Exam 4 Part VII Flashcards
Regulation of GH secretion.
Increased by GHRH from hypothalamus
Some conditions that cause GnRH secretion:
decreased fatty acids in blood
hypoglycemia
increased amino acids in blood fasting or a protein meal
stress: starvation, exercise, trauma
the first 2 hours of slow-wave sleep →↑↑ GH
low GH levels
Decreased by GHIH =
Decreased by GHIH = somatostatin from hypothalamus, also δ cells in pancreas.
growth hormone deficiency
Deficiency: in childhood: dwarfism, e.g., panhypopituitary dwarf. Much is from GH lack, also lack of TSH.
excess GH
before the epiphyses of the long bones fuse: giantism or gigantism
in adulthood: acromegaly: many soft tissues grow, bones that can grow do, other bones thicken.
acromegaly symptoms
Everything keeps growing: cardiomegaly, huge valves, feet, hands
Colon polyps → colon cancer
Had 2 hips replaced
Diabetes
Only thing painful about surgery for tumor: skin was so thick, they couldn’t get an IV in - hematomas
Iodine is preferentially pumped into the follicle cells from the blood (iodine trapping). From there iodine moves into the lumen of the follicle and combines with
thyroglobulin
thyroglobulin
Thyroglobulin is a protein stored in the lumen, and thyroxine (tetra-iodothyronine=T4) and triiodothyronine (T3) are formed from within it.
Then when T3 and T4 are needed for use, thyroglobulin is taken up by pinocytosis into the cell, and T3 and T4 are released from the
thyroglobulin molecule and travel into the blood.
There is a long latency before the effects of
There is a long latency before the effects of thyroid hormones can be seen: 12 hours to 3 days and then the effects continue for a long time (days).
B. Effects of thyroid hormones:
increased metabolic rate protein synthesis\ gluconeogenesis breakdown of fats use of glucose stimulates growth rapid cerebration
Inc. TRH from hypothalamus causes
Inc. TRH from hypothalamus causes TSH from pituitary to stimulate the thyroid gland.
condition that stimulates TRH
Condition that stimulates: cold. Obese people cold room to lose weight
conditions that suppress TRH
Conditions that suppress: Excitement & anxiety, conditions that stim. the sym. system, perhaps because they cause inc. body heat.
In childhood: cretinism:
In childhood: cretinism: failure to grow, mental deficiency becomes irreversible, may be necessary to receive certain kinds of stimulation before a certain age
In adulthood: myxedema:
In adulthood: myxedema: Low BMR, weight gain, poor cold tolerance, slow mentation: “myxedema is the one disease that can be diagnosed over the telephone.”
Hashimoto’s:
Hashimoto’s: thyroglobulin &/or thyroid peroxidase, etc., antibodies. Most common type of hypothyroidism in U.S.
iodine deficiency goiter:
iodine deficiency goiter: endemic goiter in the “goiter belts” because of lack of iodine in the soil. Central Europe & Great Lakes. Is TSH high or low?
excess TH
C. Excess: hyperthyroidism: high BMR, nervousness, irritability, weight oss, fatigue, hyperphagia, heat intolerance, fine tremor of the fingers, warm skin. One form is Grave’s disease.
Autoantibodies to TSH receptor
Autoantibodies to TSH receptor (TSI = thyroid-stimulating immunoglobulin) cause gland to hyperfunction (in 3/4 of Grave’s yield hyper-, ¼ yields hypothyroidism). Exophthalmic goiter can occur. Also causes enhanced responses to sym. stim. (increases synthesis of adrenergic receptors). Can have high C.O. failure.
adrenocortical hormone
They are steroids, formed from cholesterol, degraded in the liver
A. Mineralocorticoids:
A. Mineralocorticoids: Aldosterone – very potent; Corticosterone – intermediate between mineralocorticoid and glucocorticoid
effects of aldosterone
tubular reabsorption of sodium
tubular secretion of K+
`Regulation of aldosterone secretion
Controlled almost independently of other adrenocortical hormones
regulation of aldosterone secretion: Controlled almost independently of other adrenocortical hormones Decreasing importance:
K+ concentration of extracellular fluid
quantity of body sodium. If Na+ drops, bl. vol. drops renin
ACTH – has a permissive effect on aldosterone secretion. Without it, the gland atrophies, including to a mild extent the cells that produce aldosterone.
