Endocrinology Flashcards
secretion from neurons reach the blood stream and influence cells some distance away
neuroendocrine
Hormone classifications (3)
- proteins and peptides
- steroids (cholesterol derived)
- aa tyrosine derived (epi, norepi, dopa, thyroxine)
______ _______ usually controls secretion of hormones; less often by ________ _________ (oxytocin cervix dilation)
negative feedback,
positive feedback
adrenal medulla is modified _______ ________
neural tissue
amino acid based hormone classifications (4)
- simple aa, peptide & protein
- can’t enter cell
- 2nd messenger use
- most common
Steroid hormone classifications (5)
- cholesterol derived
- can enter cells
- direct action
- gonadal and adrenocortical
- usually slower overall effect
lab test for hormones
Challenging (small amounts)
-radioimmunoassay (bound/free ratio)
Pituitary components
- anterior pituitary (adrenohypoghysis)
2. posterior pituitary (neurohypophysis)
Posterior pituitary releases _________ and _______- both made in the ___________, particularly in the ____ _____ & ____________ nuclei. Released directly into circ.
ADH and Oxytocin,
hypothalamus,
supra optic ¶ventricular nuclei
embriologic derivation:
anterior pituitary:
posterior pituitary:
- oral cavity pouch
- down growth of 3rd ventricle
Hormones released by anterior pituitary(6)
GOAT FLAP
- Growth GH
- Ox
- adrenocorticotrophic ACTH
- Thyroid stimulating TSH (thyrotropin)
- Follicle Stimulating FSH
- Luteinizing LH
- ADH
- Prolactin
Hypothalamus controls pituitary by_________ _______ ________, released into ________-________ portal blood vessels.
hypothalamic releasing hormones, (^ concentration vs. syst)
hypothalamic-hypophysial
__________hypothalamus monitors body fluid _________ (CSF 3rd vent–directly adjacent). _____ secreted to adjust for _______ changes.
osmoreceptors,
osmolarity,
ADH,
osmolarity
ADH acts on ______ _____ of the ____ renal tubules and _____ _____ to INCREASE H2O reabsorption
Principle cells,
DISTAL,
collecting ducts
baroreceptors in the ____ _____, _____ ____, and carotid artery sense _______/ _____ and signal the hypothal via the _____ nerve to ^v ADH secretion
left atrium, aortic arch,
hypoveolemia/ hypervolemia,
vagus
Diabetes insipidus DI can be:
- central DI
2. nephrogenic DI (osmolar gradient lost)
ADH pathophys characterized by decrease in plasma osmolarity, decreased serum Na+ (too much total body water)
SIADH syndrom of inappropriate ADH secretion usually from (OAT CELL CARCINOMA of lung)
Functions: uterine contration, milk “let down”, milk ejeciton
oxytocin
oxytocin release stimulated by
- nipple stim
- sight, sound, smell infant
- cervical dilation (positive feedback)
6 anterior pituitary hormones produced by 5 cell types: (5)
- trophes:
1. thyrotrophes
2. corticotrophes
3. lactotrophes
4. gonadotrophes
Growth Hormone (GH) actions (4)
aka somatotropin
- ^ linear growth
- ^ protein synthesis
- ^ fat utilizaiton for energy
- ^ insulin resistance – DIABETOGENIC–wants body to use fats before glucose
excess GH:
deficiency in GH:
- -Acromegaly(when growth plates already closed-over ^time) vs. gigantism (^ GH before plates closed)
- -pituitary dwarf (no linear growth)
XRH
released by hypothalamus to stimulate pituitary
GH secretion stimulated by: (4)
- fasting
- starving
- ^ aa in plasm
- exercise
- -GH opposed by
- -GH mediated by
somatostatin
somatomedin
pregnancy and suckling stimulate production and release of ______. Dopamine inhibits release. Hormone inhibits _____ , and promotes ______ development.
prolactin,
ovulation,
breasts
galactorrhea cause from. This along with _______ presenting symptoms of pituitary adenoma.
