Physio 2 - Endocrinology 2

drraythe's version from 2015-06-09 01:45

Endocrine pancreas-- DIABETES MELLITUS

Question Answer
**what is the definition of diabetes mellitus (DM)?an absolute or relative lack of insulin leading to impaired carb, lipid, and protein metabolism
What is Type 1 DM?aka insulin dependent DM= IDDM= ABSOLUTE LACK OF INSULIN
what causes Type 1 DM?islet cell destruction b/o pancreatitis, senile degeneration, autoimmune dz
in Type 1 DM, what is the blood glucose level? what is the insulin level?high blood glucose, low insulin
species prone to Type 1 DM?most common in DOGS (esp. middle aged to old). (cats 20-30% of DM, middle aged to old, humans is juvenile form 10-20%)
what is Type 2 DM?aka non-insulin dependent DM= IDDM= decreased sensitivity to insulin (why=??), receptor numbers are dec, receptors are changed, faulty signal xmission--> impaired binding or insulin action= INSULIN RESISTANCE= RELATIVE lack of insulin
basic pathogenesis of Type 2 DM starting with "hyperglycemia"hyperglycemia --> constant insulin release --> hyperinsulinemia --> Beta cells become exhausted --> insulin levels can return to normal or fall below normal levels
what causes Type 2 DM?UNKNOWN, obesity is often a predisposing factor (via a lipid metabolite??) and can often be reversed with a loss of body weight
species preferences for Type 2 DM?CATS #1, 70-80% of DM (inc b/o obesity, age)
what is Secondary/ Type 3 DM?aka transient DM, it is secondary to eg) excess cortisol, growth hormone, progesterone levels causing insulin-resistance and/or activated gluconeogenesis
how common is type 3 DM in vetmed? Is it reversible?common. yes it's reversible.
which DM(s) are reversible?Type 2 is often reversible with weight loss. Type 3 is reversible if you treat the underlying cause.
what does an absolute/relative lack of insulin mean for glucagon? why?absolute/relative EXCESS OF GLUCAGON, b/c glucagon cells (A-cells) are INSULIN SENSITIVE
how does DM cause a CATABOLIC SITUATION (pathophysiology) (3)(1) persistent hyperglycemia b/o reduced cellular glc uptake and inc gluconeogenesis (2) reduced glycogenesis and prot syth (no glc in cell to make this stuff) (3) inc lipolysis and proteolysis=== catabolic situation
**box: what are the three main problems with DM?(1) hyperosmolality of plasma (lots of glc in it) (2) lipolysis exceeds energy demands (3) glc dependent tissues get too much glc
how does DM affect urinating? how?hyperglycema --> exceed renal threshold of reabsorption --> glucosuria/osmotic diuresis= POLYURIA
how does DM affect drinking? how?hyperosmolality+polyuria--> intra and extracellular dehydration--> possibly hypovolemic shock/CNS damage/anuria/coma/death, compensation by drinking= POLYDIPSIA
how does DM cause weight loss?the proteolysis causes the weight loss, mm weakness, and reduction of organ fxns
how does DM affect lipolysis? what does this lead to?excessive lipolysis --> fatty liver and ketoacidosis --> diabetic coma
what can cause a diabetic coma (not sugar related)the excessive lipolysis --> fatty liver and ketoacidosis --> diabetic coma
how does DM affect appetite? Over time what happens?INITIAL polyphagia (b/c hypothalamic satiety center is insulin-dependent) then LATER, ANOREXIA/ vomiting following tissue damages a/o acidosis
what are the 4 things that happen with long withstanding hyperglycemia?(1) formation of glycated proteins (bad) (2) cataract/lens + nerve damage (3) glycated proteins/acidosis/proteolysis/swelling (4) prone to infections, esp in urinary tract
why are glycated proteins formed? examples?excess glc is entering glc-dependent cells b/c it can't enter the independent ones. ex) defective Hb A, defective myelin in nerve sheaths, fructosamines in plasma
what is a fructosamine? why do we care?It is a glycated protein, it is DIAGNOSTICALLY IMPORTANT! signals 2+ weeks of elevated blood glc, allows the practitioner to differentiate DM from inc glc due to stress
how does DM cause cataract/lens and nerve damage?excess glc converted to SORBITOL which is osmotically active --> swelling --> cataract+lens+nerve damage
the substance responsible for cataract/lens and nerve damage in DM?sorbitol
in DM the glycated proteins/acidosis/proteolysis/swelling have two main effects(1) structural changes in blood vessels (microangiopathies- eg: glomerula) (2) nerve damage (neuropathies- eg: TIBIAL NERVE DAMAGE IN CAT, retinal problems in humans)
why are animals with DM prone to UTIs (/infections)?because the excess glucose in the urine is feeding the bacteria that live there, allowing more growth
What is the level of glucose at which it shows up in the urine?180mg/gl glc

