Chapter 20 Health Alt

Question 1

Significantly altered hormone levels due to:

Answer 1

-Inappropriate amounts of hormone delivered to target cell
->Disorders of endocrine glands
->Failure of feedback systems
->Dysfunctional hormones
->Defects in hormone delivery
-Inappropriate responses by the target cell
->Abnormalities in receptors
->Intracellular disorders

Question 2

Alterations of the Hypothalamic-Pituitary System

Answer 2

-The most common cause of apparent hypothalamic dysfunction is interruption of the pituitary stalk. Such interruptions prevent hypothalamic hormones from reaching the pituitary gland.
-Damage to the pituitary stalk can be caused by destructive lesions, rupture after head injury, surgical transection, or tumor.
-Without hypothalamic hormones, the pituitary releases inadequate amounts of follicle-stimulating hormone (FSH), luteinizing hormone (LH), adrenocorticotropic hormone (ACTH), thyroid stimulating hormone (TSH), and growth hormone.

Question 3

Diseases of the Posterior Pituitary: Part 1

Answer 3

-Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
->Hypersecretion of ADH
->Caused by ectopic production of ADH by tumors (in the lungs, stomach, pancreas, bladder, etc.), pulmonary (pneumonia, asthma, cystic fibrosis, etc.) or CNS disorders (encephalitis, meningitis, tumors, & trauma), surgery, or medications (can happen a lot in the elderly)
->Clinical manifestations are related to hyponatremia and are determined by severity
Symptoms of SIADH:
-enhanced renal free water retention
-hyponatremia
-GI symptoms include vomiting, abdominal cramps

Question 4

Diseases of the Posterior Pituitary: Part 2

Answer 4

-Diabetes insipidus (DI)
->Insufficiency of ADH causing loss of too much water in urine
->Two forms
->Neurogenic (central)—insufficient secretion of ADH
->Nephrogenic—inadequate response to ADH
->Manifestations include polyuria, nocturia, and continuous thirst

Question 5

Diabetes insipidus

Answer 5

insufficient ADH activity
1.Neurogenicorcentral DI.Caused by the insufficient secretion of ADH, it occurs when any organic lesion of the hypothalamus, pituitary stalk, or posterior pituitary interferes with ADH synthesis, transport, or release. Causative lesions include primary brain tumors, traumatic brain injury, hypophysectomy, aneurysms, thrombosis, infections, and immunologic disorders. It can also be caused by hereditary disorders that affect ADH genes or result in structural changes in the pituitary gland.
2.Nephrogenic DI.Caused by inadequate response of the renal tubules to ADH. Acquired nephrogenic DI is caused by disorders and drugs that damage the renal tubules. These disorders include pyelonephritis, amyloidosis, destructive uropathies, and polycystic kidney disease. Drugs that may induce a reversible form of nephrogenic DI include lithium carbonate, colchicine, amphotericin B, loop diuretics, general anesthetics, and demeclocycline.
-Individuals with DI have a partial to total inability to concentrate urine.
-Insufficient ADH activity causes excretion of large volumes of dilute urine, leading to increased plasma osmolality.
-In conscious individuals, the thirst mechanism is stimulated and induces polydipsia.
-Dehydration develops rapidly without ongoing fluid replacement.
-The clinical manifestations of DI include polyuria, nocturia, continuous thirst, and polydipsia.

Question 6

Diseases of the Anterior Pituitary: Part 1; Hypopituitarism

Answer 6

-Hypopituitarism
->Absence or failure of anterior pituitary hormones
->Panhypopituitarism—all hormones deficient and the person suffers from multiple complications
-Caused by
->Pituitary infarction (may occur when there is significant blood loss or hypovolemic shock. OR in women during the postpartum period (Sheehan syndrome) )
->Space-occupying lesions (include pituitary adenomas or aneurysms, which can enlarge and compress the pituitary gland)
->Traumatic brain injury
->Removal of destruction of the gland
->Infections (meningitis, syphilis, etc.)
->Autoimmune hypophysitis
-Symptoms related to cortisol insufficiency

Question 7

Anterior pituitary - Panhypopituitarism; the certain deficiencies.

Answer 7

-ACTH deficiency with associated loss of cortisol is a potentially life-threatening disorder.
-Symptoms of cortisol insufficiency include nausea, vomiting, anorexia, fatigue, and weakness.
-TSH deficiency causes cold intolerance, skin dryness, lethargy, and decreased metabolic rate. -The onset of FSH and LH deficiencies in women of reproductive age is associated with amenorrhea and atrophy of the vagina, uterus, and breasts.
-GH deficiency in children is manifested by growth failure and a condition known ashypopituitary dwarfism.