^ prolactin–headache
- v dopamine
- pituitary tumor
TSH–in response to ____
thyroid stimulating hormone (thyrotropin),
thyroid releasing hormone (TRH)
TSH actions (2)
Thyroid stimulating hormone (thyrotropin)
1. regulates growth of thyroid
2. regulates secretion T3 & T4
Negative feedback to HYPO and PIT
ACTH from ___-_______. Released by _________-______ _____
adrenocorticotrophic hormone from pro-opiomelanocortin,
corticotrophin-rleasing hormone
ACTH modulates ________ secretion from the zona __________ of adrenal _______
cortisol,
fasciculate,
cortex
FSH under control of ______.
Follicle stimulation hormone,
Release controlled by GnRH (gonadotropin releasing hormone
FSh actions (2)
- stim development of ovary follicles
2. stim spermatogenesis
LH under control by _____. Hormone stimulates development of _____ ______ in women. Stimulates ________ ______ for Leydig cells of ____ in men.
Luteinizing Hormone–GnRH,
corpus luteum,
testosterone secretion,
testis
T3 and T4 are highly _____ ______ in blood. So effects will be ______; long ____-_____. Less than __% free in serum, rest bound to ______-____ ______.
protein bound, steady, half-life, 1%, thyroxine-binding globulin
steroid hormones secreted by follicles and corpus luteum of ovaries. Negative feedback to hypothalamus ^v release of ____ and ____
Estrogen and Progesterone,
FSH & LH
T4 ==> T3 functions (slide 23)
turns into
^ Na+ K+ ATPase ^ basal Metabolic rate ^ O2 consumption ^cardiac output (think of hypo/hyperthyroidism symptoms)
__________hypothalamus monitors body fluid _________ (CSF 3rd vent–directly adjacent). _____ secreted to adjust for _______ changes.
osmoreceptors,
osmolarity,
ADH,
osmolarity
ADH acts on ______ _____ of the ____ renal tubules and _____ _____ to INCREASE H2O reabsorption
Principle cells,
DISTAL,
collecting ducts
baroreceptors in the ____ _____, _____ ____, and carotid artery sense _______/ _____ and signal the hypothal via the _____ nerve to ^v ADH secretion
left atrium, aortic arch,
hypoveolemia/ hypervolemia,
vagus
Diabetes insipidus DI can be:
- central DI
2. nephrogenic DI (osmolar gradient lost)
ADH pathophys characterized by decrease in plasma osmolarity, decreased serum Na+ (too much total body water)
SIADH syndrom of inappropriate ADH secretion usually from (OAT CELL CARCINOMA of lung)
Functions: uterine contration, milk “let down”, milk ejeciton
oxytocin
oxytocin release stimulated by
- nipple stim
- sight, sound, smell infant
- cervical dilation (positive feedback)
6 anterior pituitary hormones produced by 5 cell types: (5)
- trophes:
1. thyrotrophes
2. corticotrophes
3. lactotrophes
4. gonadotrophes
Growth Hormone (GH) actions (4)
aka somatotropin
- ^ linear growth
- ^ protein synthesis
- ^ fat utilizaiton for energy
- ^ insulin resistance – DIABETOGENIC–wants body to use fats before glucose
excess GH:
deficiency in GH:
- -Acromegaly(when growth plates already closed-over ^time) vs. gigantism (^ GH before plates closed)
- -pituitary dwarf (no linear growth)
XRH
released by hypothalamus to stimulate pituitary
GH secretion stimulated by: (4)
- fasting
- starving
- ^ aa in plasm
- exercise
- -GH opposed by
- -GH mediated by
somatostatin
somatomedin
pregnancy and suckling stimulate production and release of ______. Dopamine inhibits release. Hormone inhibits _____ , and promotes ______ development.
prolactin,
ovulation,
breasts
Zona Glomerulus affects the ______
Glomerulus of kidney (Aldosterone)
TSH–in response to ____
thyroid stimulating hormone (thyrotropin),
thyroid releasing hormone (TRH)
TSH actions (2)
- regulates growth of thyroid
- regulates secretion T3 & T4
Negative feedback to HYPO and PIT
ACTH from ___-_______. Released by _________-______ _____
adrenocorticotrophic hormone from pro-opiomelanocortin,
corticotrophin-rleasing hormone
ACTH modulates ________ secretion from the zona __________ of adrenal _______
cortisol,
fasciculate,
cortex
FSH under control of ______.
