Endocrine

Question 1

Negative Feedback

Answer 1

• probably the most important monitoring system to see if we have enough
• can only say we don’t need it anymore; it cannot help an organ that is over producing

Example: Low TSH but high T3 & T4

when we have decreases or increases in both, then we have a problem and we must determine the problem

(possible adenoma or hypothalmic issue)

Question 2

TRH is the mothership messenger that tells the anterior pituitary which says, OK, we need to send messengers to the thyroid because we don’t have enough, then TSH goes out; TSH is underboss: is is the messenger that goes to the thyroid that ways we need more T3 or T4;

Answer 2

They thyroid is the metabolic gas pedal we have increased metabolic activity, AA, etc with Less, we have let up in the gas pedal

Question 3

Negative Feedback

Answer 3

Thyroid: They hypothalmus releases thyrotropin releasing hormone TRH. TRH causes the release of TSH (thyrotropin). TSH released from the anterior pituitary targets the thyroid gland and stimulates the release of T4 and some T3. Most of T3 is converted in teh periphery. So when there is low circulating thyroid hormones, we would expect that if the negative feedback loop is working, that there would be a high level of TSH in the blood but a low actual thyroid hormone

Question 4

Hormone effects:

direct effects

&

permissive effects

Answer 4

hormone regulation

up-regulation

down regulation

Question 5

Direct Effects

Answer 5

I am releasing a hormone and it is going to have “THIS” activity

-Ex: T4 increases metabolic activity in a lot of things

Question 6

Perissive effects

Answer 6

Ex: cortisol sensitizes the tissue to epinephrine and norepinephrine

-giving a medication will: more sensitive to

and will make things more potent because of the potentiation of things

Question 7

UP REGULATION

Answer 7

• low numbers of hormones increase the number of receptors per cell
• Lipid controlling drugs work this way:

if only a little bt, receptors will up regulate because the body needs it

-initially sweep a lot of cholesterol out of the system and the liver freaks out because it needs cholesterol to make bile and hormones, especially gonadal hormones and it aus I ned more cholesterol and I don’thave it; so it upregulates hepatocytes that pull LDL out of the system, and with lipid-controlling meds the liver never catches up so the amount of availability on the system is way down because the lier is pulling it out to create what it needs

Question 8

Down Regulation

Answer 8

High concentrations decrease the number of receptors

• when there are too many hormones in concentration, we have down regulation to say we don’t need anymore and the hormones float out in circulation
• EX: insulin sensitivity:

whenever there are a loss of hormones floating around, either the upper end or too many, cells begin to say “I don’t need that much” ad they down regulate the receptors and it leaves more of that hormone out in circulation just sitting wround. Because a person is diabetic, he has a very high circulating level of glucose, there is a ton if gluose, there is a ton of insulin and hyperinsulinemia makes the tissues sy”Woah, I don’t need that much”, so the tissues actually become less sensitive to the insulin and glusoce molecule together and they take up less of it which exacerbates the problem; we know that people who have diabetes, their insulin sensitivity is a pajor part of the problem

Question 9

Hypothyroidism

Answer 9

expected:

High TSH, low T3 and T4

Question 10

Hyperthyroidism

Answer 10

Low TSH, High T3 and T4

Question 11

Hypothalmic Pituuitary axis

Answer 11

They Hypothalmic-Pituitary axis is the basis for the neuro-endocrine system. They hypothatmus and the pituitary make up the basis for this system, which includes the feedback mechanisms. When the hypothalmus targets the pituitary with particular releasing factors, it causes the release of others that then target distant organs. When those distant organs relese their hormones, catecholamine and other substances, therei presence in the blood or their actions provide negative feedbck reducing subsequent messengers and secretion. This is the Basis for HPA.

Question 12

Hypothalmic -Pituitary Axis

Answer 12

reason why many of the decadron-type drugs for 54321

-y giving ehn a glucocorticoid, creating a false negative feedback loop (exogenous); hypothalmus is saying “I have a lot of cortisol in the system, what do I need to send?”