Question 8

Diseases of the Anterior Pituitary: Part 2; Hyperpituitarism

Answer 8

-Hypersecretion of hormones
-Commonly caused by a benign, slow-growing pituitary adenoma
-Manifestations related to tumor growth and hormone hyper/hyposecretion

Question 9

Diseases of the Anterior Pituitary: Part 3; Hypersecretion of growth hormone (GH)

Answer 9

-Acromegaly
->Hypersecretion of GH during adulthood
-Giantism
->Hypersecretion of GH in children whose epiphyseal plates have not yet closed

Question 10

Diseases of the Anterior Pituitary: Part 4; Prolactinoma

Answer 10

-Prolactinoma
->Hypersecretion of prolactin
->Caused by pituitary tumors that secrete prolactin
-Manifestations
->In females, amenorrhea, galactorrhea, hirsutism, and osteopenia
->In males, gynecomastia, hypogonadism, and erectile dysfunction

Question 11

Alterations to the Thyroid Function: Part 1

Answer 11

-Primary thyroid disorders
->Dysfunction or disease of thyroid
->Increased or decreased thyroid hormone (TH)
->Idiopathic, caused by autoimmune mechanisms
-Central (secondary) thyroid disorders
->Disorders of pituitary gland thyroid stimulating hormone (TSH) production

Question 12

Alterations to the Thyroid Function: Part 2

Answer 12

-Thyrotoxicosis
->Condition due to any cause of increased TH levels
->Hyperthyroidism—increased TH levels from thyroid gland
->Primary caused by Graves disease, toxic multinodular goiter, and solitary toxic adenoma
->Central (secondary) caused by pituitary adenomas
->Manifestations are increased metabolic rate, heat intolerance, and tissue sensitivity

Question 13

Alterations to the Thyroid Function: Part 3

Answer 13

Hyperthyroid conditions
->Graves disease
->Autoimmune disease caused by stimulation of thyroid by autoantibodies against TSH receptor
->Pretibial myxedema
->Hyperthyroidism resulting from nodular thyroid disease
->Toxic multinodular goiter
->Toxic adenoma
->Thyrotoxic crisis (thyroid storm)
->TH levels rise dramatically, can be fatal

Question 14

Alterations to the Thyroid Function: Part 4

Answer 14

Hypothyroidism
->Deficient production of TH by thyroid gland
->Primary
->Loss of thyroid function
->Caused by autoimmune thyroiditis, loss of thyroid tissue, medications, and endemic iodine deficiency
->Central (secondary)
->Failure of pituitary to synthesize adequate TSH
->Caused by pituitary tumors and associated treatments
->Manifestations are decreased metabolic rate, cold intolerance, and lethargy

Question 15

Alterations to the Thyroid Function: Part 5

Answer 15

Hypothyroid conditions
->Hashimoto disease
->Autoimmune (thyroiditis) disease causing gradual destruction of thyroid tissue
->Congenital hypothyroidism
->Thyroid tissue absent
->Hereditary defects in TH synthesis
->Subacute thyroiditis (de Quervain thyroiditis)
->is a rare nonbacterial inflammation of the thyroid gland often preceded by a viral infection. It is accompanied by fever, tenderness, and enlargement of the thyroid gland and transient hypothyroidism before the gland recovers normal activity.
->Postpartum thyroiditis
->generally occurs up to 6 months after birthing with a course similar to that seen in subacute thyroiditis.
->Iatrogenic hypothyroidismresults from ablation of the thyroid gland during treatment for hyperthyroid conditions.

Question 16

Thyroid Carcinoma

Answer 16

-Most common endocrine malignancy
->Exposure to ioniz­ing radiation, especially during childhood, is the most consistent causal factor. Papillary and follicular thyroid carcinomas are the most frequent, and medullary and anaplastic thyroid carcinomas are less common. The cancer is typically discovered as a small thyroid nodule or metastatic tumor in the lungs, brain, or bone.
-Ionizing radiation most common cause
-Treated with thyroidectomy, suppression therapy, radiation, and chemotherapy

