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NURS 350 patho endoc

Patho endocrine function/alterations

QuestionAnswer
main functions of endocrine system fetal repro/cns diff/growth-devel/repro, homeostasis/corrective measures
1st messenger hormones (fat soluble) plasma carrier protein, steroid hormone binds, through cystol to DNA--> mRNA -->ribosome-->protein
Water soluble hormones use 2nd messenger. Name 2 examples cAMP and IP3-Ca (inositol triphosphate)
MOA cAMP hormone binds receptor. GTP binds G protein. ATP transformed by Adenyl cyclase to cAMP which is 2nd messenger.
Once cAMP activated, what actions does it take activates protein kinases --> activate/deactivate specific enzyems. OR direct gene transcription, protein synthesis. ----- Example ---- how epi stimulates break down of glycogen to glucose
in the IP3 inositol triposphate 2nd messenger system, what happens after G protein activated G protein uses enzyme phospholipase C --> IP3 which binds to ER. When IP3 binds it opens the Ca++ channel. Ca++ leaves ER to cystol where it may trigger ---exocytosis ---binding to calmoudulin (which alters pmem, contractile pros and enzymes)
5 mechanisms for hormonal alterations to occur * over/under secretion *receptor number decreases *Abs against receptors *receptor dysfunction (mutations, etc) *ectopic hormone release not sensitive to feedback mechanisms
hormones released by posterior pituitary oxytocin, ADH
hormones released by anterior pituitary *TSH *ACTH *FSH/LH *GH *PRL *endorphins
what causes SIADH and definition ectopic source oat cell/lung inf/drugs --> TOO MUCH ADH
what disease manifests with water retention, hyponatremia and hypoosmolality SIADH serum Na <135, osmolality <280.
Clinical manifestations of SIADH *neuro: hyponatremia --> seizures, deficits *HF *GI cramping, vomitting (no diarrhea)
What causes DI and definition neurogenic hypothal/post pit OR nephrogenic OR psychogenic --> TOO LITTLE ADH
what disease manifests with polydyspia, polyuria, dehydration, hyper serum osmolality, hypo urine osmolality diabetes insipidus - inability to concentrate urine due to low ADH
diseases of the anterior pituitary can lead to hypopituitarism or hyperpituitarism or panhypopituitarism
hypopituitarism caused by infarction, disease, trauma, infections, surgery and infections which affect anterior pit or hypothalmus primary or secondary.
panhypopituitarism absense of ALL pituitary hormones. of particular importance ACTH followed by TSH, FSH, LH
ACTH deficiency bwo panhypopituitarism results in ACTH deficiency which impacts ---cortisol (life threatening)---- aldosterone (Na reabsorption)
manifestations of ACTH deficiency n/v/anorexia ---fatigue---hypoglycemia---decreased aldosterone-->serum hyponatremia. IF ACTH completely absent may need cortisol to sustain life
hyperpituitarism - what hormones affected results in increases in GH and IGF-1 (insulin-like growth hormone-1)
hyperpituitarism-increased GH manifestations kids--> giantism. Adults --> acromegaly
manifestations of acromegaly (hyperpituitary-GH) CT proliferation --> bony proliferation (face/feet/hands), increased tongue/sebaceous/sweat. Coarse hair, skin
hyperthyroidism AKA thyrotoxicosis definition over-production of T3, T4 most commonly caused by Grave's disease
what is Graves Disease Type II autoimmune hypersensitivity - most common cause of thyrotoxicosis
MOA of Grave's disease autoimmune production of TSIs = thyroid stimulating immunoglobulins which STIMULATE HYPERPLASIA (not destroy) thyroid --> over production thyroid hormones
how does presence of TSIs effect thyroid feedback loop increased thyroid hormone levels signal to decrease TSH production. However, TSIs continue to stimulate T3/T4 release despite decreased level of TSH
