Endocrine Disorders 310

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Hypopituitarism
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Terms in this set (77)
Hypopituitarism
-Decreased secretion of hormones
-70-90% of function must be destroyed before function is obvious;
-Can be congenital or acquired;
-ACTH deficiency is most serious;
Consequence of decreased ACTH
-ACTH influences hormone secretion from the adrenal gland
-Less ACTH = Less Aldosterone and cortisol
-Decreased aldosterone= decreased Na/H2O retention ( decreased BP)
-Decreased cortisol= abnormal sugar levels/altered metabolism
Image: Consequence of decreased ACTH
Hypopituitarism symptoms
-Weakness( due to low blood sugar)
-Fatigue
-Postural Hypotension(due to reduced BP)
Hypothalamus
-Releasing and inhibiting hormones
-Controls the release of pituitary hormones
-Dopamine,
Image: Hypothalamus
Anterior pituitary hormones
Growth Hormone, ACTH, Thyroid Stimulating Hormone (TSH), FSH & LH (Gonadotropic hormones)
Image: Anterior pituitary hormones
Growth Hormone
Anterior Pituitary-
Stimulates growth of bone and muscle, promotes protein synthesis and fat metabolism, decreases carbohydrate metabolism
ACTH
-Anterior Pituitary
-Stimulates synthesis and secretion of adrenal cortical hormones
-A stress responder
TSH
Anterior Pituitary
Stimulates synthesis and secretion of thyroid hormone
FSH
Anterior Pituitary
-Female: stimulates growth of ovarian follicle, ovulation
-Male: stimulates sperm production
LH
-Anterior Pituitary
-Female: stimulates development of corpus luteum, release of oocyte, production of estrogen and progesterone
-Male: stimulates secretion of testosterone, development of interstitial tissue of testes
Posterior pituitary hormonesADH OxytocinADHIncreases water reabsorption by kidneyOxytocinStimulates contraction of pregnant uterus, milk ejection from breasts after childbirthDecreased aldosteroneInfluence of adrenal hormone: decreased Na/H2O retentionDecreased cortisolInfluence of adrenal hormone: abnormal sugar levels/altered metabolismThyroid Feedback loop1)Low levels of T3 & T4 are detected 2)Ant. pituitary releases TSH 3)TSH stimulates thyroid to release T3 & T4 4)Elevated levels of T3 and T4 are detected, feedback to pituitary to reduce the release of TSHT3 and T4-Thyroid hormones: -Increase the metabolic rate; -increase protein, fat and carb metabolism - -increase O2 consumption -Higher HR and contractility (due to epi) -Vasodilation -Increased GI motility -Neuromuscular hyperactivity - T3 is more active -T4 is more prevalentHypothyroidismDecreased function - slows metabolic process; can be congenital or acquired;primary hypothyroidismMost common- a disorder of the Thyroid -caused by destruction or dysfunction of the thyroid glandCauses of primary hypothyroidsim-Thyroidectomy, ablation or chemicals -Large amounts (too much!) Iodine which can block hormone production -Autoimmune (like hashimoto)secondary hypothyroidismsecondary to disorders of hypothalamic or pituitary originHypothyroid symptomsEVERYTHING SLOWS -Weight gain -coarse brittle hair -cold intolerance -bradycardia -constipation -delayed deep tendon reflexes -lethargy, fatigue, muscle weaknessHashimoto thyroiditits-Autoimmune diseases resulting in destruction of thyroid functional tissue leading to hypothyroidism and goiter -more common in women; -may initially start as goiter leading to hypothyroid functionHyperthyroidism-Excessive thyroid function -Causes: iodine containing agents, autoimmune (Grave's disease, most common)Primary tumorPituitary tumor that originates in the pitutitarySecondary tumorPituitary tumor that has metastasized to pituitaryAdenomas of the PituitaryHave the potential to secrete hormones 32% secrete prolactin 21% secrete GH ( increase in protein synthesis)Symptoms of hyperthyroidism-Weight loss; -muscle wasting -thin, fine hair -heat intolerance -tachycardia -diarrhea r/t increased peristalsis and increased water retention -hyperreflexivity -fine tremorDiabetes insipidus-Partial or complete deficiency of anti diuretic hormone (ADH) -caused: head trauma, neurosurgery, cancer, inherited disorderEffects of Low ADH-ADH normally promotes retention of water -Low amounts leads to a decrease in permeability in the collecting ducts of the nephron. -Less water leaves collecting duct, so its excreted out in UrineSymptoms of Diabetes insipidusPolyuria(large volume, dilute urine) Polydipsia (excessive thirst )Causes of SIADH-Neuro-infections, trauma, hemorrhage) -Cancer (primary or paraneoplastic) -Inherited -Medssyndrome of INCREASED ADH (SIADH)-Condition characterized by increased release of - -ADH from the anterior pituitary results in increased reabsorption of H2O from the renal tubulesSymptoms of SIADHdecreased urine output with concentrated urine; hemodilution and hyponatremia; neurological changes (Lethargy, confusion, seizures, coma) hypertensionHemodilutiondecreased concentration of cells and solids in the blood resulting from gain of fluidHyponatremiaWith this condition, the body holds onto too much water. This dilutes the amount of sodium in the blood and causes levels to be low. Symptoms include nausea, headache, confusion, and fatigueGrave's disease-Autoimmune disorder; -more common in women; -abnormal production of TSH receptors antibodies which stimulates releasing more thyroid hormone; -strong family association;Graves Symptomshyper metabolic state; ophthalmopathy;TSH receptor antibodiesThese are antibodies which bind to the TSH receptors on the pituitary gland and stimulate the release of TSH, leading to an increased production of T3 and T4, even after optimal levels have been reachedIncrease BPPurpose of renin-angiotensin-aldosterone mechanismAdrenal Cortex Hormones1)Mineralocorticosteroids, mainly aldosterone 2)Glucocorticoids, mainly cortisol 3)Adrenal androgens, mainly dehydroepiandrosterone (DHEA) and androstenedioneMineralcorticosteroids-Aldosterone -Adrenal Cortex -Increases sodium absorption, potassium loss by kidneyGlucocorticoids-Mainly cortisol -Adrenal Cortex -Affects metabolism of all nutrients; regulates blood glucose levels, affects growth, has anti-inflammatory action, and decreases effects of stressAdrenal medulla-Epinephrine -NorepinephrineEpinephrine and norepinephrineServe as neurotransmitters for the sympathetic nervous systemElevated cortisol (glucosteriods)Adrenal cortex: -Increased glucose production by liver; -increased breakdown of protein(AA brought to liver to produce sugars (gluconeogenesis) -altered fat metabolism (gets stored in unusually places) -influence behavior by binding and stimulated rxn in brain -suppress inflammation and immunity 1)decrease in capillary permeability, 2)reduce in cell mediated and humoral responseElevated aldosterone (mineralcorticoid)Adrenal cortex: Regulated by renin-angiotensin-aldosterone system; elevated levels result in increased Na/H2O retention and K+ excretion (too low/high can lead to afib)Elevated androgensAdrenal cortex: Promote pubertal growth of hairCortisol, aldosterone, andorgensHormone(s) released by the adrenal cortexEpinephrineHormone(s) released by the adrenal medullaThe Adrenal feedback loop1)Low levels of cortisol 2)Anterior pituitary release of ACTH 3)ACTH stimulates adrenal to release cortisol and androgens(cortisol, aldosterone) 4)Elevated levels of cortisol feedback to pituitary to reduce the release of ACTHAdrenal cortical insufficiencyAdrenal hormones are deficient and ACTH levels are high (no feedback inhibition) -Manifestation may not appear till 90% loss of functional glandAdrenal cortical insufficiency causes-autoimmune (most common, attack adrenal cells)(Addison's) -carcinoma, -drugs, -infectious agents;RAAS loop1) Low BP is detected in kidneys that stimulates release of renin 2)Renin stimulates conversion of angiotensinogen to angiotensin I 3)Angiotensin I is converted by ACE to angiotensin II 4)Angiotensin II stimulates the release of aldosterone