Chapter 21 Mechanisms Of Hormonal Regulation

Front 1

Organs that respond to a particular hormone are called:
a. target organs.
b. integrated organs.
c. responder organs.
d. hormone attack organs.
e. None of the above is correct.

Back 1

a. target organs.

Front 2

A major feature of the "plasma membrane receptor" mechanism of hormonal action is:
a. action of cyclic AMP.
b. increased lysosomal activity.
c. requirement of a second messenger. d. All of the above are correct.
e. Both a and c are correct.

Back 2

e. Both a and c are correct.

Front 3

A major feature of the "activation of genes" mechanism of hormonal action is:
a. a second messenger is used.
b. a hormone-Golgi complex is used.
c. the hormone enters the cell.
d. lysosomal activity increases.
e. All of the above are correct.

Back 3

c. the hormone enters the cell.

Front 4

A hormone having an antidiuretic effect similar to that of antidiuretic hormone (ADH) is:
a. insulin.
b. oxytocin.
c. hGH.
d. aldosterone.
e. adrenocorticotropic hormone (ACTH).

Back 4

b. oxytocin.

Front 5

The hypothalamus controls the adenohypophysis by direct involvement of:
a. nerve impulses.
b. prostaglandins.
c. cerebrocortical controlling factors (CCCFs).
d. regulating hormones.
e. None of the above is correct.

Back 5

d. regulating hormones.

Front 6

Hormones convey regulatory information by: a. endocrine signaling.
b. paracrine signaling.
c. autocrine signaling.
d. synaptic signaling.
e. All of the above are correct.

Back 6

e. All of the above are correct.

Front 7

If calcium levels in the blood are too high, thyrocalcit- onin (calcitonin) concentrations in the blood should:
a. increase, thereby inhibiting osteoclasts.
b. increase, thereby stimulating osteoclasts.
c. increase, but this change would not affect osteoclasts.
d. decrease, thereby inhibiting osteoclasts.
e. decrease, thereby stimulating osteoclasts.

Back 7

a. increase, thereby inhibiting osteoclasts.

Front 8

In the negative feedback mechanism controlling thyroid hormone secretion, which is the nonregulatory hormone?
a. thyrotropin-releasing hormone (TRH)
b. thyroid-stimulating hormone (TSH)
c. thyroxine
d. All of the above are regulatory for thyroid
hormone secretion.

Back 8

c. thyroxine

Front 9

The control of parathyroid hormone is most accurately described as:
a. negative feedback controlled by the hypothalamus.
b. positive feedback controlled by the pituitary.
c. negative feedback involving the pituitary.
d. negative feedback not involving the pituitary.
e. Both a and c are correct.

Back 9

d. negative feedback not involving the pituitary.

Front 10

The renin-angiotensin-aldosterone system begins to function when renin is secreted by the:
a. adrenal cortex.
b. adrenal medulla.
c. pancreas.
d. kidneys.
e. None of the above is correct.

Back 10

d. kidneys.

Front 11

The effects of adrenal medullary hormones and the effects of sympathetic stimulation can be described as:
a. opposites in all respects.
b. overlapping in some respects.
c. opposites in some respects.
d. variable depending on the sex involved.
e. overlapping in most respects.

Back 11

e. overlapping in most respects.

Front 12

Which best describes the respective effects of insulin and glucagon on blood glucose?
a. Insulin raises blood glucose; glucagon lowers it.
b. Both raise blood glucose.
c. Insulin lowers blood glucose; glucagon raises it.
d. Both lower blood glucose.
e. None of the above is correct.

Back 12

c. Insulin lowers blood glucose; glucagon raises it.

Front 13

The releasing hormones produced in the hypothalamus travel to the anterior pituitary via the:
a. stem neurons.
b. infundibular stem.
c. hypophyseal stalk.
d. hypophysial portal system.

Back 13

d. hypophysial portal system.

Front 14

Which anabolic hormone increases muscle protein synthesis?
a. T4
b. aldosterone
c. FSH
d. insulin

Back 14

d. insulin

Front 15

Aldosterone maintains electrolyte balance by:
a. retention of potassium.
b. elimination of sodium.
c. retention of both Na+ and K+.
d. Both a and b are correct.
e. None of the above is correct.

