Sleepexercisephysiologic stressfasting/hypoglycemiasex steroidsAlpha-agonists (Norepinephrine)Beta-blockers
|Phospholipase C mechansim||
-severe adult hypothyriodism
-Symptoms: enlarged tongue, puffiness of hands and feet
inflammation of a gland
|Regulation of GH secretion||
|amines are synthesized from||
-abnormally low blood sugar
Amylin analog - Diabetes
|causes of hypoglycemia||
Post op complication of gastric surgery
Function: Activate LCAT; ABCA-1.Production site: Intestine; LiverLipoprotein location: HDLGets pushed of and cleared by kidney when triglycerides get too high. Loss of A-1 Makes HDL unable to participate in reverse cholesterol transfer
Anterior Pituitary hormone regulated by Hypothalamic release of Dopamine (-) inhibitory.
Target Organ: Breast.
Act through JAK/STAT receptors.
sympathomimetic serotonin and norep reuptake inhibitor
|Do neurosecretory cells synthesize hormones?||
Severe, end-stage hypothyroidism
-Tx: maintain airways, meds, corticosteroids (for suppressed adrenal gland), correct BG and electrolyte levels, conserver body heat
|hypo/hyper causes..levels of binding proteins||
|Melanocyte-Stimulating Hormone (MSH)||
-From Anterior Pituitary
-stimulates melanocytes to secrete and deposit melanin
|antimicrosomal and antithyroglobulin antibodies||
enzyme in glycolysis pathways
found only in hepatic cells and allows them to unphosphorylate glucose which allows glucose into circulation.
Gland- Parathyroid glandTarget Organ- osteoclastsAction- increase bone break down
similar early morning hyperglycemia but due to waning of basal insulin effect
With paternal transmission of a mutated GNAS1 gene, Albright's hereditary osteodystrophy occurs without hypocalcemia, since the normal maternal allele results in the maintenance of renal responsiveness to PTH
surger perfomed on the thyroid gland
|The zona glomerulosa cells constitute 5% of the adrenal and they exclusively synthesize..||
|The hormone that stimulates milk production in the mammary gland is:||
3- hGH, melanocyte- stimulating hormone, PRL
|peptide/protein hormone synthesis||
often start as preprohormones cleaved to prohormone in rough ER and packaged by golgi cleaved to active hormone
↑ urine Na & urine osmolarity
|thyroid major protein molecule||
thyroid binding globulin
|Antidiuretic Hormone (ADH)||
-From Posterior Pituitary
-increases the reabsorption of water in the nephrons
-decreases urine volume
|What is ADH also known as?||
|What are the mineralocorticoid drugs?||
|Hydrophilic hormone examples||
pepties, catecholamines, includes storage, released as active form
secondary - ACTH is insufficient
primary - adrenal is damaged. all hormones are reduced. includes addison's
GI problems, MSH increase along with ACTH, anorexia, weight loss, nausea, vomiting, diarrhea. reduced cardiac contractility and sodim losses lead to low bp. inability to excrete water.
90% of adrenal cortex needs to be non-functional for clincal syptoms
MOA: increase target cell response to insulin
Use: monotherapy in T2DM or combined with above agents
AEs: weight gain, edema, hepatotoxicity
Are often microadenomas; most appear basophilic with H&E stain. Cause Cushings disease. Diagnostic tests include elevated ACTH, dexamethasone suppression test, ACTH elevation with metyrapone (which blocks cortisol synthesis), and MRI.
|Calcium sensing receptor||
Activates PLC, PLD, PLA2 Stimulation of PLC leads to activation of PKC and ITP, which releases intracellular calcium CSR is found in parathyroid, renal tubules, bone, GI and c-cells Cell membrane G protein receptor (intra, extra and cell membrane domains Calcium binds to the extracellular domain
|BP control in DM||
300) use an ARB.
How many amino acids make up Prolactin?
What is the critical cell specific factor that activates PRL gene transcription?
