Study BIOL 472 Topic 18 Flash Cards
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BIOL 472 Topic 18
BIOL 472 Topic 18
| exubera |
| -inhaled insuin powder from Pfizer |
| insulin pumps |
|
-deliver various forms of insulin w/ computer programmable pump -constantly infuses insulin and adjusts |
| metaformins |
|
-(avandia, glucophage) -drugs that enhance insulin sensitivity in peripheral storage tissue -take w/ insulin for maximum effectiveness |
| HbA1C test |
|
-test for glycated Hb, gives a longterm "batting avg" for blood sugar levels -normal person: 5% -diabetic as high as 30% |
| androgenital syndrome |
|
-excessive output of androgens causes mascularization of female -ambiguous genitals -pseudohermaphrodism |
| conn's syndrome |
|
(primary hyperaldosteronism) -adrenal tumor or oversecretion of aldosterone from zona -elevated blood pressure -K+ depletion and muscle weakness |
| addison's disease |
|
-lack of adrenocortical functions -anorexia, fatigue, hypoglycemia -poor stress tolerance -lack of negative feedback from adrenal hormones on pituitary -causes hypersecretion of ACTH -excessive ACTH stimulates melanocytes, causing localized dark skin pigment |
| cushing's syndrome |
|
-excessive cortisol production -muscle atrophy -osteoporosis -thin skin w/ blood vessels visible -accumulation of fat in abs -capillary rupture and straie |
| DHEA replacement |
|
-as body ages, sex hormone production declines -anti-aging effects |
| these are converted to testosterone |
|
androsternedione DHEA |
| adrenal cortex |
|
endocrine organ essential for life(w/ parathyroid gland) -mediate stress responses -3 distinct zones: 1. zona glomerulosa: produces aldosterone, a mineralocorticoid) 2. zona fasiculataa: produces glucocorticoids, cortisol compounds 3. zona reticularis: andorgens and sex hormone precursors; androstenedione; DHEA |
| cortisol responses |
|
-immune system inhibition -decrease in muscle, bone, CT mass -glycogenolysis, gluconeogenesi, FFA release -increased arterial tone (increase BP) -increase GFR -anti-inflammatory agents following joint injury |
| regulatory and secretory control for adrenal cortex |
|
CRH from hypothalamus -stimulates release of ACTH from pituitary -ACTH stimulates secretion of hormones from the adrenal cortex (cortisols and androgens) -adrenal hormones negatively feed back at the levels of both the pituitary and hypothalamus to shut down ACTH production |
| adrenal gand |
|
cortex and medulla cortex: -mineralocorticoids -sex steroid hormones -glucocorticoids medulla: -extension of the symapthetic nervous system -E and NE production/release |
| 1 identified orexin |
|
-grehlin -released by hypothalamus and stomach -stimulates hunger -releases hormones like gastrin |
| orexins |
|
-released by hypothalmus in response to low blood sugar and increase appetite -"hunger" -anorexia= w/o hunger |
| leptin |
|
"fat burning" hormone -linked to satiety |
| levels of insulin and leptin determined by |
|
amt of adipose tissue -plasma leptin and insulin feed back to hypothalmus, causing decreased food intake -stimulates satirety -increased catabolic pathway activity |
| body weight regulated by,... |
| ...hypothalamus, neurotransmitters, fat cells, hormones |
| obesity |
|
BMI -lbs x 703/ht^2 21-24 healthy 25-29 overweight 30+ obese |
| stem cell treatment |
| -pancreatic stem cells injected or transplanted |
| exubera |
| -inhaled insuin powder from Pfizer |
| insulin pumps |
|
-deliver various forms of insulin w/ computer programmable pump -constantly infuses insulin and adjusts |
| metaformins |
|
-(avandia, glucophage) -drugs that enhance insulin sensitivity in peripheral storage tissue -take w/ insulin for maximum effectiveness |
| HbA1C test |
|
-test for glycated Hb, gives a longterm "batting avg" for blood sugar levels -normal person: 5% -diabetic as high as 30% |
| Type II diabetes |
|
-adult onset -obesity -strong genetic component -insulin resistance: peripheral tissues resistant to insulin -reduced insulin output by B cells treatment: -low fat, low cal diet -exercise -can reverse disease -Sulfonlurea drugs (depolarize B cells, elevate intracellular Ca++, enhance insulin release by B cells) |
| complications of Type I diabetes |
|
