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41 Cards in this Set

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Peptide hormones and small molecules
use cell surface receptors and second messengers
Steroids and Thyroxine
intracellular receptors
Endocrine Diseases
ither undrproduction, overproduction, or mass lesions
Anterior Lobe productions
TSH, ACTH, FSH, LH, GH, PRL
Posterior Lobe productions
ADH, oxytocin
Adenoma (hyperpituitary)
-most common cause of hyperpituitarism in the anterior lobe
- can be functional or silent
- G protein mutations
- S&S: occasional acute hemorrhage, enlargement of lesion (apoplexy)
Hypopituitarism
loss of 75% of parenchyma due to tumors, mass lesions, pituitary surgery, apoplexy, necrosis, or genetic defects
Local Mass Effects
include radiographic abnormalities of sella turcica, visual field abnormalities, S&S of elevated intracranial pressure, hypopituitarism
Posterior Pituitary syndrome
ADH deficiency = diabetes insipidus, polyuria
Thyroid gland
-connected by thyroid isthmus
-T3, T4, calcitonin
Thyrotoxicosis
hypermetabolic state caused by excess T3 and T4

Hyperthyroidism
3 most common causes of thyrotoxicosis

Clinical Sx
diffuse hyperplasia, hyperfunctional multinodular goiter, adenoma of thyroid

nervousness, weight loss, heat intolerance, increased pulse pressure, exophthalmos
Treatment of hyperthyroidism
-beta blockers
-thionamide to block new hormone synthesis
-iodine solution
-thiourylenes (methimazole)
Hypothyroidism
causes: developmental, resistance syndrome, autoimmune (hashimoto's), iodine deficiency, congenital factors
Cretinism: hypothyroidism in infancy causing dwarfism
Myxedema: hypothyroidism in older child or adult
Presents with husky slow voice
Pancreas
-islets of langerhaans
-Insulin and glucagon
-somatostatin
-pancreatic polypeptide
Diabetes Mellitus
hyperglycemia
diagnosed via random glucose, fasting glucose, and abnormal glucose tolerance test
Type I diabetes: deficiency in insulin (autoimmune)
Leads to: diabetic ketoacidosis, severe depletion, diabetic coma, death
Type 2 diabetes: peripheral resistance and inadequate secretion
Metabolic defects (type II): beta cell dysfunction, insulin resistance
Pancreatic endocrine neoplasms
2% of all neoplasms
clinical syndromes:
-Hyperinsulinism (beta cell tumors)
-Hypergastrinemia/Zollinger-Ellison Syndrome: hypersecretion of gastric acid and severe peptic ulceration
-Glucagnomas: alpha cell tumors causing high plasma glucagon levels
Exocrine pancreas
2-2.5 L of enzymes a day
secretin and CCK
Enzymes: trypsin, chymotrypsin, aminopeptidase, elastase, amylase, lipase, phospholipase, and nucleases
Disorders of exocrine pancreas
cystic fibrosis, acute and chronic pancreatitis, and tumors
Congenital anomalies: agenesis, pancreas divisum, annular pancreas
Acute pancreatitis
inflammation of pancreas associated with acinar cell injury
acute onset of abdominal pain due to enzymatic necrosis
Pathogenesis: autodigestion activated by trypsinogen
Chronic Pancreatitis
repeated bouts of mild-moderate pancreatic inflammation
Pathogenesis: ductal obstruction, secreted proteins, oxidative stress, interstitial fibrosis
Clinical Features: abd pain with fever and mild-moderate elevations of serum amylase
Cysts and Tumors
Cysts: congenital cysts are believed to result dvlpmn't of pancreatic ducts
Pseudocysts: localized collections of pancreatic secretions due to inflammation
Tumors: solid, malignant, glandular tumors
Cystic Tumors: most often in elderly women
Carcinoma: 5th most frequent
GI
gastrointestinal system, digestion, absorption, abnormalities
Esophagus
Lower esophageal sphincter: critical to esophageal function, maintenance of sphincter tone is neccessary to prevent reflux of gastric contents
Congenital anomalies: esophageal atresia, tracheoesophageal fistulas, esophageal Webs, esophageal Rings, esopnageal stenosis
Motor Disorders: achalasia, hiatal hernia, diverticulum
Esophagitis: inflammation of mucosa, Reflux esophagitis (GERD), Barrett esophagus, Infectious and chemical esophagitis
Benign Tumors: mostly within esophageal wall
Malignant Tumors
Squamous cell carcinoma: most common
Adenocarcinomas: malignant epithelial tumors
Stomach
Congenital abnormalities: congenital hypertrophic pyloric stenosis (males more than females, projectile vomit)