aldosterone deficiency
Deficiency: Part of Addison’s disease: autoimmune destruction of adrenals often. Orthostatic hypotension (volume contraction = volume depletion), hyperkalemia (→ cardiac arrest, fibrillation). Without salt therapy, or mineralocorticoid therapy, the person will tend to die from blood volume loss & low cardiac output within 3 days to 2 weeks. Small boy consumed huge quantities of salt
aldosterone excess
Excess: Conn’s syndrome: primary aldosteronism: hypokalemia (secreting too much) also cardiac arrhythmias, and muscle weakness (comes from low K+, has an effect to dec. excitability), often hypertension (from inc. Na+ reabsorption).
glucocorticoids
cortisol (=hydrocortisone) – very potent
corticosterone: intermediate between mineralo- & glucocorticoids
prednisone, dexamethasone – synthetic, more potent than cortisol
Effects of glucocorticoids
increase gluconeogenesis
decreases glucose utilization by cells
decreases protein synthesis (except in liver and GI tract)
increases removal of fat from adipose tissue
increase glycogenesis in liver
Amino acids and fats are used by most tissues, glucose is conserved for the CNS.
anti inflammatory
glucocorticoids Regulation of secretion: “stress”
Regulation of secretion: “stress”
CRH from hypothalamus causes ACTH release from the anterior pituitary
glucocorticoids and stress: conditions that cause secretion
hypoglycemia
any injury or disease
extremes in temperature or any other physiological stress, e.g., sleep deprivation
peaks about 8 AM
Deficiency of both mineralocorticoids and glucocorticoids:
Deficiency of both mineralocorticoids and glucocorticoids: Addison’s disease (hypoadrenalism). The mineralocorticoid treatment will prevent immediate death, but the inability to mobilize energy resources to combat stress can make the person susceptible to any stress or disease.
excess glucocorticoids
Excess: Cushing’s syndrome could be both often cortisol
(hyperadrenalism). Lack of protein deposition: muscle weakness, fractures, poor wound-healing; “buffalo hump and moon face;” adrenal diabetes” due to hyperglycemic effect of glucocorticoids, (17 –hydroxysteroids increased in urine); psychosis – megalomaniacal type. Increased appetite (hyperphagia).
Cortisol, by preventing glucose utilization by cells, can
Cortisol, by preventing glucose utilization by cells, can cause starvation & death of some brain cells, particularly in the hippocampus, involving memory.
In the Metabolic Syndrome,
cortisol is probably a part. Metabolic Syndrome: Htn, truncal obesity, diabetes, poor lipid profile. Consider metabolic syndrome as contributing to type II diabetes??
C. Sex steroids – small amounts of mostly androgens (DHEA = dehydroepiandrosterone, and androstenedione) are produced by the
dehydroepiandrosterone, and androstenedione) are produced by the adrenal cortices. These may be involved in the growth spurt, and female libido has been attributed to adrenal and ovarian androgens.
Adrenogenital syndrome caused by a
Adrenogenital syndrome caused by a tumor or can be caused by 21B-hydroxylase deficiency → no cortisol produced → ↑ ACTH → ↑ androgens = congenital adrenal hyperplasia, has masculinizing effects. [17-ketosteroids] Metabolites from androgens increased in urine.
A. Insulin,
A. Insulin, a small protein produced by the beta cells of the endocrine pancreas (islets of Langerhans)
insulin effects
increases glucose transport into cells (brain not dependent)
increases glycogenesis in liver and muscles decreases gluconeogenesis in liver
inc. amino acid & fatty acid transport into cells (used for synthesis
insulin stimulated by
Stim. by hyperglycemia, as after a meal “pushes” FAs, AAs. & glucose into cells (facilitated diffusion).
Overall, insulin is a
Overall, insulin is a “hormone of plenty.” It promotes synthesis of protein & fats & glucose utilization. (Insulin, along with thyroid hormones and GH is necessary for normal growth.)
regulation/secretion of insulin stiumlated by
blood glucose
certain amino acids potentiate the ability of high blood glucose to stimulate secretion
food → ↑ parasym. activity, CCK, GIP = glucose-dependent insulinotropic peptide
excess insulin Excess: 1° maybe rare, 2° to hyperglycemia from
Excess: 1° maybe rare, 2° to hyperglycemia from insulin resistance
excess insulin
hyperinsulinism
insulin shock: Hypoglycemia from administering too much insulin.
insulin shock
Causes increased excitability of the nervous system that can lead to convulsions. Also the hypoglycemia can cause brain damage → coma
Type 1 – Insulin-dependent (IDDM), also called juvenile diabetes –
Autoimmune destruction of pancreatic Beta cells. Some people get this later. If uncorrected early, small in stature – illustrates the fact that is necessary for growth
Type 2 – Non insulin-dependent (NIDDM)
Maturity – onset diabetes” (now occurring in children as young as 10.): more genetic of the 2 types. Obesity is a risk factor (Obesity may be a sign of the genetic difficulty of getting glucose into cells: starved cells cause overeating?)
