Chapter 16: Endocrine System Disorders
1) A: Pituitary gland
B: Pineal gland
C: Four parathyroid glands on posterior thyroid
D: Thyroid gland
E: Thymus
F: Adrenal gland
G: Pancreas
H: Kidney
I: Ovary in female
J: Testis in male.
2) Hormones are chemical messengers and can be classified by:
-Action: control or hormone levels; blood calcium levels.
-Source: endocrine organ; adrenal gland.
-Chemical structure: amino acid derivatives or steroids.
3) Negative feedback
4) An excessive amount of hormone or a hormonal deficit.
5) Radioimmunoassay and immunochemical assays.
Diabetes Mellitus
6) Familial history (Type 1); obesity, advancing age (Type 2)
7) -Type 1: genetic factor (family history); autoimmune destruction of pancreatic beta cells.
-Type 2: familial, lifestyle, and environmental factors, especially obesity.
8) An insulin deficit leads to the following sequence of events and can be categorized into the initial
stage and progressive effects:
Initial stage -Decreased transportation and use of glucose -Hyperglycemia -Glucosuria -Polyuria
with loss of fluid and electrolytes -Fluid loss through the urine and high blood glucose levels;
dehydration -Polydipsia due to dehydration -Lack of nutrients entering the cells, stimulating
appetite and leading to polyphagia
Progressive effects -Catabolism of fats and proteins due to lack of glucose in cells; resulting in
ketosis as metabolites accumulate; ketoacidosis -Ketonuria -Glomerular filtration drops, resulting
in decompensated metabolic acidosis
9) The lack of glucose in cells results in catabolism of fats, leading to excessive buildup of fatty acids
and their metabolites, ketone (ketoacidosis).
10) Warning signs include: -Polyuria: hyperglycemia results in excess glucose in the urine as renal
tubular reabsorption capacity is exceeded; the glucose in the filtrate exerts osmotic pressure,
increasing the volume of urine produced.
-Polydipsia: fluid and electrolyte loss due to glucosuria results in dehydration and stimulation of
the thirst response (hypothalamus).
-Polyphagia: lack of nutrients in cells stimulates appetite; weight loss: particularly with type 1,
due to fat catabolism.
11) Diagnosis is established from the following: fasting blood glucose level, glucose tolerance test,
and glycosylated hemoglobin test.
, 12) Dietary modifications include dieting to reduce weight or maintain optimum weight; adding
more complex carbohydrates, getting adequate protein, and taking in low saturated fats and
fiber to reduce cholesterol levels; having minimal intake of simple and refined sugars; and
balancing and reducing food intake to match insulin availability, metabolic needs, and activity
level.
13) Oral hypoglycemics act in a number of different ways to lower blood sugar; some stimulate beta
cells to release more insulin, others reduce insulin resistance of cells and hepatic glucose
production, and another type increases cell sensitivity to insulin.
14) -Hypoglycemia
-Gastrointestinal disturbances; anorexia, nausea, vomiting
-Anemia
-Pruritus (itching)
-Liver and kidney damage
-Metallic taste (with metformin)
15) The various forms of insulin differ in onset of action, peak insulin levels, and duration of action.
16) Insulin can be administered by subcutaneous injections, continuous subcutaneous infusion
(“insulin pump”), or inhalation, which was just approved by the U.S. Food and Drug
Administration (FDA).
17) Factors that could precipitate a hypoglycemic or insulin reaction include increased physical
exercise, skipping a meal or fasting, delayed or inadequate food intake, insulin overdose (too
much insulin), and nutritional and/or fluid and electrolyte imbalances due to nausea and
vomiting.
18) Verify that patients have eaten and taken the appropriate medications.
19) Macroangiopathy: -Myocardial infarction (heart attack)
-Cerebrovascular accident (stroke)
-Peripheral vascular disease (ischemia, gangrene, and amputation affecting the legs)
-Atherosclerosis in large arteries related to hyperlipidemia, hypertension, and degenerative
changes in the intimal layer of the arterial wall
Microangiopathy: Kidneys: -Diabetic nephropathy
-Chronic renal failure
**Thickening of the capillary basement membrane, leading to occlusion of rupture**
Eyes: -Retinopathy
**Microaneurysms, neovascularization, and fibrosis; leads to blindness** Nervous system: -
Neuropathy in the CNS and peripheral nerves
-Decreased function of the sensory, motor, and ANS fibers
**In addition to ischemia, there is also a metabolic abnormality that causes degeneration of
myelin and deficit of myo-inositol, essential in the conduction of nerves impulses**
20) Diabetic neuropathy is a disorder of peripheral nerves that produces impaired sensation,
numbness, tingling, weakness, and muscle wasting. It results from ischemia and altered
metabolic process. There is a risk of tissue trauma and infection.
21) Risk of infection is greatly increased when vascular and sensory impairment coexist.
