NUR PC 705 MODULE 3 ENDOCRINE & NEURO CHAPTERS 17-22 QUESTIONS
AND WELL-EXPLAINED ANSWERS
1. Discuss the etiology of endocrine disorders in general.
Alterations in the function of the endocrine system are thought to be caused by
hypersecretion or hyposecretion of the various hormones, leading to abnormal
hormone concentrations in the blood. Also, dysfunction of the endocrine system
may result from abnormal receptor function or from altered intracellular response
to the hormone-receptor complex. Dysfunction of an endocrine gland may involve
the gland’s failure to produce adequate amounts of biologically free or active
hormone forms. A gland may also synthesize or release excessive amounts of
hormone.
2. Explain the feedback-loop systems in thyroid disorders and how
laboratory testing is based on feedback loop communications. (Page
690-691 Chapter 21)
Endocrine feedback is described in terms of short and long term feedback loops.
Feedback systems provide precise monitoring and control of the cellular
environment. Hormones have specific negative and positive-feedback
mechanisms. Most hormone levels are regulated by negative feedback, in which
tropic hormone secretion raises the level of a specific hormone. The elevated level
of the specific hormone then causes negative feedback, decreasing secretion of the
tropic hormone.
Ex. PG 691 Figure 21-2. Thyroid Stimulating Hormone (TSH) secretion from
anterior pituitary is stimulated by Thyrotropin-releasing hormone (TRH) from the
hypothalamus. Secretion of TSH stimulates the synthesis and secretion of thyroid
hormones. Increasing levels of T4 (thyroxine) and T3 (triiodothyronine) then
generate negative feedback on the pituitary and hypothalamus to inhibit TRH and
TSH synthesis.
3. Compare and contrast the etiology, pathogenesis, and clinical
manifestations of hypo and hyperthyroidism. (Pages 724-731)
Hypothyroidism: Elevated TH and suprpressed TSH
Pathophysiology: Thyrotoxicosis is a condition that results from any cause
of increased amounts of TH. Hyperthyroidism is a form of thyrotoxicosis in which
excess amounts of TH are secreted from the thyroid gland. Common diseases that
cause primary hyperthyroidism: graves disease (50-80% cause), toxic
multinodular goiter, solitary toxic adenoma, follicular thyroid carcinoma.
Central (secondary) hyperthyroidism is caused by TSH-secreting pituitary
adenomas.
,Clinical Manifestations: Increased metabolic rate with heat intolerance and inc.
tissue sensitivity to stimulation by the autonomic nervous system.
● Normal or Enlarged Thyroid Gland (goiter): Diffuse (warm on palpation),
Nodular, Solitary (toxic nodule)
● Thin Hair
● Exophthalmos (protruding eyeballs)
● Heart Failure (tachycardia)
● Weight Loss
● Diarrhea
● Warm Skin, sweaty palms
● Hyperreflexia
● Pretibial myxedema (subq swelling on the anterior portions of the legs,
indurated and erythematous skin)
Systemic Manifestations on Pg 727 Table 22-2
,Hypothyroidism: Caused by a deficient production of TH by the thyroid gland.
Most common disorder of thyroid function. Primary is the most prevalent. Central
(secondary) includes conditions that cause either pituitary or hypothalamic failure
with failure to stimulate normal thyroid function.
Pathophysiology: The loss of functional thyroid tissue leads to a decreased
production of TH. Causes in adults include autoimmune thyroiditis (Hashingmoto
disease), iatrogenic loss of thyroid tissue after surgical or radioactive treatment for
hyperthyroidism, head and neck radiation therapy, medications, and endemic
iodine deficiency.
Clinical Manifestations: Generally affects all body systems and occurs
insidiously over months or years. The lower levels of TH result in decreased
energy metabolism and decreased heat production. Person develops low basal
metabolic rate, cold intolerance, lethargy, tiredness, and slightly lowered basal
body temp. May also have diastolic hypertension.
● Loss of hair
● Coarse, brittle hair
● Periorbital edema
● Puffy Face
● Normal, enlarged, or small thyroid
● Heart Failure (bradycardia)
● Constipation
● Cold Intolerance
● Muscle Weakness
● Decreased bone mineral density (osteoporosis)
● Edema of the extremities
Characteristic sign of severe or long-standing hypothyroidism is myxedema, it is a
result of an alteration in the composition of the dermis and other tissues.
4. Differentiate the modifiable risk factors from the non-modifiable
risk factors for the different diabetes types. (Pages 735-737; 739;
742-743)
Type 1 Diabetes
Modifiable Risk Factors:
Non-Modifiable Risk
Factors: Type 2 Diabetes
Modifiable Risk Factors:
Non-modifiable Risk Factors:
5. Compare and contrast the etiology, pathogenesis, clinical
manifestations and acute complications of type 1, type 2, and
gestational diabetes mellitus. (Pages 734-746)
Type
1
Type 2
, polyuria, polyphagia, weight loss, fatigue
Pathop Acute Complications:
hysiolog
y: Pathophysiology:
Clinical
Clinical
Manifes
tations: Manifestations:
Polydips Acute
ia,
Complications:
Gestational Diabetes
Pathophysiology:
AND WELL-EXPLAINED ANSWERS
1. Discuss the etiology of endocrine disorders in general.
Alterations in the function of the endocrine system are thought to be caused by
hypersecretion or hyposecretion of the various hormones, leading to abnormal
hormone concentrations in the blood. Also, dysfunction of the endocrine system
may result from abnormal receptor function or from altered intracellular response
to the hormone-receptor complex. Dysfunction of an endocrine gland may involve
the gland’s failure to produce adequate amounts of biologically free or active
hormone forms. A gland may also synthesize or release excessive amounts of
hormone.
