NR283 EXAM 3 STUDYGUIDE
CHAPTER 18 ENDOCRINE
All right guys here is endocrine! Overview- functions of the endocrine system provide growth &
reproductive capabilities. Dysfunction of the endocrine system includes excessive or insufficient
function of the endocrine gland with alterations in hormone levels caused by either
hypersecretion or hyposecretion of hormone abnormal hormone levels.
Dysfunction of an endocrine gland can also be due to: 1) feedback systems failure to function or
respond to inappropriate signals, 2) decreased hormone delivery caused by inadequate blood
supply to the gland or target tissues, or an insufficient amount of the appropriate carrier proteins
in the serum. Ectopic sources of hormones (hormones produced by nonendocrine tissues) may
cause abnormally elevated hormone levels w/o the benefit of normal feedback system for
hormone controls---ectopic production is autonomous.
Look at (Table 18-1)
Diseases of the Posterior Pituitary: Related to abnormal secretion of ADH. An excess of this
hormone results in water retention and a hypoosmolar state, whereas deficiencies in the amount
or response to ADH result in serum hyperosmolarity.
1) Syndrome of inappropriate ADH secretion (SIADH), also known as vasopressin
dysregulation, occurs with high levels of ADH without normal physiologic stimuli for
release. Most common cause is the ectopic production of ADH by tumors such as small
cell carcinoma of the duodenum, stomach, and pancreas, bladder, prostate and
endometrium CA, lymphomas, and sarcomas. Pulmonary disorders: bronchogenic
carcinoma, pneumonia, asthma, cystic fibrosis, and respiratory failure requiring
mechanical vent. CNS disorders: encephalitis, meningitis, intracranial hemorrhage,
tumors and trauma. Surgery can result in increased ADH secretion. This is related to
fluid and volume changes, the amount and type of IV fluids given and narcotic
analgesics. Examples of medication causes include: hypoglycemic meds, narcotics,
general anesthetics, chemo agents, NSAIDs, synthetic ADH analogs.
PATHO: Enhanced water retention. ADH increases renal collecting duct permeability to
water by inducing the insertion of (aquaporin-2), a water channel protein, into the tubular
luminal membrane---increasing water reabsorption by the kidneys. Resulting in
expansion of extracellular fluid volume----dilutional hyponatremia, hypoosmolarity, and
urine is inappropriately concentrated with respect to serum osmaolarity.
CLINICAL MANIFESTATION: * Thirst,
● impaired taste,
● anorexia,
● dyspnea on exertion (DOE),
, ● fatigue and dulled sensorium all due to
hyponatremia.
● Vomiting, abd cramping (130-120 NA level).
● Levels below 110=confusion, lethargy, muscle
twitching, convulsions, irreversible neurologic
damage.
2) Diabetes Insipidus: Insufficient activity of ADH leading to polyuria and polydipsia. 2
Forms include:
1) Neurogenic or central DI- insufficient secretion of ADH
occurring when any organic lesion of the hypothalamus, pituitary
stalk, or posterior pituitary interferes with ADH synthesis,
transport or release. Lesions include primary brain tumors,
hypophysectomy, aneurysms, thrombosis, infections, and
immunologic disorders, closed head injury. Also caused by
hereditary disorders affecting ADH genes or structural changes in
the pituitary gland.
2) Nephrogenic DI: inadequate response of the renal tubules to
ADH, usually acquired or genetic. Acquired: disorders and drugs
that damage the renal tubules or inhibit the generation of cAMO in
the tubules. Disorders include, pyelonephritis, amyloidosis,
destructive uropathies, polycystic kidney disease---all leading to
irreversible diabetes insipidus. Drugs: lithium carbonate,
colchicines, amphotericin B, loop diuretics, general anesthetics and
demeclocycline. Genetic: mutation in the gene that codes for
aquaporin-2.
PATHO: Partial/total inability to concentrate urine. Insufficient ADH activity
causes excretion of large volumes of dilute urine----increased plasma osmolality.
CLINICAL MANIFESTATIONS: * Polyuria, Nocturia, Continued thirst,
polydipsia, hydronephrosis.
DIABETES MELITUS: Metabolic disease, defect in insulin secretion.
● Diagnosis based on HbA1C levels:
Glycosylated hemoglobin is a form of
hemoglobin that is measured primarily to
identify three-month average plasma glucose
concentration.
DIABETES TYPE I: Most common among pediatrics.
