Endocrine Flashcards
1
Q
Thyroid development
- derived from
- connections to tongue and what it turns into
- thyroglossal duct cyst: sxs
- thyroid follicular and parafollicular cells derived from
A
- primitive pharynx
- thyroglossal duct -> normally disappears but can persist as pyramidal lobe
- anterior midline neck mass that moves w/ swallowing
- endoderm
2
Q
Adrenal Cortex
- derived from
- glomerulosa: primary reg, hormone produced, hormone class
- fasiculata
- reticularis
A
- mesoderm
- Angiotensin II, Aldosterone, mineralcorticoids
- ACTH, cortisol, glucocorticoids
- ACTH, DHEA, androgens
3
Q
Adrenal Medulla
- dervied from
A
- neural crest
4
Q
Ant pit
- secretes
- derived from
- basophila
A
- FSH, LH, ACTH, TSH, prolactin, GH,
- oral ectoderm
- FSH, LH, ACTH, TSH
5
Q
Post pit
- secretes
- created
- transported
- derived
A
- vasopressin and oxytocin
- hypothalamus
- post pit via neurophysins
- neuroectoderm
6
Q
Endocrine Pancreas
- alpha cell
- beta cell
- delta cell
- arise from
A
- glucagon
- insulin
- somatostatin
- pancreatic buds
7
Q
Insulin
- synthesis: 1st product, 2nd product, final product
- function: binds, next steps
- anabolic effects: muscle, adipose, glycogen, triglyceride, Na, proteins, K and AA, glucagon, lipolysis
- insulin dependent glucose transporters: location
- organs with non insulin dependent glucose transporters: BRICK LIPS
- regulation
- insulin binding pathway
- insulin release pathway
A
- preproinsulin -> cleavage of presignal -> proinsulin -> cleavage of proinsulin -> exocytosis of insulin and C peptide
- binds insulin receptor -> induce glucose uptake -> gene transcription
- increase glucose in muscle and adipose, glycogen synthesis and storage, triglyceride synthesis, Na retention, protein synthesis, cellular uptake of K and AA; decreased glucagon release, and lipolysis
- GLUT 4: adipose and muscles
- Brain, RBC, Intestine, Cornea, Kidney, Liver, Iselt cells, Placenta, Spermatocyte
- controlled by glucose concentration in blood, increase in glucose causes increase in insulin
- insuling binds receptor -> PIP 3 activated -> glut 4 to membrane -> glucose into cell
- glucose binds glut2 -> ATP/ADP ratio increased -> K channels close -> voltage gated Ca channel open -> increase in intracellular Ca -> exocytosis of insulin
8
Q
Glucagon
- made by
- function
- regulation
A
- alpha cells of pancrea
- glycogenolysis, gluconeogenesis, lipolysis, ketogenesis -> elevates blood sugar to maintain homeostasis
- secreted in response to hypoglycemia
9
Q
Hypothalamic - Ant Pit Hormones
- ADH: function,
- CRH: function
- Dopamine: function
- GHRH: function
- GnRH
- MSH
- Oxytocin
- Prolactin
- Somatostatin
- TRH
A
- ADH: increase in water permeability to DCT and collecting guct -> increase water reabsorption
- CRH: Increase ACTH and beta endorphin
- Dop: decrease in prolactin
- GHRH: increase GH
- GnRH: increase FSH, LH
- MSH: increase melanogenesis by melanocytes
- Oxy: causes uterine contraction during labor, responsible for milk letdown reflex
- Prolactin: decrease in GnRH
- Somato: decrease in GH, TSH
- TRH: Increase in TSH, prolactin
10
Q
Prolactin
- source
- function: breast milk, fertility
- reg: inhibition,
A
- ant pit
- stimulates milk production, inhibits ovulation and spermatogenesis by inhibiting GnRH synthesis and release
- inhibited by dopamine; prolactin inhibits own secretion by increasing dopamin synthesis
11
Q
Growth Hormone
- other name
- production
- function
- regulation: released in response to, inhibited by
- excess secretion of GH causes -> TX
A
- somatotropin
- ant pit
- linear growth and muscle mass
