Endocrine Disorders

physiological systems responsible for homeostasis

autonomic nervous system, endocrine system

automonic nervous system regulates homeostatis through

direct neural innervation (rapid)

endocrine system

network of glands and organs producing hormones to control bodily functions

secreting cells

in glands, make and secrete hormones to deliver in the blood

receiving cells

only respond with the specific receptor to that hormone

specificity of hormonal response is based on

which cells have the receptor for that hormone (we dont pick where they go)

blood vessels are known as the

highways of the endocrine system

endocrine system issues are usually in

magnitude of secretion or error in number or function of receptors

hypothalamic pituitary axis (HPA)

communication system connecting neurological signals to the endocrine response

hypothalamus

area of brain producing hormones to control various functions, connects the nervous system and endocrine system by the pituitary gland

pituitary gland

sends out the signal to the body via hypothalamic control

HPA is regulated by

negative feedback loops to produce exactly the right amount for your body - effector hormone in blood inhibits its own production

posterior pituitary gland

controlled by neural connections to hypothalamus and releases anti-diuretic hormone and oxytocin

anti-diuretic hormone (vasopresin)

increases Na and H20 reabsorption which increases blood volume, potent vasoconstrictor - increases BP (effector hormone)

anterior pituitary gland

reponds to releasing hormone secreted from the hypothalamus via blood vessel conection

effector hormones

physiological action - dont need a target gland

anterior pituitary effector hormones

growth hormone and prolactin

growth hromone

increases growth in multiple tissues, stimulates liver to release insulin-like growth factor

prolactin

lactation/milk generation

stimulating hormones

have to go to target gland to tell that gland to make a hormone

anterior pituitary stimulating hormones

adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone (TSH), luteinizing hormone (LH), follicle-stimulating hormone (FSH)

ACTH stimulates

adrenal gland

TSH stimulates

thyroid gland

LH stimulates

gonads

FSH stimulates

gonads

primary endocrine disorder

dysfunction of peripheral gland itself

hypersecreting primary endocrine disorder

target gland starts producing way too much effector hormone, lots of negative feedback: HIGH effector, LOW stimulating

hyposecreting primary endocrine disorder

loss of target glandular tissue, no negative feedback at all: LOW effector, HIGH stimulating

secondary endocrine disorder

system controlling gland is dysfunctional (usually pituitary gland)

hypersecreting secondary endocrine disorder

pituitary gland is secreting lots of stimulating hormone, causing high release of effector hormone: HIGH effector, HIGH stimulating

hyposecreting secondary endocrine disorder

signal from pituitary gland is lost, no stimulus to produce is occurring regardless of negative feedback: LOW effector, LOW stimulating

thyroid stimulating hormone causes what release from thyroid gland

thyroxine T4 and triiodothyronine T3

thyroxine T4 is

converted to T3 in the blood

triiodothyronine T3 causes

enhanced SNS activity (increased metabolic rate, increased HR/contractility, increased muscular excitability, increased GI motility)

hyperthyroidism

autoimmune cells producing thyroid stimulating immunoglobulins that attach to TSH receptors and cause hypersecretion of T3 and T4 (grave's disease)

clinical manifestations of hyperthyroidism

goiter, nervousness, heat intolerance, hyper-metabolism, elevated SNS activity, exopthalamos

goiter

visible bulge in anterior neck

hypermetabolism from hyperthyroidism

weightloss, diarrhea, nutritional deficiency

exopthalmos

swelling behind eyes pushes eye forward and causes bulging eyes

medical diagnosis of TSH is via

TSH or TSI levels, or via radioactive iodine uptake (thyroid cells are the only ones to take up iodine - hyperactive will light up)

hyperthyroidism treatment

anithyroid medication (inhibits thyroid hormone release), radioactive iodine ablation, surgery

PT implications of hyperthyroidism

neuromuscular manifestations - chronic peri-arthritis, calcific tendonitis, proximal muscle weakness, respiratory muscle weakness - reduced exercise tolerance

parathyroid removal would

cause hypocalcemia (parathyroid regulates Ca2+)

hypothyroidism

usually primary via loss of thyroid tissue

clinical manifestations of hypothyroidism

fatigue, sensitivity to cld, weight gain, diffuse muscle tenderness and trigger points, carpal tunnel syndrome, proximal muscle weakness, muscle/joint swelling, bradycardia, decreased BF, myxedema

myxedema

increased water in layers of the skin, nonpitting/boggy edema, thickened tongue, laryngeal/pharyngeal structures (dermis has too much sugars and draws H20 - not starlings)

medical diagnosis for hypothyroidism

low TH, high TSH

treatment for hypothyroidism

hormone replacement therapy

PT implication for hypothyroidism

non-inflammatory joint effusion, skin prone to tears (pressure ulcers), decreased exercise tolerance, replacement therapy should reduce musculoskeletal symptoms