Back 15

e. None of the above is correct.

Front 16

Mineralocorticoids

Back 16

Conserve sodium

Front 17

Glucocorticoids

Back 17

Antiinflammatory

Front 18

ACTH

Back 18

Adrenal cortex

Front 19

TSH

Back 19

Thyroid gland

Front 20

TRF

Back 20

Adenohypophysis

Front 21

prolactin

Back 21

Mammary glands

Front 22

Epinephrine

Back 22

Cause(s) fight-or-flight response

Front 23

Glucocorticoids

Back 23

Influence(s) inflammatory response

Front 24

Mineralocorticoids

Back 24

Control(s) Na+, H+, and K+ levels

Front 25

Gonadocorticoids

Back 25

Act(s) as minor sex hormone(s)

Front 26

Hypothalamus - Releasing hormones

Back 26

Act on anterior pituitary to stimulate release or inhibit synthesis and release of hormones

Front 27

Posterior pituitary - Antidiuretic hormone (ADH)Oxytocin

Back 27

Causes conservation of body water, reduces serum osmolality, may regulate CNS functions

Front 28

Posterior pituitary - Oxytocin

Back 28

Stimulates uterine contraction and lactation, has antidiuretic activity, may have a role in sperm mobility

Front 29

Anterior pituitary - Adrenocorticotropic hormone (ACTH)

Back 29

Stimulates production of glucocorticoids (gluconeogenesis, inhibits immunity, anti-inflammatory) by adrenal cortex

Front 30

Anterior pituitary - Melanocyte-stimulating hormone (MSH)

Back 30

Stimulates darkening of skin color

Front 31

Anterior pituitary - Growth hormone (GH)

Back 31

Promotes growth of body tissues

Front 32

Anterior pituitary - Thyroid-stimulating hormone (TSH)

Back 32

Stimulates production and release of thyroid hormones (growth and maturation of tissues)

Front 33

Anterior pituitary - Follicle-stimulating hormone (FSH)

Back 33

Initiates maturation of ovarian follicles; stimulates spermatogenesis

Front 34

Anterior pituitary - Prolactin

Back 34

Stimulates secretion of breast milk

Front 35

Anterior pituitary - Luteinizing hormone (LH)

Back 35

Causes ovulation and stimulates ovary to produce estrogen and progesterone; stimulates androgen production by interstitial cells of testes

Front 36

Thyroid - Thyroxine (T3, T4)

Back 36

Increases rate of cellular metabolism

Front 37

Thyroid - Calcitonin

Back 37

Osteoblastic—lowers serum calcium

Front 38

Parathyroid - Parathyroid hormone (PTH)

Back 38

Osteoclastic—raises serum calcium

Front 39

Pancreatic islets of Langerhans - Insulin

Back 39

Promotes utilization of glucose; lowers serum glucose

Front 40

Pancreatic islets of Langerhans - Amylin

Back 40

Delays nutrient uptake and suppresses glucagon after meals

Front 41

Pancreatic islets of Langerhans - Glucagon

Back 41

Promotes utilization of glycogen; raises serum glucose

Front 42

Adrenal cortex - Glucocorticoids, mostly cortisol

Back 42

Antagonize effects of insulin; inhibit inflammatory response and fibroblastic activity, protein catabolic

Front 43

Adrenal cortex - Mineralocorticoids, mostly aldosterone

Back 43

Promote retention of sodium by renal tubules

Front 44

Adrenal cortex - Androgens and estrogens

Back 44

Promote secondary sex characteristics

Front 45

Adrenal medulla - Catecholamines (epinephrine and norepinephrine)

Back 45

Regulate blood pressure through effects on vascular smooth muscle and heart

Front 46

Pineal gland - Melatonin

Back 46

Regulates circadian rhythms and reproductive systems

Front 47

Disorders of the endocrine system are based on

Back 47

hyposecretion

hypersecretion

abnormal receptor function

altered intracellular response to the hormone-receptor complex

Front 48

Cause of most common hypothalamic diseases

Back 48

Interruption in the infundibular stem caused by trauma or tumor.