Question 17

Alterations of Parathyroid Function: Part 1

Answer 17

Hyperparathyroidism
->Increased secretion of parathyroid hormone (PTH)
->Classified as:
->Primary— excess secretion of PTH from one or more parathyroid glands
->Secondary—increase in PTH secondary to chronic hypocalcemia; parathyroid glands to chronic hypocalcemia, which is commonly associated with decreased activation of vitamin D in individuals with renal failure. caused by renal disease.
->Tertiary—develops after a long period of hypocalcemia; such as is seen with chronic dialysis, renal transplantation, or gastrointestinal malabsorption.
->Hallmark manifestations are hypercalcemia and hypophosphatemia
-(PTH hypersecretion enhances renal phosphate excretion and results in hypophosphatemia and hyperphosphaturia)

Question 18

Alterations of Parathyroid Function: Part 2

Answer 18

Hypoparathyroidism
->Abnormally low PTH levels
->Usually caused by parathyroid damage in thyroid surgery.
->Hypomagnesemia is another cause of low PTH levels bc it inhibits PTH secretion.
->Manifestations are primarily those of hypocalcemia.

Question 19

Hypercalcemia

Answer 19

-Hypercalcemia means that the renal tubules must filter large amounts of calcium, leading to hypercalciuria and production of an abnormally alkaline urine.
-its when there in an abnormally high amount of calcium in the blood

Question 20

Diabetes Mellitus Type 1

Answer 20

Type 1 diabetes (caused by autoimmune beta-cell destruction, usually leading to absolute insulin deficiency)
->Idiopathic Type1: Idiopathic type 1 diabetes mellitusis far less common than autoimmune diabetes, has a strong genetic component, and occurs mostly in people of Asian or African descent. Affected individuals have no evidence of beta-cell autoimmunity and have varying degrees of insulin deficiency.

->Autoimmune Type 1: Autoimmune type 1 diabetes mellitusis a slowly progressive disease that destroys beta cells of the pancreas. There are strong genetic associations with histocompatibility leukocyte antigen (HLA) class II allelesHLA-DQandHLA-DR.
->Immunologically mediated Beta cell destruction and apoptosis
80%-90% cells lost, insulin synthesis declines, hyperglycemia develops
->Alterations in insulin, amylin, glucagon
->Insulin normally suppresses secretion of glucagon, and thus hypoinsulinemia leads to a marked increase in glucagon secretion. In addition to the decline in insulin secretion, there is decreased secretion ofamylin(another beta-cell hormone), which also leads to an increase in glucagon.Glucagon,a hormone produced by the alpha cells of the islets, acts in the liver to increase the blood glucose level by stimulating glycogenolysis and gluconeogenesis.. Thus both a lack of insulin and a relative excess of glucagon contribute to hyperglycemia in type 1 diabetes.

Question 21

Type 1 Diabetes Mellitus Clinical Manifestations

Answer 21

Manifestations result from insulin deficiency:
->Hyperglycemia
->Polydipsia (inc thirst)
->Polyuria (inc urination)
->Polyphagia (inc hunger)
->Weight loss
->Fatigue
->Recurrent infections
->Prolonged wound healing
-The common clinical manifestations of type 1 diabetes result from both insulin deficiency and hyperglycemia. Acute complications also may include hypoglycemia and DKA. Chronic complications include renal, nervous system, cardiac, peripheral vascular, retinal, and bony tissue dysfunction.

Question 22

Diabetes Mellitus Type 2

Answer 22

Type 2 diabetes (caused by progressive loss of beta-cell insulin secretion, frequently with a background of insulin resistance)
-Initial insulin resistance
->Compensatory hyperinsulinemia prevents clinical appearance
->A decrease in beta-cell mass and a reduction in normal beta-cell function develops and leads to a relative deficiency of insulin activity. The glucagon concentration is increased in type 2 diabetes because pancreatic alpha cells become less responsive to glucose inhibition, resulting in an increase in glucagon secretion.
-Later loss of beta cells causing deficiency of insulin activity
-GI hormones play role in insulin resistance
->Hormones released from the gastrointestinal (GI) tract play a role in insulin resistance, beta-cell function, and diabetes.Ghrelinis a peptide produced in the stomach and pancreatic islets that regulates food intake, energy balance, and hormonal secretion. Theincretinsare a class of peptides that are released from the GI tract in response to food intake and function to increase the secretion of insulin and have many other positive effects on metabolism.