retinopathy neuropathy atherosclerosis |
| If Type I let untreated... |
|
high [glucose] -glucose can't reach tissues w/o insulin -body burns fats/proteins -ketoacidosis (acid + dehydration can lead to coma, death) "hyperglycemic coma" -if inject insulin w/o food, -hypoglycemic coma -"insulin shock" -glucose administration will cure it |
| Type I diabetes |
|
-no genetic link -insulin dependent -only 10% diabetics -autoimmune disorder causes antibodies to destroy B cells -eventually no insulin produced -Epstein-barr virus? -treat w/ insulin |
| glucose tolerance test |
|
-12 hr fast -administer glucose -normal adult: peaks, then returns to normal in 2 hours -diabetic: resting glucose already high, soars way up, doesn't really come down |
| can produce insulin deficiency by... |
|
...pancreatectomy ...Streptozocin (zots out B cells, causes diabetes in 3 days in rats) |
| insulin deficiency |
|
1. polyurea (too much urine) 2. polydipsea (have to drink a lot) 3. polyphagia (high blood glucose, but tissues can't access it) |
| Diabetes Mellitis |
|
-sweet urine - |
| insulin mode of action |
|
insulin receptors have tyrosine kinase activity -initiate intracellular cascade -adds GLUT transporters to cell membrane -allows glucose entry into the cell -7 different types of GLUTs |
| insulin effects |
|
-increased transport of glucose, AA, K+ into insulin-sensitive areas (muscle, fat, liver) -anabolic effects (glycogen synthetase, protein synthesis, increase lipogenic enzymes, inhibit protein breakdown, inhibit gluconeogenic enzymes) |
| insulin |
|
-produced by pancreatic B cells -clip SS bonds to get active form -binds to receptors -internalized -degraded by insulin proteases -degraded by liver/kidney |
| non supressible insulin-like activity |
|
-activity not suppressed by insulin antibodies -somatomedins (IGF 1, 2) |
| liver |
|
-endocrine organ -stores glucose as glycogen -generates glucose thru glucose 6 phosphate |
| pancreas |
|
-endo and exocrine functions alpha: secrete glucagon, increase plasma glucose (fasting) beta: insulin, decrease plasma glucose (feasting) Delta: somatostatin; inhibits A, B, F F cells: pancreatic polypeptide; slows food absorption; questionable function |
| if no Vit D... |
|
-poor intestinal Ca++ absorption -rickets or osteomalcia |
| D3 |
|
-calcitrol -1, 25 dihydroxycholecaliferol -synthesized w/ sun -fortified in milk -1st modief in liver -2nd modified in kidneys -allows Ca++ absorption by SI -stimulates Ca++ reabsorption by kidneys -shuts down PTH release |
| calcitonin |
|
-opposite PTH -produced by parafollicular C cells of thyroid gland -decreases plasma [Ca++] -decreases bone reabsorption -decreases kidney reabsorption |
| that damn estrogen |
|
-estrogen tends to decrease PTH -after monopause, low estrogen, so increased PTH -increased bone dissolving -osteoporosis -treated w/ estrogen replacement therapy |
| if no PTH... |
|
-low [Ca++] -causes increase in Na+ permeability -hyperexcitable nerves -hypocalcemic tetany, Trousseau's sign |
| PTH |
|
-4 pea-sized parathyroid glands on thyroid -low [Ca++] causes PTH release -increase bone reabsorption -increase Ca++ -increase kidney DCT reabsorption of Ca++ -stimulates Vit D3 production |
| regulators of body Ca++ |
|
-parathyroid hormone (PTH) -calcitonin (CT) -Vit D3 |
| osteoclasts |
|
-mvt of Ca++ out of hydroxyapatite and into ioned Ca++ pool -dissolve bone -responds to PHT |
| osteoblasts |
| -Ca++ deposition on bone (calcitonin) |
| plasma Ca++ |
|
-regulated in narrow range -45% bound to albumin -10% in phosphate/citrate complexes -45% free, subject to hormonal control |
| calcium homeostasis |
|
99% Ca++ found in bone -in form of hydroxyapatite crystals |
| exophthalamus |
|
-bug-eyed appearance -immune-mediated enlargement of muscles and tissues in eyes -often in Grave's disease |
| creatinism |
|
-hypothyroidism in infants -deficient TH secretion |
| goiters |
|
-enlarged thyroid glands -caused by either: hyperthyroidism (overstimulation) hypo (gland increases in size due to I deficiency, little T3, T4, high TSH stimulates gland) |
| exopthalamos |
| swelling of muscles and fat (autoimmune attack); protruding eyes |
| Grave's disease |
|