Front 49

Another cause of hypothalamic diseases

Back 49

The absence of hypothalmic hormones - due to lack of stimulation of the pituitary.

Front 50

Diseases due to absence of hypothalamic hormones

Back 50

• Diabetes insipidus - lack of ADH
• Cessation of menses, and sperm production - lack of gnrh
• Low levels of ACTH - lack of corticotropin-releasing hormone (CRH)
• Low levels of growth hormone - absence of growth hormone regulatory hormones
• Hyperprolactinemia - lack of usual inhibitory controls

Front 51

Diseases of the Posterior Pituitary

Back 51

Diseases that cause clinically observable symptoms are rare. When they occur they usually involve abnormal ADH secretion.

Front 52

Syndrome of inappropriate ADH secretion (SIADH)

Back 52

Characterized by high levels of ADH in the absence of normal physiologic stimuli for its release.

Front 53

The most common causes of SIADH

Back 53

• Ectopically produced hormone due to cancer
• Losses following pituitary surgery
• Medications - especially psychiatric

Front 54

Pathophysiology of SIADH includes

Back 54

• Water retention leading to edema - due to increased tubule permeability to water

• Hyponatremia due to expanded extracellular volume causing suppression of renin and aldostserone secretion (hyperosmolarity of urine)

Front 55

Symptoms of SIADH due to hyponatremia

Back 55

thirst
impaired taste
anorexia
dyspnea on exertion
fatigue
dulled sensorium
vomiting and cramps confusion
lethargy
muscle twitching
convulsions

Front 56

Treatment of SIADH

Back 56

Correction of underlying causal problems
Administration of hypertonic saline and fluid restriction

Front 57

Diabetes insipidus

Back 57

Related to insufficiency of ADH, leading to polyuria and polydipsia

Front 58

3 forms of Diabetes Insipidus

Back 58

• Neurogenic - insufficient amounts of ADH

• Nephrogenic - inadequate response to ADH

• Psychogenic - extremely large volumes of fluid intake

Front 59

Pathophysiology of Diabetes Insipidus

Back 59

• Partial to total inability to concentrate urine

• Chronic polyuria and polydipsia

• Low urine specific gravity (1.00 to 1.005)

Front 60

Treatment of Diabetes Insipidus

Back 60

Must be distinguished from other polyuric states and may require ADH replacement.

Front 61

Diseases of the Anterior Pituitary

Back 61

Disorders may involve either hypofunction or hyperfunction of the gland

Front 62

Hypopituitarism

Back 62

May range from absence of selective hormones to complete failure of all hormonal functions. Most common causes are pituitary infarction as seen in Sheehan syndrome (postpartum pituitary necrosis), head trauma and infections.

Front 63

Pathophysiology of Hypopituitarism

Back 63

The pituitary is extremely vulnerable to infarction due to vasospasm of the artery supplying it, as well as the fact that the supplying portal system is already partly deoxygenated.

Front 64

Clinical manifestations of Hypopituitarism

Back 64

• Lack of ACTH (cortisol) - loss of functional maintenance of adrenal gland and decreased aldosterone

• Lack of TSH - thyroid deficiency

• Lack of ADH - diabetes insipidus

• Lack of FSH and LH - gonadal failure, loss of second-degree sexual characteristics

• Lack of GH (HGH) - dwarfism

Front 65

Treatment of Hypopituitarism

Back 65

Correction of underlying disorder, replacement therapy

Front 66

Hyperpituitarism

Back 66

Often caused by primary adenoma. Incidence may be as high as 22% - many are asymptomatic.

Front 67

Pathophysiology of Hyperpituitarism

Back 67

Local expansion - tumor may impinge on optic chiasma, hypothalamus or other secretory cell of anterior pituitary. Secretory tumor - maybe hypersecretion or hyposecretion due to pressure changes.
• hyposecretion of GH is asymptomatic in adults
• gonadotropic hyposecretion results in menstrual irregularity, decreased libido and receding second-degree sexual characteristics
• hypersecretion of GH in childhood causes giantism
• hypersecretion of GH in the adult causes acromegaly

Front 68

Hyperthyroid Function

Back 68

Thyrotoxicosis is a condition in which thyroid hormones (TH) from any source exert greater than normal responses. This results in increased metabolic rate with heat intolerance and increased sensitivity to stimulation by the sympathetic division of the ANS.