2. Explain the feedback-loop systems in thyroid disorders and how
laboratory testing is based on feedback loop communications. (Page
690-691 Chapter 21)
Endocrine feedback is described in terms of short and long term feedback loops.
Feedback systems provide precise monitoring and control of the cellular
environment. Hormones have specific negative and positive-feedback
mechanisms. Most hormone levels are regulated by negative feedback, in which
tropic hormone secretion raises the level of a specific hormone. The elevated level
of the specific hormone then causes negative feedback, decreasing secretion of the
tropic hormone.
Ex. PG 691 Figure 21-2. Thyroid Stimulating Hormone (TSH) secretion from
anterior pituitary is stimulated by Thyrotropin-releasing hormone (TRH) from the
hypothalamus. Secretion of TSH stimulates the synthesis and secretion of thyroid
hormones. Increasing levels of T4 (thyroxine) and T3 (triiodothyronine) then
generate negative feedback on the pituitary and hypothalamus to inhibit TRH and
TSH synthesis.
3. Compare and contrast the etiology, pathogenesis, and clinical
manifestations of hypo and hyperthyroidism. (Pages 724-731)
Hypothyroidism: Elevated TH and suprpressed TSH
Pathophysiology: Thyrotoxicosis is a condition that results from any cause
of increased amounts of TH. Hyperthyroidism is a form of thyrotoxicosis in which
excess amounts of TH are secreted from the thyroid gland. Common diseases that
cause primary hyperthyroidism: graves disease (50-80% cause), toxic
multinodular goiter, solitary toxic adenoma, follicular thyroid carcinoma.
Central (secondary) hyperthyroidism is caused by TSH-secreting pituitary
adenomas.
,Clinical Manifestations: Increased metabolic rate with heat intolerance and inc.
tissue sensitivity to stimulation by the autonomic nervous system.
● Normal or Enlarged Thyroid Gland (goiter): Diffuse (warm on palpation),
Nodular, Solitary (toxic nodule)
● Thin Hair
● Exophthalmos (protruding eyeballs)
● Heart Failure (tachycardia)
● Weight Loss
● Diarrhea
● Warm Skin, sweaty palms
● Hyperreflexia
● Pretibial myxedema (subq swelling on the anterior portions of the legs,
indurated and erythematous skin)
Systemic Manifestations on Pg 727 Table 22-2
,Hypothyroidism: Caused by a deficient production of TH by the thyroid gland.
Most common disorder of thyroid function. Primary is the most prevalent. Central
(secondary) includes conditions that cause either pituitary or hypothalamic failure
with failure to stimulate normal thyroid function.
Pathophysiology: The loss of functional thyroid tissue leads to a decreased
production of TH. Causes in adults include autoimmune thyroiditis (Hashingmoto
disease), iatrogenic loss of thyroid tissue after surgical or radioactive treatment for
hyperthyroidism, head and neck radiation therapy, medications, and endemic
iodine deficiency.
Clinical Manifestations: Generally affects all body systems and occurs
insidiously over months or years. The lower levels of TH result in decreased
energy metabolism and decreased heat production. Person develops low basal
metabolic rate, cold intolerance, lethargy, tiredness, and slightly lowered basal
body temp. May also have diastolic hypertension.
● Loss of hair
● Coarse, brittle hair
● Periorbital edema
● Puffy Face
● Normal, enlarged, or small thyroid
● Heart Failure (bradycardia)
● Constipation
● Cold Intolerance
● Muscle Weakness
● Decreased bone mineral density (osteoporosis)
● Edema of the extremities
Characteristic sign of severe or long-standing hypothyroidism is myxedema, it is a
result of an alteration in the composition of the dermis and other tissues.
4. Differentiate the modifiable risk factors from the non-modifiable
risk factors for the different diabetes types. (Pages 735-737; 739;
742-743)
Type 1 Diabetes
Modifiable Risk Factors:
Non-Modifiable Risk
Factors: Type 2 Diabetes
Modifiable Risk Factors:
Non-modifiable Risk Factors:
5. Compare and contrast the etiology, pathogenesis, clinical
manifestations and acute complications of type 1, type 2, and
gestational diabetes mellitus. (Pages 734-746)
Type
1
Type 2
, polyuria, polyphagia, weight loss, fatigue
Pathop Acute Complications:
hysiolog
y: Pathophysiology:
Clinical
Clinical
Manifes
tations: Manifestations:
Polydips Acute
ia,
Complications:
Gestational Diabetes
Pathophysiology:
