Endocrine patho s2010

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  • Water intoxication - cause edema and thirst\nSIADH - caused by tumor (small cell pulm, gi, \n
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  • Hyptherthyroid vs. Thyrotoxicosis\nHyperthyroid is ONE cause of thyrotoxicosis.\nHyperrefexia and clonus. \n\nThyroid storm - have hyperthyroid and then get major stressor.\nHyperthermic, tachy, a-fib, high output CF, agitation and delirious, NV, coma, death. \n
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  • Sever dyslipidemia\nDelayed return on reflexes. \n
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  • Hb gets glycosylate stuck to it, for 120 days (life of red blood cell).\n
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  • Lose K because compensating for H out due to increased acidosis. \n
  • Diabetic keotacidosis - shows signs and symptoms with underlying mechanism. \n
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  • Syndrome - regardless of cause, #1 iatrogenically. \nACTH - dependant: sourse of ACTH\nACTH inpendant - She’s just pumping, without. \n
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  • Endocrine patho s2010

    1. 1. Alterations of Hormonal Regulation Reference: Pathophysiology by Kathryn McCance Mindy Milton, MPA, PA-C July 29, 2010 1Mosby items and derived items © 2006 by Mosby, Inc.
    2. 2. Elevated or Depressed Hormone Levels Failure of feedback systems Dysfunction of an endocrine gland Secretory cells are unable to produce, obtain, or convert hormone precursors The endocrine gland synthesizes or releases excessive amounts of hormone Increased hormone degradation or inactivation Ectopic hormone release 2Mosby items and derived items © 2006 by Mosby, Inc.
    3. 3. Target Cell Failure Receptor-associated disorders  Decrease in number of receptors  Impaired receptor function  Presence of antibodies against specific receptors  Antibodies that mimic hormone action  Unusual expression of receptor function 3Mosby items and derived items © 2006 by Mosby, Inc.
    4. 4. Alterations of the Hypothalamic-Pituitary System 4Mosby items and derived items © 2006 by Mosby, Inc.
    5. 5. Diseases of the Posterior Pituitary Syndrome of inappropriate antidiuretic hormone secretion (SIADH)  Hypersecretion of ADH  Without physiologic stimulus  Most common etiology ectopically produced ADH  Malignant tumors  For diagnosis, normal adrenal and thyroid function must exist  Clinical manifestations are related to enhanced renal water retention, hyponatremia, and hypoosmolarity 5Mosby items and derived items © 2006 by Mosby, Inc.
    6. 6. Diseases of the Posterior Pituitary  Diabetes insipidus  Insufficiency of ADH  Partial or total inability to concentrate the urine  Neurogenic - MOST COMMON cause  Destruction of stalk  Insufficient amounts of ADH  Nephrogenic  Inadequate response to ADH  Clinical manifestations  Polyuria and polydipsia  Low urine sp gravity  Hypernatremia (loss of fluid)  Increased plasma osmolarity 6Mosby items and derived items © 2006 by Mosby, Inc.
    7. 7. Diseases of the Anterior Pituitary Hypopituitarism  Pituitary infarction  Sheehan syndrome - post-partum hemorrhage.  Hemorrhage  Shock  Others: head trauma, infections, and tumors  Decrease secretion of all or some hormones  Clinical manifestations  Depends on severity of each individual hormone deficiency 7Mosby items and derived items © 2006 by Mosby, Inc.
    8. 8. Diseases of the Anterior Pituitary Hypopituitarism  Panhypopituitarism  ACTH deficiency  TSH deficiency  FSH and LH deficiency  GH deficiency 8Mosby items and derived items © 2006 by Mosby, Inc.
    9. 9. Diseases of the Anterior Pituitary Hyperpituitarism  Commonly due to a benign, slow-growing pituitary adenoma  Adenoma secretes the hormone of the origin cell type without physiological need or control of negative feedback  Manifestations due to local expansion of tissue  Headache and fatigue  Visual changes (optic chiasm or cavernous sinus)  Hyposecretion of neighboring anterior pituitary hormones  GH, LH, and FSH-secreting cells most sensitive to pressure 9Mosby items and derived items © 2006 by Mosby, Inc.
    10. 10. Diseases of the Anterior Pituitary Hypersecretion of growth hormone (GH)  Acromegaly  Hypersecretion of GH during adulthood  Gigantism  Hypersecretion of GH in children and adolescents  Most common etiology is due to primary pituitary adenoma  Also see increased release of insulin-like growth factor 1 with increase GH  Both lead to increase growth of bone and connective tissue 10Mosby items and derived items © 2006 by Mosby, Inc.
