Anatomy and Physiology 2 Chapter 18 - Hormonal Imbalances

hyposecretion

underproduction

hypersecretion

overproduction

hyposecretion of ADH leads to

diabetes insipidus (AVP-D and AVP-R)

2 things about diabetes insipidus (AVP-D and AVP-R)

1. ADH deficiency due to hypothalamus or posterior pituitary gland damage or resistance of receptor

2. excess urination leads to dehydration

hypersecretion of ADH leads to

SIADH (syndrome of inappropriate ADH secretion)

2 things about SIADH (syndrome of inappropriate ADH secretion)

1. too much ADH leads to high blood pressure

2. retention of fluid and headache occur

hyposecretion of GH leads to

pituitary dwarfism (Lionel Messi): decrease in bone and muscle growth

hypersecretion of GH leads to what 2 things

1. gigantism (children) = excessive growth and height

2. acromegaly (adults) = excessive growth to hands, feet, facial features, etc.

hyposecretion of gonadotropins leads to what 2 things

1. no sexual maturity (children)

2. no functional sperm or eggs (adults)

hypersecretion of ACTH leads to what 2 things and is stimulated by what

1. GAS (general adaptation syndrome)

2. CRH rhythms off

*stimulated by stress, fever, and hypoglycemia

hyposecretion of the TH leads to what 2 things

1. cretinism (children) = mental and physical retardation

2. myxedema (adults) = low basal metabolic rate (BMR); lethargic, swelling

hypersecretion of the TH leads to what

Grave’s disease

2 things about Grave’s disease

1. > 160% basal metabolic rate (BMR) = hungry, weight loss, edgy

2. protruding eyes from sockets due to using all lipid reserves

hyposecretion of the PTH causes

muscular weakness, neurological problems (requires greater excitability)

hypersecretion of the PTH leads to

weak and brittle bones, gall and kidney stones

hyposecretion of the adrenal glands leads to

Addison’s disease

3 things about Addison’s disease

1. involves deficits in mineralocorticoids (aldosterone)

2. decrease in glucose and Na+ levels

3. weight loss, severe dehydration, and hypotension

hypersecretion of the adrenal glands leads to

Crushing’s disease

3 things about Crushing’s disease

1. depresses cartilage and bone formation

2. inhibits inflammation

3. depresses immune system

hypersecretion of gonadocorticoids leads to

congenital adrenal hyperplasia

4 things about congenital adrenal hyperplasia

1. not noticeable in adult males

2. females and prepubertal males:

   1. females = facial hair, masculine pattern of body hair, clitoris resembles small penis

   2. prepubertal males = maturation of reproductive organs, secondary sex characteristics emerge early

what is GAS

a stress response that can cause short-term and long-term effects and has 3 phases

5 short-term effects of GAS

1. heart rate increases

2. blood pressure increases

3. bronchioles dilate

4. blood flow changes, reducing GI activity, and urine output

5. metabolic rate increases

5 long-term effects of GAS

mineralocorticoids (aldosterone)

1. kidneys retain Na+ and water

2. blood volume and blood pressure rise

glucocorticoids (cortisol)

1. proteins and fats converted to glucose or broken down

2. blood glucose increases

3. immune system suppressed

3 phases of GAS

1. alarm phase: use epinephrine and norepinephrine; used for fight or flight response and for a very short time

2. resistance phase: use glucocorticoids (cortisol); last longer than a few hours

3. exhaustation phase: last for weeks or months; use proteins for energy due to using lipid reserves

what are the 4 cell types of the pancreas

1. alpha cells: glucagon

2. beta cells: insulin

3. delta cells: identical GH-IH hormone; suppresses release of glucagon and insulin by other islet cells and slows food absorption and enzymes secretion rates

4. PP cells: pancreatic polypeptide cells; inhibits gallbladder contractions and regulates pancreatic enzyme release

what is diabetes mellitus and 3 things about it (generalized)

accumalation of glucose in blood and urine due to faulty glucose (hyperglycemia and glycosuria)

1. more fatty acid metabolism means we can’t make ATP from glucose

2. more protein break down (starving tissue)

3. insulin dependent cells drowing in glucose

how does type I diabetes mellitus occur and 3 things about it

beta cells destroyed (hyposecretion)

1. injury, autoimmune

2. insulin pump to survive

3. most cases occur in childhood

how does type II diabetes mellitus occur and 3 things about it

beta cells are good, but insulin receptor issues (hypoactivity due to down-regulation)

1. often associated with obesity

2. seems to be a genetic component

3. potential environmental factors

2 long term problems of diabetes mellitus

1. more fatty acids in the blood

2. capillary proliferation because of so much glucose:

   1. blindness (retinopathy)

   2. pain (neuropathy)

   3. kidney failure (nephropathy)

   4. reduced peripheral circulation (tissue death, ulceration, susceptible to infections)

   5. heart attacks

3 signs of diabetes mellitus

1. polyuria: high volume urine output

2. polydipsia: excessive thirst

3. polyphagia: excessive hunger and food consumption