clinical manifestions of Graves --> thyrotoxicosis exophthalmos from infiltration of orbital contents --> visual abnormalities. PRETIBIAL myxedema (doughy, non-pitting)
thyrotoxic crisis or thyroid storm dangerous hyperthyroidism results in death if not treated within 48 hours
what causes toxic nodular goiter results from abnormal stimulation of thyroid or compensatory hypersecretion of TSH in presence of thyroid hormone deficiency
under what circumstances to goiters develop iodine deficiency, pregnancy, autoimmune disorders. may disappear with return of normal thyroid levels. smooth or nodular
manifestations of thyrotoxicosis INCREASED METABOLIC RATE (CO, HR), heat intolerance, goiter usually present, increased tissue sensitivity to SNS stimulation
what causes hypothyroidism inflammatory disease of thyroid OR secondary to pituitary failure --- bacterial (acute thyroiditis) --- post-viral inflamm (subacute) ---
What is Hashimoto disease first autoimmune disease recognized where thyroid gland is destroyed by cell and/or antibody mediated immune process. One cause of hypothyroidism
manifestations of hypothyroidism myxedema characteristic, slow metabolic (brady, decreased CO), heat intolerance, lethargy
myxedema MOA CT separated by increased pro and mucopolysaccharides. These bind water --> nonpitting, boggy edema. in tongue, pharyngeal, laryngeal --> slurred speech/hoarseness
myxedema coma state of decompensated hypothyroidism that may or may not present actual myxedema. Primary symptoms altered mental status, hypothermia. Also hypoglycemia, hypotension, brady, hypovent
action of PTH parathyroid hormone maintain normal SERUM Ca++ levels by stimulating clasts for bone resorption. Also stim GI/renal for Ca++ resporption
hyperparathyroidism --> hypercalcemia bwo primary - adenoma of chief cells. Secondary - RF where kidney can't activate Vit D3 resulting in Ca++ not reabsorbed.
clinical manifestations hyperparathyroidism hypercalcemia manifestations (neuro, gastric, muscular. xs bone resorp --> osteopenia, pathalogic fractures. hypercalcemia/hyercalciuria --> renal calculi
hypoparathyroidism results from removal of parathyroid gland --> these manifestations hypocalcemia and HYPERphosphatemia. tetany, alopecia, dry skin, skeletal deformity as bond resorption is decreased
General definition diabetes mellitus group of disorders characterized by hyperglycemia, numerous target organ effects. Type 1 = absolute insulin def. Type 2 = insulin resistance/insulin secretory deficit. Secondary forms - genetic beta cell defects, pnacreatic diseases, gestational et al
Lab diagnostics for DM fasting glucose > 140. Elevated glucose tolerance test. random glucose >200 presenting with the 3 polys. Glycosolated Hgb for long term monitoring (120 day RBC life cycle)
Fun facts IDDM type 1 10% of all diabetes. genetic/environmental. associate with HLA (human leukocyte Ag II). Requires environmental trigger like EBV, CMV, mumps
Diabetes type 1-A cell mediated destruction of Beta cells associated with HLD-DR4
Diabetes type 1-B uncommon autoimmune associated with Hashimot's, Graves, myasthenia gravis. associated with HLA-DR3
DKA occurs when when theres relative/absolute insulin deficiency AND an increase in insulin counterregulatory hormones
NIDDM Type 2 DM 90% of diabetes. obesity and insulin resistance
NIDDM type 2 DM MOA decreased Beta-cell responsiveness to plasma glucose. Alos abnormal glucagon secretion. strong inheritance pattern, no single gene identified - may be a group of genes
name 5 acute complicatons of DM hypoglycemia, DKA, hyperosmolar nonacidotic diabetic coma, Somogyi effect, Dawn phenomenon
hypoglycemia AKAinsulin shock/reaction. plasma glucose < 45-60. Occurs 90% of time in Type 1.