Follicle stimulation hormone,
Release controlled by GnRH (gonadotropin releasing hormone
FSh actions (2)
- stim development of ovary follicles
2. stim spermatogenesis
LH under control by _____. Hormone stimulates development of _____ ______ in women. Stimulates ________ ______ for Leydig cells of ____ in men.
Luteinizing Hormone–GnRH,
corpus luteum (temporary structure in women’s follical during luteal phase, releases ^ progesterone/estrodial),
testosterone secretion,
testis
T3 and T4 are highly _____ ______ in blood. So effects will be ______; long ____-_____
protein bound,
steady,
half-life
steroid hormones secreted by follicles and corpus luteum of ovaries. Negative feedback to hypothalamus ^v release of ____ and ____
Estrogen and Progesterone,
FSH & LH
T4 ==> T3 functions (slide 23)
turns into
^ Na+ K+ ATPase ^ basal Metabolic rate ^ O2 consumption ^cardiac output (think of hypo/hyperthyroidism symptoms)
Hormone affects every organ system in body, mediate cellular metabolic rate.
Thyroid Hormones:
- T3-triodothyronine – ^active than T4
- T4 -thyroxin–target tissue converts to T3
Thyroid gland composed of ^# of _____ filled with _____ _____, made up of thyroglobulin containing ______ ______
follicles,
colloid material,
thyroid hormone
_______ _____ of thyroid concentrates ______ in gland (30X greater than in blood).
iodide pump,
iodide,
Thyroid hormone affects ____, increasing _______. Effects last several days. Effects:
DNA, transcription 1. ^ thermogenesis, sweating 2. ^ rate /depth of respiration 3. ^cardiac output 4. etc. ^ metabolic excitation
hyperthyroidism aka
Graves’ Disease–autoimmunce process destroying negative feedback receptors
read abt symptoms
Hypothyroidism symptoms:
v metabolic rate resulting in:
- cold intolerance
- weight gain
- lethargy
- hyxedema (puffiness of skin)
deficient dietary iodine resulting in decreased T3/T4 secretion there for high TSH levels –> stimulate thyroid growth =
thyroid goiter
Adrenal gland CORTICAL Zones and products mnemonic (steroid hormones)
Go Find Rex, Make Good Sex
- Zona Glomerulosa = Mineralocorticoids (aldosterone)
- Zona Fasciculata = Glucocorticoids (cortisol)
- Zona Reticularis = Androgens
Adrenal Medulla makes ___________: _______ & ________
catecholamines:
epinephrine & norepinephrine
ACTH stimulated by ____ from hypothalamus. ACTH stimulates the SYNTHETIC pathways to make the _______ _____ derived from ________.
CRH (corticotrophin releasing hormone),
adrenocortical hormones,
cholesterol
secretion of ______ from Zona glomerulosa stimulated by ____–also stimulated by ______ __
aldosterone,
Renin,
angiotensin II
PRODUCTION and SECRETION from Zona fasciculate and Zona reticularis under direct control of _____.
ACTH
*T3 and T4 need _______ for synthesis
IODINE (for test should know at which level problem is (hyp, pit, thyroid, diet) in relation to symptoms and lab test values)
Glucocorticoid(cortisol) /androgen secretion from adrenal glad controlled by _____ ______ of _______ to pituitary. Release peaks in early _______.
negative feedback,
cortisol,
morning
Zona Glomerulus affects the ______
Glomerulus of kidney (Aldosterone)
- Cortisol (glucocorticoid) is the _____ hormone. Peaks in ____. Functions: (5)
Study actions deeply!