PATHO: Autoimmune T-cell mediated disease that destroys beta cells of the
pancreas. Destruction of beta cells is related to genetic susceptibility and
environmental factors. Strongest genetic association is with histocompatibility
,leukocyte antigen (HLA). Environmental factors=exposure to certain drugs,
foods and viruses. Cellular immunity and humoral immunity are stimulated,
resulting in beta-cell destruction and apoptosis. Insulin synthesis
declines=hyperglycemia. Insulin-secreting beta cells of the islet of Langerhans
must be destroyed. Glucagon, a hormone produced by the alpha cells of the islets,
acts in the liver to increase blood glucose level by stimulating glycogenolysis and
glucogenesis. In addition to decline in insulin secretion---decreased secretion of
amylin (beta-cell hormone). Amylin suppresses glucagon release from the alpha
cells. Thus both alpha-call and beta-cell functions are abnormal and both a lack
of insulin and a relative excess of glucagon contribute to hyperglycemia.
CLINICAL MANIFESTATIONS: Affects fat, protein and carb metabolism.
(TABLE 18-5)!
● polyuria
● polydipsia 3P’s
● polyphagia
● Thirst
● Weight loss
● DKA
● Fatigue
● Visual changes
DIABETES TYPE II: (non-insulin dependent) Risk factors: age, obesity,
hypertension, physical activity and family history. Individuals with metabolic
syndrome (obesity, dyslipidemia, prehypertension, and hyperglycemia).
PATHO: Insulin resistance and decreased insulin secretion by beta cells.
Insulin resistance- suboptimal response of insulin-sensitive tissues to insulin and
assoc with obesity. Mechanisms of obesity: 1) obesity results in increased serum
levels of leptin and decreased levels of adiponectin. These changes associated
with inflammation and decreased insulin sensitivity. 2) elevated levels of serum
free fatty acids and intracellular deposits of triglycerides and cholesterol
interfering with intracellular insulin signaling and decreases tissue responses to
insulin and contribute to beta-cell apoptosis. 3) inflammatory cytokines and
interleukin-6 are released and induce insulin resistance and are cytotoxic to beta
cells. 4) obesity is correlated with hyperinsulinemia and decreased insulin
receptor density. LOOK AT FIG 18-12!
● Beta-cell dysfunction develops and leads to a
relative deficiency of insulin activity. The islet
dysfunction is caused by a combination of a
decrease in beta-cell mass and reduction in
normal beta-cell function.
● Glucagon concentration is increased due to
pancreatic alpha cells becoming less responsive
, to glucose inhibition >>increase in glucagon
secretion. These high levels of glucagon
increase blood glucose level by stimulating
glycogenolysis and gluconeogenesis.
● Hormones released from GI tract play a role in
insulin resistance, beta-cell function. (Gherlin)
CLINICAL MANIFESTATIONS: * overweight
* dyslipidemic
● hyperinsulinemic
● hypertensive
● polyuria
● polydipsia
● fatigue
● pruritus
● recurrent infections
● visual changes
● neuropathy symptoms
ACUTE COMPLICATIONS OF DIABETES MELLITUS
3 Major Acute complications:
1) Hypoglycemia: (insulin shock or insulin reaction) more common in type 1 DM.
Symptoms: pallor, tremor, anxiety, tachycardia, palpitations, diaphoresis,
headache, dizziness, irritability, fatigue, poor judgement, confusion, visual
disturbances, hunger, seizures, and coma.
2) Diabetic Ketoacidosis (DKA): SERIOUS complication related to a deficiency of
insulin and an increase in the levels of insulin counterregulatory hormones
(catecholamines, cortisol, glucagon, growth hormone). More common in type I
because insulin is more deficient. DX criteria: 1) serum glucose level >250, 2)
serum bicarb level <18, 3) serum Ph <7.30, 4) presence of anion gap, and 5) presence
of urine and serum Insulin deficiency enhances lipolysis therefore; increasing amount
of nonesterfied fatty acids delivered to the liver. This results in increased
glyconeogenesis which contributes to hyperglycemia and production of ketones
bodies by mitochondria of the liver at a rate that exceeds peripheral use.
Accumulation of ketone bodies causes drop in pH>>metabolic acidosis.
3) Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS): Sig complication of
type II, occurring more often in elderly with infections or cardiovascular or renal
disease. **differs from DKA in the degree of insulin deficiency and the degree of
fluid deficiency***
Clinical Features: 1) serum glucose level >600, 2) serum Ph >7.30, 3) serum bicarb
level >15, 4) serum osmolarity >320, 5) either absent or small numbers of ketones in
the urine and serum.
