Patho endocrine function/alterations
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| main functions of endocrine system | fetal repro/cns diff/growth-devel/repro, homeostasis/corrective measures
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| 1st messenger hormones (fat soluble) | plasma carrier protein, steroid hormone binds, through cystol to DNA--> mRNA -->ribosome-->protein
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| Water soluble hormones use 2nd messenger. Name 2 examples | cAMP and IP3-Ca (inositol triphosphate)
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| MOA cAMP | hormone binds receptor. GTP binds G protein. ATP transformed by Adenyl cyclase to cAMP which is 2nd messenger.
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| 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
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| 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)
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| 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
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| hormones released by posterior pituitary | oxytocin, ADH
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| hormones released by anterior pituitary | *TSH
*ACTH
*FSH/LH
*GH
*PRL
*endorphins
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| what causes SIADH and definition | ectopic source oat cell/lung inf/drugs --> TOO MUCH ADH
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| what disease manifests with water retention, hyponatremia and hypoosmolality | SIADH serum Na <135, osmolality <280.
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| Clinical manifestations of SIADH | *neuro: hyponatremia --> seizures, deficits
*HF
*GI cramping, vomitting (no diarrhea)
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| What causes DI and definition | neurogenic hypothal/post pit OR nephrogenic OR psychogenic --> TOO LITTLE ADH
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| what disease manifests with polydyspia, polyuria, dehydration, hyper serum osmolality, hypo urine osmolality | diabetes insipidus - inability to concentrate urine due to low ADH
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| diseases of the anterior pituitary can lead to | hypopituitarism or hyperpituitarism or panhypopituitarism
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| hypopituitarism caused by | infarction, disease, trauma, infections, surgery and infections which affect anterior pit or hypothalmus primary or secondary.
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| panhypopituitarism | absense of ALL pituitary hormones. of particular importance ACTH followed by TSH, FSH, LH
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| ACTH deficiency bwo panhypopituitarism | results in ACTH deficiency which impacts ---cortisol (life threatening)---- aldosterone (Na reabsorption)
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| manifestations of ACTH deficiency | n/v/anorexia ---fatigue---hypoglycemia---decreased aldosterone-->serum hyponatremia. IF ACTH completely absent may need cortisol to sustain life
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| hyperpituitarism - what hormones affected | results in increases in GH and IGF-1 (insulin-like growth hormone-1)
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| hyperpituitarism-increased GH manifestations | kids--> giantism. Adults --> acromegaly
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| manifestations of acromegaly (hyperpituitary-GH) | CT proliferation --> bony proliferation (face/feet/hands), increased tongue/sebaceous/sweat. Coarse hair, skin
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| hyperthyroidism AKA thyrotoxicosis definition | over-production of T3, T4 most commonly caused by Grave's disease
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| what is Graves Disease | Type II autoimmune hypersensitivity - most common cause of thyrotoxicosis
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| MOA of Grave's disease | autoimmune production of TSIs = thyroid stimulating immunoglobulins which STIMULATE HYPERPLASIA (not destroy) thyroid --> over production thyroid hormones
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| 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
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| clinical manifestions of Graves --> thyrotoxicosis | exophthalmos from infiltration of orbital contents --> visual abnormalities. PRETIBIAL myxedema (doughy, non-pitting)
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| thyrotoxic crisis or thyroid storm | dangerous hyperthyroidism results in death if not treated within 48 hours
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| what causes toxic nodular goiter | results from abnormal stimulation of thyroid or compensatory hypersecretion of TSH in presence of thyroid hormone deficiency
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| under what circumstances to goiters develop | iodine deficiency, pregnancy, autoimmune disorders. may disappear with return of normal thyroid levels. smooth or nodular
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| manifestations of thyrotoxicosis | INCREASED METABOLIC RATE (CO, HR), heat intolerance, goiter usually present, increased tissue sensitivity to SNS stimulation
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| what causes hypothyroidism | inflammatory disease of thyroid OR secondary to pituitary failure --- bacterial (acute thyroiditis) --- post-viral inflamm (subacute) ---
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| 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
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| manifestations of hypothyroidism | myxedema characteristic, slow metabolic (brady, decreased CO), heat intolerance, lethargy
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| myxedema MOA | CT separated by increased pro and mucopolysaccharides. These bind water --> nonpitting, boggy edema. in tongue, pharyngeal, laryngeal --> slurred speech/hoarseness
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| 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
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| action of PTH parathyroid hormone | maintain normal SERUM Ca++ levels by stimulating clasts for bone resorption. Also stim GI/renal for Ca++ resporption
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| hyperparathyroidism --> hypercalcemia bwo | primary - adenoma of chief cells. Secondary - RF where kidney can't activate Vit D3 resulting in Ca++ not reabsorbed.
