Patho Test 2 Book Summary Study Ch 21, 22

Front 1

Water soluble hormones circulate throughout body unbound or bound?

Back 1

unbound…bc they are WATER soluble…they don't need to be on a carrier protein to float around. Lipid soluble hormones are bound to carrier proteins...

Front 2

receptors for hormones are? and where are they found

Back 2

proteins

ON the plasma membrane…INSIDE the cytosol, or in the nucleus.

Front 3

what are the second messengers you know of?

Back 3

cAMP, cGMP, calcium

these activate certain regulatory proteins…what are they?: cAMP: adenylyl cyclase, cGMP: guanayyl cyclase, calcium: calmodulin

Front 4

lipid soluble hormones act?

Back 4

they can bind to the plasma protein or they can do directly into the nucleus

Front 5

hypothalamus regulates many hormones including: dopamine which inhibits ____, CRH which releases ____ and substance P which inhibits ____

Back 5

prolactin…, ACTH and endorphins, acth

Front 6

ADH does what?

Back 6

yea it holds water in …but how? by increasing serum osmolalaity.

Front 7

hormones of anterior pitutitary

Back 7

AM LFT P.G. ACTH, MSH, LH, FSH, TSH, PROLACTIN, GROWTH HORMONE.

Front 8

WHAT IS ONE of the ways TSH makes TH to make

Back 8

stimulating uptake of iodine intracellular

Front 9

the thyroid gland is made of ____ which also have _ cells that release____ and __ hromones

Back 9

follicles, C, somatostatin, calcitonin (odd fact, if calcitonin is high or low doesn't do anything to humans….)

Front 10

islets of langerhans have what type of cells

Back 10

alpha, beta, delta, and F cells

Front 11

beta cells make the ____ in pancreas

Back 11

insulin

Front 12

alpha cells make ___ in pancreas

Back 12

glucagon

Front 13

incretin hromones do what

Back 13

if sugar high in body they will secrete insulin, but inhibit glucagon synthesis, and delay gastric emptying

Front 14

delta cells

Back 14

>>>stops glucagon and insulin somatostatin

Front 15

adrenal medulla secretes? and adrenal cortex secretes?

Back 15

medulla-catecholamines; epi/norepi

cortex- steroid hormones (aldosterone, adrenal androgens, estrogens) all made of ??? cholesterol

Front 16

glucocorticoids

Back 16

2 MAIN FUNCTIONS: 1. immuno supression2.) anti inflmaatory = cortisol is a glucocorticoid

Front 17

mineralcorticoids

Back 17

aldosterone….are steroid hormones…..keep na//lose K

Front 18

SIADH

Back 18

tOOOO MUCH ADH (usually from some tumor that keeps secreting ADH)

DI- too little ADH

Front 19

IN siadh IF YOU HAVE too much ADH…u are holding in a lot of water right/ this leads to what?

Back 19

hyponatremia/hypomolaity

Front 20

DI can be neurogenic/nehphrogenic..what does that mean

Back 20

(principal feautre---polyuria/polydipsia, not able to concentrate urine)neurogenic…is what the disease is….not enough ADH…nephrogenic means NOT GOOD ENOUGH RESPONSE to ADH….

Front 21

dipsogenic DI

Back 21

when upkeep drinking a lot of water to the point you will drop ADH below normal

Front 22

hypopituitarism

Back 22

dysfunction of ANTERIOR pituitary…not working well enough….ss/ depends on which hormone is not working

Front 23

hyperpituitarism

Back 23

anterior pituitary has tumor….pushes on other structures….causing HYPOsecretino of certain hormones…interesting

Front 24

too much GROWTH hormone? in adults and children causes

Back 24

adults- acromegaly

children- gigantism

these ppple have prolonged high levels of GH can cause screw up in connective tissue. all systems delveop SLOWLY.. (renal, cardiac), etc.

Front 25

GRaves disease manifestations… (we know how this occurs…)

Back 25

hyperthyroidism caused by autoimmune response…antibodies stick to th receptors and prevent negative feedback…..

ss: thyroid enlargement, enlargement of extra ocular muscles, pretrial myxedema (swelling of legs/hands)

Front 26

autoimmune thyroidits (Hashimotos disease)

Back 26

the thyroid tissue gets destroyed slowly by lymphocyte infiltration, antibody activation of natural killer cells, and apoptosis; this is HYPOTHYROIDISM and u may still see a goiter

Front 27

subacute thyroidits

Back 27

first the follicular cells are damaged…causingHYPERthyroidism due to the leak of T3 AND T 4 = hyperthyroidism

then hypothyroidism happens….so this is classified as a hypothyroidism and it is nonbacterial

Front 28

secondary hypothyroidism

Back 28

hypothalmus and pituitary dysfunction= TSH not making enough in body

Front 29

hypothyroidism main ss

Back 29

low metabolism and low heat production (always cold)

Front 30

myxedema is characteristic sign of?

Back 30

HYPOthyroidism

Front 31

myxedema is?

Back 31

what it is says…EDEMA… caused MAINLY in hypothyroidism ….of legs and sometime shands...

Front 32

what is a myxedema coma

Back 32

a medical emergency…..of hypothyroidism

Front 33

what kind of carcinoma is common of the thyroid

Back 33

papillary/follicular

Front 34

primary hyperparathyroidism is usually caused by??

Back 34

a tumor….and this will manifest as TOO MUCH chronic calcium in body…and increased bone reabsorption, and increased calcium in urine thats how much calcium is floating around

Front 35

calcium and______ have ___ relationship

Back 35

phosphate ;inverse

Front 36

which other hormone is insulins sidekick

Back 36

amylin it has 3 functions

it stops glucagon from forming and breaking down

it keeps u full after meals

and after meals it helps slow down gastric motility….therefore, if the food stays in the stomach longer then it will slowly enter blood stream also

Front 37

ghrelin and who does the opposite action

Back 37

ghrelin is secreted in gi cells when ur stomach is hungry….therefore, it will cause u to eat….and increases gastric acid secretion, etc. it is in the hypothalamus

Front 38

leptin has opposite effect..it makes u feel FULL AND GHRELIN

Back 38

secreted when u are hungry

Front 39

insulin resistance is associated with increased/decreased ghrelin

Back 39

decreased

Front 40

somogyi effect...

Back 40

basically u take some insulin at night with dinner, and in middle of night around 3 am …bs will be low, then the body reacts and releases stress hormones causes the blood glucose to rise at 7am…..it will be high! you may want to increase NPH but its dangerous to patient..so measure ….treatment…decrease dose NPH…..so then body doesn't have to compensate

Front 41

dawn phenomenon

Back 41

high blood glucose early in the morning due to growth hormone secretion in am!!!!!! thats..all…but how do u differentiate between this and somogyi? the 3AM blood glucose…will be normal here in the dawn phenomenon ….everything is normally going until 7 am….but with somogoyi at 3 am the blood sugar is LOW; TREATMENT FOR dawn? increase NPH...

Front 42

DKA can occur in both types of diabetes?

Back 42

yes

Front 43

microvascular complications from dm are associated with

Back 43

endothelial alterations and basement membrane alterations s well as thrombosis

Front 44

describe the feedback loop of cortisol

Back 44

hypothalamus>>>CRH>>pituitary gland>>> ACTCH>>>>adrenal gland>>>cortisol>>

Front 45

cushiness disease

Back 45

excessive acth= too much cortisol = immunosupression

Front 46

too much adrenal medulla function =?

Back 46

pheochromocyotoma usually causes this, which is a catecholamine producing tumor…so ss of SNS; palpitations, constipation, hypertension, glucose intolerance….