neurogenic symptoms of hypoglycemia hypothal senses low glucose --> increased HR, palpitations, diaphoresis, tremors, pallor, anxiety
cell malnutrition symptoms of hypoglycemia HA, dizz, irritability, fatigue, poor judgement, conf, visual changes, hunger, seizures, coma
what are the insulin counterregulatory hormones that are increased in DKA those whose actions are to increase glucose levels ---catecholamines, cortisol, glucagon and GH
symptoms of DKA Kussumaul breathing, dizz, decreased CNS, ketonuria, abd pain, N, thirst, polyuria
in which type of DM do we see DKA complication almost exclusively in DM type 1 due to insulin insufficiency
hyperosmolar nonacidotic diabetic coma labs DM Type 2 complication cuz insulin deficiency is not as profound as in Type 1. NORMAL ketones but glucose OVER > 600. HYPERosmolality >310. BUN 70-90
manifestations hyperosmalr nonacidotic diabetic coma due to high blood sugar, this hyposomolal state --> glycosuria, polyuria and causes severe volume depletion & intracellular dehydration --> 15% mortality rate
Somogi effect Common in Type 1 DM & Kids: hypoglycemia at night stimulates glucose counter-regulatory hormoes to increase glucose levels - which are high in the morning
Dawn phenomenon late night insulin dose wanes, so GH elevated to increase glucose metab by muscle/fat. Result is an early morning in glucose levels
name 4 CHRONIC complications of DM microvascular disease, large blood vessel disease, infections, neuropathies
MOA of DM chronic complication microvascular diseases thickening of basement membrane effects microciruclation to eye/kidney --> retinopathy, nephropathy. Diabetes most common cause of end stage renal disease
MOA of DM chronic complicaton large vessel disease CAD, CVAs, peripheral vascular disease. CAD is most common cause of death of those with Type II DM
MOA infections DM chronic complications sensory impairment, hypoxia. increased pathogen growth in presence of high glucose and decreased blood supply
can neuropathies of DM chronic complications be revers some are progressive while others, such as foot/wrist drop, can be reversed.
Actions of Adrenal Gland Cortex --> cortisol & aldosterone. Medulla --> catecholamines
What is Cushing Syndrome (may or may not involve pituitary) results from primary disease of adrenal cortex -->hyercortisolism OR from ectopic production of ACTH from tumor elsewhere (small cell lung cancer)
What is Cushing Disease (pituitary involvement) when the hypocortisolism is SECONDARY to pituitary adenoma --> increased ACTH
How do Cushing Syndrome/Disease present *elevated cortisol changes metabolism *CV = HTN, CAD, CHF *immunosupression important complication
symptoms of Cushing syndrome *moon face, supraclavicular fat pads, trunk obesity-thin extremeties, increased facial/body hair, thin scalp hair
Cushing disease lose ability to increase ACTH and cortisol with stress, which presents these symptoms *weight gain, glucose intolerance *bone disease, muscle wasting *immunosuppression *hyperpigmentation
what is hyperaldosterosonism excess aldosterone production bwo primary adrenal adenoma or secondary RAA system condition such as HF, RF, HTN, hepatic cirrhosis
manifestations of hyperaldosteronism hypernatremia, hypervolemia, hypokalemia are manifestations of this adrenal disorder
what is hypocortisolism decreased adrenal stimulation by ACTH or primary cortisol hyposecretion
What is Addison disease high ACTH and inadequate cortisol synthesis/release (think feedback on ACTH)
What causes Addison disease autoimmune disease, TB of adrenal, familial insufficiency, cancer/hemorrhage of adrenals
what characterizes secondary hypocortisolism commonly due to withdrawal of exogenous glucocorticoids that have been administered for a long period of time and therefore have suppressed the production of ACTH by the pituitary
when hypocortisolism is due to secondary decrease corticosteroid treatment, is it Addisons no, it is secondary hypocortisolism
symptoms of hypocortisolism/Addisons weakeness, low BS, poor response stress, hypovolemia, hyperkalemia
take home message Addisons vs hypocortisolism *Addisons = high ACTH low cortisol *hypocortisolism = low ACTH, low cortisol
what is pheochromocytoma tumor (usually benign) of adrenal medulla that results in hypersecretion of catecholamines - especially in response to a stressor
symptoms of pheochromcytoma high BP, HR, sweating/flushing, constipation, glucose intolerance
Created by: lorrelaws