Exam 4 Eggena Case 22-1

Question 1

Secretion of T3 and T4 is regulated by the release of

Answer 1

thyrotropin from thyrotophs of the anterior pituitary

Question 2

biological activity of TSH is in the

Answer 2

beta subunit

Question 3

TSH enhances

Answer 3

iodide uptake
formation of MIT and DIT
release of T3 and T4
hyperplasia and hypertrophy of follicular cells

Question 4

TSH exerts effects on follicular cells by

Answer 4

increasing cAMP after binding to receptors and stimulating adenylate cyclase.

Question 5

TSH secretion is regulated by

Answer 5

TRH (from the hypothalamus)

Question 6

the plasma levels of free T3 and T4 is self reglated by

Answer 6

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.

Question 7

desensitizatio of thyrotrophs is due to

Answer 7

decreased TRH receptpor synthesis in the presence of T3

Question 8

The feedback signal that stops thyroid horome synthesis is not generated by the amount of inorganic iodide in follicular cels, but rather by

Answer 8

the amount of organic iodine in colloid, which limits cAMP formation in cyclic cells.

Question 9

Wolff Chaikoff effect

Answer 9

high doses of iodide inhibit iodide organification and stop T3 and T4 release into the circulation.

Question 10

iodide is used in the treatment of

Answer 10

thyroid storm (a surge in thryoid hormones in a person with thyroid disease during period of stress)

Question 11

In hypeprthyroid patient test, serum levels of T4, TSH and iodine

Answer 11

T4 increased
serium TSH decreased
iodine increased

Question 12

treatment of hyperthyroidism

Answer 12

young: propylthiouracil

adults over 40: iodine

Question 13

grave’s disease is characterized by a

Answer 13

diffused toxic goiter (an enlarged thryoid gland that secretes excess T3 and T4)

Question 14

features of grave’s disease

Answer 14

diffuse toxic goiter
exophthalmos (protruding eyes)
pretibial myxedema (non pitting edema on the dorsal surfaces of legs and feet).

Question 15

thyroid gland enlargemnt and hyperthyroidism result when

Answer 15

circulating antibodies bind to receptors for TSH. (thyroid stimulating immunoglobulin)

Question 16

hyperthyroidism symptoms

Answer 16

weight loss
excessive sweating
breakdown proteins (cause muscle weakness)

Question 17

TBG levels increase when

Answer 17

pregnant or taking oral contraceptives.

It is usually necessary to meausre the free concentration of T3.

Question 18

many of the symptoms of increased hyperthyroidism are caused by

Answer 18

increased sympathetic activity.

Question 19

treatment of hyperthyroidism

Answer 19

propanolol
propothiouracil)
MIT, DIT
thyroidectomy

Question 20

after a thyroidectomy

Answer 20

patients are useually hypothyroid and require L thyroixin

Question 21

low circulating levels of T3 or T4 may be due to

Answer 21

decreased synthesis of T3 and T4, seen in Hashimoto’s disease.

Question 22

a cause of hypothyroidism is

Answer 22

iodine deficiency

Question 23

hypothyroidism due to decreased circulating levels of TSH is most commonly associated with

Answer 23

most commonly associated with tumors of the pituitary gland or postpartem necrosis of the pituitary (Sheehan’s syndrome).

Question 24

when serum concentrations of free T3 and T4 drop, more TSH is secreted by

Answer 24

thyrotrophs of the anterior pirtuitary.

Question 25

if hypothyroidism is not detected early and treated

Answer 25

the child will fail to grow and will develop the characterists of cretinism: short stature, coarse features, thick tongue, dry skin and mental retardation.

Question 26

ketoacidosis

Answer 26

hyperventilating (Kussmaul breating)

hyperkalemia

Question 27

calcium gluconate raises the threshold of cardiac muscle and protects the heart from the

Answer 27

depolarizing action of hyperkalemia

Question 28

Emergency measures for reducing plasma potassium are aimed at shifting potasssium iions into cells, this can be accomplished by

Answer 28

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.