- pulsatile, released in response to growth hormone releasing hormone, which is increased during exercise, deep sleep, puberty, hypoglycemia; inhibited by glucose and somatostatin
- acromegaly of gigantism; TX w/ somatostatin analogs
12
Q
Appetite Reg
- Ghrelin: function; produced by; sleep deprivation/ prader willi causes; location of effect
- Leptin: function; produced by; mutation causes; sleep deprivation or starvation causes
- Endocannabinoids: location; function; exogenous
A
- stimulates hunger and GH release; produced by stomach; sleep deprivation or prader willi causes increased ghrelin production; lateral area of hypothalamus
- satiety hormone; produced by adipose tissue; congenital obesity; decrease in leptin production
- act at cannabinoid receptor in hypothalamus to increase appetite; reason why exogenous cannabinoid causes the munchies
13
Q
Anti-diuretic Hormone
- other name
- production
- function
- regulation
- central diabetes insipidus vs nephrogenic
A
- vasopressin
- hypothalamus and stored and secreted in post pit
- reg serum osmolality and blood pressure via reg of aquaporin channel insertion in principal cells
- plasma osmolality/ hypovolemia
- ADH decreased vs ADH normal
14
Q
Cortisol
- source
- function: increases, decreases
- regulation
A
- adrenal zona fasiculata
- increase appetite, DP, insulin resistance, gluconeogenesis/lypolysis/proteolysis; decreases fibroblast activity, inflammatory and immune responses, bone formation
- CRH stimulates ACTH release causes cortisol
15
Q
Ca homeostasis
- forms
- increased pH
- decreased pH
A
- ionized, hound to albumin, bound to anions
- albumin binds more Ca -> decrease free Ca -> increase PTH
- albumin binds less Ca -> increase in free Ca -> decrease PTH
16
Q
PTH
- source
- function
- reg: increases PTH; decreases PTH
A
- chief cells of parathyroid
- increase bone resorption of Ca and PO4, kidney reabsorption of Ca in DCT, and D3 production; decrease reabsorption of PO4 in PCT
- decreased serum Ca, high PO4, low serum MG; very low MG
17
Q
Calcitonin
- source
- function
- reg
A
- parafollicular cells of thyroid
- decrease bone resorption of Ca
- increase serum Ca -> calcitonin secretion
18
Q
Thyroid Hormones
- source
- secreted form vs activated form
- function- 6 B’s
- reg
- TBG: what is it, function, increased by, decreased by
A
- follicles of thyroid
- T4 vs T3
- Brain maturation, bone growth, beta adrenergic effects, increase basal met rate, increase blood sugar, breaks down lipids
- TRH -> TSH -> T4 -> T3 -> w/ neg feeback from T3/T4
- thyroxine binding gobulin; binds T3 and T4 making it inactive in blood -> will increase w/ estrogen, heaptic failure, steroid use, nephrotic syndrome
19
Q
Signaling Pathways of endocrine hormones
- cAMP: pathway; FLAT ChAMP CGGH
- cGMP: BAD GraMPa
- IP3: GOAT HAG
- Intracellular receptor: PEE CAT TV
- Tyrosine Kinase: Get Found In the MAP
- Non TK: PIGGlET
A
- G-alpha-s -> AC -> cAMP -> PKA; FSH, LH, ACTH, TSH, CRH, hCG, ADH, MSH, PTH, calcitonin, GHRH, glucagon, histamine
- BNP, ANP, NO
- GnRH, Oxytocin, ADH, TRH, histamine, angiotensin II, Gastrin
- Progesterone, estrogen, tetosterone, cortisol, aldosterone, T3/T4, Vit D
- Insulin, IGF-1, PDGF
- Prolactin, Immunomodulators, GH,G-CSF, Erythropoeitin, Thrombopoeitin
20
Q
Adrenal Steroid Synthesis
- aldosterone
- glucocorticoids: 2 pathways; inhibited by
- androgens
- estrogen
A
- chol -> pregnenolone -> progesterone + 21- hydroxylase -> 11-deoxycorticosterone + 11 beta hydroxylase -> corticosterone -> aldosterone
- chol -> pregnenolone -> 17 hydroxy pregnenolone -> 17 hydroxy progesterone -> 11 deoxy cortisol -> cortisol –OR– Chol -> pregnenolone -> progeterone -> 17 hydroxy progesterone -> de oxy cortisol -> cortisol; metyrapone
