Term
TRH (Thyrotropin-releasing hormone)
Gland of origin
Major actions
Disorders |
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Definition
Hypothalamus
Stimulates secretion of TSH and prolactin
Tertiary hypothyroidism – TRH producing areas of hypothalamus are impaired (by tumor, infarction, congenital, etc) which effects TSH levels (low) which effects T3/4 levels (low) |
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Term
Corticotrophin-releasing hormone
CRH
Gland of origin
Major actions |
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Definition
Hypothalamus
Stimulates secretion of ACTH, maintins the ability of corticotrophs to make & secrete ACTH in acute response to CRH |
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Term
Gonadotropin-releasing hormone
GnRH
Gland of origin
Major actions
Disorders |
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Definition
Hypothalamus
Stimulates secretion of LH and FSH |
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Term
Growth hormone releasing hormone
GHRH
Gland of origin
Major actions
Disorders |
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Definition
Hypothalamus
Stimulates secretion of growth hormone |
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Term
Somatotropin release-inhibiting hormone
(somatostatin)
SRIF
Gland of origin
Major actions |
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Definition
Hypothalamus
(also found in delta cells in pancreatic islet tissue)
Inhibits secretion of growth hormone
Inhibits secretion of insulin, glucagon
Normal or elevated in diabetes (hyperglycemia, ketosis) |
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Term
Prolactin-inhibiting factor
(dopamine)
PIF
Gland of origin
Major actions |
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Definition
Hypothalamus
Inhibits secretion of prolactin |
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Term
Thyroid stimulating hormone
TSH
Gland of origin
Stimulus/suppresion
Major actions
Disorders |
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Definition
Anterior pituitary
Stimulated by cold, suppressed by stress or i/c FT3
Stim siz, # of follicular cells
Tropic (stim T3/T$ synth & sec)
Trophic (maintains gland health)
Stimulates all steps in hormone synth & sec - effects primarily mediated by membrane receptors, Gs-alpha, cAMP, PKA
I/c the efficiency of the iodine pump with dietary I intake is low
Secondary Hyperthyroidism – too much TSH leads to excess T3/4 (pituitary in origin)
- Graves’ dz due to ab against TSH; always presents with exophthalmos; Grave’s is most common cause for hyperthyroidism
- due to iodine excess, has an anti-TSH-like effect
Secondary Hypothyroidism – too little TSH leads to def T3/4 (pituitary in origin: tumor, infarction, congenital)
- due to iodine deficiency – low TSH leads to goiter b/c no T3/4 can be produced |
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Term
Follicle-stimulating hormone
FSH
Gland of origin
Major actions
Disorders |
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Definition
Anterior pituitary
Stimulates growth of ovarian follicles and estrogen secretion
Promotes sperm maturation in the testes
Excess –amenorrhea, impotence
Insufficiency –hypogonadism, delayed adolescence |
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Term
Luteinizing hormone
LH
Gland of origin
Major actions |
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Definition
Anterior pituitary
Stimulates ovulation, formation of corpus luteum, and synthesis of extrogen and progesterone (ovary)
Stimulates synthesis and secretion of testosterone (testes) |
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Term
Growth hormone
(somatotropin)
GH
Gland of origin
Stimuli for release
Inhibitors (neg feedback)
Major actions
Disorders |
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Definition
Anterior pituitary
AA (esp arginine)
ingestion of protein meal
starvation (i/c ghrelin)
hypoglycemia
exercise, stress, trauma
sleep
IGF-I
Somatostatin
Cell growth in size and #
Protein synthesis (i/c AA transport into cells, i/c ribosomal pr synth, i/c RNA synth, d/c protein catabolism)
Lipolysis (HSL), "spares blood glucose"
Inhibits CHO use (blood glucose rises)
-inhibition of glucose uptake into m
-stim of gluconeogenesis in liver
Release of IGF-I (somatomedin) from liver & kidney --> bone growth
Osmotic diuresis secondary to i/c [glucose]
Secretion of somatostatin
Gigantism – excess GH in childhood
Acromegaly – excess GH in adult (octreotide used in treatment)
Dwarfism – lack of GH
Lorons dwarfism - GH levels are normal, but receptors are defective/absent |
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Term
Prolactin
Gland of origin
Major actions
Disorders |
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Definition
Anterior pituitary
Stimulates milk production and breast development
Panhypopituitarism –ALL anterior pituitary hormones are destroyed
Excess –galactorrhea, amenorrhea, impotence
Insufficiency –no lactation |
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Term
Adrenocorticotropic hormone
ACTH
Gland of origin
Major actions
Disorders |
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Definition
Anterior pituitary
Stimulates synthesis and secretion of adrenal cortical hormones (membrane R, adenylylcyclase, cAMP_
Secondary Cushing’s – too much ACTH due to pituitary tumor leading to hypercortisolism; *hyper-pigmentation often present*
Secondary Addison’s/adrenal insufficiency – enzyme deficiencies lead to excess ACTH |
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Term
β-endorphin
What class of hormones does this belong to?
