Exam 4 Eggena Case 22-1 Flashcards
Secretion of T3 and T4 is regulated by the release of
thyrotropin from thyrotophs of the anterior pituitary
biological activity of TSH is in the
beta subunit
TSH enhances
iodide uptake
formation of MIT and DIT
release of T3 and T4
hyperplasia and hypertrophy of follicular cells
TSH exerts effects on follicular cells by
increasing cAMP after binding to receptors and stimulating adenylate cyclase.
TSH secretion is regulated by
TRH (from the hypothalamus)
the plasma levels of free T3 and T4 is self reglated by
feedback inhibition of TSH secretion. As circulating T3 and T4 rise, thyrotophs synthesize less TSH and become insensitive to TRH stumulation, but TRH secretion is not affected.
desensitizatio of thyrotrophs is due to
decreased TRH receptpor synthesis in the presence of T3
The feedback signal that stops thyroid horome synthesis is not generated by the amount of inorganic iodide in follicular cels, but rather by
the amount of organic iodine in colloid, which limits cAMP formation in cyclic cells.
Wolff Chaikoff effect
high doses of iodide inhibit iodide organification and stop T3 and T4 release into the circulation.
iodide is used in the treatment of
thyroid storm (a surge in thryoid hormones in a person with thyroid disease during period of stress)
In hypeprthyroid patient test, serum levels of T4, TSH and iodine
T4 increased
serium TSH decreased
iodine increased
treatment of hyperthyroidism
young: propylthiouracil
adults over 40: iodine
grave’s disease is characterized by a
diffused toxic goiter (an enlarged thryoid gland that secretes excess T3 and T4)
features of grave’s disease
diffuse toxic goiter
exophthalmos (protruding eyes)
pretibial myxedema (non pitting edema on the dorsal surfaces of legs and feet).
thyroid gland enlargemnt and hyperthyroidism result when
circulating antibodies bind to receptors for TSH. (thyroid stimulating immunoglobulin)
hyperthyroidism symptoms
weight loss
excessive sweating
breakdown proteins (cause muscle weakness)
TBG levels increase when
pregnant or taking oral contraceptives.
It is usually necessary to meausre the free concentration of T3.
many of the symptoms of increased hyperthyroidism are caused by
increased sympathetic activity.
treatment of hyperthyroidism
propanolol
propothiouracil)
MIT, DIT
thyroidectomy
after a thyroidectomy
patients are useually hypothyroid and require L thyroixin
low circulating levels of T3 or T4 may be due to
decreased synthesis of T3 and T4, seen in Hashimoto’s disease.
a cause of hypothyroidism is
iodine deficiency
hypothyroidism due to decreased circulating levels of TSH is most commonly associated with
most commonly associated with tumors of the pituitary gland or postpartem necrosis of the pituitary (Sheehan’s syndrome).
when serum concentrations of free T3 and T4 drop, more TSH is secreted by
thyrotrophs of the anterior pirtuitary.
if hypothyroidism is not detected early and treated
the child will fail to grow and will develop the characterists of cretinism: short stature, coarse features, thick tongue, dry skin and mental retardation.
ketoacidosis
hyperventilating (Kussmaul breating)
hyperkalemia
calcium gluconate raises the threshold of cardiac muscle and protects the heart from the
depolarizing action of hyperkalemia
Emergency measures for reducing plasma potassium are aimed at shifting potasssium iions into cells, this can be accomplished by
insulin or beta 2 adrenergic agonsists that stimulate sodium potassium ATPase or with sodium bicarbonate that draws hydrogen ions out of cells on hydrogen/sodium antiporters.
contributing factors to type II diabetes
stress
excess glucagon, growt hormone, cortisol, somatostatin
drugs: prednisone (cortisol), thiazide diuretics
counterregulatory hormones such as excessive growth hormone or excessive cortisol
can induce a diabetes like condition with high plasma glucose by opposing the actions of insulin.
stress from surgery or infections
raises plasma glucose in diabetic diabetic patients: glucose returns to normal when the stress busides.
polyphagia results when cells in the hypothalamic satiety center sense
plasma glucose to be too low.
the reason for inappropriate hunger drive is that
insulin is required for glucose entry into cells of the satiety center.
if glucose cannot enter satiety center neurons becuase insulin is lacking, hypothalamic feeding centers are released from
tonic inhibition by the satiety center, the person feels hungry, seeks food and eats.
diabetes and blurred glucose resulted when
plasma glucose was high, pulling water with it and distorting the lens. Once glucose had diffused back out and the lens was no longer swollen, his vision returned back to normal.
diabetes and fatigue was caused
by insufficient glucose entry into muscle cells and partly muscle wasting, as proteins were broken down and amino acids converted to glucose in the absence of insulin.
