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ENDOCRINE DISEASE

CUSHINGS DISEASE -metabolic disorder;excessive anterior pituitary secretion of ACTH -hypersecretion of cortisol, androgens & aldosterone ETIOLOGY: -ACTH production by nonpituitary tumors(Ectopic tumors-prim lung tumors) -ACTH production by pituitary tumors -Adrenal tumors producing cortisol S/S(commonly caused by hypercortisolism)
weight gain(buffalo hump)

(*Na&h20 retention due to mineralocorticoid effects of cortisol,exhibited when high cortisol)


-glucose intolerance (due to cortisol-induced insulin resistance and increased gluconeogenesis and glycogen storage by liver Elevated Cortisol, glucocorticoids results in muscle wasting, accumulation of adipose tissue, in face and trunk and increased blood proteins and glucose levels.

Elevated mineralocorticoids aldosterone in conjunction with the increased androgens promotes edema, a form called pitting edema. Hyperpigmentation POMC ACTH&MSH.

*elevated cortisol levels, vascular sensitivity to catecholamines is increased significantly, leading to vasoconstriction and hypertension. PATHOGENESIS: Without treatment 50% of the patients die within 5 years of onset. Due to: Overwhelming Infection Suicide Complications from arteriosclerosis and Hypertensive disease TREATMENT: Medication;radiation therapy and surgery IDIOPATHIC ADDISONS DISEASE(ORGAN-SPECIFIC AUTOIMMUNE) -Adrenal atrophy and hypofunction ETIOLOGY:
Abnormally low levels of Cortisol and Aldosterone Hypocortical Functioning, Dysfunction of the adrenal cortex, caused by an autoimmune

mechanism, autoimmune destruction of the adrenal cortex

Primarily women, 30 60 years of age Associated with TB (tuberculosis)adrenals are attacked by the TB irreversible and progressive loss of the adrenal cortex. Amyloidosis and Familial adrenal deficiency, Adrenoleukodystrophy and adrenomyeloneuropathy are other causes. ****May be inherited as an autosomal recessive trait S/S Failure of negative feedback causes an increase in ACTH Possible hyperpigmentation ... POMC ACTH&MSH. Weakness, anorexia, diarrhea, hypoglycemia, fatigue, apathy, hypotension PATHOGENESIS: Other autoimmune diseases predispose one to Addisons. Autoantibodies are present in 50%-70% of the individuals with idiopathic Addisons disease, the % increases in younger patients and those with other autoimmune diseases. Requires long-term daily glucocorticoid replacement therapy.

GRAVES(THYROTOXICOSIS)(TYPE V AUTOIMMUNE DISEASE) ETIOLOGY:


HYPERTHYROIDISM (elevated TH & suppressed TSH) occurs more commonly in women producing an antibody that looks like TSH enlarged thyroid gland(goiter) opthalmopathy (bulging eyes) dermopathy (pretibial edema) surgery, radiation, drug therapy(can reverse thyroid)

S/S

PATHOGENESIS

HASHIMOTOS THROIDITIS(AUTOIMUNE THYROIDITIS)


HYPOTHYROIDISM destruction of thyroid tissue by infiltration of lymphocytes and circulating thyroid autoantibodies (antithyroid peroxidase and antithyroglobulin antibodies). Failure of negative feedback

S/S

Goiter Baggy edema Pharalaryngeal Gain weight PATHOGENESIS: Female-fetus.mental retardation Hormone replacement therapy(T4 hormone)

POST GASTROECTOMY SYNDROME -S/S that occur after gastric resection -caused by changes in motor and control functions of the stomach and upper small intestines

CELIAC SPRUE W/ DUODENAL AND JEJUNAL INVMNT(AUTOIMMUNE) ETIOLOGY:


damages the small intestinal villous epithelium when there is ingestion of gluten (gliadin), the protein component of cereal grains.

*gluten-sensitive enteropathy BILROTH I & II GASTRECTOMY BILROTH I:


pylorus is removed and the distal stomach is anastomosed directly to the duodenum. greater curvature of the stomach is connected to the first part of the jejunum in a side-to-side manner.

