NR 283 EXAM 3 STUDY GUIDE (LATEST)
****PLEASE NOTE THAT THESE STUDY GUIDES SHOW DIFFERENT
CHAPTER NUMBERS (BOOK EDITION WAS CHANGED) BUT MATERIAL
SHOULD BE THE SAME!
***ALSO THIS STUDY GUIDE IS ALREADY DONE BY MY SOURCE, THIS IS
WHY IT'S SUPPEERRRRRRR LONG! SORRY GUYS BUT FEEL FREE TO USE ;)
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-
****PLEASE NOTE THAT THESE STUDY GUIDES SHOW DIFFERENT
CHAPTER NUMBERS (BOOK EDITION WAS CHANGED) BUT MATERIAL
SHOULD BE THE SAME!
***ALSO THIS STUDY GUIDE IS ALREADY DONE BY MY SOURCE, THIS IS
WHY IT'S SUPPEERRRRRRR LONG! SORRY GUYS BUT FEEL FREE TO USE ;)
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-
