1. BIO 139 Anatomy & Physiology II
Endocrine Disorders
BIO 139 Anatomy & Physiology II

2. Think of the normal function of the hormone.
What would you expect with hypo- or hyper-secretion?

3. Hypothyroidism Possible causes of hypothyroidism
Failure of the thyroid gland to make hormone
Deficiency of TRH, TSH or both
Dietary iodine deficiency

4. Hypothyroidism
Symptoms are related to a reduction in overall metabolic rate
Poor tolerance to cold
Tendency to gain weight
Easily fatigued
Slow, weak pulse (↓ HR)
↓ BP and Cardiac output
Impaired memory and slow speech
↓ GI Motility

5. Treatment for Hypothyroidism
Daily use of synthetic hormone
Levothroid, Levoxyl, Synthroid, Unithroid

6. Hypothyroidism
Cretinism results if have thyroid deficiency since birth
Dwarfism
Mental retardation
Preventable with EARLY treatment
Myxedema
Puffy apperance of hands, face & feet

7. Hyperthyroidism Possible causes of hyperthyroidism Grave’s disease
TRH or TSH excess
Thyroid tumor

8. Grave’s Disease Autoimmune disease
Abnormal presence of thyroid stimulating immunoglobulin (TSI)
TSI has similar structure to TSH
Stimulates growth of thyroid and TSH secretion
Not subject to negative feedback

9. Hyperthyroidism
Symptoms related to Elevated basal metabolic rate (BMR is # of calories you’d burn if you just rested for 24 hrs)
Increased heat production
Body weight falls
Loss of skeletal muscle protein & weakness
Cardiovascular abnormalities (↑ BP, HR and CO)
↑ Respiratory rate

10. Treatments for Hyperthyroidism
Anti-thyroid medication
Removal of thyroid tissue
Radioactive iodine therapy

11. Goiter Enlarged thyroid gland May accompany hypo- or hyperthyroidism
Due to increased stimulation of thyroid gland
↑ in cell size and number

12. Diabetes Mellitus
2 types that result from abnormal insulin production, impaired insulin utilization (sensitivity to insulin) or both
Symptoms are grouped according to effects on glucose, amino acid & fat metabolism
17 million people with DM in US (6.2%)
5th leading cause of death in US

13. Normal Insulin Function
Insulin levels rise after meals
Stimulates storage of glucose as glycogen
Inhibits gluconeogenesis
Enhances fat deposition in adipose tissue
Increases protein synthesis

14. Type I Diabetes Mellitus (5-10%)
Juvenile onset (usually), peak between 11-13yrs of age
Autoimmune destruction of ß-cells
Rapid onset of symptoms
↓Insulin = ketone bodies made (from ↑ Lipolysis) = ↓pH
Diabetic Ketoacidosis can occur (↓blood pH)
This will lead to metabolic acidosis
Requires exogenous insulin treatment = Insulin dependent

15. Type II Diabetes Mellitus (90%)
Non-insulin dependent
Adult onset, (over 40) often associated with obesity
Insulin receptor not sensitive to normal levels of insulin or an insufficient amount made
Left untreated over time, insulin level decreases
Can be treated by diet and weight management

16. Effects of Uncontrolled Hyperglycemia
See additional handout!

17. Complications of Diabetes Mellitus
Damage to large and small vessels
Diabetic retinopathy
Damage to capillaries and arterioles of retina
Diabetic nephropathy
Damage to small vessels that supply kidney glomeruli
Diabetic neuropathy: Nerve damage
Sensory neuropathy – loss of protective sensation in lower extremities
Reduced nerve conduction and demyelination

18. Growth Hormone Disorders
Pituitary Dwarfism
Pituitary Gigantism
Acromegaly

19. Growth Hormone Deficiency
Pituitary Dwarfism
GH deficiency in children
Short stature from retarded skeletal growth
Normal body proportions

20. Growth Hormone Excess Acromegaly
GH excess in adulthood (3/1 million people in US)
Bones become thicker & soft tissues proliferate
Enlargement of tongue, cardiomegaly
Disfuguring
Overproduction of GH can result from a benign pituitary tumor

21. Growth Hormone Excess Pituitary Gigantism
GH excess in childhood before epiphyseal plates have closed
Rapid growth in height
May grow to 8 feet tall

22. Antidiuretic Hormone Abnormalities
ADH deficiency: Diabetes Insipidus
Hypersecretion of ADH: SIADH
Syndrome of inappropriate antidiuretic hormone

23. Causes of Diabetes Insipidus
Central Diabetes Insipidus
Damage to hypothalamus or pituitary
Nephrogenic Diabetes Insipidus
Kidney tubules not responsive to ADH