Front 69

Diseases that can cause hyperthyroidism

Back 69

Grave's disease
Toxic multinodular goiter
Thyroid cancer and secretion

Front 70

Grave's disease

Back 70

an autoimmune disorder associated with genetic predisposition. The syndrome may consist of one or more of the following:
1. Hyperthyroidism - increased metabolism
2. Diffuse thyroid enlargement - goiter
3. Ophthalmopathy - exophthalmus or protruding eyes
4. Dermatopathy-myxedema - indurated (hardening) and erythematous skin
5. Effects on extremities - pretibial swelling

Front 71

Nodular goiter

Back 71

Certain autonomously functioning cells producing larger amounts of TH may cause the remainder of the gland to undergo involution.

Front 72

Toxic Nodular Goiter

Back 72

Nodular goiter with resulting hyperthyroidism

Front 73

Thyrotoxic Crisis

Back 73

Thyroid storm - usually a dangerous worsening of a severe hyperthyroidism condition due to excessive stress. Death occurs within 48 hours without treatment.

Front 74

Hypothyroidism

Back 74

Deficient production of TH

Front 75

Primary hypothyroidism causes

Back 75

Congenital defects or loss following treatment, or defective synthesis resulting from autoimmune disease

Front 76

Secondary hypothyroidism causes

Back 76

Usually due to insufficient stimulation from pituitary or hypothalamus and/or peripheral resistance to TH

Front 77

Clinical manifestations of hypothyroidism

Back 77

• Decreased BMR

• Cold intolerance

• Slightly lowered basal body temperature

• Excessive TSH production and goiter

• Myxedema - non-pitting, boggy edema

Front 78

Treatment of Hypothyroidism

Back 78

Replacement therapy

Front 79

Hypothyroid conditions usually due to inflammation

Back 79

• Myxedema coma - diminished level of consciousness associated with severe hypothyroidism

• Congenital hypothyroidism - found in infants as a result of absent thyroid tissue and hereditary defects in synthesis

• Thyroid carcinoma - increased risk factor may be exposure to ionizing radiation, especially during childhood

Front 80

Hyperparathyroidism

Back 80

Causes demineralization of bone. Condition may be called osteitis fibrosa cystica because areas of bone are replaced by cavities that fill with fibrous tissue. The bones become deformed and highly susceptible to fracture - usually caused by a tumor.

Front 81

Types of hyperparathyroidism

Back 81

• Primary - PTH secretion autonomous and not under usual feedback control

• Secondary - response due to chronic hypocalcemia usually due to renal failure

• Tertiary - hyperplasia of gland and loss of sensitivity to circulating calcium levels. May be due to renal failure.

Front 82

Treatment of hyperparathyroidism

Back 82

Done by excluding all other causes of hypercalcemia. Surgical removal of some or all glands may be necessary.

Front 83

Hypoparathyroidism

Back 83

Commonly caused by damage to the glands during thyroid surgery or as a result of hypomagnesemia. Low levels of PTH cause neurons to depolarize without the usual stimulus. Nervous impulses increase and result in muscle twitches, spasm and convulsions or tetany.

Front 84

Effects of hypoparathyroidism can be observed in:

Back 84

• Trousseau sign - binding of a cuff around the upper arm produces contraction of the fingers and inability to open the hand

• Chvostek sign - contraction of the facial muscle is elicited by tapping the facial nerves at the angle of the jaw.

Front 85

Treatment of hypoparathyroidism

Back 85

Involves elimination of secondary causes if possible, parenteral administration of calcium, and maintenance with oral doses of calcium and vitamin D.

Front 86

Dysfunctions of the Endocrine Pancreas

Back 86

Hyperinsulinism

Hypoinsulinism

Front 87

Hyperinsulinism

Back 87

Usually the result of a malignant tumor. Causes decreased blood glucose levels which stimulates secretion of epinephrine, glucagon and HGH.

Symptoms include anxiety, sweating, tremor, increased heart rate and weakness. The brain is deprived of glucose and it may cause disorientation, convulsions, shock and death.