Is PRL secreted in bursts that increase in frequency and amplitude with sleep?
|Amine hormones are derived from?||
TyrosineThyroid, epi, norep
|Examples of thymic hormones||
ThymosinThymic humoral factor (THF)Thymic factorThymopoietin
ADH secretion by osmolarity & ECF volume
-Normalize BG (regulare insulin given IV)
-Replace Potassium (unless hyperkalemia or no urine output)
|usual first sign of DM in children||
|Parathyroid Hormone (PTH)||
-from the parathyroids
-target bone, kidney, digestive tract
-promote breakdown of bone to increase blood calcium
-promote retention and absorption of calcium in kidneys and digestive tract
|What are the normal values for epinephrine?||
|Diagnosis of hyperparathyroidism?||
Diagnostic workup for hypercalcemia often includes testing the PTH levels. Ultrasound of the neck area may reveal enlarged glands. Occasionally, scintigraphy with MIBI is necessary to identify adenomas or hyperplastic parathyroids.
- most common cause of hyperpituitarism
- can be functional or nonfunctional
- 35-60 yo
- soft, well circumscribed lesion
- histologically cells look homogenous
- up to 30% have no capsule and become an invasive adenoma and invade into local structures.
|Type I Pseudohypoaldosteronism||
high renin, angiotensin II and aldosterone
tyrosine (tyrosine hydroxylase - rate limiting) -> DOPA -> dopamine -> NE (glucocorticoid stimulated PNMT) -> epi
must be solubilized (3 g water/g glycogen)
normal human ~ 80g in liver, 400g in muscle
small posterior part of pituitary connected to the brain.
|Tiny but complex portion of the brain, which is attached to the pituitary by means of the infundibular (hypophyseal) stalk||
impairs PTH secretion and PTH action leading to hypocalcemia, Malabsorption, chronic alcoholism, and cisplatintherapy are currently the most common causes of hypomagnesemia
a tumor of chromaffin cells of the adrenal medullaa. remember 10%: this describes the number of pheos that are malignant, extra-adrenal, part of multiple endocrine neoplasia syndromes, bilateral, and pediatric.
one of two hormones produced in the pancreas
|What is the preferred treatment for IHA?||
A bilobed organ where T cells develop immunocompetence
|amino acid derivatives||
EPI, NE, DA, T3, T4 derived from tyrosine - thyroid hormones 2 rings; catecholamines 1 ring
|(3) signs of gh excess||
Overgrowth of tissue
|Water soluble hormones dissolved in plasma & transported to target tissue via the interstitial space 2||
peptide and catecholamines
|What indication would make the nurse suspect damage to the laryngeal nerve?||
|Once treatment has begun, what should the urine look like?||
|pt with weakness, polyuria, polydipsia, lethargy, confusion, convulsions, and coma||
hyperosmolar nonketotid coma (HONK)
|what does inositol triphosphate do?||
decreases release of PTH
genetic loci with the largest risk of T2DM
|gestational diabetes mellitus||
caused by metabolic stress of pregnancy causes diabetes in women with an inherent predisposition for diabetes
hyperglycemia results in macrosomia (increased fetal size) and perinatal morbidity
a polypeptide hormone, produced by the anterior lobe of the pituitary gland, that stimulates the cortex of adrenal glands.
Hyperthyroid patients are treated with
Propylthiouracil (PTU), which inhibits the peroxidase enzyme, thereby decreasing thryroid hormone synthesis at oxidation
|Primary adrenal insufficiency||
– Defect in adrenal gland– Dx: ↓cortisol ↑ ACTH– Treat: glucocorticoids, mineralcorticoids, ± androgens
|Clinical Presentation of Cushings disease or syndrome||
Caused by elevated glucocorticoids a. hypertensionb. truncal obesity and “moon facies”, buffalo humpc. proximal muscular weakness and atrophy of Type II fibersd. thin skin, capillary fragility, loss of collagene. osteoporosis, often with compressed vertebral fracturesf. hyperpigmentation (if Cushing disease)g. acne, hirsutism, amenorrheah. glucose intolerance (diabetes)i. immune suppressionj. mental status changes, depression
What are the three major functions they can have?
Antagonists to treat conditions caused by excess production of hormones.
