puberty (estrogen, test), exercise, stress, stage 3 and 4 sleep, alpha adrenergic agonist
-INHIBIT- somatostatin, somatomedins, GH, increase glucose, increase fatty acids, obesity, menopause, beta adrenergic agonist, pregnancy

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9
Q

dwarfism/acromegaly

A

-dwarfism- GH deficient, delayed puberty, failed growth, mild obesity
-GH excess (GH secreting pituitary adenoma)
-prior to puberty -> gigantism- linear growth
-after puberty ->acromegaly- increase organ size, insulin resistant, course features

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10
Q

prolactin

A

-TRH + dopamine -> prolactin -> breast -> milk, breast growth, ovulation suppression
-dopamine > TRH in males and non-pregnant females
-STIMULATE- pregnancy, suckling, dopamine antagonist, stress, sleep, TRH
-INHIBIT- prolactin (stimulates dopamine), dopamine, somatostatin
-prolactin deficiency- caused by destruction of anterior pituitary
-prolactin excess*** -> hypothalamic-pituitary stalk damage causes loss of dopamine and its inhibition -> galactorrhea and infertility

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11
Q

posterior pituitary: ADH*

A

-hypovolemia -> decrease MAP -> vagus -> posterior pituitary -> ADH -> increase H2O reabsorption (decrease osmolarity) AND smooth muscle contraction (vasoconstriction)
-STIMULATE- increase osmolarity, low ECF, angiotensin 2, pain, nausea, hypoglycemia, nicotine, opiate
-INHIBIT- decrease osmolarity, alpha agonist, ANP
-central diabetes insipidus** (damage to stalk)- cant secrete ADH -> excess dilute urine, thirst, dehydration, high osmolarity
-nephrogenic diabetes insipidus**- ADH normal but collecting ducts are unresponsive -> same S&S
-SIADH- excess ADH due to lung tumor -> increase water reabsorption, decrease osmolarity, concentrated urine

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12
Q

posterior pituitary: oxytocin

A

-dilation of cervix, orgasm, suckling, conditioned response -> oxytocin -> uterine contraction and lactation
-STIMULATE- suckling, dilation of cervix, orgasm, sight/sound/smell of infant
-INHIBIT- opiates

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13
Q

thyroid hormone

A

-TRH -> TSH -> thyroid -> T3 (active),T4 (inactive) -> cardiovascular (increase CO and O2), growth, BMR (increase O2 consumption and heat), metabolism (increase glucose), nervous system
-STIMULATE- TSH, thyroid stimulating immunoglobulin, TBG (pregnancy)
-INHIBIT- iodine deficiency/excessive, decrease TBG (liver disease)

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14
Q

hyperthyroidism

A

-causes: neoplasm, excessive TRH/TSH, exogenous T3/T4
-high T3, T4
-hyperexcitablity, hyperreflexia, irritabilty, wt loss, increase foot intake, heat, high BMR, tachy, high CO, weak, tremor
-goiter, exophthalmos
-high TSH if anterior pituitary defect
-decrease TSH due to neg feedback
-graves disease- increase thyroid stimulating immunoglobulin -> hypertrophy (low TSH)

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15
Q

hypothyroidism

A

-causes: thyroiditis (hashimoto), thyroidectomy, iodine deficiency, congenital (cretinism), decrease TRH/TSH
-decrease BMR, wt gain, decrease heat, decrease CO, hypoventilation, tired, mental slowness, drooping eyelids, slow growth, mental retardation
-myxedema- severe
-goiter
-child- cretinism- mental retardation
-adult- slow, impaired memory, decrease mental capacity (all other symptoms)
-high TSH from negative feedback in thyroid gland (hashimoto)
-low TSH from defect in hypothalamus or anterior pituitary
-low T3, T4*

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16
Q

ACTH

A

-CRH -> ACTH -> adrenal cortex -> cortisol
-STIMULATE- decrease cortisol, sleep-wake transition, stress (hypoglycemia, surgery, trauma, psych), ADH, alpha agonist, beta antagonist, serotonin
-INHIBIT- high cortisol, opiods, somatostatin
-Conn syndrome
-addisons
-cushings
-21beta-hydroxylase deficiency
-17 alpha-hydroxylase deficiency

17
Q

glucocorticoids

A

-cortisol
-increase gluconeogenesis
-increase proteolysis
-increase lipolysis
-decrease glucose use- high blood sugar
-decrease insulin sensitivity
-inhibit inflammatory response
-suppress immune system
-enhance vascular response to catecholamines- hypertension
-inhibit bone formation-osteoporosis
-increase GFR
-decrease REM- tired

18
Q

action of mineralocorticoids

A

-aldosterone
-increase Na reabsorption
-increase K secretion
-increase H secretion
-frequent urination
-hypertension
-thirst
-weakness
-tingling, cramps

19
Q

adrenal androgens

A

-DHEA, androgens
-females- stimulate growth of pubic and armpit hair, stimulate libido
-males- same as test

20
Q

Conn syndrome

A

-mineralcorticoids
-aldosterone secreting tumor -> increase Na reabsorption, K and H secretion
-hypertension*
-hypokalemia*
-metabolic alkalosis
-decrease renin*
-frequent urination, increase thirst
-weakness, tingling, cramping

21
Q

Addisons Disease

A

-primary adrenocortical insufficiency
-increase ATCH* (negative feedback)
-autoimmune destruction of adrenal cortex
-decrease cortisol- hypoglycemia, anorexia, wt loss, nausea, vomiting, weakness
-decrease aldosterone- hyperkalemia, metabolic acidosis, hypotension
-decrease androgens- decrease pubic hair, decrease libido
-orange pigment to skin

