exam 3 physio even better

Thymus

Helps t-cells fight, after 40, it becomes nonexistnet

Pancreatic islets

part endocrine/exocrine

Pineal gland

produces melatonin in darkness. Sun inhibits

Diabetes

Type1: juvenile diabetes, plasama insulin

type 2: adult onset, insulin resistence, sometimes malfunction insulin which is when they would take insulin

the big three: polyuria, polydipsia, polyphagia

Victoza

medicine for diabetes

Saxenda (liraglutide)

for obesity

Numbers for diabetes

anything greater than or equal to 6.5% A1C, greater than or equal to 126 mg.dl, look for numbers abover 200 or above for everything else

Interleukins-6

low grade inflammation due to obsesity, hypertensive

Herring bodies

in the antieror pitutary, buldged terminals that contain ADH and OT in the pars nervosa from the superoptic nuceli (ADH) and the paraventricular nuceli (OT)

Exocrine

duct

endocrine

system

short loop

pituitary back to hypothalamus. TSH inhibiting TRH, and ACTH inhibiting CRH

Hypothalamic-hypophyseal-Thyroid axis

Hypothalamus→ TRH→pituitary gland→ thyroid gland →cells

Hypothalamic-hypophyseal-adrenal axis

same but CRH —> ACTH → ACTCh stimulates cortisol release

Issues with growth

not enough secretion of IGF-1 from liver

Achondroplasia

dwarfism, epiphyseal plates have cells and these plates cause growth because cartilage is growing. Cells are not dividing with achondroplasia

Acromegaly

overproduction of Gh and IGF-1. Tumors. bone growth in girth, not linear . The happy gilmore guy

Central diabeted insipidus

not enough ADH.AVP being made

Nephrogenic diabetes insipidus

When ADH binds to v2r, it allows it to become permable and AQP2 can pass through. AQP3 and 4 are always expressed, but you can’t move water from lumen to apical side without ADH. This condition is when you lose water and ADH does not do its job.

V2 and V2 for nephrogenic

V1 blood vessels, V2 kidneys

Secondary active transporter for thyroid gland

Na/I symporter. We only need iodide for thyroid hormone GO OVER THE CYCLE

Deiodinase

makes t3 from t4. t4 is a t3 reservoir. More t4 than t3, t3 is the only active one, but we cut out both

Hyperthyroidism

high t3/t4 graves disease. Treatment: antithyroid agents, radioiodine therapy, thyroidectonmy. Take methimazole

hypothyroidism

low t3/t4 Hasimotos, Take synthroid (we wanna cause spike in T4 NOT t3).

Catabolic

Breaks down molecules and releases energy, like vitamin D, cataboklic because it breaks down bones

Anabolic

Drives growth and repair and protein synthesis

Bones are composed of

hydyoxyaptite (too much of this causes brittle bone disease) and collagen (too much of this causes osteomylagia, rickets. Bones bend too much)

Tendon

epi and perimycim, dense connective tissue

Osteoblast

rank ligand

osteoclast

rank receptor

OPG

dummy receptor, stops clast

Evisa

increases bone density for women and increases OPG/RANKL because the dummy receptor makes clast not bind to RANk receptor and prevents clast

pulsed PTH

calcium release, anabolic, helps with osteoporosis because you’re pulsing stuff.

calcitrial

pth goes throug kidney and goes. to cacitriol which is the active form of vitamin D3 and helps parathyroids

Hyperparathyroidism

weakness, bone pain, osteoporosis, a lot of plasma calcium. Cause is more plasma parathyroid due to parathyroid adeoma. Treatment:parathyroiddectomy

Hypoparathyroidism

presentation: LESS calcium, cramping, twitching, tetany. Cauase: down plasa due to thyroiddectomy or autoimmunity. Treatment: more calcium, PTH therapy

Islets of Langerhans

the 1% of pancreas that is endocrine.

Zone Glomerulosa Cells

Produces miniralocorticoid aldosterone Stimulated by ACTH and ang 2. Effector cells are in DCT and collecting ducts of kidney. NA+ and K+ goes up, Na+ reabsorption up, H20 reabsorbtion up.

Zona Fasciculata Cells.

Produce cortisol. Stimualted by ACTTH. glucose up, cortisol up. antagonizes insulin reception. Involved in Addisons disease. and adrenal insufficiency.

Zona reticularis

produces androgens, DHEA and androstendedione. stimulated by ACTH. weak masuclizing effects and intermediates for testosterone and estrogen production. Performance enhancing and Congenital adrenal hyperplasic. similar to PCOS. ANDROSTENEDIONE IS BANNED NOW.

Adrenal insufficiency

Weakness, hypotension, hyperpigmentation, salt craving, Causes: low cortisiol bc of sterioid withdrawl. Addisons disease. Treatment: hydrocortisone and fludorcortisone. Primary: adrenal cortex is damaged, low cortisol, high ACTH, high CRH. Secondary:pituitary not producing enough ACTH, cortisol is low, ACTH is low, CRH is high because of reduced cortisol feedback. Tertitary: everything low.

Adrenal Excess

Round face, red cheeks, humpback, obsesity, hypertension, osteoporosis. Cortiisol up, cushings syndrome and disease. Treatment: tumor resection, mineralcorticoid biosysnthesis inhibitors. inverse relationship, everything is high.

Muscle cells

true syncytion, many cells fused together, we have the same muscle we were born with

Sarcolemma

myotcites excitible with RMP of -85mv. established by k+ leak and CIC-1 chloride channels

Motor end-plate

region of sarcolemma and the convoutions are junctional folds. nACHrRs and ligand gated channels are inside. VOLTAGE GATED ARE OUTSIDE MOTOR END PLATE

Lateral sacs at the end of sarcopalsmic reticulium

calcium leaves and helps the fibers slide. Get calcium oiut by alpha motor neuron and graded potentials. t-tubules (which are sarcolemma) helo it. You could fall out the end of the t-tubule

calsequestirian

protein binding calcium to lateral sac

What is resposbile for the piveting?

ADP and P falling off of myosin head

Muscle dystophy

dystrophin is bad

What does calcium bind to once released from SR WILL BE ON EXAM

troponin