stress, morning, Functions: 1. catabolism--glycogen storage 2. antiinflammatory-- (v response to hist, sero, protag) 3. suppresses immune response 4. ^ GFR 5. inhibits bone formation
Aldosterone functions:(3)
- ^ Na+ reabsorption–ECF vol expansion
- ^ renal K+ secretion
- ^ renal H+ secretion–metabolic alkalosis
Adrenal Androgens & function: (video) (4)
- dehydro-epiandrosterone DHE and androstenedione
- DHE minor role in males
- DHE major androgen in females
- may cause “masculinization” in females
Leptin made by _______ ______. Adjusts ______ _____ & _______ ______
adipose tissue/ fat cels,
hunger sensation,
Energy expenditure
Failure of adrenal gland (causes: autoimmune, cancer) – disease and symptoms
(PRIMARY) Addison's disease (adrenal insufficiency) symp: 1. hypoglycemia 2. anorexia 3. weakness 4. HYPERPIGMENTATION
Failure to stimulate adrenal gland (causes: iatrogenic, pit tumor, hypo disorder): disease, symptoms, and RX
(SECONDARY) Addison’s disease–adrenal insufficiency
Symp:
1. same as primary minus hyperpigmentation
RX: replace steroids
Excess glucocorticoids aka–caused by?
Cushing’s syndrome:
- iatrogenic
- pituitary adenoma w/ ^ ACTH release
- Adrenal adenoma
- Cushing’s syndrome symp + RX
Symp: 1.hyperglycemia 2. HTN 3. muscle wasting 4. moon face 5. buffalo hump 6. abdominal striae RX depends on cause: 1. adrenalectomy 2. pit surgery
makes MSH melanocyte stimulating hormone
pituitary gland–overproduction can cause hyperpigmentation
Primary hyperaldosteronism aka–tumor–RX
Conn’s syndrome–Spironolactone (aldo antagonist)/ surg
Main extracellular buffer (alkaline)
Bicarb CO3—released by pancreas into small intestines
CO2 + H2O –> H2CO3 (carb acid) –> CO3- + H2
Pancreas hormones and cell mnemonic GIS
AG (starvation)
BI (plenty)
DS (inhibitory)
Hormone that regulates insulin and glucagon–
also known at Growth Hormone Inhibitory Hormone
Somatostatin
empty sella syndrome
pituitary sits in sella tersica–
iodine needed for synthesis of ____ & _____. Thus low levels in diet will lead to higher release of _____ from pituitary. And ______ will result.
T3& T4,
TSH,
goiter
to check integrity of pituitary-adrenal axis (based on negative feedback loop)
Dexamethasone suppression test (pituitary will react to dex same way as cortisol–then check cortisol next morning) If you give dex and cortisol down next day = normal. If you give dex and cortisol high next day = adrenal producing cortisol on its own=disfunction
negative feedback for FSH and LH controlled by
levels of progesterone/ estrodile in blood – intermediary in contrast to T3/T4 feedback for thyroid/pit/hypo system
opposes aldosterone–need to be wary of ________ due to interplay of Na+ and K+ by aldo in kidney (to keep me electrically neutral)
spironolactone,
hyperkalemia (K+ not be excreted by aldo)
Symptoms of Conn Syndrome (3) + treatment
- hypertension
- hypokalemia
- metabolic alkalosis
- RX w/ spironolatone (aldo antagonist)
Hormone of abundance + actions (4)
Insulin,
- decrease blood glucose
- decrese blood lipid levels
- decrease blood aa concentration
- ^ K+ uptake by cells
Preproinsulin –>
proinsulin –> insulin
Diabetes type I aka; cause
Insulin dependent diabetes mellitus IDDM–inadequate insulin secretion secondary to DESTRUCTION of BETA cells
Type I diabetes characterized by (7)
- hyperglycemia
- polyuria
- ketoacidosis (because using fat/aa for energy)
- polydipsea
- polyphagia (cellular starvation)
- hyperkalemia (insulin promotes K+ cell uptake)
- diabetic ketoacidosis, coma
Type II diabetes mellitus aka + cause
Non-insulin dependent diabetes lmellitus NIDDM,
–adequate insulin secretion–cells “insulin resistant”
(not prone to ketosis because insulin working somewhat)
Type II diabetes mellitus characterized by (2)
- abnormal glucose levels
2. metabolic derangements of Type I
Diabetic coma caused by
hyperosmolarity cause neurons not to work right
Hormone of starvation (____), stimulated by _______ blood glucose. Increases blood glucose concentraiton by: (3)
glucagon, decreased, 1. glycogenolysis (break down glycogen) 2. gluconeogenesis 3. increased lipolysis
________ produced and released from hypothalamus stimulated by food ingestion. Modulates response of _____/____ to food ingestion–affects rest of body in _______ manner.