-autoimmune disease -antibodies resemble TSH -stimulate thyroid -essentially no TRH, high T3, T4 levels -exopthalamos: swelling of muscles and fat (autoimmune attack); protruding eyes |
| hypertyroidism |
|
-symptoms opposite of hypo -Grave's disease most common form -treatment: -drugs that block iodine uptake by follicular cells -drugs that block iodination -destruction of thyroid gland -TH replacement |
| Hashimoto's disease |
|
-autoimmune disease -antibodies attack thyroid gland |
| hypothyroidism |
|
-underactive -I deficiency -hypothalamus problem (decrease TRH) -ant. pit. problem (decrease TSH, no response to TRH) -Hashimoto's disease -decreased matabolism -decreased HR, CO, SV -cold, clammy, lethargic -decreased nail, bone growth -raspy voice -weight gain in children: cretinism in adults: myxendema |
| RT3 |
|
-also deiodenation product -biologically inactive |
| T3 and T4 are usually bound to... |
|
...Tyroxine binding globuin -or albummin -inactive -lipophilic so limited solubility in plasma -unbound state active, but small quantity -constant pool or supply |
| T3 |
|
-3 iodines -lower plasma [] -most biologically active -most formed from deiodonated T4 |
| T4 |
|
-4 iodines -DIT + DIT -most biologically active -most plasma [] -essentially a "pre-hormone" -de-iodenated to form more active T3 |
| thyroid gland |
|
-bilobed -centered at isthmus - |
| intermediate pitiuitary lobe |
|
MSH: melanocyte stimulating hormone no function in humans oversecretion causes bronzing of skin |
| acromegaly |
| -oversecretion of GH |
| somatomedins |
|
IGF (insulin-like gorwth factors) from liver -negative feedback on GH secretion -act on anterior pi. and hypothalamus -stimulates bone growth -stimulates cell proliferation |
| GH |
|
-insulin-like actions: muscle: increases aa uptake to grow liver: increases protein synthesis -anti-insulin actions: muscle: decrease glucose uptake liver: increase gluconeogenesis fats: increase lypolysis, decrease glucose uptake nt effect: increase plasma glucose increase protein synthesis triggers somatomedin from liver |
| ACTH |
| adrenal stimulating cortex |
| TSH |
| thyroid stimulating hormone |
| FSH, LH |
| -stimulates gonads |
| anterior pituitary |
|
-hypophyseal portal system -secretes 6 hormones -secretion regulated by hypothalmus regulatory hormones (CRN, GnRH, RH means "releasing hormone") -true endocrine gland (acidophil and basophils produce own hormones) |
| hypophyseal portal system |
| to grow beneath |
| acidophils, basophils |
|
in anterior pituitary -produce own hormones |
| oxytocin |
|
-stimulates uterine contractions -administration can trigger labor (not naturally) -milk ejection -hugging effect? |
| diabetes insipidus |
|
-tasteless urine (no sugar) -large volumes of dilute urine 1. neurogenic cause: no ADH release 2. nephrgenic cause: failure of tubules to respond to ADH |
| ADH |
|
-small peptide (9 aa) -action modes: 1. increase water reabsortion by DCT, collecting duct; sweat glands and GI tract 2. bind to receptors on smooth muscle; stimulates Ca++ entry and contraction--> vasoconstriction--> increases BP release dictated by: 1. changes in osmolarity (osmoreceptors shrink to detect 1% change) 2. drop in plasma volume (hemmoraging or bleeding); more powerful response triggered 10-15x more |
| posterior pituitary gland releases |
|
1. ADH 2. oxytocin -both made in hypothalmus |
| posterior pituitary |
|
-derived from brain tissue -supra and paraventricular nuclei in hypothalamus -secrete hormones, stores in posterior pi. -ADH, oxytocin |
| Rathke's Pouch |
| -mouth lining that forms anterior pituitary |
| anterior pituitary |
|
-derived from mouth lining (Rathke's Pouch) -synthesis of releasing factor and growth factors -blood portal syste, |
| steroid hormone action |
| -affects nucleus directly via transcription/translation |
| peptide/amine hormone action |
|
1. cAMP 2. IP2/DAG 3. direct membrane Ca++ channel activation |
| classes of hormones |
|
1. protein (peptide) 2. amines (neurohormones and thyroxine) 3. steroids |
| endocrine system |
|
-cells release messanger substances into blood stream that has action on specific target tissue -messengers include: 1. hormones 2. nuerohormones 3. prostaglanins |
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