If the fasting blood sugar is greater than 140 mg/dL
the person has diabetes melltus
if fasting blood sugar is leass than 140 mg/dL, but more than 115 mg/dL, a person
may or may not have diabetes. In this situation, a glucose tolerance test is usually performed.
glucose satiety test
the test subject eats a high carbohydrate diet for 3 days and on the morning of the test drinks a solution with glucose. blood samples are collected at 30 min intervals.
the amount of glycohemoglobin is proportional to the
average plasma glucose level in the preceding 1 to 2 months.
When more than 10% of hemoglobin is glycosulated
plasma glucose concentrations have been at unacceptably high levels and closer control is warranted.
because circulating insulin is degreaded more rapidly than C peptide,
C peptides are higher than insulin. The evaluate patients with hypoglycemia.
cardiac output increases by as much as 50% during the second trimester due to an
increase in stroke volume and heart rate.
This is caused by venous retrun, primarily from shunting of blood through low resistance placental vessels.
in pregnancy, because of the decrease in total peripheral resistance,
blood pressure decreases during pregnancy. The changes in vascular resistance are accompanied by increased plasma volume and increased production of red blood cells.
The increased velocity of blood flow together with decreased viscosity of blood leads to
turbulence that is detected as a midsystolic flow murmur.
rising concentrations of progesterone increase the
sensitivity of central chemoreceptors to carbon dioxide, resulting in hyperventilation and respiratory alkalosis.
why was the pregnant thyroid gland enlarged?
unbound thyroid hormone increases slightly, most of the hormone is bound to thryoid binding proeins that are stimulated by estrogens during pregnancy.
why did the pregnant patient’s blood pressure increase upon lying supin in her third trimester?
In the supine position, the baby rests on the inferior vena cava, which diminishes venous return and triggers a compensatory increase in cicrulating concenrations of angiotension II.
the hyperreactivity of the cardiovascular system serves as a warning sign that the patient is developing
ecclampsia
why did she have nocturia in the 36th qweek?
gravity caused accumulation of edema fluid in her legs during the daytime. At night, this fluid was mobilized and the increased circulting plasma volume inhibited ADH and aldosterone.
Increased pressure diruesis
why was the pregnant patient unable to breat feed her newborn?
the anterior pituitary was not producing prolactin.
Why did the pregnant patient’s menses not return?
anterior pituitary failure caused decreased LH FSH
Why did the pregnant patient’s pubic hair not grow?
they are dependent upon testoserone, which is dependent on ACTH, which was deficient because of anterior pituitary.
why was the pregnant patient hypothenisve 3 months after her postpartum hemorrhage?
lack of ACTH and cortisol decreases vascular responsiveness to vasoconstrictions, resulting in decreased peripheral vascular resistance and a fall in blood pressure.
why was the pregnant patient cold?
due to decreased concentrations of T3 and T4. Decreased thyroid hormones were depressed because of TSH deficiency secondary to anterior pituitary.
Why was the pregnant patient given injection of insulin, TRH and GnRH?
insulin allowed glucose to diffuse into muscle cells, causing them serves as a potent stimulus, for secretion of ACTH, growth hormone and prolactin, from the anterior pituitary. TSH, FSH and LH, failure to increase the release of these hormones.
why did the pregnant patient have panhypopituitarism?
by infarction of the anterior pituitary (sheehan’s syndrome). During pregnancy, the anterior pituitary hypertrophies. When blood flow was decreased due to hemorrhage, the anterior pituitary cells died. treatment was replacing only the essential hormones. growht hormone, is not essential in adulthood.