Front 88

Hypoinsulinism

Back 88

Diabetes Mellitus - A heterogeneous group of hereditary diseases which leads to an elevation of blood glucose and excretion of glucose in the urine.

Front 89

Type I diabetes mellitus (IDDM)

Back 89

Usually found in those under 20, with an abrupt onset. It is characterized by a marked decline in the number of beta cells in the pancreas, leading to a deficiency of insulin and elevation of glucose in the blood.

Other changes include:
ketosis - accelerated fat breakdown causes production of organic acids which lowers the pH of the blood and can result in death. Accelerated atherosclerosis and sugar depositon leads to early clogging of the arteries.

Front 90

Causes of IDDM

Back 90

Genetic predisposition (HLA - human leukocyte antigens)

Exposure to antigenic triggers (virus)

Autoimmune - islet cell antibodies.

Front 91

Evaluation of IDDM

Back 91

polydipsia
polyuria
polyphagia
weight loss
hyperglycemia

Front 92

Treatment of IDDM

Back 92

Injection of insulin

Diet - 55% carbohydrates, <30% fats, 15% proteins

Exercise - diminishes insulin requirements

Transplantation - still experimental

Front 93

Type II Diabetes Mellitus (NIDDM)

Back 93

Most common type.
Most often found in people over 40 and overweight. Clinical symptoms are mild, and high glucose levels in the blood can usually be controlled by diet. In most cases there is not a shortage of insulin in the blood, but a lack of response to the insulin by its target cells. This may be due to decreased numbers of insulin receptors.

Front 94

Clinical manifestations of NIDDM

Back 94

May show some of the classic type I symptoms, but usually symptoms are insidious and nonspecific and include:
Purritus
Recurrent infections
Visual changes
Paresthesia

Front 95

Treatment of NIDDM

Back 95

Restore euglycemia by dietary measures, weight loss, oral hypoglycemic agents and exercise.
In some cases insulin may have to be used.

Front 96

Gestational Diabetes

Back 96

Glucose intolerance whose first onset is during third trimester of pregnancy. Obese women are at greater risk. Increased chance of developing NIDDM later.

Front 97

Acute Complications of Diabetes Melliltus

Back 97

• Hypoglycemia

• Diabetic ketoacidosis

• Hyperosmolar hyperglycemic nonketotic coma (HHNK)

• Dawn phenomenon

• Somogyi (so mo'gee)

Front 98

Hypoglycemia

Back 98

Lowered blood sugar due to exogenous, endogenous or functional causes.
Symptoms are the result of adrenergic reaction and from cellular malnutrition.

-also called insulin shock or insulin reaction

Front 99

Hypoglycemia symptoms

Back 99

Symptoms include: tachycardia, diaphoresis, tremors, pallor, hunger, headache, irritability and confusion leading to seizure or coma

Front 100

Hypoglycemia treatment

Back 100

Raise glucose levels

Front 101

Diabetic ketoacidosis

Back 101

A serious complication of diabetes, in which we see increased release of fatty acids, accelerated gluconeogenesis and ketogenesis due to insulin deficiency.

Front 102

Diabetic ketoacidosis clinical manifestations

Back 102

Clinical manifestations - polyuria and dehydration, glycosuria, electrolyte disturbances, Kussmaul respirations, postural dizziness, ketonuria, anorexia, nausea, abdominal pain, thirst and acetone odor on the breath.

Front 103

Diabetic ketoacidosis treatment

Back 103

Treatment - administration of insulin to lower glucose levels, and restore fluids and electrolytes

Front 104

Hyperosmolar hyperglycemic nonketotic coma (HHNK)

Back 104

Glycosuria and polyuria result from extreme blood glucose elevation. Neurologic changes such as stupor, correlate with the degree of hyperosmolarity.

Front 105

Hyperosmolar hyperglycemic nonketotic coma (HHNK) treatment

Back 105

Treatment - rehydration and electrolyte replacement are vital

Front 106

Dawn phenomenon

Back 106

Early morning rise in blood glucose may be related to surge in HGH activity, decrease in insulin sensitivity or normal circadian variation.

