Alt Of Endo Function 1

Question 1

Syndrome of Inappropriate ADH (SIADH)

Answer 1

Kidneys exposed to excessive amounts of ADH - high concentrations

From pituitary - secretes multiple hormones into bloodstream. Too much/little GH. ADH affects kidney cells (reabsorption)

Question 2

Causes of SIADH

Answer 2

Post-surgery: increased ADH secretion 5-7 days after general anesthesia. Hyponatremic, not severe

Ectopic production by cancers (pulmonary) - ectopic pregnancy; not smoking from the place it should (implantation in Fallopian tube)

Pulmonary infections: tuberculosis and other bacterial pneumonias (don’t know why)

CNS disorders (head traumas, infections, stroke) - in pituitary, cells dump ADH when there is trauma or infection

Question 3

Pathophysiology and clinical consequences of SIADH

Answer 3

Increased secretion of ADH - ADH allows kidneys to re absorb more pure water

Increased perm of renal tubules to water - increases water reabsorption by kidneys

Excretion of concentrated urine - antidiurese; not peeing, urine input goes down

Results in hyponatremia and reduced plasma osmolarity (only for SIADH or diabetes insipidus patients)

Increased blood volume/blood pressure - edema, weight gain

Question 4

Diabetes Insipidus (DI)

Answer 4

When kidneys are exposed to REDUCED amts of ADH

Question 5

Types of diabetes insipidus (DI)

Neurogenic

Answer 5

Nervous system

Insufficient amts of ADH secreted due to lesions of hypothalamus or posterior pituitary

Caused by brain tumors, stroke, infections, head trauma

Question 6

Nephrogenic (kidney)

Answer 6

Inadequate response to ADH due to renal tubule damage

Caused by several renal diseases and drug toxicity (lithium)

Question 7

Pathophysiology and consequences of Neurogenic DI

Answer 7

Acute damage to hypothalamus or posterior pituitary leads to loss of ADH secretion

Decreased permeability of renal tubules to water - decreases water reabsorption by kidneys

Excretion of large volumes of dilute urine

Results in high plasma osmolarity and hypernatremia

Hypovolemia and hypotension

Decreased adh secretion -> decreased water reabsorption -> low BV -> low BP -> increased plasma osmolarity [Na+]

Question 8

Patho of nephrogenic DI

Answer 8

Damage to renal tubules leads to decreased response to adh

Excretion of large volumes of dilute urine

Results in high plasma osmolarity and hypernatremia

Hypovolemia and hypotension

Question 9

Thyroid hormone

Answer 9

Produced by follicle cells of the thyroid gland

Hormones produced are thyroxine (T4) and triiodothyronine (T3)

Question 10

Physiological effects of thyroid hormone

Answer 10

Stimulates metabolism - increases metabolism, increases metabolic rate of all cells, promotes thermogenesis, hyper = hot, hypo = cold

Normal maturation of the nervous system and promotes effects of growth hormone - in children and infants = short stature, brain doesn’t develop, need thyroid hormone meds

Increases target cell responsiveness to catecholamines - epinephrine and norepinephrine released by sympathetic nervous system (fight or flight)

Catecholamines - raise heart rate and blood pressure due to fight or flight response

TH present: bp goes up
No TH: bp goes down

Question 11

Feedback and regulation of T3/T4

Answer 11

Thyroxine releasing hormone (TRH) - released by the hypothalamus; doesn’t circulate throughout the body; hormone that causes another hormone to be released (TSH)

Thyroid stimulating (TSH) - released by the anterior pituitary; causes thyroid hormone to grow

Question 12

Effects of TRH and TSH

Answer 12

Increased TRH -> high TSH -> 1) high iodide uptake -> high t3&t4 production

2) high thyroglobulin production -> high t3&t4 production
3) high follicle growth -> high number of follicles and size of glands

Question 13

Negative feedback mechanisms of Thyroid hormone (bring levels to normal)

Answer 13

High TH (t3/t4) -> low tsh/trh -> low production of t3/t4

Low th (t3/t4) -> high trh -> high tsh -> high production of t3/t4

Continuous to keep t3/t4 level

Question 14

Hyperthyroidism

Answer 14

When tissues are exposed to excessive amounts of thyroid hormone (T3/T4)