Question 23

Type 2 Diabetes Mellitus: Manifestations and risk factors

Answer 23

-Genetic abnormalities combined with environmental influences result in the basic pathophysiologic mechanisms of type 2 diabetes, which are insulin resistance and decreased insulin secretion by beta cells. The most well-recognized risk factors are family history, age, obesity, hypertension, poor diet, and physical inactivity.
-Obesity is one of the most important contributors to insulin resistance and diabetes
-Manifestations (nonspecific): fatigue, pruritus, recurrent infections, visual changes, or symptoms of neuropathy; often overweight, dyslipidemic, and hypertensive
-3 P’s as well
-The metabolic syndrome is a constellation of disorders (central obesity, dyslipidemia, prehypertension, and an elevated FBG) that together confer a high risk of developing type 2 diabetes and associated cardiovascular complications.

Question 24

Gestational Diabetes Mellitus

Answer 24

-Gestational diabetes mellitus (GDM) (diabetes diagnosed in the second or third trimester of pregnancy that was not clearly overt diabetes prior to gestation)
-Gestational diabetes mellitus (GDM)
->Any degree of glucose intolerance with onset or first recognition during pregnancy
-Maturity onset diabetes of youth (MODY)
->Beta-cell function or insulin action affected by autosomal dominant mutations

Question 25

Acute Complications of Diabetes Mellitus

Answer 25

-Hypoglycemia
->Hypoglycemiain diabetes is sometimes calledinsulin shockorinsulin reaction.Individuals with type 1 diabetes require insulin to manage their diabetes and are at more risk for hypoglycemia than those with type 2 diabetes because they have more severe deficits in their ability to control serum glucose levels. Significant drops in blood sugar most often occur when there is an unexpected change in caloric intake or exercise without appropriate modification of insulin dosing. Hypoglycemia sometimes occurs in type 2 diabetes during treatment with oral hypoglycemic medications. Symptoms include pallor, tremor, anxiety,tachycardia, palpitations, diaphoresis, headache, dizziness, irritability, fatigue, poor judgment, confusion, visual disturbances, hunger, seizures, and coma.
-Diabetic ketoacidosis (DKA)
->Diabetic ketoacidosis (DKA)is a serious complication related to a deficiency of insulin and an increase in the levels of insulin counterregulatory hormones (catecholamines, cortisol, glucagon, GH). DKA is much more common in type 1 diabetes because insulin is more deficient. It is characterized by hyperglycemia, acidosis, and ketonuria. Insulin normally stimulates lipogenesis and inhibits lipolysis, thus preventing fat catabolism.Symptoms of DKA include Kussmaul respirations (hyperventilation in an attempt to compensate for the acidosis), postural dizziness, central nervous system depression, ketonuria, anorexia, nausea, abdominal pain, thirst, andpolyuria. DKA is managed with a combination of fluids, insulin, and electrolyte replacement.

-Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)
->Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)is an uncommon but significant complication of type 2 diabetes mellitus with a high overall mortality. It occurs more often in elderly individuals who have other comorbidities, including infections or cardiovascular or renal disease. HHNKS differs from DKA because type 2 diabetes is characterized by a lesser degree of insulin deficiency, which therefore prevents lipolysis and the production of ketones. However, hyperglycemia is usually more profound in HHNKS leading to more polyuria and fluid deficiency. Therefore the clinical features of HHNKS include a very high serum glucose concentration and osmolarity without metabolic acidosis. Clinical manifestations include severe dehydration; loss of electrolytes (especially potassium); and neurologic changes, such as stupor. Management includes fluid, insulin, and electrolyte replacement