Hypothalamic/ pituitary system

Question Answer
what is the major integrating link between the nervous and endocrine systems?hypothalamus
where does the hypothalamus receive input from?various other CNS regions (thalamus, limbic system, cortex, RAS, and sensory signals from visera and eye)
what does the hypothalamus largely control?HOMEOSTASIS (eg osmolality, body temp, ANS)
what controls body homeostasis?hypothalamus
what is involved with emotions/stress/fear/control of hunger/thirst/sexual behavior?the hypothalamus
**box. What is the important thing to know about the hypothalamus and the endocrine system?it is a MASTER endocrine gland- its many neuroendocrines influence other CNS areas as well as various peripheral endocrine glands VIA the pituitary
what does "-tropin" mean?stim an endocrine gland to secrete their own hormone
what does "-trophic" mean?stim growth (there's an h in growth)
how are the hypothalamus and the pituitary physically related to each other?they are connected by the hypophyseal stalk
what are the portions of the pituitary gland?anterior, posterior, pars intermedia
describe the anterior pituitary gland"Adenohypophysis", formed from rathke's pouch= GLANDULAR epithelium which produces/secretes hormones under hypothalamic control
describe the posterior pituitary gland"neurohypophysis", EXTENSION of the hypothalamus= NERVOUS tissue which stores and releases the two hypothalamic hormones produced in the nucleus supraopticus and nucleus paraventricularis (ADH and OXYTOCIN)
what does the HYPOTHALAMUS produce/secrete upon stimulation, which do what? (what two kinds of hormones, which are released where and go where?)Releasing hormones (RH) and/or Inhibiting hormones (IH) which are released into the hypothalamic-hypophyseal portal system--> RH/IH reach the anterior pituitary gland (adenohypophysis)
what happens when RH/IH reaches the anterior pituitary?they stim/inhibit production and release of hormones from the ant. pituitary gland into circulation= Tropic hormones (mostly)
what kind of hormones does the ant pituitary release (mostly)?Tropic (have other endocrine glands as targets)
name the three steps of the hypothalamic-pituitary system in order?Hypothalamus--(hormones)--> Ant. pituitary --(hormones)--> peripheral endocrine glands (release their own hormones)
what are the parts of the hypothalamic-pituitary-endocrine axis?hypothalamus, ant. pituitary, peripheral endocrine glands
what are the 7 main hormones of the hypothalamus?TRH (thyrotropin releasing hormone), CRH (corticotropin releasing hormone), GnRH (gondadotropin releasing hormone), GHRH (growth hormone releasing hormone), GHIH (growth hormone inhibiting hormone--=somatostatin), PIH (prolactin inhibiting hormone--=DOPAMINE), PRH (prolactin releasing hormone)
what is somatostatin, where does it come from?aka growth hormone inhibiting hormone, released from hypothalmus
what are the 6 hormones of the anterior pituitary?Thyrotropin (thyroid stim hormone aka TSH), Corticotropin (adrenocorticotropic hormone aka ACTH), Follicle stimulating hormone (FSH), Luteninizing hormone (LH), Growth hormone (somatotropin aka somatotropic hormone aka ST(H) ), prolactin
what are the 4 glands which the hypothalamic-pituitary system target?thyroid, adrenal cortex, gonads, liver (there are also some which don't have a peripheral gland, just direct effects)
if the thyroid gland is targeted, what hormone(s) is released/inhibited?thyroid hormones
is the adrenal cortex is targeted, what hormone(s) is released/inhibited?glucocorticoids
if the liver is targeted, what hormone(s) is released/inhibited?somatomedins
describe path if hypothalamus releases TRHthyrotropin releasing hormone released from hypothalamus --> thyrotropin (TSH, thyroid stim hormone) released from ant pituitary --> stim thyroid gland to release thyroid hormones --> target mult tissues
describe path if hypothalamus releases CRHcorticotropin releasing hormone from hypo. --> corticotropin (adrenocorticotropic hormone, ACTH) released from ant pit --> adrenal cortex releases glucocorticoids --> target mult tissues
describe path if hypothalamus releases GnRHgonadotropin releasing hormone from hypo --> FSH and/or LH (follicle stim, leutinizing) from ant pit --> gonads release sex hormones --> target mult tissues
describe path if hypothalamus releases GHRH/GHIHgrowth hormone releasing (or inhibiting) hormone from hypo --> inhibit or stim growth hormone (somatotropin/STH) from ant pit --> those target liver (there are also direct effects) which releases somatomedins --> targets mult tissues
describe path if hypothalamus releases PIH or PRHprolactin (inhibiting/releasing) hormone from hypo --> stim prolactin release/inhibition in ant pit --> gives direct effects onto mammary gland