Front 107

Somogyi (so mo'gee)

Back 107

A rebound phenomenon occurring in diabetes - over-treatment with insulin induces hypoglycemia which initiates the release of epinephrine, ACTH, glucagon and HGH, which stimulates lipolysis, gluconeogenesis and glycogenolysis, resulting in rebound hyperglycemia and ketosis.

Front 108

Chronic Complications of Diabetes Mellitus

Back 108

• Diabetic neuropathies

• Microvascular disease

• Nephropathy

• Macrovascular disease

Front 109

Diabetic neuropathies

Back 109

Mechanism may be vascular and/or metabolic - results in a form of "dying back" in which distal portions of neurons are the most severely affected. Conduction velocity, electromyopathy and sensory perception may all show abnormalities.

Front 110

Microvascular disease

Back 110

Thickening of the capillary membrane results in decreased tissue perfusion and is often proportional to the duration of the disease.

Front 111

Nephropathy

Back 111

Renal glomerular enlargement and basement membrane thickening result in intercapillary glomerulosclerosis. Proteinuria is first manifestation. Impaired kidney function accelerates retinopathy. Death from renal failure is common.

Front 112

Macrovascular disease

Back 112

Most common cause of morbidity and mortality found in type II patients. It appears that fibrous plaques result from proliferation of the smooth muscle in the arterial wall.

Front 113

Macrovascular disease results in:

Back 113

1. Coronary artery disease - accounts for 75% of the deaths for type II diabetics, and results in myocardial infarction and congestive heart failure.
2. Cerebral atherosclerosis is greater in type II diabetics. Survival rate after a massive stroke is shorter. Hypertension is a risk factor.
3. Peripheral vascular disease - because of the occlusion of the small arteries and arterioles, foot lesions leading to gangrene and amputation are common.
4. Infection - the individual with diabetes is at greater risk for infection because:
• Impaired vision - diminished prevention, or lack of awareness of breaks in the skin
• Hypoxia - vascular changes cause decreased oxygen to tissues and glycosylated hemoglobin impedes release of oxygen
• Pathogens proliferate more rapidly because of increased glucose in body fluids, decreased blood supply, decreased white blood cells to affected area. Chemotaxis and phagocytosis is defective.

Front 114

Disorders of the Adrenal Cortex

Back 114

• Cushing's Disease
• Cushing's Syndrome
• Hyperaldosteronism

Front 115

Cushing's Disease

Back 115

Caused by excessive anterior pituitary secretion of ACTH
- more common in females

Front 116

Cushing's Syndrome

Back 116

Chronic hypercortisolism caused by hyperfunction of the adrenal cortex, with or without pituitary involvement, or from ectopic ACTH secretion.
- More common in older males

Front 117

Clinical manifestations of Cushing's syndrome

Back 117

• Excessive secretion of cortisol causes redistribution of fat, resulting in spindly legs accompanied by a characteristic "moon face", "buffalo" hump on the back and pendulous abdomen.
• Facial skin is flushed (high blood pressure), skin covering abdomen develops stretch marks
• Individual bruises easily and wound healing is poor
• Approximately 1/2 develop mental status changes from irritability to severe psychiatric disturbance
• Females may experience changes due to increased androgen levels

Front 118

Hyperaldosteronism

Back 118

Hyper-secretion of mineralocorticoid aldosterone characterized by a decrease in the body's potassium concentration and excessive retention of sodium and water. If potassium depletion is great, neurons cannot depolarize and muscular paralysis results. The increased water volume in the blood causes high blood pressure and edema.

Front 119

Hyperaldosteronism treatment

Back 119

Treatment - glucocorticoid and electrolyte replacement

Front 120

Disorders of the Adrenal Medulla

Back 120

Hypersecretion of medullary hormones is normally due to tumors or the chomaffin cells, called pheochromocytomas. This causes excessive production of catecholamines (norepinephrine and epinephrine), which causes a prolonged version of the fight-or-flight response with:
• high blood pressure
• increased metabolic rate
• nervousness
• sweating
The condition eventually wears out the body and general weakness results.

Front 121

Adrenal Medulla disorders treatment

Back 121

TX - Surgical excision of the tumor