ACTH

Question 13

They Hypothalmus

Pituitary

and target hormones

Answer 13

AXIS

Question 14

Goes down in line:

Hypothalmus to pituitary to target hormones

Question 15

Posterior Pituitary

(neurohpyohysys)

Answer 15

stores and releases oxytocin and ADH

(both produced in they hypothalmus and stored in the posterior pituitary)

Question 16

Anterior Pituitary

(adenohypophysis)

Answer 16

stores multiple hormones including the trophic hormones

Question 17

Any hormones labeled trophic or tropic:

Answer 17

targets another endocrin hormone

Question 18

b endorphins

Answer 18

these hormones form a complex with other substances (they are ligands) to bind with other opiod receptors

Question 19

b lipotropin

Melanocyte stimulating hormone (MSH)

Answer 19

stimulate the production and release of skin pigments from the melanocytes

Question 20

FSH

Answer 20

stimulates egg maturation and sperm production. When low in women, it tends to cause amenorrhea. If low in men, loss of facial hair, decreaed libido and erectile dysfunction

Question 21

Prolactin

(luteotrophic hormone…VERY close to lutotropic)

Answer 21

Doesn’t have a known particular releasing factor, but it does have an inhibiting factor in the hypothalmus (most likely dopamine)

It is presumed that there is a releasing factor, but it hasn’t been isolated. Prolactin is also produced in other tissues in the body. Stiulates lactation and normal sexual function.

Supresses ovaian function

Question 22

Lutenizing hormone (LH)

Lutotropin

Answer 22

• increases the production and release of teroid hormones. -Surge in women releasing egg at ovulation
• defiency in women may cuse wt gain, heavy period, insomnia, irritibility

low in men-reduced testosterone

Question 23

Growth Hormone (GH)

(somatotropin)

Answer 23

Bone and muscle growth, release of insulin-like factors from the liver

Question 24

Adrenocorticotrophic hormone (ACTH)

Answer 24

The “Stress” messenger: stimulated the release of glucocorticoids (cortison which increases protein and CHO metabolism, increes anti-inflammatory factors and causes gluconeogenesis (the reason BS elevated when on steroids) and mineralocorticoid (aldosterone) and causes reabsorption of sodium

Question 25

Hyper/hypo thyroidism

Answer 25

Primary: dysfunction or disease of the thyroid gland Hyper/hypo thyroidism Thyrotoxicisis aka hyperthyroidism

Question 26

Graves Disease

Answer 26

Most common cause of hypothyroidism Pretibial myxedema - auto-immune driven - body creates antibodies to thyroid itself; diseases they thyroid and creates an over production of thyroid)

Question 27

Hyperthyroidism resulting from nodular thyroid disease

Answer 27

Goiter

Question 28

Secondary

Answer 28

alteration if pituitary TSH production

Question 29

Primary Hypothyroidism

Answer 29

Subacute thyroiditis (DeQervain's thyroiditis)=uncommon -painful, fever, inflammation, they look systemically ill -

Question 30

Autoimmune thyroiditis Hashimotos, chronic lymphocytic thyroiditis)

Answer 30

Hashimotos's is the most common cause of hypothyroidism in the USA -immune driven that almost always follows a viral infection

Question 31

Painless thyroiditis

Answer 31

Pathology says its viral (similar to hashimoto) BUT they are inflammatory with systemic symptomatology

Question 32

Postpartum Thyroiditis

Answer 32

Immune complexes attack thyroid for a short period of time usually resolves on their own

Question 33

Myxedema Coma

Answer 33

Long-standing hypothyroidism that has been untreated

Question 34

Both are disorders of the posterior pituitary

Question 35

SIADH

Answer 35

-Ectopic Secretion of ADH is the most common cause (too much ADH); will hold onto water also common after surgery For Diagnosis: normal adrenal and thyroid function must exsist - Clinical Manifetations - r/t enhanced renal water retention - hyponatremia (almost all cases = dilutional hyponatremia) Hypoosmolarity/hyperosmolarity - little solute being diluted by all the water - specific gravity would be HIGH because the urine in concentrated K+ is generally unaffected -N/V, anorexia are symptoms that will develop when fluid retention occurs

Question 36

Diabetes Insipidious

Answer 36

- insufficient of lack of ADH (dumping water without regard to how much fluid is on board) - polyuria and polydipsia - partial or total inability to concentrate the urine Specific gravity of the urine would be very low; because a lot of water beingpumped through kidneys

Question 37

Neurogenic

Answer 37

Insufficient amounts of ADH May result from head trauma water deprivation does not help

Question 38

Nephrogenic

Answer 38

inadequate response to ADH

Question 39

Hormones released

Answer 39

ACTH TSH (THYROTROPIN) GRH OR GRF (SOMATOTROPIN) B-LIPOPROTEIN Prolactin (no known releasing factor/dopamine is antagonist) Leutinizing hormone FSH B-endorphins