    11. 11. Diseases of the Anterior Pituitary Acromegaly  Pathophysiology  Increased reabsorption of phosphate at the kidney tubule  Increased metabolic rate  Impaired glucose metabolism  Inhibition of peripheral glucose uptake  Increased glucose production 11Mosby items and derived items © 2006 by Mosby, Inc.
    12. 12. Acromegaly Clinical manifestation  Enlarged tongue  Coarse skin and body hair  Enlarged bones of the face, hands, and feet  Elongation of the ribs – barrel chest  Elevated blood glucose  Signs of tumor expansion  Visual changes 12Mosby items and derived items © 2006 by Mosby, Inc.
    13. 13. Hypersecretion of GrowthHormone (GH) 13Mosby items and derived items © 2006 by Mosby, Inc.
    14. 14. Diseases of the Anterior Pituitary Hypersecretion of prolactin- 30% of tumors  Caused by prolactinomas  In females, increased levels of prolactin cause amenorrhea, galactorrhea, hirsutism, and osteopenia  In males, increased levels of prolactin cause hypogonadism, erectile dysfunction, impaired libido, galactorrhea, oligospermia, and diminished ejaculate volume 14Mosby items and derived items © 2006 by Mosby, Inc.
    15. 15. Alterations of Thyroid Function Hyperthyroidism - Thyrotoxicosis  Graves disease – most common  Autoimmune  Goiter  Exophthalmos - infiltration of smooth muscle around eye.  Pretibial myxedema  Toxic multinodular Goiter  Pregnancy  Increased TSH  Puberty  Iodine deficiency - stimmulation  Toxic adenoma of thyroid  Goiter with one hyperfunctioning nodule  Mutation of TSH receptor  TSH secreting pituitary adenoma Thyroid Storm  Medical emergency 15Mosby items and derived items © 2006 by Mosby, Inc.
    16. 16. Hyperthyroidism Clinical Manifestations Subjective  Objective  Heat intolerance  Muscle wasting  Wt loss  Wt loss  Fatigue  Diaphoresis  Diarrhea  Flushed warm skin  Irritability  Tachycardia  Tremors  Atrial dysrhythmias  Dyspnea  Hyperreflexia  Anxiety  Exophthalmos  Menstrual irregularities  Goiter  Soft fine hair  incresed sensitivity to catacholamines. 16Mosby items and derived items © 2006 by Mosby, Inc.
    17. 17. Hyperthyroidism – Lab Dx Pituitary  Thyroid  Elevated TSH  Decreased TSH  Elevated T3  Elevated T3  Elevated T4  Elevated T4 17Mosby items and derived items © 2006 by Mosby, Inc.
    18. 18. Alterations of Thyroid Function Hypothyroidism  Primary hypothyroidism  Subacute thyroiditis - can follow viral infection. Tender neck.  Autoimmune thyroiditis (Hashimoto disease - opposite of Graves, both #1.)  Postpartum thyroiditis  Myxedema  Severe or long-standing  Congenital hypothyroidism  Cretinism  Post therapy for hyperthyroidism Myxedema coma  Medical emergency 18Mosby items and derived items © 2006 by Mosby, Inc.
    19. 19. Hypothyroidism Clinical Manifestations Subjective  Objective  Weakness  Decreased cardia output  Tiredness  Decreased bp  Cold intolerance  Increased blood cholesterol  Dry, flaky skin  Anemia  Brittle nails  Bradycardia  Goiter  Amenorrhea  Slightly lower temp  Confusion/dementia  Reflex delayed return  Constipation  Wt gain  Wt gain  Cool skin  Dyspnea  Memory loss 19Mosby items and derived items © 2006 by Mosby, Inc.
    20. 20. Hypothyroidism – Lab Dx Pituitary  Thyroid  
 
 
TSH  Elevated TSH  Decreased T3  Decreased T3  Decreased T4  Decreased T4 20Mosby items and derived items © 2006 by Mosby, Inc.
    21. 21. Alterations of Parathyroid Function Hyperparathyroidism  Primary hyperparathyroidism  Excess secretion of PTH from one or more parathyroid glands - etiology unknown.  Secondary hyperparathyroidism  Increase in PTH secondary to a chronic disease - think renal failure Hypoparathyroidism  Abnormally low PTH levels  Usually caused by parathyroid damage in thyroid surgery 21Mosby items and derived items © 2006 by Mosby, Inc.