Diagnostic tools for identifying endocrine abnormalities.
|distinguish Addison's from secondary cause||
Addison's has hyperpigmentation from MSH from excess ACTH production from POMC
|Long: superior hypophysial arteries form capillary network in median eminence (1 capillary plexuses) converge & form it. travel down infundibulum to deliver venous blood to anterior lobe.||
Short hypothalamic hypophysial portal blood vessel
|treatment for thyroid storm||
esmolol IV propranalol, .5 mg increments
250-500 mg/hr q6 IV or by NG
followed by sodium iodide, I IV/12 hrs
cortisol 100mg q 8 to prevent associated adrenal suppresion
|inside the thyroid, iodide is oxidized back to iodine which is bound to||
amino acid tyrosine
|Trousseau's sign =||
occlude brachial artery and get carpal spasm (sign of hypocalcemia)
|What is the source of thyroid hormones?||
Thyroid follicular cells
|Will a pt. with Cushings disease gain or lose wt.?||
|hypoglycemia, high immunoreactivity, insulin, and suppressed plasma C peptide||
--> pathognomonic of exogenous insulin administration
|Main causes of hyperthyroidism are:||
1. Graves disease
2. toxic multinodular goiter
3. functioning thyroid adenoma
|palmar and tubo-eruptive xanthomas||
occur with remnant accumulation in remnant removal disease
|what does vasopressin do?||
An antidiuretic with stimulated the reabsorption of fluids at kidney. Also causes vasoconstrition and elevated BP
|What does the parenchyma of medulla secrete?||
Epinephrine and nor-epinephrine
|Somatostatin has what effect on hormone release from the ant. pituitary||
Inhibits GH and TSH Release
|TESTS FOR GROWTH HORMONE SECRETION||
• Basal levels:– GH, IGF-1, IGFBP-3• Stimulated:– Arginine– Insulin– GHRH– Estrogen/beta-blockers; L-DOPA• Suppression:– OGTT
|what are the cardinal manifestations of hyperprolactinemia in young adult women?||
Inappropriate lactation, together with oligomenorrhea (irregular menses) or amenorrhea (absent menses).
|What is the first stage of mitosis?||
PROPHASE, metaphas, anaphase, telophase.
|Special Considerations for HRT||
-May takes weeks to feel better
-Take medications daily
-Tx can speed up body functions causing problems for pts with:
*Corinary Artery Disease
|GH causes growth only when||
There is adequate insulin
There is adequate CHO in the diet
|17-a-hydroxylase deficiency manifests with:||
Low cortisol, low sex hormones, high aldosterone! --> HTN, hypokalemia, phenotypically female but no maturation
|Who is more at risk of developing hyperparathyroidism?||
Women between 60-70
|What is the primary function of mineralocorticoids (aldosterone)?||
regulation of sodium balance
|what is myxedema coma and how to treat?||
long-standing hypothyroidism, untreated. cold exposure/trauma/infxn/CNS depressants --> hypothermia, stupor --> CO2 retention --> respiratory depression --> fatal. tx with very high T3 and T4
|Surgery for Cushing's Disease||
- usually highly effective, but give low doses of glucocorticoids
|How does hypocalcemia manifest itself in sheep and goats?||
Mild hyperexcitability in early stages, tetany (stiffness in legs), flaccid paralysis (weak and recumbent)
|Zona reticularis physical description||
between zona fasciulata and medulla,. They are polyhedral cells, some darker some lighter
|What are the parafollicular cells? What is their function?||
Cells within the thyroid gland follicles. Also known as C-cells. Synthesize and secrete calcitonin, an inhibitor of bone resorption.
|Following a precipitous delivery with substantial blood loss from a placenta previa, a 24-year-old primigravida is in stable condition. However, she is unable to breastfeed the baby. Then, over the next few months she notes a failure to return to normal||
post-partum pituitary necrosis led to the loss of pituitary hormones and hypogonadism, hypothyroidism, and finally secondary adrenal insufficiency. e
|What is the mechanism by which glucocorticoids mediate lipid metabolism chronic effect (Central fataccumulation with chronic excess of cortisol)?||
Uncertain, associated with increased insulin levels which may interactwith cortisol to increase lipogenesis at central sites.
|which tissues don't need insulin to take up Glu?||
Brain and RBCshave GLUT1 trasporter
|inhibition of gluconeogenesis leads to||
↓ amount & activity of liver enzymes
↓ release of amino acids from muscle & other tissues
|unlike MH, thyroid storm is not associated with||
acidosis, muscle rigidity, elevated CK
|What is the major action of Luteinizing hormone LH?||
Female: stimulates development of corpus luteum, release of oocyte, production of estrogen and progesterone.