Question 40

Posterior Pituitary Hormones

Answer 40

- these hormones are produced in the hypothalmus and stored in the posterior pituitary until the appropriate signals tell them to release - Hormones STORED: ASH and OXYTOCIN - HORMONES RELEASED: - ADH (formerly called vasopressin) - controls plasma osmolality 1-strikes VI receptors in the periphery, causing vaso constriction because it releases calcium; calcium is important in any type of contraction becaue it binds to troponin and tropamycin which allows actin and mysin, which shorten and contraction occurs - 2- acts on V2 receptors in renal tubules: causes renal tubule to hold on to sodium, and wehre salt goes, wa-wa goes - OXYTOCIN- uterine contractions and milk ejection in lactating women/let down - Prolactin causes the production of milk - reduces the brains responsiveness to stressful stimuli, especially in the pregnant and postpartum states

Question 41

-pituitary is vascular and therefore vilnerable to ischemia and infarction

Question 42

Hypopituitarism

Answer 42

Pituitary infarction - sheehan syndrome - hemorrhage - shock Others: Head trauma, infections and tumors (post-partum hemorrhage is an example) Panhypopituitarism: all hormones are absent ACTH defiency TSH defiency FSH and LH defieciency GH deficiency (-no feedback looping is working at al, electrolyte imbalances, malaise, muslce weakness:major endocrinopathies)

Question 43

Hyperpituitarism

Answer 43

Commonly due to a benign, slow-growing pituitary adenoma -Manifestations: Headache and fatigue visual changes hyposecretions or hyper secretions of neighboring anterior pituitary hormones

Question 44

Hypersecretion of growth Hormone ACROMEGALY

Answer 44

hypersecretion of GH during adulthood - slowly progressive - Mortality: cardiac hypertrophy, HTN, athersclerosis, Type II leading to coronary artery disease - malignancies are common

Question 45

Clinical manifestations of acromegaly

Answer 45

connection tissue proliferation - enlarged tongue, interstitial edema, increase in the size and function of sebaceous and sweat glands, coarse skin and body hair - Bony proliferation: large joint arthropathy - periosteal vertebral growth - Kyphosis - enlargement of facial bones and hands and feet - protrusion of lower jaw and forehead - need for increasingly large sizes of shoes, hats, rings and gloves

Question 46

Giantism

Answer 46

GH hypersecretion in children and adolescents

Question 47

Hypersecretion of prolactin

Answer 47

- caused by prolactinomas - most common hormonally active pituitary tumor - in females, increased levels of prolactin causes amenorrhea, galactorrhea, hirsutism and osteopenia - in males, increased levels of prolactin cause hypoginadism, erictile dysfunction, impaired libido, oligospermia, and diminished ejaculate volume

Question 48

Causes: primary adrenal insufficiency (addison disease)

Answer 48

Secondary: inadequate stimulatin of the adrenal glands by ACTH or a primary inability of the adrenals to produce and secrete the adrenocortical hormones

Question 49

Cushing;s Disease

Answer 49

Causes: excessive anterior pituitary secretion of ACTH Cushing Syndrome: excessive level of cortisol, regardless of cause

Question 50

Clinical Manifestations of Cushing's

Answer 50

weight gain is the most common accumulation of adipose tissue in the trunk, facial and ervical areas (truncal obesity, moon face, buffalo hump) transient weight gain from Na and water retention may be present - Glucose inolerance - ,etabolic syndome with abdominal obesity, HTN, glucose intolerance and dyslipidemia is a common complication 50% experience an alteration in mentl status -Women may experience increased hair growth and oligomenorrhea

Question 51

Addison's Disease

Answer 51

Cause: Primary adrenal insufficiency adrenocortical hypofunction

Question 52

Clinical manifestations of Addison's

Answer 52

result from hypocortisolism and hypoaldosteronism -weakness and easy fatigability hyperpigmentation and vitiligo hypoglycemia as condition progresses=anorexia, n/v. diarrhea greatest concern is hypotension that can progress to complete vascular collapse and shock disturbances in mood and motvation are common -women may lose axilarru and pubic hair

Question 53

Causes of hyperfunction of the adrenal medulla

Answer 53

caused by tumors fromthe chromaffin cells of the adrenal medulla - pheochromocytomas (tachycardia, HTN, palpitations, A-Fib) - secrete catecholamines on a continious or episodic basis