ACTH from anterior pituitary causes

adrenal gland release of cortisol and aldosterone

aldosterone acts to

increase Na/H2O and blood vol at kidney

cortisol acts to do what at liver

increase gluconeogenesis (need sugar to fuel metabolism to heal)

cortisol acts to do what at blood vessels

vasoconstrict with NE

cortisol does what at bone

increases resorption

cortisol does what at adipose

increases lipolysis

cortisol does what at all tissues

antiinflammation to decrease amount of response (decrease side effects), increase protein breakdown, block glucose entry at non essential tissue

adrenal insufficiency

problem with gland and cant produce aldosterone or cortisol

primary adrenal insufficiency includes

addison's disease, adrenal radiation, adrenal neoplasm

secondary adrenal insufficiency

steroid-induced ACTH suppression, body perceives it as cortisol and inhibits ACTH via negative feedback

steroid induced ACTH suppression drugs should be

weened off of to get the glands ready to get cortisol levels back, 1:1 ratio of time on drug to time of cortisol return, >1 year on drug may never get cortisol levels back

addison's disease

autoimmune disease that destroys the adrenal gland

adrenal gland atrophy leads to

low cortisol and aldosterone

glucocorticoid insufficiency

decreased gluconeogenesis, resistance to infections/trauma/stress, loss of negative feedback causing increased ACTH and melanocyte stim hormone (pigmentation of skin)

mineralcorticoid insufficiency

fluid and electrolyte imbalance without Na/H20 reabsorption

clinical manifestations of addison's disease (primary adrenal insufficiency)

weak, weight loss/nausea, depression, hypoglycemia, hyperpigmentation, dehydration/HTN, reduced stress tolerance

medical diagnosis for adrenal insufficiency

blood and urine labs, cortisol response to synthesic ACTH (fail to release = positive finding for primary adrenal insufficiency)

treatment for adrenal insufficiency

synthetic cortisol and aldosterone

PT implications for adrenal insufficiency

minimize stress response, no aquatic therapy, risk of adrenal crisis (acute shutdown sx)

cushing's syndrome

somethign causing elevated cortisol (common from taking steroids)

primary hypercortisolism

ACTH independent, from corticosteroid use or adrenal tumors

secondary hypercortisolism

ACTH dependant, cushing disease: tumor on pituitary gland stimulating ACTH release and increasing cortisol release

clinical manifestations of cushings syndrome

obestiy/moon face, buffalo hump, osteoporosis, cardiac hypertrophy/hypertension, thin skin, ammenorrhea, muscle weakness

obesity/moon face and buffalo hump are because

increased cortisol causes fat resdistribution - accumulates at face, neck, back, etc.

osteoporosis with hypercortisolism

cortisol stimulates osteoclasts and inhibits osteoblasts, permitting bone breakdown

cardiac hypertrophy/hypertension with hypercortisolism

increased cortsiol acts like aldosterone at high amounts, increasing Na/H2O reabsorption

thin/wrinkled skin and abdominal striae with hypercortisolism

from low protein, prone to pressure ulcers, purple streaks on abdomen - differential diagnosis from stretch marks/obesity

medical diagnosis of hypercortisolism

blood levels of cortisol and ACTH, dexamethasone stress test - fail to suppress is a positive finding for unregulated cortisol production

treatment for hypercortisolism

radiation, drug therapy, surgery, high protein diet

PT implications with hypercortisolism

watch for sx, monitor vitals, precatiosn (osteoporosis), pressure ulcers risk

somatopause

decreased growth hormone production with age - causes more adiposity and less lean muscle mass

menopause

decreased sex hormones with age, low estrogen causes decreased bone health, icnreased risk of heart disease and UTI

adrenopause

decreased ability to release adrenal gland hormones with age, low cortisol causes increased pain response to trauma, low tolerance of physiological stress/infection

postural hypotention

blunted baroreceptors with age, slower neural feedback, vulnerable for dehydration