Insulin resistance:
Insulin resistance: impairment of biologic responses to insulin, can be due to defects from insulin abnormalities to insulin action cascade in target cells. Often considered a problem with the receptor, not necessarily.
diabetes type 2 symptoms
Symptoms: Polyuria, polydipsia, polyphagia, weight loss in IDDM, acidosis. Diabetic coma can come from the acidosis & exacerbated by the dehydration.
. Some complications of chronic diabetes:
. Some complications of chronic diabetes: retinopathy, neuropathy, peripheral vascular problems (some associated with atherosclerosis) including foot ulcers, nephropathy, susceptibility to infection, poor wound-healing.
B. Glucagon,
B. Glucagon, a polypeptide produced by alpha cells of endocrine pancreas
glucagon effects
increases glycogenolysis in liver
increases gluconeogenesis in liver
increases use of fats for energy
Glucagon is a hyperglycemic agent.
Regulation of glucagon secretion:
Regulation of secretion: stimulated by hypoglycemia, exercise
C. Somatostatin,
polypeptide from delta cells of the islets of Langerhans. It has been suggested that its role is to slow the assimilation of food from the gut. It is the same as hypothalamic GHIH. Also inhibits insulin and glucagon release. (The “Oh, shut up.” hormone.)
Hormonal control of blood glucose
liver – blood glucose buffer system
hypoglycemic hormone: insulin
hyperglycemic hormones (4): Glucagon and epinephrine ( glycogenolysis), GH and cortisol, (glucose util. by cells)
hyperglycemic hormones (4):
hyperglycemic hormones (4): Glucagon and epinephrine ( glycogenolysis), GH and cortisol, (glucose util. by cells)
The 5 hormones that increase the removal of fat from adipose tissue & increase its use for energy:
glucagon, epinephrine, GH, cortisol, T3/T4
The 2 hormones that increase glycogenolysis:
Glucagon and epinephrine
The 2 hormones that promote the use of all 3 types of food for energy:
Glucagon and T3/T4
The 3 hormones that increase glycogenesis:
Cortisol and GH (by glucose util. hyperglycemicglycogenesis) & insulin (stim. by eating)
3 hormones necessary for growth:
Insulin, T3/T4 (protein anabolic at normal levels), GH (panhypopituitary dwarfism is partly low GH). Sex hormones? NO: Castrati – very tall, unimpeded effect of growth hormone. Testosterone (or estrogen) caps your final height. Precocious puberty in either sex → short in stature.
spermatogenesis
It begins occurring at puberty and continues throughout life. In meiosis, the precursors to germ cells go from the diploid number of chromosomes to the haploid number, taking about 75 days to go from germinal cell to sperm.
Hormones that stimulate spermatogenesis
Testosterone, produced by the interstitial cells(=Leydig cells), is necessary for sperm development.
LH: stimulates the interstitial cells
FSH: stimulates the Sertoli cells (=nurse cells) to providenutrition for the developing sperm and to convert spermatids into sperm (spermiation)
Seminal vesicles
Their secretions form part of the semen. The secretions contain mucoid material including:
seminal vesicles Their secretions form part of the semen. The secretions contain mucoid material including:
fructose and other nutrients for sperm
prostaglandins – aid fertilization:
prostaglandins – aid fertilization:
react with cervical mucus to make it more receptive to sperm
maybe cause reverse peristalsis in uterus and fallopian tubes – tohelp sperm move toward ovaries (Guyton mentions that a few reach the upper end of the fallopian tube in 5 minutes.)
Prostate gland
It secretes a thin, alkaline fluid. Alkalinity is important for successful fertilization. The fluid in the vas deferens is acidic (sperm end-products), the vagina is acidic (3.5 – 4.0), and a too acidic environment immobilizes the sperm.