Question 15

Primary hyperthyroidism

Answer 15

Genetic predisposition causing a variety of familial hyperthyroid disorders - occurs in primary (thyroid) gland

Thyroiditis - gets inflamed, maybe from bacterial or viral infection

Toxic modular or multinodular goiter (Pulmmer disease) - abnormal, benign growth of the gland, more tissue; goiter is cause of the disease

Thyroid adenomas (benign tumors)

Thyroid cancer (adnocarcinoma) - sometimes cancer cells will over produce TH; spread and causes other problems

Question 16

Secondary hyperthyroidism

Answer 16

TSH-secreting pituitary adenomas - located in the brain, some become very large and suppress brain tissue and can cause blindness

Graves’ disease (70%)

Overdose of thyroid medication (thyrotoxicosis)

Question 17

Patho of primary hyperthyroidism

Answer 17

Increased t3/t4 secretion from thyroid gland leads to thyroid-stimulating hormone suppression

Question 18

Patho of secondary hyperthyroidism

Answer 18

Increased TSH secretion from anterior pituitary gland leads to increased t3/t4 secretion

Question 19

Clinical consequences due to increased t3/t4

Answer 19

Increased metabolic rate - weight loss, very thin

Increase neuromuscular activity - can have a tremor or insomnia

Increased SNS stimulation - fast heart rate and high blood pressure; risk for heart failure cause of it being overworked, can die

Question 20

Clinical consequences due to increased tsh

Answer 20

Goiter possible with secondary hyperthyroidism

Question 21

Graves’ disease

Special case of hyperthyroidism

Answer 21

Overproduction of thyroid autoantibodies called thyroid stimulating immunoglobulin (TSI)

TSIs mimic effect of TSH

Elevated levels of TSIs stimulate excess of t3/t4 secretion

Elevated plasma levels of t3/t4 cause TSH suppression

Question 22

Clinical consequences of Graves’ disease

Answer 22

Problems due to hyperthyroidism

Goiter due to TSH-like effects of TSI and accumulation of TSI in thyroid gland tissue

Effects of thyroid stimulating immunoglobulins on ocular tissue (95% incidence) - degeneration of extraocular muscles and edematous fluid accumulation in orbit

Extraocular muscle dysfunction

Exophthalmos (protruding eyeball)

Retinal and optic nerve damage

Question 23

Hypothyroidism

Answer 23

Primary hypothyroidism - loss of thyroid tissue leads to decreased t3/t4

Secondary hypothyroidism - failure of pituitary to synthesize adequate TSH; decreased tshirt secretion from anterior pituitary gland leads

Question 24

Etiologies of primary hypothyroidism

Answer 24

Iodine deficiency

Congenital lack of thyroid tissue: born w partial or without; required for growth of brain and muscle

Hashimoto’s thyroiditis: production of autoantibodies that block TSH receptors

Question 25

Etiologies or secondary hypothyroidism

Answer 25

Stroke to hypothalamus or pituitary; TRH and TSH (permanent loss)

Pituitary tumor (benign or cancerous)

Postpartum pituitary necrosis; similar to stroke (pituitary cells die)

Question 26

Patho of primary hypothyroidism

Answer 26

Decreased t3/t4 secretion from thyroid gland leads to increased TSH secretion

decreased th (t3/t4) -> increased TRH -> increased TSH

Question 27

Patho of secondary hypothyroidism

Answer 27

Decreased TSH secretion from anterior pituitary gland leads to decreased t3/t4 secretion

no neg feedback

decreased TSH -> decreased production of t3/t4

Question 28

Patho of general hypothyroidism

Answer 28

Myxedema: collagen in connective tissues is replaced by other proteins and mucopolysaccarhides creating a complex that binds to water

Attracted to water

Accumulates in heart, diaphragm and other organs

Question 29

Clinical consequences of hypothyroidism due to decreased t3/t4

Answer 29

Decreased metabolic rate - no energy, 50% of atp to control impulses

Decreased neuromuscular activity - reflexes

Decreased SNS activity - decrease in bp, cardiac function; severe = heart failure; respiratory rate

Question 30

Clinical consequences of hypothyroidism due to increased TSH

Answer 30

Goiter possible with primary hypothyroidism from iodine deficiency - low iodine -> low t3/t4 -> high tsh -> follicle growth + accumulation of thyroglobulin