BILROTH II:

EXOCRINE DISEASE

CYSTIC FIBROSIS (Autosomal recessive inherited disorder) ETIOLOGY: Intrinsic genetic chromosome 7 affects chloride ion channels resulting in enhanced sodium resorption and dehydrated secretions S/S Caucasian 1/3500, nonwhite 1/12,000 Chronic cough, sputum production, labored ventilation. Hypoxia, clubbing of the fingers and cyanosis. Maldigestion and malabsorption PATHOGENESIS: CF is a multiorgan disease; pulmonary failure is the most common cause of death. Mean life expectancy is now about 30 years, when compared with high death rates when it was described in 1936. Gene therapy is promising for the future. CROHNS DISEASE(TYPE IV-CELL MEDIATED) ETIOLOGY:
idiopathic inflammatory disorder that affects any part of the gastrointestinal tract but commonly on the distal small intestine and proximal large colon elevated IgG-caused severity of disease. associated with genetic factors alterations in epithelial cell barrier functions immunopathology related to abnormal T-cell reactions to commensal microflora and other luminal antigens Risk factors include family history, tobacco use, Jewish ethnicity, urban residency, and the CARD15/NOD2 (nucleotide-bindingoligomerization-domains) gene mutations

PATHOGENESIS

overly aggressive response to normal flora bacteria in genetically predisposed individuals. Immunomodulatory agents Surgery TNF delta blocking agents-tx of fistulas and maintain remission

GASTRITIS
A. CHRONIC FUNDAL GASTRITIS(AUTOIMMUNE)

ETIOLOGY:
Gastric mucosa degenerates extensively in the body and fundus of the stomach,leading to gastric atrophy Loss of chief cells & parietal cells.diminishes secretion of pepsinogen, HCl, and intrinsic factors. Elevated plasma levels of gastrin- acid secretion is insufficient(achlorydia) Pernicious anemia- cant facilitate vit B12 absorption B. CHRONIC ANTRAL GASTRITIS Involves in antrum only Factors that are associated: 1. use of alcohol, tobacco, and NSAIDS 2. *****H. pylori-major causative factor activation of T and B lymphocytes w/ infiltration of neutrophils CagA(H. pylori gene)-produces vacuolating toxin

S/S

Anorexia, vomiting,nausea,fullness,, and epigastric pain Gastric bleeding Gastric carcinoma- w/ chronic H. pylori infection Combinations of antibiotics(treat h. pylori) Vit B12 supplement for pernicious anemia

PATHOGENESIS: POST GASTRECTOMY

MALTASE DEFICIENCY
autosomal recessive disorder, with the gene located on the long arm of chromosome 17. accumulation of glycogen in the lysosomes of muscle cells and the cells of other tissues absence of the enzyme acid maltase is responsible for the abnormality in glycogen metabolism

LACTASE DEFICIENCY(INTESTINAL LACTASE)


common cause of osmotic diarrhea and loss of pancreatic enzymes Nonabsorbable substance is milk sugar, or lactose. Lactose remains in the intestinal lumen because it is not digested or absorbed

CELIAC SPRUE W/ DUODENAL AND JEJUNAL INVMNT BILROTH I & II GASTRECTOMY MALABSORPTION CYSTIC FIBROSIS CROHNS ULCERATIVE COLITIS ETIOLOGY:
chronic inflammatory disease that causes ulceration of the colonic mucosa and extends proximally from the rectum into the colon. individuals between 20 and 40 years of age. Risk factors: jewish descent and prevalent to white populations & Northern Europeans.

S/S

Loss of absorptive mucosal surface- diarrhea Mucosal destruction-bleeeding, cramping pain & urge to defecate Most common*** frequent diarrhea, w/ small amts of blood Therapy-5-aminosalicylic acid (mesalazine) Steroids and salicylates-suppress inflammatory response Immunosuppresive agents, cyclosporine, tacrolimus, and infliximab(chronic UC) Broad spectrum antibiotics/ probiotics can modulate intestinal flora Surgical resection of the colon/ colostomy may be performed

PATHOGENESIS:

* crohns have skip lesions while UC has continuous colonic invmnt, beginning in rectum GASTRITIS POST GASTRECTOMY MALTASE DEFICIENCY LACTASE DEFICIENCY CELIAC SPRUE, SOLELY JEJUNAL INVMNT CELIAC SPRUE, W/ DUODENAL AND JEJUNAL INVMNT BILROTH I& II GASTRECTOMY