from adrenal 5)Aldosterone promotes Na+/H2O retention to elevate BP (which leads to reflex bradycardia)Angiotensin 1Is a weak vasoconstrictorAngiotensin 21)Potent vasoconstrictor 2)Stimulates release of aldosteroneEffects of adrenal cortical insufficiency-Mineralocorticoid deficiency (Na+ & H2O excretion, K+ retention); -glucocorticoid deficiency (risk for hypoglycemia, metabolic abnormalities), -hyperpigmentation (due to elevated levels of ACTH)Symptoms of Adrenal COrtical InsufficiencyAnorexia and weight loss Fatigue and weakness Orthostatic hypotension (loss of fluid) Hyponatremia (Increased urinary losses of sodium, chloride, and water) Hyperkalemia(increased retention of K+) Hyperpigmentation Associated autoimmune conditionHypercortisolismGlucocorticoid excess seen in Cushing's syndromeCauses of Cushing syndrome-Pituitary adenoma (Cushing's DISEASE); -adrenal tumor -ectopic Cushing syndrome - ACTH secreting tumor (Small cell lung cancer)Symptoms of glucocorticoid excess-Cushing Syndrome -Altered fat metabolism-Deposits of fat on top of back, around face and abdomen -thin extremities -osteoporosis -development of DM (elevated blood sugar) -excess aldosterone -increased BPPheochromocytomaTumor predominantly of adrenal medulla -releases catecholamines; -leads to HTN, nervousness, massive/chronic headachesDiabetes mellitusDisorder of carbohydrate metabolism, protein and fat metabolism -imbalance between insulin availability and insulin neededCauses of diabetes mellitus1. Inadequate production of insulin 2. Insensitive insulin receptors (usually obses) 3. Inadequate functioning following receptor activation 4. Destruction of insulin prior to exerting it's effect (less common)Beta cellsPancreas cells Insulin produced hereGluconeogenesisProduction of glucose from amino acids, glycerol and lactic acid when body sugar levels is too lowFunction of insulin-promote glucose uptake in cells -prevents breakdown of fat and glycogen -inhibits gluconeogenesis -increases protein synthesisType 1 diabetes mellitusDestruction of pancreatic beta cells; -usually immune related which is a genetic predisposition with an environmental trigger -or idiopathic cause -absolute absence of insulinDM type 1 Insulin absenceThe absolute absence of insulin that leads to the breakdown of fats and decreased protein synthesis. Fatty acids are converted to ketones by the liver to compensateDiabetic ketoacidosis-A severe manifestation of insulin deficiency; - life threatening complication of type 1 - -hyperglycemia (glucose>200), - hemoconcentration, and -production of ketones which are acidic caused by altered glucose and fat metabolism;Treatment of DKA1)Fluid and electrolyte replacement via IV 2)Insulin 3)Use of bicarbonate (controversial)3 Polys of DMPolyuria (i.e., excessive urination) Polydipsia (i.e., excessive thirst) Polyphagia (i.e., excessive hunger)type 2 diabetes mellitus-Hyperglycemia due to relative insulin deficiency; 1)not enough insulin to meet the need , 2) resistance to insulin (free fatty acids, exhausted beta cells), 3) Destruction of insulin Treated with hypoglycemic agentsDM Type 2 causesGenetic component and acquired trigger (like obesity or lack of activity)Not enough insulin leads to...-Either form reduced number of beta cells or beta cell exhaustion. -This leads to cells not taking in enough glucose -Too much sugar in the blood -increased glucose production by the liver -Must be treated with insulin injectionsResult of hyperglycemic state-Although there is enough sugar in the blood, cells begin to starve from lack of fuel -Liver recognizes cell starvation and stimulates gluconeogenesis which further increased blood glucose levels -Excess glucose is excreted into urine -Cells begin to metabolize protein for EnergyHyperglycemic hyperosmolar non-ketosis HHNK-More common in DM Type 2 - characterized by hyperglycemia, hemoconcentration and dehydration without significant ketoacidosis -Treat with IV fluid and Insulin