NR 283: PATHOPHYSIOLOGY FINAL EXAM STUDY GUIDE
WITH ANS
ENDOCRINE SYSTEMS DISORDERS
• Hypoparathyroidism
- Leads to hypocalcemia
o Weak cardiac muscle contractions
o Increased excitability of nerves—spontaneous contractions of skeletal muscle
• Endocrine disorder causes
- Excess hormone level of deficit/decrease hormone level
• Hyperparathyroidism
-Bone demineralization (Hypercalcemia)
,• Diabetes (cellular level in kidney)
*******-decrease in transport in kidney resulting in glucosuria
- Diabetes mellitus—basic problem is inadequate insulin effects in receptor tissues
o Deficit of insulin secretion
o Production of insulin antagonists
- Diabetes results in abnormal carbohydrate, protein, and fat metabolism.
- Some tissues can transport glucose in the absence of insulin:
o CNS, kidney, myocardium, gut, skeletal muscle
▪ Skeletal muscle can partially meet tissue needs without insulin.
- Type 1 (mostly in children)
o Autoimmune destruction of beta cells in pancreas (Insulin)
o Insulin replacement required
o Acute onset in children and adolescents
o Not linked to obesity
o Genetic factors may play a role.
o Metabolic changes
▪ Catabolism of fats and proteins
• Excessive amounts of fatty acids and metabolites
• Ketones in the blood
▪ Ketonuria
• Decreased serum bicarbonate
• Decrease in pH of body fluids
• Ketoacids excreted in urine
▪ Decompensated metabolic acidosis
, - Type 2 (Occurs in adults)
o Non–insulin-dependent
o Oral hypoglycemic medications may be used.
o Caused by decreased production of insulin and/or increased resistance by body cells to
insulin
o Onset is slow and insidious, usually in those older than 50 years
o Associated with obesity
o Component of metabolic syndrome
o Increasing incidence in teens and young adults
o Control of Type 2
▪ Diet should contain:
• Increased fiber
• Reduced lipids and simple carbohydrates
▪ Regular exercise to reduce glucose levels
▪ Reduce insulin resistance by reducing BMI to normal range
▪ Monitoring blood glucose levels as ordered
▪ Medication to stimulate the beta cells of the pancreas to produce more insulin
▪ If insulin-dependent—proper administration of insulin to maintain glucose
levels in normal range
▪ Routine follow-up and blood testing
- General Manifestations
o Insulin deficit results in decreased transport and use of glucose in many cells.
▪ Polyphagia
▪ Fatigue
o Blood glucose levels rise—hyperglycemia
WITH ANS
ENDOCRINE SYSTEMS DISORDERS
• Hypoparathyroidism
- Leads to hypocalcemia
o Weak cardiac muscle contractions
o Increased excitability of nerves—spontaneous contractions of skeletal muscle
• Endocrine disorder causes
- Excess hormone level of deficit/decrease hormone level
• Hyperparathyroidism
-Bone demineralization (Hypercalcemia)
,• Diabetes (cellular level in kidney)
*******-decrease in transport in kidney resulting in glucosuria
- Diabetes mellitus—basic problem is inadequate insulin effects in receptor tissues
o Deficit of insulin secretion
o Production of insulin antagonists
- Diabetes results in abnormal carbohydrate, protein, and fat metabolism.
- Some tissues can transport glucose in the absence of insulin:
o CNS, kidney, myocardium, gut, skeletal muscle
▪ Skeletal muscle can partially meet tissue needs without insulin.
- Type 1 (mostly in children)
o Autoimmune destruction of beta cells in pancreas (Insulin)
o Insulin replacement required
o Acute onset in children and adolescents
o Not linked to obesity
o Genetic factors may play a role.
o Metabolic changes
▪ Catabolism of fats and proteins
• Excessive amounts of fatty acids and metabolites
• Ketones in the blood
▪ Ketonuria
• Decreased serum bicarbonate
• Decrease in pH of body fluids
• Ketoacids excreted in urine
▪ Decompensated metabolic acidosis
, - Type 2 (Occurs in adults)
o Non–insulin-dependent
o Oral hypoglycemic medications may be used.
o Caused by decreased production of insulin and/or increased resistance by body cells to
insulin
o Onset is slow and insidious, usually in those older than 50 years
o Associated with obesity
o Component of metabolic syndrome
o Increasing incidence in teens and young adults
o Control of Type 2
▪ Diet should contain:
• Increased fiber
• Reduced lipids and simple carbohydrates
▪ Regular exercise to reduce glucose levels
▪ Reduce insulin resistance by reducing BMI to normal range
▪ Monitoring blood glucose levels as ordered
▪ Medication to stimulate the beta cells of the pancreas to produce more insulin
▪ If insulin-dependent—proper administration of insulin to maintain glucose
levels in normal range
▪ Routine follow-up and blood testing
- General Manifestations
o Insulin deficit results in decreased transport and use of glucose in many cells.
▪ Polyphagia
▪ Fatigue
o Blood glucose levels rise—hyperglycemia