    22. 22. Alterations of Parathyroid Function Hyperparathyroidism  Hypoparathyroidism Increased bone resorption  Decreased bone resorption by osteoclasts by osteoclast  Pathologic fractures  Decreased calcium  Kyphosis reabsorption from renal  Hypercalcemia tubules  Hypophosphatemia  Hypocalcemia  Hyperphosphatemia  Alkaline urine, Hypercalciuria, and  Lower threshold for nerve hyperphosphaturia and muscle irritability  Renal stones  Calcium moves out of cells  Decrease response to ADH  Muscle spasms  Mild insulin resistance  Hyperreflexia  NV - direct stimulation to  seizure CNS.  Must give Vit D. 22Mosby items and derived items © 2006 by Mosby, Inc.
    23. 23. Type 1 Diabetes Mellitus Genetic susceptibility Environmental factors Demonstrates pancreatic atrophy and specific loss of beta cells  No insulin Two types  Immune  Cell mediated destruction of beta cells  Macrophages, T and B lymphocytes, and natural killer cells are present  Production of auto-antibodies to islet cells or to insulin  HLA-DR3 and DR4 associated with higher risk of disease  Non-immune  Pancreatitis 23Mosby items and derived items © 2006 by Mosby, Inc.
    24. 24. Type 1 Diabetes Mellitus Diagnosis  Fasting blood glucose > 126 on two occasions OR  R(andom)BS > 200 on two occasions with AND symptomatic. Tracking progression and treatment effectiveness  HgbA1c – glycosylated hemoglobin (%)  RBC 120 d life span  Irreversible binding  Goal is 7, normal < 6 24Mosby items and derived items © 2006 by Mosby, Inc.
    25. 25. Type 1 Diabetes Mellitus Manifestations Hyperglycemia, polydipsia, polyuria, polyphagia, weight loss, and fatigue Ketoacidosis (metabolic acidosis)  Secondary to increased lipolysis with by-product formation of acetone bodies from FFA catabolism  Acetoacetic acid, hydroxybutyric acid, and acetone  Blood and urine  Glycosuria when renal threshold met (180 mg/dl) 25Mosby items and derived items © 2006 by Mosby, Inc.
    26. 26. Type 1 Diabetes Mellitus 26Mosby items and derived items © 2006 by Mosby, Inc.
    27. 27. Type 1 Diabetes Mellitus 27Mosby items and derived items © 2006 by Mosby, Inc.
    28. 28. Dysfunction of the Pancreas Type 2 diabetes mellitus  Maturity-onset diabetes of youth (MODY)  Mutation of gene for insulin secretion or action  Gestational diabetes mellitus (GDM)  During pregnancy  Majority go on to have DMII later  Common form of diabetes mellitus type 2  Insulin resistance  Less receptors  Compensatory hyperinsulinemia until beta cell burn out  Dyslipidemia  hypertension 28Mosby items and derived items © 2006 by Mosby, Inc.
    29. 29. Type 2 Diabetes Mellitus 29Mosby items and derived items © 2006 by Mosby, Inc.
    30. 30. Acute Complications of DM Hypoglycemia - #1 complication of DMII  Increased insulin or oral medications in the presence of decreased glucose availability (too much insulin or no food or increased exercise)  Glucose 45-60 mg/dl  Result in SNS stimulation DANGEROUS!  Diaphoresis To the brain.  Tachycardia Self control is  Palpitations dangerous, especially if  Tremors, pallor too tight, for this  Altered mental status Diabetic ketoacidosis  No insulin and counter regulatory hormones: cortisol and catecholamines  Triggered by infection, illness, surgery, or interruption of insulin therapy  Gluconeogenesis and Ketogenesis = ketone bodies = metabolic acidosis  Clinical manifestations  Dehydration due to osmotic diuresis and hyperglycemia Total K stores are down,  Glucosuria but may not be noticable,  hypokalemia so have to be careful  Kussmaul respirations treating.  Ketonuria Look at K!!! 30  ALOC - comaMosby items and derived items © 2006 by Mosby, Inc.
    31. 31. Diabetic Ketoacidosis 31Mosby items and derived items © 2006 by Mosby, Inc.
    32. 32. Acute Complications of DM Somogyi effect  Drop in blood sugar causes stimulation of body’s glucose counter regulation measures  Nocturnal hypoglycemia  Nightmares  Morning headache  Glucagon, cortisol, GH, and epinephrine  Gluconeogenesis  glycogenolysis  Result is rebound am hyperglycemia  Too much insulin!!! Many will want to over treat. Dawn phenomenon  Morning hyperglycemia due to decreased available insulin  No nocturnal hypoglycemia  Nocturnal elevation of GH  Hyperglycemia by decreasing peripheral tissue glucose uptake  Faster insulin clearance 32Mosby items and derived items © 2006 by Mosby, Inc.