Question 29

contributing factors to type II diabetes

Answer 29

stress
excess glucagon, growt hormone, cortisol, somatostatin
drugs: prednisone (cortisol), thiazide diuretics

Question 30

counterregulatory hormones such as excessive growth hormone or excessive cortisol

Answer 30

can induce a diabetes like condition with high plasma glucose by opposing the actions of insulin.

Question 31

stress from surgery or infections

Answer 31

raises plasma glucose in diabetic diabetic patients: glucose returns to normal when the stress busides.

Question 32

polyphagia results when cells in the hypothalamic satiety center sense

Answer 32

plasma glucose to be too low.

Question 33

the reason for inappropriate hunger drive is that

Answer 33

insulin is required for glucose entry into cells of the satiety center.

Question 34

if glucose cannot enter satiety center neurons becuase insulin is lacking, hypothalamic feeding centers are released from

Answer 34

tonic inhibition by the satiety center, the person feels hungry, seeks food and eats.

Question 35

diabetes and blurred glucose resulted when

Answer 35

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.

Question 36

diabetes and fatigue was caused

Answer 36

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.

Question 37

If the fasting blood sugar is greater than 140 mg/dL

Answer 37

the person has diabetes melltus

Question 38

if fasting blood sugar is leass than 140 mg/dL, but more than 115 mg/dL, a person

Answer 38

may or may not have diabetes. In this situation, a glucose tolerance test is usually performed.

Question 39

glucose satiety test

Answer 39

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.

Question 40

the amount of glycohemoglobin is proportional to the

Answer 40

average plasma glucose level in the preceding 1 to 2 months.

Question 41

When more than 10% of hemoglobin is glycosulated

Answer 41

plasma glucose concentrations have been at unacceptably high levels and closer control is warranted.

Question 42

because circulating insulin is degreaded more rapidly than C peptide,

Answer 42

C peptides are higher than insulin. The evaluate patients with hypoglycemia.

Question 43

cardiac output increases by as much as 50% during the second trimester due to an

Answer 43

increase in stroke volume and heart rate.

This is caused by venous retrun, primarily from shunting of blood through low resistance placental vessels.

Question 44

in pregnancy, because of the decrease in total peripheral resistance,

Answer 44

blood pressure decreases during pregnancy. The changes in vascular resistance are accompanied by increased plasma volume and increased production of red blood cells.

Question 45

The increased velocity of blood flow together with decreased viscosity of blood leads to

Answer 45

turbulence that is detected as a midsystolic flow murmur.

Question 46

rising concentrations of progesterone increase the

Answer 46

sensitivity of central chemoreceptors to carbon dioxide, resulting in hyperventilation and respiratory alkalosis.

Question 47

why was the pregnant thyroid gland enlarged?

Answer 47

unbound thyroid hormone increases slightly, most of the hormone is bound to thryoid binding proeins that are stimulated by estrogens during pregnancy.

Question 48

why did the pregnant patient’s blood pressure increase upon lying supin in her third trimester?

Answer 48

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.

Question 49

the hyperreactivity of the cardiovascular system serves as a warning sign that the patient is developing

Answer 49

ecclampsia

Question 50

why did she have nocturia in the 36th qweek?

Answer 50

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

Question 51

why was the pregnant patient unable to breat feed her newborn?

Answer 51

the anterior pituitary was not producing prolactin.

Question 52

Why did the pregnant patient’s menses not return?

Answer 52

anterior pituitary failure caused decreased LH FSH

Question 53

Why did the pregnant patient’s pubic hair not grow?

Answer 53

they are dependent upon testoserone, which is dependent on ACTH, which was deficient because of anterior pituitary.

Question 54

why was the pregnant patient hypothenisve 3 months after her postpartum hemorrhage?

Answer 54

lack of ACTH and cortisol decreases vascular responsiveness to vasoconstrictions, resulting in decreased peripheral vascular resistance and a fall in blood pressure.

Question 55

why was the pregnant patient cold?

Answer 55

due to decreased concentrations of T3 and T4. Decreased thyroid hormones were depressed because of TSH deficiency secondary to anterior pituitary.

Question 56

Why was the pregnant patient given injection of insulin, TRH and GnRH?

Answer 56

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.

Question 57

why did the pregnant patient have panhypopituitarism?

Answer 57

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.