Male: stimulates secretion of testosterone, development of interstitial tissue of testes.
|What can be done to manage SIADH?||
Eliminate underlying cause, restrict fluid intake, Furosemide (Lasix) - if hyponatremia is present
|The parathyroid gland chief cell Ca receptor has 2 signal transducers... what are they?||
1. inositol triphosphate --> reduces PTH release
2. cAMP --> increases PTH release
|What would a C-cell tumor do to calcium in a bull?||
Hypocalcemia d/t increased calcitonin
|what does chromophobe cells do?||
believe to be inactive form of chromophile cells
|What is the order of activation for Vit D? Which form is an accurate predictor of calcium storage?||
Synthesized from 7 dehydro-cholesterol and sunlight in skin; 25 hydorxylation in live; 1 hydroxylation in kidney (active form)
|what are the signs of ACTH deficiency?||
Common symptoms are fatigue, muscle weakness, anorexia and weight loss. Hyponatremia and hypoglycemia may be present, but severe dehydration and hyperkalemia do not occur.
|What does "Coupling" refer to during the process of thyroid hormone formation?||
“Coupling” refers to a still mysterious process in which TG folds upon itself allowing iodo-tyrosines in its N- and C-regions to come in contact, transferring the iodo-phenyl group of one tyrosine to the phenyl ring of another iodo-tyrosine within TG.
|What is the strict definition of hormones?||
\"Chemical messengers that travel in the bloodstream\"
|why are hyperth pts prone to an exagerated response to induction||
because they are chronically vasodilated and hypovolemic
|What are some interventions for hyperpituitarism?||
Parlodel: reduces tumor size, but can cause hypotension
Hypophysectomy: removal of anterior pituitary to decrease hormone levels.
|What signs could the family watch for to notify the dr. that the dose of hormone is to low?||
wt. loss , postural hypotension
|What does the thyroid do?||
The function of the thyroid is to regulate the body's metabolism by making thyroid hormone.
|what happens when you lose cortisol?||
- catecholamines do not exert their normal vasoconstrictive effects
- inability to readily mobilize energy sources.
|what does pars intermedia do?||
not sure, but may be involved with melanocyte stimulating hormone
|What is his yearly risk of developing diabetes if you have prediabetes||
Patients with prediabetes have a vastly increased risk of progressing to type 2 diabetes---5-10% per year
|What are some of the drugs that induce aldosterone deficiency or resistance states w/Hyperkalemia?||
Inhibition of synthesis/secretion of A (↓PA; ↑PRA) ACE inhibitors/Ang II receptor blockers CyclosporineSuppression of renin release (↓PA; ↑PRA) β-blockers Cyclooxygenase inhibitors (NSAIDs)Interference with renal actions of A (↑PA; ↑PRA)- MR blockers Spironolactone Eplerenone - ENaC blockers Amiloride Triamterene
|Uterus progesterone down regulates it own receptors & receptors for estrogen (menstration). Thyroid: T3 decreases senstivity for TRH receptors in anterior pit. High T3 decreases overall response hypothalamus, pitutary and thyroid axis.||
What is up-regulation and how does it occur?
|What do mineral corticoids do?||
They have an effect on F & E balance, specifically aldosterone (controlled by the RAAS system and controls fluid volume)
|When is measurment of TSH levels indicated in the elderly?||
When pts. have unexplained physical or mental deterioration
|What is the function of the parathyroid.||
The sole purpose of the parathyroid glands are to regulate the calcium level in our bodies within a very narrow range so that the nervous and muscular systems can function properly.
|what is the equation for calculating the LDLs from TGs?||
LDL = TC – (TG/5 + HDL)
|Which glucose transporter acts as a sensor? Which cells express this transporter?||
The liver and beta cells’ GLUT2 has a low affinity for glucose, allowing those tissues to sense and respond to graded levels of serum glucose.
|Pituitary dwarfishm. Failure to grow, short tature, mild obesity, delayed puberty. Caused by hypothalamic dysfxn so decrease GHRH, lack of anterior pit GH, Can't generate IGF in liver & GH receptor deficiency/defect.||
GH excess in adults causes what and what are the symptoms?
|Who is at higher risk of developing Graves' disease?||
Women, usually between the second and fourth decades
|What are the 2 principal cell types||
1) Dark cheif cells 2) light chief cells
|If angina is detected in a patient, what is the nurses first action?||
Must report finding and treat at once to avoid a fatal myocardial infarction, thyroid hormone administration must be discontinues immediately
|What is different in T3 and T4?||
T 4 is weak, T3 is 5x stronger than T4.
|what to do first if you have pt with solitary nonfunctioning thyroid nodule?||
TSH --> if nl TSH, then U/S, then FNA for cytology