22
Q

cushing disease

A

-excess glucocorticoids (cortisol)* -> hypersecretion of ACTH* from pituitary adenoma
-hyperpigmentation
-hyperglycemia*
-thin extremities
-central obesity
-round face
-supraclavicular fat
-buffalo hump
-poor wound healing
-osteoporosis
-striae
-virilization and menstrual disorders

23
Q

administration of Synthetic Glucocorticoid (Dexamethasone) to a Normal Person

A

-cushing syndrome
-spontaneous or pharmacologic
-decrease ACTH (neg feedback)
-primary adrenal hyperplasia
-high cortisol*
-same S&S as cushing disease

24
Q

21 beta-hydroxylase deficiency

A

-congenital adrenal hyperplasias
-decrease cortisol* and aldosterone*
-causes increase in androgens (DHEA- androgen precursor increase)*
-increase ATCH* (neg feedback)
-DECREASED deoxycorticosterone (DOC - aldosterone precursor)*
- INCREASED urinary 17-ketosteroids (androgen precursor)
-virilization in females
-early growth (linear)
-early pubic hair
-symptoms of cortisol and aldosterone deficiency
-hypotension
-hyperkalemia
-salt wasting -> low Na

25
Q

insulin

A

-beta cells
-storage and abundance
-STIMULATE- increase glucose, increase AA, increase fatty acid and ketoacid, glucagon, cortisol, GIP, K, vagal stim (ACh), obesity
-INHIBIT- decrease glucose, fasting, exercise, somatostatin, alpha agonist
-increase glucose into cells, increase glycogen, increase protein, increase fat deposition, decrease lipolysis, increase K into cells
-decrease blood glucose, amino acid, fatty acid, ketoacid, K
-diabetes mellitus type 1- decrease insulin* -> high blood glucose, fatty acid, and K
-diabetes mellitus type 2- insulin resistance of target tissue

26
Q

glucagon

A

-utilization and starvation
-STIMULATE- fasting, decrease glucose, increase AA, CCK, beta agonist, ACh
-INHIBIT- insulin, somatostatin, increase fatty acid and ketoacid
-increase blood glucose, fatty acid, ketoacid

27
Q

calcium

A

-60% is ultrafilterable and 50% of that is ionized (active)
-bone resorption - PTH and vitamin D
-calcitonin - inhibits bone resorption
-reabsorption from kidney- PTH
-absorption from SI -> vitamin D
-decrease Ca -> increase PTH -> increase bone resorption, increase Ca reabsorption from kidney, decrease phosphate reabsorption from kidney, increase Ca absorption from intestine (indirect via vitamin D) -> increase Ca

28
Q

Surgical Hypoparathyroidism

A

-Thyroidectomy / Parathyroidectomy
-decrease PTH
-hypocalcemia- decrease bone resorption, decrease renal and intestinal absorption
-hyperphosphatemia- decrease urine phosphate
-decrease vitamin D
-(same as congenital hypoparathyroidism)
-hyperreflexia, twitching, cramps. tingling, weakness
-chvostek sign- facial twitching when tapping on facial nerve
-trousseau sign- carpopedal spasm upon inflation of BP cuff
-low urine cAMP

29
Q

primary hyperparathyroidism

A

-parathyroid adenoma
-excessive PTH
-hypercalcemia* (and uria)- high bone resorption, renal and intestinal absorption
-hypophosphatemia- decrease renal phosphate reabsorption -> phosphaturia
-stone, bones, groans
-high vitamin D
-High Ca -> inhibits ADH -> polyuria and dipsia
-Lung Cancer Producing Parathyroid Hormone–Related Peptide (PTH-rp)- SAME BUT PTH IS LOW* (suppressed by hypercalcemia)
-stones (hypercalcemia), bones (increase bone resorption), groans (constipation/nausea), and psychologic overtones (hyporefelxia, lethargy, coma, death)
-high cAMP

30
Q

secondary hyperparathyroidism

A

-AKA vitamin D deficiency/chronic renal failure
-excessive PTH secondary to hypocalcemia -> increase bone resorption
-low vitamin D -> osteomalacia
-low phosphaturia

31
Q

vitamin D

A

-1alpha hydroxylase
-increase Ca absorption in kidney and intestine, increase bone resorption
-increase Ca
-rickets- child -> low vitamin D -> bone growth failure and deformity due to low Ca and phosphate
-osteomalacia -adult -> low vitamin D -> new bone fails to mineralize -> bending and softening of bones
-vitamin D resistance -> congenital absence of 1 alpha-hydroxylase OR chronic renal failure -> osteomalacia

32
Q

Car Accident That Severs the Hypothalamic-Pituitary Stalk

A

-prolactin- excess -> loss of dopamine and therefore inhibition -> Galactorrhea and infertility result
-ADH- Central diabetes insipidus -> failure to secrete ADH -> excess dilute urine, high serum osmolarity, thirst and dehydration
-orthostatic hypertension
-serum osmolarity high
-PTH- Initially ↑ serum Ca2+ (thru bone resorption) → once serum Ca2+ is high enough, becomes neg feedback to inhibit PTH release → usually high Ca2+ stimulates calcitonin release from hypothalamus to decrease Ca2+ ⇒ now DECREASED calcitonin → hyperCa2+ → PTH forever inhibited from secretion

33
Q

alpha agonist and beta agonist

A

-STIMULATES:
-growth hormone (inhibited by beta agonist)
-ACTH (and beta antagonist)

-INHIBITS:
-ADH
-insulin

-beta agonist - stimulates glucagon

Physiology (24 decks)

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