22) -Tuberculosis
-Infections in the feet and hands
-Fungal infections
1) A: Pituitary gland
B: Pineal gland
C: Four parathyroid glands on posterior thyroid
D: Thyroid gland
E: Thymus
F: Adrenal gland
G: Pancreas
H: Kidney
I: Ovary in female
J: Testis in male.
2) Hormones are chemical messengers and can be classified by:
-Action: control or hormone levels; blood calcium levels.
-Source: endocrine organ; adrenal gland.
-Chemical structure: amino acid derivatives or steroids.
3) Negative feedback
4) An excessive amount of hormone or a hormonal deficit.
5) Radioimmunoassay and immunochemical assays.
Diabetes Mellitus
6) Familial history (Type 1); obesity, advancing age (Type 2)
7) -Type 1: genetic factor (family history); autoimmune destruction of pancreatic beta cells.
-Type 2: familial, lifestyle, and environmental factors, especially obesity.
8) An insulin deficit leads to the following sequence of events and can be categorized into the initial
stage and progressive effects:
Initial stage -Decreased transportation and use of glucose -Hyperglycemia -Glucosuria -Polyuria
with loss of fluid and electrolytes -Fluid loss through the urine and high blood glucose levels;
dehydration -Polydipsia due to dehydration -Lack of nutrients entering the cells, stimulating
appetite and leading to polyphagia
Progressive effects -Catabolism of fats and proteins due to lack of glucose in cells; resulting in
ketosis as metabolites accumulate; ketoacidosis -Ketonuria -Glomerular filtration drops, resulting
in decompensated metabolic acidosis
9) The lack of glucose in cells results in catabolism of fats, leading to excessive buildup of fatty acids
and their metabolites, ketone (ketoacidosis).
10) Warning signs include: -Polyuria: hyperglycemia results in excess glucose in the urine as renal
tubular reabsorption capacity is exceeded; the glucose in the filtrate exerts osmotic pressure,
increasing the volume of urine produced.
-Polydipsia: fluid and electrolyte loss due to glucosuria results in dehydration and stimulation of
the thirst response (hypothalamus).
-Polyphagia: lack of nutrients in cells stimulates appetite; weight loss: particularly with type 1,
due to fat catabolism.
11) Diagnosis is established from the following: fasting blood glucose level, glucose tolerance test,
and glycosylated hemoglobin test.
, 12) Dietary modifications include dieting to reduce weight or maintain optimum weight; adding
more complex carbohydrates, getting adequate protein, and taking in low saturated fats and
fiber to reduce cholesterol levels; having minimal intake of simple and refined sugars; and
balancing and reducing food intake to match insulin availability, metabolic needs, and activity
level.
13) Oral hypoglycemics act in a number of different ways to lower blood sugar; some stimulate beta
cells to release more insulin, others reduce insulin resistance of cells and hepatic glucose
production, and another type increases cell sensitivity to insulin.
14) -Hypoglycemia
-Gastrointestinal disturbances; anorexia, nausea, vomiting
-Anemia
-Pruritus (itching)
-Liver and kidney damage
-Metallic taste (with metformin)
15) The various forms of insulin differ in onset of action, peak insulin levels, and duration of action.
16) Insulin can be administered by subcutaneous injections, continuous subcutaneous infusion
(“insulin pump”), or inhalation, which was just approved by the U.S. Food and Drug
Administration (FDA).
17) Factors that could precipitate a hypoglycemic or insulin reaction include increased physical
exercise, skipping a meal or fasting, delayed or inadequate food intake, insulin overdose (too
much insulin), and nutritional and/or fluid and electrolyte imbalances due to nausea and
vomiting.
18) Verify that patients have eaten and taken the appropriate medications.
19) Macroangiopathy: -Myocardial infarction (heart attack)
-Cerebrovascular accident (stroke)
-Peripheral vascular disease (ischemia, gangrene, and amputation affecting the legs)
-Atherosclerosis in large arteries related to hyperlipidemia, hypertension, and degenerative
changes in the intimal layer of the arterial wall
Microangiopathy: Kidneys: -Diabetic nephropathy
-Chronic renal failure
**Thickening of the capillary basement membrane, leading to occlusion of rupture**
Eyes: -Retinopathy
**Microaneurysms, neovascularization, and fibrosis; leads to blindness** Nervous system: -
Neuropathy in the CNS and peripheral nerves
-Decreased function of the sensory, motor, and ANS fibers
**In addition to ischemia, there is also a metabolic abnormality that causes degeneration of
myelin and deficit of myo-inositol, essential in the conduction of nerves impulses**
20) Diabetic neuropathy is a disorder of peripheral nerves that produces impaired sensation,
numbness, tingling, weakness, and muscle wasting. It results from ischemia and altered
metabolic process. There is a risk of tissue trauma and infection.
21) Risk of infection is greatly increased when vascular and sensory impairment coexist.
22) -Tuberculosis
-Infections in the feet and hands
-Fungal infections