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| clinical manifestations hyperparathyroidism | hypercalcemia manifestations (neuro, gastric, muscular. xs bone resorp --> osteopenia, pathalogic fractures. hypercalcemia/hyercalciuria --> renal calculi
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| hypoparathyroidism results from removal of parathyroid gland --> these manifestations | hypocalcemia and HYPERphosphatemia. tetany, alopecia, dry skin, skeletal deformity as bond resorption is decreased
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| 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
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| 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)
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| 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
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| Diabetes type 1-A | cell mediated destruction of Beta cells associated with HLD-DR4
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| Diabetes type 1-B | uncommon autoimmune associated with Hashimot's, Graves, myasthenia gravis. associated with HLA-DR3
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| DKA occurs when | when theres relative/absolute insulin deficiency AND an increase in insulin counterregulatory hormones
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| NIDDM Type 2 DM | 90% of diabetes. obesity and insulin resistance
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| 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
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| name 5 acute complicatons of DM | hypoglycemia, DKA, hyperosmolar nonacidotic diabetic coma, Somogyi effect, Dawn phenomenon
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| hypoglycemia | AKAinsulin shock/reaction. plasma glucose < 45-60. Occurs 90% of time in Type 1.
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| neurogenic symptoms of hypoglycemia | hypothal senses low glucose --> increased HR, palpitations, diaphoresis, tremors, pallor, anxiety
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| cell malnutrition symptoms of hypoglycemia | HA, dizz, irritability, fatigue, poor judgement, conf, visual changes, hunger, seizures, coma
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| what are the insulin counterregulatory hormones that are increased in DKA | those whose actions are to increase glucose levels ---catecholamines, cortisol, glucagon and GH
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| symptoms of DKA | Kussumaul breathing, dizz, decreased CNS, ketonuria, abd pain, N, thirst, polyuria
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| in which type of DM do we see DKA complication | almost exclusively in DM type 1 due to insulin insufficiency
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| 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
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| 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
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| 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
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| 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
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| name 4 CHRONIC complications of DM | microvascular disease, large blood vessel disease, infections, neuropathies
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| 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
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| 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
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| MOA infections DM chronic complications | sensory impairment, hypoxia. increased pathogen growth in presence of high glucose and decreased blood supply
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| can neuropathies of DM chronic complications be revers | some are progressive while others, such as foot/wrist drop, can be reversed.
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| Actions of Adrenal Gland | Cortex --> cortisol & aldosterone. Medulla --> catecholamines
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| 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)
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| What is Cushing Disease (pituitary involvement) | when the hypocortisolism is SECONDARY to pituitary adenoma --> increased ACTH
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| How do Cushing Syndrome/Disease present | *elevated cortisol changes metabolism
*CV = HTN, CAD, CHF
*immunosupression important complication
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| symptoms of Cushing syndrome | *moon face, supraclavicular fat pads, trunk obesity-thin extremeties, increased facial/body hair, thin scalp hair
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| 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
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| what is hyperaldosterosonism | excess aldosterone production bwo primary adrenal adenoma or secondary RAA system condition such as HF, RF, HTN, hepatic cirrhosis
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| manifestations of hyperaldosteronism | hypernatremia, hypervolemia, hypokalemia are manifestations of this adrenal disorder
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| what is hypocortisolism | decreased adrenal stimulation by ACTH or primary cortisol hyposecretion
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| What is Addison disease | high ACTH and inadequate cortisol synthesis/release (think feedback on ACTH)
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| What causes Addison disease | autoimmune disease, TB of adrenal, familial insufficiency, cancer/hemorrhage of adrenals
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| 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
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| when hypocortisolism is due to secondary decrease corticosteroid treatment, is it Addisons | no, it is secondary hypocortisolism
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| symptoms of hypocortisolism/Addisons | weakeness, low BS, poor response stress, hypovolemia, hyperkalemia
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| take home message Addisons vs hypocortisolism | *Addisons = high ACTH low cortisol
*hypocortisolism = low ACTH, low cortisol
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| what is pheochromocytoma | tumor (usually benign) of adrenal medulla that results in hypersecretion of catecholamines - especially in response to a stressor
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| symptoms of pheochromcytoma | high BP, HR, sweating/flushing, constipation, glucose intolerance
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