CHAPTER 18 ENDOCRINE
All right guys here is endocrine! Overview- functions of the endocrine system provide growth &
reproductive capabilities. Dysfunction of the endocrine system includes excessive or insufficient
function of the endocrine gland with alterations in hormone levels caused by either
hypersecretion or hyposecretion of hormone abnormal hormone levels.
Dysfunction of an endocrine gland can also be due to: 1) feedback systems failure to function or
respond to inappropriate signals, 2) decreased hormone delivery caused by inadequate blood
supply to the gland or target tissues, or an insufficient amount of the appropriate carrier proteins
in the serum. Ectopic sources of hormones (hormones produced by nonendocrine tissues) may
cause abnormally elevated hormone levels w/o the benefit of normal feedback system for
hormone controls---ectopic production is autonomous.
Look at (Table 18-1)
Diseases of the Posterior Pituitary: Related to abnormal secretion of ADH. An excess of this
hormone results in water retention and a hypoosmolar state, whereas deficiencies in the amount
or response to ADH result in serum hyperosmolarity.
1) Syndrome of inappropriate ADH secretion (SIADH), also known as vasopressin
dysregulation, occurs with high levels of ADH without normal physiologic stimuli for
release. Most common cause is the ectopic production of ADH by tumors such as small
cell carcinoma of the duodenum, stomach, and pancreas, bladder, prostate and
endometrium CA, lymphomas, and sarcomas. Pulmonary disorders: bronchogenic
carcinoma, pneumonia, asthma, cystic fibrosis, and respiratory failure requiring
mechanical vent. CNS disorders: encephalitis, meningitis, intracranial hemorrhage,
tumors and trauma. Surgery can result in increased ADH secretion. This is related to
fluid and volume changes, the amount and type of IV fluids given and narcotic
analgesics. Examples of medication causes include: hypoglycemic meds, narcotics,
general anesthetics, chemo agents, NSAIDs, synthetic ADH analogs.
PATHO: Enhanced water retention. ADH increases renal collecting duct permeability to
water by inducing the insertion of (aquaporin-2), a water channel protein, into the tubular
luminal membrane---increasing water reabsorption by the kidneys. Resulting in
expansion of extracellular fluid volume----dilutional hyponatremia, hypoosmolarity, and
urine is inappropriately concentrated with respect to serum osmaolarity.
CLINICAL MANIFESTATION: * Thirst,
● impaired taste,
● anorexia,
● dyspnea on exertion (DOE),
, ● fatigue and dulled sensorium all due to
hyponatremia.
● Vomiting, abd cramping (130-120 NA level).
● Levels below 110=confusion, lethargy, muscle
twitching, convulsions, irreversible neurologic
damage.
2) Diabetes Insipidus: Insufficient activity of ADH leading to polyuria and polydipsia. 2
Forms include:
1) Neurogenic or central DI- insufficient secretion of ADH
occurring when any organic lesion of the hypothalamus, pituitary
stalk, or posterior pituitary interferes with ADH synthesis,
transport or release. Lesions include primary brain tumors,
hypophysectomy, aneurysms, thrombosis, infections, and
immunologic disorders, closed head injury. Also caused by
hereditary disorders affecting ADH genes or structural changes in
the pituitary gland.
2) Nephrogenic DI: inadequate response of the renal tubules to
ADH, usually acquired or genetic. Acquired: disorders and drugs
that damage the renal tubules or inhibit the generation of cAMO in
the tubules. Disorders include, pyelonephritis, amyloidosis,
destructive uropathies, polycystic kidney disease---all leading to
irreversible diabetes insipidus. Drugs: lithium carbonate,
colchicines, amphotericin B, loop diuretics, general anesthetics and
demeclocycline. Genetic: mutation in the gene that codes for
aquaporin-2.
PATHO: Partial/total inability to concentrate urine. Insufficient ADH activity
causes excretion of large volumes of dilute urine----increased plasma osmolality.
CLINICAL MANIFESTATIONS: * Polyuria, Nocturia, Continued thirst,
polydipsia, hydronephrosis.
DIABETES MELITUS: Metabolic disease, defect in insulin secretion.
● Diagnosis based on HbA1C levels:
Glycosylated hemoglobin is a form of
hemoglobin that is measured primarily to
identify three-month average plasma glucose
concentration.
DIABETES TYPE I: Most common among pediatrics.