24. Diabetes Insipidus: ADH Deficiency
SYMPTOMS:
↑ urinary output (polyuria)
↑ plasma osmolality
↓ ECF volume or ↑ solute concentration
↑ thirst (polydipsia)
Hypernatremia
TX: ADH like drugs

25. Treatment for Diabetes Insipidus
Central Diabetes Insipidus
Use of synthetic ADH
Hypotonic fluids
Nephrogenic Diabetes Insipidus
Low salt diet
Drink enough water to prevent dehydration

26. SIADH
Overproduction or over- secretion of ADH, even when plasma osmolality is low or normal
Causes:
CNS disease
Some cancers
Drugs

27. SIADH SYMPTOMS: Hypoosmolality
Hyponatremia (as a result of excess water)
Muscle cramps and weakness
Concentrated urine produced
↑ Blood volume and ↑ ECF volume
↑ GFR
TX: Restrict Fluids, Diuretics

28. Adrenocortical Disorders: Deficiency of Adrenocortical hormones
Symptoms related to decreased aldosterone and cortisol secretion
Possible causes
Autoimmune destruction of adrenal cortex
Decrease in ACTH secretion (cortisol only)

29. Deficiency of Aldosterone and Cortisol: Addison’s disease
Cortisol Effect
Poor response to stress
Low blood glucose
Increased urine production & Weight loss
Alsosterone Effect
Reduced Na+ levels & increased K+ levels in blood
Acidosis, tremors and tetany (↑ K+)
Treatment:
Hormone replacement therapy

30. Hypersecretion of Adrenocortical Hormones
Possible of causes of hypersecretion :
Adrenal tumor
Pituitary tumor
Inappropriate over-activity of renin system (aldosterone only)

31. Hypersecretion of Cortisol
Cushing’s syndrome – hypersecretion of cortisol
Hyperglycemia accompanied by protein shortage & abnormal fat distribution
Weight gain
‘Moon face’ (adipose in trunk, face and cervical area)
Depressed immune system
Also decreases ACTH release

32. Treatment of Cushing’s
Surgery (Tumor)
Radiation (Tumor)
Cortisol Inhibiting Drugs

33. Hypersecretion of Aldosterone
Conn’s syndrome – hypersecretion of aldosterone
High levels of sodium (hypernatremia)
Hypertension
↓ potassium levels (hypokalemia)
Metabolic Alkalosis (increased bicarbonate ion concentration)

34. Treatment of Conn’s
Surgery (if a tumor)
Monitor salt and water intake

35. Why could some of these symptoms be fatal?

36. Adrenogenital Syndrome

37. Adrenal Androgens
Adrenal cortex secretes androgens, mineralocorticoids and glucocorticoids
All are derived from cholesterol by different enzyme catalyzed reactions

38. Steroidogenic Pathway: All are Derivatives of Cholesterol

39. Adrenal Androgens
DHEA is an adrenal androgen, derived from cholesterol
Is weaker than testosterone
DHEA important in females
Responsible for growth of axillary and pubic hair
Enhancement of pubertal growth spurt
Development and maintenance of female sex drive

40. DHEA Release DHEA is released under the control of ACTH
DHEA and cortisol output parallel each other
BUT…
DHEA inhibits GnRH release and not ACTH/CRH release
Levels surge in puberty, peak between 25 and 30 and then begin to decrease

41. Adrenogenital Syndrome
Excess secretion of adrenal androgens is called adrenogenital syndrome or congenital adrenal hyperplasia
Results from inherited defect in cortisol steroidogenic pathway
From this defect, Cortisol is not produced under influence of ACTH but adrenal androgens are
Results in inappropriate masculinization in all but adult males

42. Steroidogenic Pathway: All are Derivatives of Cholesterol

43. Characteristics of Adrenogenital Syndrome in Adult Females
Hirsutism = male pattern of body hair
Male secondary sex characteristics
Deepening of voice
More muscular arms & legs
Breasts become smaller
Menstruation may cease

44. Characteristics of Adrenogenital Syndrome in Infant Females
Male type genitalia develop
Enlarges clitoris (homologous to the penis)
‘Ambiguous genitalia’
Internal structures develop properly
Failure to menstruate
This is called female pseudohermaphroditism

45. Characteristics of Adrenogenital Syndrome in Pre-Puberty Males
Premature development of secondary sex characteristics
May appear to enter puberty at 2-3 years of age
This is called precocious pseudopuberty
No effect is seen in adult males!!!
Why?

46. Treatment of Adrenogenital Syndrome
All symptoms can be reversed by glucocorticoid therapy
Suppresses CRH & ACTH release
Less DHEA made & GnRH release not suppressed