Gland of origin
Synthesis? |
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Definition
An endogenous opioid - analgesia, i/c GI tone, tolerance, physical dependence
Anterior pituitary
Synth as part of POMC (along with ACTH are released during stress, suppressed by cortisol) |
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Term
Melanocyte-stimulating hormone
MSH
Gland of origin
Major actions
Disorders |
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Definition
Anterior pituitary (POMC)
Stimulates melanocytes to secrete melanin
circulating MSH activity is regulated along with ACTH; secretion is inhibited by cortisol
Patients with disorders resulting in high ACTH secretion develop hyperpigmentation (b/c of relationship b/t cortisol, ACTH, and MSH) |
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Term
Oxytocin
Gland of origin
Stimulus for release
Major actions
Disorders |
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Definition
Originates in the PVN/SON, stored in the posterior pituitary
Suckling
distention of the uterus & cervix and mvmts of infant during pregnancy
stimulation of cervix during sex
Milk ejection/letdown
Parturition (freq & force of uterine contractions i/c in presence of estrogen)
Sperm transport
Too much oxytocin could lead to premature delivery
Oxytocin’s weak ADH activity can cause water intoxication during long infusions and can precipitate HTN during acute administration |
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Term
Antidiuretic hormone – vasopressin
ADH
Gland of origin
Stimulus for release
Major actions
Disorders |
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Definition
Synth in SON & PVN, stored in posterior pituitary
I/c ECF osmolarity (esp NaCl)
D/c BP or volume
Trauma, pain, anxiety, nicotine, barbiturate anesthetics
Stimulates H2O reabsorption by renal collecting ducts (V2 receptors)
Venous constriction (V1 receptor, IP3)
Factors that increase ADH secretion:
↑ serum osmolarity, volume contraction, pain, nausea, hypoglycemia, nicotine, opiates, antineoplastic drugs
Factors that decrease ADH secretion:
↓ serum osmolarity, ethanol, α-agonists
Too little ADH: diabetes insipidus -> idiopathic; surgical, traumatic and secondary to hypothalamus tumors or vascular lesions; nephrogenic (no renal ADH receptors); psychogenic polydypsia
Too much ADH: syndrome of inappropriate ADH secretion -> usually due to non-pituitary tumor secreting excess ADH |
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Term
Thyroxine (T4)
Triiodothyronine (T3)
Gland of origin
Major actions
Inhibitors
Disorders |
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Definition
Thyroid gland
Skeletal growth
↑ O2 consumption
Heat production
↑ protein , fat, and carbohydrate use
Maturation of nervous system (perinatal)
Block organification: goitren (cabbage), propylthiouracil (PTU)
Compete for iodine pump: thiocyanate, perchlorate, lithium
Primary Hyperthyroidism – excess hormone secretion (thyroid in origin)
-> Graves: autoimmune form; exophthalmous, pretibial myxedema
-> Thyroiditis caused by leakage of T3/4 due to damage to thyroid
-> iodine excess blocks T4 synthesis and acts as anti-TSH
-> thyroid adenomas (single nodular goiters) secrete excess T3/4 w/o pituitary control
-> enhanced beta adrenergic activity
Primary Hypothyroidism – reduced T3/4 secretion (usually due to an attack on the thyroid)
- primary: iodine def, genetic loss, bacterial/viral damage (Hashimoto's, de Quervain's - deQ can start out as hyper, end up hypo), surgical/radioactive damage
- secondary: pit problem/low TSH - brain/AP tumor crowds or destroys TSH producing regions; pit infarc due to trauma/hemorrhage/post-partum hemorrhage (Sheehans), congenital
- tertiary - TRH producing regions of HT are impaired
-> Cretinism (congenital) – neonatal hypothyroidism, leads to permanent mental retardation
-> Hashimoto’s throiditis due to no T3/4 and high TSH caused by autoimmune dz that destroys the thyroid
-> iodine deficiency can lead to low T4 (high T3) |
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Term
Calcitonin
Gland of origin
Major actions
Disorders |
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Definition
Thyroid gland – parafollicular cells
↓ serum [Ca2+]
promotes bone formation (osteoblasts)
Ca++ filtration -> renal excretion |
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Term
Parathyroid hormone
PTH
Gland of origin
Major actions
Disorders (hypo-/hypercalcemia) |
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Definition
Parathyroid gland (chief cells)
↑ serum [Ca2+]
↓ serum [Pi]
bone resorption, renal Ca reabsorption
Hypocalcemia sx: hyper-reflexia, paraesthesias, m cramps, laryngeal spasm
Hypocalcemia caused by:
- hypoparathyroidism, due to low PTH
- Pseudo-hypoparathyroidism – secondary hyperparathyroidism due to resistance to PTH
- Mg deficiency (d/c ability to secrete PTH, common in alcoholic liver disease)
- Vit D deficiency (nursing home pts)
- Renal failure (-> vit D def, tx give active 1,25 form)
Hypercalcemia sx: hypophosphatemia, skeletal wasting, personality/neural/GI disturbances
Causes:
– primary hyperparathyroidism, caused by parathyroid adenoma or glandular hyperplasia
- hypervitaminosis D
- non-endocrine causes |
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Term
Catecholamines
Epi
NE
DA
Gland of origin
Synthesis
Major actions
Disorders |
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Definition
Adrenal medulla
Tyrosine -TH-> LDopa --> DA -DBH-> NE -PNMT-> Epi
NE
i/c HR, contractility, CO, constricts peripheral blood vessels, i/c systolic + diastolic -> i/c MAP
Epi
i/c HR, contractility, CO, dilation of skeletal BV, constriction of GI & skin BV, slight i/c systolic + d/c diastolic -> n/c MAP
inhibits insulin secretion
DA
inhibits prolactin
same CV effects as Epie & NE
can support circulation during shock with fewer episodes of secondary renal failiure
Relax intestines & bladder, contract sphincters
Stimulate axillary sweating
Denervation super sensitivity
Orthostatic HTN – can result from degeneration of preganglionic SNS nerves -> secondary lack of catecholamines
Pheochromocytoma – causing excess catecholamines - tx adrenergic blockers
Thyrotoxicosis – similar to catecholamine excess - tx beta-blockers |
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Term
Glucocorticoids
(cortisol)
Gland of origin
Activator
Major actions
Disorders
What happens when there are enzyme deficiencies in tfhe cortisol pathway?
which drug blocks 11-beta hydroxylase? |
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Definition
Adrenal cortex (zona fasciculata)
Stress (--> CRH -> ACTH -> cortisol)
Stimulates gluconeogenesis (i/c [glucose])
Anti-inflammatory (suppresses COX)
Immunosuppression
Inhibits pr synth (except in liver) --> negative N balance
Lipolytic
Stabilizes lysosomal membranes
Helps effects of catecholamines
Reduces effects of histamine
Primary Cushing’s syndrome – hypercortisolism due to adrenal hyperplasia; *pigmentation will be normal*
Addison’s dz - low/absent cortisol, can lead to Addisonian crisis
Adrenogenital syndrome – excess secretion of adrenal androgens due to enzyme defect w/ subsequent ACTH induced adrenal hyperplasia
; i/c intermediates (androgens, estrogens, progestins, mineralcorticoids)
super excess ACTH -> hyperpigmentation
11-b HL converts 17-OH DOC to cortisol
METYRAPONE blocks it
prevents cortisol synth -> adrenal i/c 11-DOC (precursor), confirms secondary adrenocortical insufficiency |
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Term
Aldosterone (mineralcorticoid)
Gland of origin
Major actions
Stim for secretion
Inhibitors (drugs)
Disorders |
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Definition
Adrenal cortex (zona glomerulosa)
↑ renal Na+ reabsorption
↑ renal K+ secretion
↑ renal H+ secretion
*Ang II* -> zona glomerulosa -> stim aldo
I/c K+ -> zona glomerulosa
SNS i/c renin release
(D/c Na, ACTH, peptidase-ATIII)
Losartin - ang-II R antagonist
Captropril - ACE inhibitor
Spironolactone - aldo antagonist
Conn’s: primary hyper-aldosteronism -> increased aldosterone levels; increased Na+, GFR, blood pressure; continued K+ loss
Addison’s dz – adrenocortical insufficiency -> due to no aldosterone |
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Term
1,25-dihydroxycholecalciferol
(Vitamin D3 active form)
Gland of origin
Major actions
Disorders |
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Definition
Kidney (activation site)
↑ intestinal Ca2+ absorption
↑ bone resorption
*calbindin* synthesis (an intestinal transport pr, facilitates absorption of dietary Ca++)
activated in kidneys by low Pi (created by PTH)
1-alpha-hydroxylase generates 1,25 dihydroxy-D3 |
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Term
Insulin
Stimulus for secretion
Inhibitors of secretion
Gland of origin
Major actions
Disorders |
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Definition
Pancreas (β cells)
I/c blood glucose, AA (esp arg)
Vagal (ACh) stimulation
Glucagon
Catecholamines (via alpha R)
Somatostatin
↓ blood [glucose], [amino acid], [fatty acid]
stimulates transport of glucose into cells via facilitated diffusion (i/c glut-4 receptors on muscle, adipose)
glucose utilization
glycogen synthesis (muscle)
AA transport (active)
protein synthesis (muscle)
lipogenesis (adipose)
K+, Mg+ transport into cells
decreases catabolic processes |
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Term
Glucagon
Gland of origin
Stimulus for secretion
Inhibitors of secretion
Major actions
Disorders |
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Definition
Pancreas (α cells)
falling blood [glucose]
i/c [AA] (protective)
Catecholamines (via beta R)
PNS stimulation
Circulating ketones
Somatostatin
↑ blood [glucose], [fatty acid]
glycogenolysis
gluconeogenesis
HSL: provides FA
stimulates insulin release |
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Term
Estradiol
Gland of origin
Major actions
Disorders |
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Definition
Ovary
Growth and development of female reproductive organs
Follicular phase of menstrual cycle |
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Term
Progesterone
Gland of origin
Major actions
Disorders |
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Definition
Ovary
Luteal phase of menstrual cycle |
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Term
Testosterone
Gland of origin
Major actions
Disorders |
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Definition
Testes
Spermatogenesis
Male secondary sex characteristics |
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Term
Human chorionic gonadotropin
HCG
Gland of origin
Major actions
Disorders |
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Definition
Placenta
↑ estrogen and progesterone synthesis in corpus luteum |
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Term
Human placental lactogen
HPL
Gland of origin
Major actions
Disorders |
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Definition
Placenta
Stimulates protein synthesis and overall growth, and milk production and breast development during pregnancy |
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Term
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Definition
Peptide GF, i/c glucose utilization by connective tissues
IGF-1: plasma conc doesn't d/c like insulin during hypoglycemia |
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Term
Hypopituitarism
causes
defects? |
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Definition
congenital, necrosis secondary to vascular failure/hemorrhage (Scheehans Syndrome), space occupying tumors, head trauma
lack of GH in childhood - dwarfism
non pituitary origins of dwarfism:
- Laron's dwarfism - resistance to hormone, production OK
- bad/poor IGF-I
- inadequate thyroid production
- inadequate insulin production
- too much androgen in childhood (causes premature closure of epiphyseal plates) |
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Term
Effect of iodine def on TSH
Effect of iodine excess on TSH |
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Definition
Def:
more MITs, fewer DITs --> i/c T3 synth --> d/c T3 (more severe def) --> i/c TSH --> trophic, thyroid enlarges into a GOITER
excess:
blocks thyroid hormone synth, has an anti-TSH-like effect, used prior to surgery to minimize operative complications (thyroid storm) |
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Term
Estrogen: effect on thyroid hormone
Androgen effect?
Estrogen's effect on cortisol |
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Definition
Stimulate i/c in TBG --> more T3/T4 is bound, less is free --> i/c TSH --> normal FT3/FT4 (euthyroid), but bound hormone remains i/c
Opposite to estrogen - lowered TBF - ultimately euthyroid, but low totals
I/c CBG -> d/c fCortisol (also raises central set point of cortisol neg feedback -> i/c fCortisol & totals
men treated with estrogens > pregnancy > contraceptives |
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Term
Catecholamine receptors:
Alpha-1
Role in fight-or-flight response
effects, catecholamine(s) |
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Definition
primarily via IP3
vasoconstriction
intestinal smooth m relaxation
D/c blood flow to nonessential vascular beds - fast - NE
Epi, NE |
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Term
Catecholamine receptors:
Alpha-2
effects, catecholamine(s) |
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Definition
mainly presynaptic
inhibition of NE release via inhibition of cAMP
Epi, NE
inhibit insulin secretion |
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Term
Catecholamine receptors:
beta-1
Role in fight-or-flight response
effects, catecholamine(s) |
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Definition
via i/c cAMP
cardiostimulatory
lipolytic (HSL)
provide i/c blood flow, HR, contractility, SV, CO all i/c
Epi, NE |
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Term
Catecholamine receptors:
beta-2
Role in fight-or-flight response
effects, catecholamine(s) |
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Definition
via i/c cAMP
bronchodilatory
open vascular beds in skeletal m
dilate airway to i/c O2 delivery
provide energy: release of stored glucose & FA, stim cAMP, i/c glycogenolysis & lipolysis
Epi
vasodilatory (skeletal m)
lipolytic, glycogenolytic, gluconeogenesis (liver) |
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Term
Catecholamine receptors:
beta-3
effects, catecholamine(s) |
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Definition
via i/c cAMP
most important in adipose
Little bit of both, more NE
lipolytic, lower glucose uptake |
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Term
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Definition
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Term
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Definition
prazocin (alpha1)
phentolamine (alpha1&2) |
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Term
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Definition
isoproterenol
salbutamol (beta2)
dobutamine (beta1 |
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Term
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Definition
propranolol, atenolol (beta1)
metoprolol (beta1&3)
esmolol (beta1)
pindolol (beta1&2) |
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Term
| Termination of catecholamine effects |
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Definition
1. Neuronal reuptake (Type I) - blocked by cocaine, psych meds
2. Non-neuronal reuptake (type 2) - blocked by corticosteroids
3. COMT - transfers donor methyl groups to catechol rings --> metanephrine, normetanephrine, 3-methoxytyramine
4. MAO - oxidative deamination - MAOI available |
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Term
| How to predict Ca++ correction |
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Definition
| Difference in albumin x 0.8 + measured Ca++ |
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Term
Dexamethasone Suppression Test
Normal?
Cushing's?
ACTH producing tumor? |
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Definition
Normal: low dose suppresses cortisol levels
Cushing's: low dose has no effect, high dose suppresses cortisol
ACTH tumor: neither high nor low suppresses cortisol |
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