Question 26

Chronic Complications of Diabetes Mellitus

Answer 26

-Microvascular disease: Diabetic microvascular complications are characterized by occlusion of capillaries, with associated ischemia of tissues. It is a leading cause of blindness, end-stage kidney failure, and various neuropathies.
->Diabetic retinopathy: Diabetic retinopathyis a leading cause of blindness worldwide and is a common complication of type 2 diabetes because of the likelihood of long-standing hyperglycemia before diagnosis. Diabetic retinopathy results from relative hypoxemia, damage to retinal blood vessels, red blood cell (RBC) aggregation, and hypertension. Macular edemais the leading cause of blurred vision among persons with diabetes.
->Diabetic nephropathy: Diabetes is the most common cause of chronic kidney disease and end-stage kidney disease, and nearly halfof individuals with diabetes mellitus develop diabetic kidney disease.Renal glomerular changes occur early in diabetes mellitus, occasionally preceding the overt manifestation of the disease.There is progressive glomerulosclerosis and decreased glomerular blood flow and glomerular filtration that can progress to renal failure. Microalbuminuriais the first manifestation of diabetic kidney dysfunction and signals the onset of systemic diabetic complications.
->Diabetic neuropathies: Diabetic neuropathyis the most common complication of diabetes. The underlying pathologic mechanism includes metabolic and vascular factors related to chronic hyperglycemia with ischemia and demyelination contributing to neural changes and delayed conduction.Loss of pain, temperature, and vibration sensation is more common than motor involvement and often involves the extremities first in the hands and feet.
-Macrovascular disease: Macrovascular disease (lesions in large- and medium-sized arteries) increases morbidity and mortality and increases the risk for hypertension, accelerated atherosclerosis, cardiovascular disease, stroke, and peripheral vascular disease, particularly among individuals with type 2 diabetes mellitus.
->Cardiovascular disease: Cardiovascular disease is the primary cause of death of people with diabetes, with higher risk for women. Hypertension often coexists with diabetes mellitus. Diabetes also is associated with deleterious changes in serum lipids, including highlevels of low-density lipoproteins (LDLs), and low levels of high-density lipoproteins (HDLs). The incidence ofcongestive heart failureis higher in individuals with diabetes, even without myocardial infarction.
->Stroke: Stroke is twice as common in those with diabetes (particularly type 2 diabetes) as in the nondiabetic population. As in CAD, accelerated atherosclerosis of the cerebral vessels results from insulin resistance and hyperglycemia, especially when associated with hypertension and hyperlipidemia.
->Peripheral vascular disease: Diabetes mellitus increases the incidence of peripheral vascular disease (PVD). Age, duration of diabetes, genetics, and additional risk factors (smoking, hyperlipidemia, hypertension) influence the development and management of PVD. PVD in those with diabetes is more diffuse and often involves arteries below the knee. Occlusions of the small arteries and arterioles can lead to claudication (pain from reduced blood flow during exercise), ulcers, gangrene, and amputation. The lesions begin as ulcers and progress to osteomyelitis or gangrene, requiring amputation.
-Infection

Question 27

Disorders of the Adrenal Cortex Part 1:

Answer 27

-Hypercortical function (inc cortisol secretion)
->Cushing syndrome
->Manifestations resulting from chronic excess cortisol, regardless of cause
->Cushing disease
->Excessive anterior pituitary secretion of ACTH; excess endogenous secretion
->Manifestations
->Weight gain in trunk (“truncal obesity”), facial (“moon face”), cervical areas (“buffalo hump”)
->Glucose intolerance and protein wasting: Glucose intolerance occurs because of cortisol-induced insulin resistance and increased gluconeogenesis and glycogen storage by the liver. Protein wasting is caused by the catabolic effects of cortisol on peripheral tissues. Muscle wasting leads to muscle weakness. In the skin, loss of collagen leads to thin, weakened integumentary tissues through which capillaries are more visible and are easily stretched by adipose deposits.

Question 28

Disorders of the Adrenal Cortex Part 2:

Answer 28

-Congenital adrenal hyperplasia (Congenital adrenal hyperplasiaresults from an inherited deficiency of an enzyme that is critical in cortisol biosynthesis. Because cortisol is not produced efficiently, the concentration of ACTH increases and causes adrenal hyperplasia, which results in the overproduction of mineralocorticoids or androgens, or both.)
->Deficiency in cortisol production causing increase in ACTH concentration
-Hyperaldosteronism
->Primary hyperaldosteronism (Conn syndrome)
->Increased aldosterone secretion from abnormality in adrenal cortex
->Secondary hyperaldosteronism
->Extra-adrenal stimulus of aldosterone secretion
->Manifestations
->Hypertension, hypokalemia, and hypervolemia

Question 29

Disorders of the Adrenal Cortex Part 3:

Answer 29

-Hypersecretion of adrenal androgens
->Feminization (female secondary sex characteristics)
-Hypersecretion of adrenal estrogens
->Virilization (male secondary sex characteristics)
-hypersecretion of adrenal androgens and estrogens may be as a result of adrenal tumors.

Question 30

Disorders of the Adrenal Cortex Part 4:

Answer 30

-Adrenocortical hypofunction (hypocortisolism): low levels of cortisol secretion
->Addison disease (Addison disease is characterized by inadequate corticosteroid and mineralocorticoid synthesis and elevated levels of serum ACTH (loss of negative feedback).)
->Primary adrenal insufficiency
->Autoimmune mechanisms destroy adrenal cortical cells
->Addisonian crisis—hypotension leading to vascular collapse and shock
->Secondary hypocortisolism
->Decreased ACTH, adrenal atrophy
->Often results from prolonged exposure to exogenous glucocorticoids