    33. 33. Chronic Complications of DiabetesMellitus Microvascular disease = Glycosylation end-products  Retinopathy  Retinal ischemia and RBC aggregation  Progression from non-proliferative to proliferative disease  Neovascularization and fibrous tissue formation  Macula and optic disk = vision loss  Diabetic nephropathy  Glomeruli damage – hypertension and hyperglycemia  Basement membrane thickening, hypertrophy = decrease GFR  Microalbuminuria – first sign 3300.  Diabetic neuropathy  “dying back” – effects distal portions of nerves significantly  Toes, feet, ankles  Axon degeneration  Involves sensory, motor, autonomic 33Mosby items and derived items © 2006 by Mosby, Inc.
    34. 34. Chronic Complications of DM Macrovascular disease = large vessel  Damage due to elevated LDL, triglycerides, and AGE  Coronary artery disease  Stroke  Peripheral arterial disease Infection  Hyperglycemia  Poor circulation 34Mosby items and derived items © 2006 by Mosby, Inc.
    35. 35. Alterations of Adrenal Function Disorders of the adrenal cortex  Cushing disease - acth microadenoma.  Excessive anterior pituitary secretion of ACTH  Mineralocorticoids and glucocorticoids  Cushing syndrome  Excessive level of cortisol, regardless of cause  Exogenous  Steroid treatment for chronic inflammatory conditions  Endogenous  ATCH secreting pituitary microadenoma (C. disease)  Adrenal cortex tumor  Ectopic secretion of ACTH by Lung cancer 35Mosby items and derived items © 2006 by Mosby, Inc.
    36. 36. Cushing Syndrome Subjective:  Objective:  Sx of gastritis, ulcer disease  General – buffalo hump,  Acne truncal obesity, moon facies  Wt gain  Wt changes/distribution  Mental status – depressed  Increased facial hair with mood swings  Thinning of scalp hair  Skin- atrophy, poor wound  Bruising healing, purple striae,  Decreased muscle strength ecchymosis, increase facial or body hair  MSK- muscle wasting, decreased strength and tone  Hypertension  Hyperglycemia  Glycosuria  Hypokalemia 36Mosby items and derived items © 2006 by Mosby, Inc.
    37. 37. Cushing Disease 37Mosby items and derived items © 2006 by Mosby, Inc.
    38. 38. Alterations of Adrenal Function Disorders of the adrenal cortex  Hyperaldosteronism  Primary hyperaldosteronism (Conn disease)  Benign, single adrenal adenoma (80-90%)  Hypertension  Hypokalemia  Secondary hyperaldosteronism  Most common due to angiotensin II (Renin mechanism) 38Mosby items and derived items © 2006 by Mosby, Inc.
    39. 39. Primary Hyperaldosteronism 39Mosby items and derived items © 2006 by Mosby, Inc.
    40. 40. Alterations of Adrenal Function Disorders of the adrenal cortex  Adrenocortical hypofunction  Primary adrenal insufficiency (Addison disease)  Idiopathic Addison disease - autoimmune  Elevated ACTH with inadequate corticosteriod synthesis and output  Decrease mineralocorticoids, glucocorticoids, and androgens  Secondary hypocortisolism  Low or absent ATCH and low cortisol  Pituitary hypofunction  Sheehan syndrome  Panhypopituitarism  Hypophysectomy  Isolated ATCH deficiency 40Mosby items and derived items © 2006 by Mosby, Inc.
    41. 41. Addison Disease  Subjective:  Objective:  Anxiety  Wt loss  Restlessness  Postural hypotension  Fatigue/weakness  Increased pigmentation  Dizziness of skin  Nausea/vomiting  Hypoglycemia  diarrhea  Hyponatremia  Hyperkalemia 41Mosby items and derived items © 2006 by Mosby, Inc.
    42. 42. Adrenocortical Insufficiency:Laboratory Pituitary  Cortex  Low ACTH  High ACTH  Low Cortisol  Low Cortisol 42Mosby items and derived items © 2006 by Mosby, Inc.
    43. 43. Alterations of Adrenal Function Disorders of the adrenal medulla  Adrenal medulla hyperfunction  Caused by tumors derived from the chromaffin cells of the adrenal medulla  Pheochromocytomas  Secrete catecholamines on a continuous or episodic basis 43Mosby items and derived items © 2006 by Mosby, Inc.
    44. 44. Pheochromocytoma  Clinical manifestations:  Hypertension  episodic  Diaphoresis  Palpitations  Headache  Heat intolerance  Wt loss  constipation 44Mosby items and derived items © 2006 by Mosby, Inc.
    45. 45. The End  Questions? 45Mosby items and derived items © 2006 by Mosby, Inc.

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