chapter 41 pathos exam 6

endocrine system

ALWAYS on negative feedback loop

pituitary gland

master gland,

anterior - most hormones are coming out of here - 2nd portal system we have

posterior - only 2 are released directly into nervous system. disconnects to axon

hypothalamus

detects state of body and monitors everything that goes on and on a negative feedback loop

problem

primary problem- the target gland is the issue

secondary - problem in the anterior pituitary

WORST tertiary- problem with hypothalamus

GH secretion

hypothalamus secretes GHRH which stimulates GH

stimulates the anterior pituitary - GH secretion

inhibits the anterior pituitary - GHIH secretion

if growing too much then you will release GHIH

growth hormone deficiency

idiopathic GH deficiency - don’t know hat caused it

MATT Laron-type dwarfism : genetic mutation where receptor does not work (does not accept growth hormone)

DO NOT give mr jones with Laron-type dwarfism GH bc will not work

everything is smaller - hands feet, proportionate

AMY and ZACK 70% of dwarfism is achondroplasia - axial skeleton is normal size but appendicular Skelton does not grow

TX- supportive, shunt - no cure

growth hormone excess

usually always associated with pituitary tumor (80% of the time).

before puberty - gigantism (80% are cured with surgery)

during puberty your ephiseal plates close- which means you’re as small as pull ever get. if you have too much GH and they go into ephiseal plates while open, you’ll keep growing. this is gigantism

TX: surgery to remove tumor. then medication to block production of GH

acromegaly (after puberty)

big hands and feet, thicker skin , enlarged face, tongue

after epipheseal plates have closed.

tx: to remove tumor and medication to block production of GH

thyroid gland hormones

anterior pituitary releases thyroid stimulation hormone

hypothyroidism

Hashimoto’s - most common thyroid underfunction disease. autoimmune

surgery could cause this, tumor removal- maybe removed too much thyroid. maybe not enough iodine.

tx- treatment all life - levothyroxine/synthroid

hyperthyroidism

graves disease - most common cause- caused by tumor

very fast

ss- prominent eyes, tachycardia, shaking , HTN, restlessness.

tx- antithyroid medication that blocks , take out some thyroid , or radioactive iodine to make t3 and t4- radioactive iodine kills the thyroid. if given too much radioactive iodine then willl be hypothyroid

goiter -

hypertrophy of the thyroid.

euthyroid - normal function

tx for hyper goiter - radioactive iodine

tx for hypo goiter - not making enough thyroid hormone, so the hypothalamus says you have to make more, hypertrophy of cells

only reason for hyperthyroid goiter is if it becomes untreated

can have goiter if normal, hyper or hypo

cortisol

increases

Addison’s disease

insufficiency of cortisol adrenal gland - primary problem

bc of trauma, damage, autominnune disease,

s/s- fatigued - no fight or flight , no appetite , darkening of the skin - JFK had Addisons was TAN. increased melanin production

tx- oral corticosteroids- bc im not making enough steroids.

Cushing syndrome

too much cortisol- stops metabolism of nutrients

s/s/- weight gain, slow healing injuries, moon face, does not break down things, anxiety and depression, extra face and body hair, irregular periods.

fragile skin bc fat in subcutaneous layer, if too much cortisol the fat layer diminishes so not enough fat to protect blood vessels, likely to be damaged skin, thinner, UNDER EYES

tx- surgery to remove tumor, or medication to inhibit cortisol,

diabetes

#7 cause of death , #1 cause of renal failure - blood glucose damages capillaries

glucose metabolism

glucose is the preferred method of metabolism, if not then fat.

insulin makes sure that glucose can get from blood to cell

cells are not permeable to glucose- need transporter

pancreas - 20% alpha - 70% beta

as endocrine function - 20% are alpha cells, 70% are beta cells, 10% are delta cells

beta- release insulin and amylin (amylin suppresses glucagon)

somatostatin - released during physiologic stress

insulin

increased blood glucose-

either used immediately for ATP or stored

insulin prevents- glycogen breakdown , fat breakdown, and protein breakdown

geek bonus

1921 insulin was discovered

1922 was mass produced

2 tons of pig and cattle pancreas to get 8 oz of insulin

beta cells of pancreas release insulin

insulin binds to insulin binding site. signals protein to move glucose transporter

glucagon

alpha cells release

it says you have to release glucose in the blood

tells us to get glucose in the blood

case scenario

insulinoma - tumor secretes too much insulin. take every last bit of glucose out of blood to cells. low glucose levels

glucagon- tells liver to release glucose for energy source. a lot of glucose ! do not give glucagonoma corticosteroids.

corticosteroids increase blood glucose

insulin makes blood glucose levels lower

insulin

lowers blood glucose levels. give corticosteroids to insulinoma

types

type 1Aand B- autoimmune - 5-10% of ppl

type 2 - beta cells of pancreas don’t work or underfunctioning -

gestational diabetes (pregnant woman has diabetes) - checked between 24-28 weeks - more likely to develop type 2 diabetes later.

type 1 DM

quarter of people w type 1 genetics.

go to doctor bc thirty all the time, hungry all the time and have to pee all the time.

losing weight bc cells can’t use glucose bc don’t have insulin

tx: insulin inject

not making insulin . can’t take pill bc would be broken down In GI tract

type 2 -90-95%

mostly lifestyle things or genetics. insulin resistance.

TX: first be told lifestyle changes, lose weight eat better. then be put on meds,

pill -need to know they all work to decrease blood glucose levels

then start taking insulin

metabolic syndrome

3/5 things to be metabolic snydome

insulin resistance, high blood pressure, high triglyceride levels, low HDL cholesterol, central obesity

tx; lifestyle changes, medication statins, beta blockers

hyperglycemia

bc insulin resistance.

complications of diabetes

diabetic ketoacidosis - most likely ICU

low insulin levels , fatty acids breakdown

only TX: insulin

exogenous insulin acts the same as endogenous insulin

hypoglycemia - not enough glucose in blood - mainly side affect of anti diabetic meds

tx: sugar

nephropathy

kidney disease - caused by systemic inflammation. glucose will damage cells, complication of diabetes. too much glucose bc not enough insulin to get rid of it

neuropathy complication

nerve damage cause by persisntely high blood glucose level.

hyperglycemia for so long it damaged nerves

tx: manage blood glucose levels frequently

diabetic foot ulcer

the most common complication of DM leading to hospitalization. caused by neuropathy.

Dm impedes the normal steps in wound healing