Question 54

SXS

Answer 54

R/t chronic affects of catecholamine secretion HTN most commoon sign (r/t increased pvr) (HTN may be sustained or paroxysmal) diaphoresos, tachycardia, palpitations and severe headache

Question 55

causes acute complications:

Answer 55

Acute compliations of DM: -hypoglycemia -DKA \*insulin deficiency \*decreased glucose use, ketosis, metabolic acidosis, osmotic diuresis \*usually treated with Type I \*illness, trauma, surgery, emotions \*total body (not serum) potassium defiency cerebral edema, especially in children

Question 56

Hyperosmolar hyperglycemic nonketotic syndrome

Answer 56

usually associated with type 2 higher glucose less ketosis severe dehydration and potassium deficit greater fluid loss

Question 57

Chronic complications of DM

Answer 57

Hyperglycemia and nonenzymatic glycosylation hyperglycemia and polyol pathway -sorbitol and fructose increase intracellular osmotic pressure (attracts water leading to cell imjury cecause increased tonicity sucks fluid in) Evident in Kinase C -enzyme inappropriately activated by hyperglycemia \_RBC's, eyes, kidneys can utilize sugar without insulin MICROvascular disease: Retinopathy diabetic nephropathy Lab Values

Question 58

Type I DM 2 Types: Immune and non-immune

Answer 58

Demonstrates pancreatic atrophy and loss of beta cells =macrophages, T & B Lymphocytes, and natural killer cells are present

Question 59

genetic susceptibility 15% of family memner with DM type I will have it environmental factors immunolocigallu mediated destruction of beta cells

Question 60

Clnical manifestations of type I DM

Answer 60

hyperglycemia - 80-90% of the function of insulin secreting beta cells in the islet of Langerhans is lost - polydipsia, polyuria, polyphagia, weight loss an fatigue

Question 61

Type 2 DM

Answer 61

dysfunction of the pancreas affects adults and children genetic environmental interaction increased insulin resistance decreased secretion of insulin metabolic syndrome Treatment: exercise, treatment of obesity, medication manifestations: recurrent infections, vision problems, neuropathy

Question 62

Hypoglycemia

Answer 62

Hypo SXS cold, clammy skin tremblinig or nervousness loss of motor coordination and function irritabilty or confusion blurred vision headache -nausea/stomach pain fainting/unconsciousness

Question 63

Hyperglycemic

Answer 63

SXS increased thirst and urination sweet odor to breath fatigue agitation and confusion high levels of ketones in the urine weight loss

Question 64

DKA

Answer 64

insulin deficiency decreased glucose use, ketosis, metabolic acidosis, osmotic diuresis usually treated with type I illness, trauma surgery, emotions Total body (not serum) potassium deficiency cerebral edema, especially in children

Question 65

HHNK hyperosmolor hyperglycemic nonketotic syndrome

Answer 65

usually associated with type II higher glucose less ketosis severe dehydration and potasium deficit greater fluid loss

Question 66

Difference with DKA and HHNK

Answer 66

patient with HHNK will have sufficient insulin to take care of enough glucose getting in the tissues and to suppress lipolysis (breakdown of fat)=get hyperglycemia dn superdehrdrated; no ketosis and usually not acidoic DKA: Uses fat as a source, does have metabolic acidosis, do become ketotic -CMP-High CO2 and a large anion gap; tells you that there are other anions that are NOT being accounted for CO2 is really a measure of Bicarn -bicarb+dissolved CO2+carbonic acid; 95% bicarb

Question 67

Macro-vascular changes in DM

Answer 67

coronory artery disease (most common ause of death in personw with type 2 and prevalence increases with duration of the disease) - Stroke - peripheral arterial disease

Question 68

Micro-vascular complications with DM

Answer 68

retinopathy diabetic nephropathy

Question 69

Insulin

Answer 69

regulated by chemical, hormonal, neural mechanisms - synthesized from proinsulin - cleaved into c peptide and insulin - can check c peptide levels and get an accurate measure of insulin levels - Secretion promoted by increased blood glucose levels - Purpose of insulin as intracellular transport mechansim - facillitates intracellular transport of K+ - facilitates the rate of glucose uptake into body's cells - sensitivity of the insulin receptor is key in maintaining normal cellular function (insulin resistance) - electrolytes that insulin transports - facilitates intracellular transport of K+