somatostatin,
glucose/glucagon,
inhibitory
drug for Type II diabetes that ^ tissue usage of insulin
metformin
Ca ++ concentrations:
Protein bound: 40% (unfilterable)
Ion complexed: 10% (ultafilterable)
Active ionized form: 50% (ultrafilterable + active)
*hyocalcemia causes: (6)
- hyperreflexia
- muscle cramping
- spontaneous twitching
- tingling/ numbness
- chvostek sign (facial twitch when CN 7 tapped)
- Trosseau sign (carpopedal spasm–w/ BP cuff inflation)
*Hypercalcemia causes: (5)
- polyuria
- polydipsia
- hyporeflexia
- consipation
- lethargy, coma, death
Ca++ and H+ both bind to _________, so ^v H+ (pH change) in blood can can alter ____ binding, and ^v levels in blood, (____________/__________) symptoms
albumin,
Ca++,
(Hypo/hypercalcemia)
*GIP/GLP-1
Gastric inhibitory peptide
Glucagon-like peptide (glucagon analog)
INCREASE insulin secretion,
OPPOSE actions of glucagon
(for type II diabetes)
serum _______ stimulates release of insulin–if Beta cells get worn out by overuse, a ____ __ ________ will start to look like a ____ __ ________
glucose,
Type II diabetic
Type I diabetic
Increased ________ concentration increases complexed Ca++, decreasing free ______ concentrations
phosphate,
Ca++
Decreased _______ concentration increases _______ Ca++, increasing free Ca++ concentrations
phosphate,
complexed
Somatostatin made in:
aka growth hormone inhibiting hormone GHIH
- hypothalamus
- liver
- GI tract
Stimulated by food ingestion
Secretion of _______ ______ stimulated by decreased serum Ca++ concentration
parathyroid hormone
Parathyroid hormone effects:(3)
- Bone (^ resorption–>^ Ca++ & phosphate in ECF)
- kidney (^ Ca++ reabsorption; v phosphate reabsorption)
- small intestine (^ Ca++ absorption via VITAMIN D)
PRIMARY Hyperparathyroidism, as from ______ ______, may cause (3) ______, _______ ______, and ________
parathyroid ADENOMA,
- hypercalcemia,
- kidney stone (Ca++/Phosphate)
- hypophosphatemia
SECONDARY hyperparathyroidism, as from excessive ___ ______ secondary hypocalcemia as from: (3) _______, _______, _________
PTH secretion,
- Vit D deficiency
- Renal failure
- PTH secretion tumor
PTH wants to increase:
Ca++ concentration in serum
Hypoparathyroidism usually from: clincaly we’ll see
treatment of thyroid gland resulting in destruction of parathyroid glands.
-hypocalcemia/hyperphosphatemia
2nd major regulatory hormone for Ca++ & phosphate
Vitamin D aka cholecalciferol
_____ modifies vitamin-D to make inactive form then ______ further modifies into _______ or ______ form
liver,
kidney,
active/inactive
Actions of active vitamin-D derivative (4)
- ^ mineralization of new bone
- ^ Ca++ / phosphate absorption by SMALL INTESTINES
- Kidney–^ reabsorption of Ca++ & phosphate
- Bone–stim bone “REMODELING”
ppl with chronic renal failure will have _______ due to inability to excrete _________, thus ____ will be taken out of bones. SECONDARY HYPERPARATHYROIDISM
osteoporosis,
phosphate,
Ca+
Vitamin D deficiency will cause:
______ in children:
______ in adults:
- Rickets (can’t mineralize bones)
- osteomalacia, osteoporosis (from renal failure–no active D)
_______ opposes PTH by lowering serum free ____. Made in thyroid–stims Ca++ into bones.
calcitonin,
Ca++
^v Ca++ chart on pg 17 of outline
*
bones made of–thus vitamin D wants to save ______
calciumphosphate –bound,
both