- chol -> pregnenolone -> 17 hydroxy pregnenolone -> DHEA -> androstenidione -> testosterone -> DHT –OR – chol -> pregnenolone -> progesterone -> 17 hydroxy pregnenolone -> androstenidion -> testosterone
- aromatase, from androstenidione or testosterone
21
Q
Androgen Enzyme Deficiencies
- 17 alpha hydroxylase: amount of mineral corticoids, amount of cortisol, amount of sex hormone, BP, [K], labs, presentation
- 21 hydroxylase: amount of mineral corticoids, amount of cortisol, amount of sex hormone, BP, [K], labs, presentation
- 11 beta hydroxylase: amount of mineral corticoids, amount of cortisol, amount of sex hormone, BP, [K], labs, presentation
A
- used to make 17 hydroxy pregnenolone and progesterone -> will result in lots of mineral corticoids, low cortisol and androgens , high BP, low K; XY: ambiguous genitalia w/ undescended testes and XX lacks seconday sex development
- low mineral corticoids, low cortisol, high sex, low, BP, high K, high renin and 17-hydroxy progesterone; salt wastin or precocious puberty w/ virilization in women
- low aldosterone but high deoxycorticosterone, low cortisol, high sex, high BP (deoxycoritco), decreased K, decreased renin, virilization in women
22
Q
Cushing syndrome
- etiology
- causes (3 ish)
- findings
- DX
- Exogenous glucocorticoids or adrenal tumor
- Ectopic ACTH
- Cushing DX
A
- increased cortisol
- exogenous corticosteroids, adrenal adenoma/ hyperplasia/ carcinoma; ACTH secreting pit adenoma
- hypertension, weight gain, moon face, buffalo hump, skin changes, hirsutism, amenorrhea
- increased free cortisol on 24 hr UA, increased late night salivary cortisol, no suppression w/ low dose dexamethasone
- suppressed ACTH test
- elevated ACTH w/ no suppression on dexamethasone test and no increase in ACTH and cortisol w/ CRH
- elevated ACTH w/ adequate suppression on dexamethason test and an increase in ACTH and cortisol on CRH stim test
23
Q
Nelson Syndrome
- what is it
- sequalae
- sxs
- tx
A
- removal of cortisol feedback after bilateral adrenalectomy for refractory cushing dx
- enlargement of existing ACTH secreting pit adenoma
- hyperpigmentation, headache, bitemporal hemianopia
- pit radiation or resection
24
Q
Adrenal insufficiency
- what is it
- sxs
- tx
A
- inability of adrenal gland to generate enough glucocorticoids +/- mineralcorticoids
- weakness, fatigue, orthostatic hypotension,
- glucocorticoid and mineralcorticoid replacement
25
Q
Primary Adrenal Insufficiency
- what is it// caused by
- acute
- addisons dx
- waterhouse- friedrichsen: what is it
A
- deficiency of aldosterone and cortisol production because of loss of gland function
- hypotension, hypekalemia, metabolic acidosis, skin/mucosal hyperpigmentation
- sudden, presents w/ shock in acute adrenal crisis
- caused by adrenal atrophy/destruction by DX (Autoimmune or TB)
- acute primary adrenal insuff bc of adrenal hemmorrhage associated w/ septicemia, DIC and endotoxin shock from N meningitidis
26
Q
Secondary Adrenal insufficiency
- caused by
- sxs
A
- decreased in pit ACTH production
- no hyperpigmentation and no hyperkalemia bc aldosterone is intact
27
Q
Tertiary Adrenal insufficiency
- caused by
- adlosterone
A
- chronic use of exogenous steroids w/ abrupt withdrawal
- aldosterone unaffected so K and htn should be fine
28
Q
Hyperaldosteronism
- what is it
- sxs
- primary: caused by; aldosterone vs renin levels; main sxs
- secondary:
A
- increased secretion of aldosterone from adrenal gland
- hypertension, decreased K, met alkalosis
- caused by adrenal adenoma or bilateral adrenal hyperplasia; increase in aldosterone with decrease in renin; treatment resistant HTN w/o edema
- pts w/ renovasc HTN, juxtaglomerular tumors and edema