PATHO: Autoimmune T-cell mediated disease that destroys beta cells of the
pancreas. Destruction of beta cells is related to genetic susceptibility and
environmental factors. Strongest genetic association is with histocompatibility
,leukocyte antigen (HLA). Environmental factors=exposure to certain drugs,
foods and viruses. Cellular immunity and humoral immunity are stimulated,
resulting in beta-cell destruction and apoptosis. Insulin synthesis
declines=hyperglycemia. Insulin-secreting beta cells of the islet of Langerhans
must be destroyed. Glucagon, a hormone produced by the alpha cells of the islets,
acts in the liver to increase blood glucose level by stimulating glycogenolysis and
glucogenesis. In addition to decline in insulin secretion---decreased secretion of
amylin (beta-cell hormone). Amylin suppresses glucagon release from the alpha
cells. Thus both alpha-call and beta-cell functions are abnormal and both a lack
of insulin and a relative excess of glucagon contribute to hyperglycemia.
CLINICAL MANIFESTATIONS: Affects fat, protein and carb metabolism.
(TABLE 18-5)!
● polyuria
● polydipsia 3P’s
● polyphagia
● Thirst
● Weight loss
● DKA
● Fatigue
● Visual changes
DIABETES TYPE II: (non-insulin dependent) Risk factors: age, obesity,
hypertension, physical activity and family history. Individuals with metabolic
syndrome (obesity, dyslipidemia, prehypertension, and hyperglycemia).
PATHO: Insulin resistance and decreased insulin secretion by beta cells.
Insulin resistance- suboptimal response of insulin-sensitive tissues to insulin and
assoc with obesity. Mechanisms of obesity: 1) obesity results in increased serum
levels of leptin and decreased levels of adiponectin. These changes associated
with inflammation and decreased insulin sensitivity. 2) elevated levels of serum
free fatty acids and intracellular deposits of triglycerides and cholesterol
interfering with intracellular insulin signaling and decreases tissue responses to
insulin and contribute to beta-cell apoptosis. 3) inflammatory cytokines and
interleukin-6 are released and induce insulin resistance and are cytotoxic to beta
cells. 4) obesity is correlated with hyperinsulinemia and decreased insulin
receptor density. LOOK AT FIG 18-12!
● Beta-cell dysfunction develops and leads to a
relative deficiency of insulin activity. The islet
dysfunction is caused by a combination of a
decrease in beta-cell mass and reduction in
normal beta-cell function.
● Glucagon concentration is increased due to
pancreatic alpha cells becoming less responsive
, to glucose inhibition >>increase in glucagon
secretion. These high levels of glucagon
increase blood glucose level by stimulating
glycogenolysis and gluconeogenesis.
● Hormones released from GI tract play a role in
insulin resistance, beta-cell function. (Gherlin)
CLINICAL MANIFESTATIONS: * overweight
* dyslipidemic
● hyperinsulinemic
● hypertensive
● polyuria
● polydipsia
● fatigue
● pruritus
● recurrent infections
● visual changes
● neuropathy symptoms
ACUTE COMPLICATIONS OF DIABETES MELLITUS
3 Major Acute complications:
1) Hypoglycemia: (insulin shock or insulin reaction) more common in type 1 DM.
Symptoms: pallor, tremor, anxiety, tachycardia, palpitations, diaphoresis,
headache, dizziness, irritability, fatigue, poor judgement, confusion, visual
disturbances, hunger, seizures, and coma.
2) Diabetic Ketoacidosis (DKA): SERIOUS complication related to a deficiency of
insulin and an increase in the levels of insulin counterregulatory hormones
(catecholamines, cortisol, glucagon, growth hormone). More common in type I
because insulin is more deficient. DX criteria: 1) serum glucose level >250, 2)
serum bicarb level <18, 3) serum Ph <7.30, 4) presence of anion gap, and 5) presence
of urine and serum Insulin deficiency enhances lipolysis therefore; increasing amount
of nonesterfied fatty acids delivered to the liver. This results in increased
glyconeogenesis which contributes to hyperglycemia and production of ketones
bodies by mitochondria of the liver at a rate that exceeds peripheral use.
Accumulation of ketone bodies causes drop in pH>>metabolic acidosis.
3) Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS): Sig complication of
type II, occurring more often in elderly with infections or cardiovascular or renal
disease. **differs from DKA in the degree of insulin deficiency and the degree of
fluid deficiency***
Clinical Features: 1) serum glucose level >600, 2) serum Ph >7.30, 3) serum bicarb
level >15, 4) serum osmolarity >320, 5) either absent or small numbers of ketones in
the urine and serum.