Gastritis: inflammation of mucosa
-Acute: neutrophilic infiltration
-NSAID use
-epigastric pain, nausea, vomitting, overt hemorrhage
Chronic Gastritis
Peptic Ulcer Dz
chronic mucosal inflammatory changes with lymphocytes or plasma cell infiltrates leading to mucosal atrophy and intestinal metaplasia

Pathogenesis: H pylori, alcohol, cigarette smoking, granulomatous conditions (chron)

PUD: breach in mucosa of alimentary tract, chronic often solitary, imbalance btwn gastroduodenal mucosal defense mechanisms and mucoal damaging forces (acid)
accelerated by NSAIDs, infection, ischemia, shock, etc; burning or aching pain that is worse at night
gastric polyp
nodule or mass the projects above the level of surrounding mucosa
seen with chronic gastritis
pathogenesis: major factors are environment, diet, low socioeconomic status, host factors, and genetic factors
Gastric carcinoma
weight loss, abdominal pain, anorexia,vomiting, altered bowel habits, anemic Sx
clinical prognosis: depends on depth of tumor invasion
Small Intestine
congenital anomalies: obstruction may be complete (atresia) or incomplete (stenosis)
Small and large intestine pathology
Malabsorption syndromes: presents with steatorrhea

Whipple disesae: strong caucasion male predominance

Disaccharidase deficiency: lastase deficiency, common in NA and AA, osmotic diarrhea

IBD: Chron's and ulcerative colitis

Chrons: autoimmune, granulomatos disease, sharp demarcation of deceased bowel segments

Ulcerative colitis: ulceroinflammatory disease limited to the colon, continuous fashion from the rectum, recurrent bloody mucoid diarrhea for days, weeks, or months
Tumors of small intestine
adenomas
adenocarcinomas: associated with Chron's disease, alcohol and tobacco
Tumors of the colon
polyps, adenomas, colorectal carcinomas,

Polyps: tumorous masses that protrude into lumen of gut

Adenomas: intraepithelial neoplasms that are usually sessile

Colorectal carcinoma: most common malignancy of western countries, 98% of cancers of the colon
-btwn 60-79
- US, Australia, New Zealand, Eastern Europe
-dietary practices implicated
-asymptomatic for years
Cell death
results from ischemia, infection, toxins, or immune reaction

necrosis: occurs after ischemia and chemical injury, always pathologic

Apoptosis: suicide program
Hyperplasia
increase in number of cells causing increased volume of organ/tissue

usually occurs with hypertrophy

occurs if cellular population capable of synthesizing DNA

Hypertrophy involves cell enlargement without DNA division

physiologic or pathologic

Physiologic hyperplasia: hormonal or compensatory

Mechanism: local production of growth factors, increased growth factor receptors, activation of particular intracellular signaling pathways

Pathologic hyperplasia: excesive hormonal stimulation or growth factors, risk factor for cancer
Hypertrophy
increase in size of cells
more structural components
striated and cardiac muscle
increased workload

Mechanism:
Atrophy
shrinkage in size of cell
physiologic: early development or return after pregnancy
Pathologic: underlying cause

Common causes: decreased workload, deinnervation, ischemia, malnutrition, loss of endocrine stimulation, aging, pressure

Mechanisms: balance btwn protein synthesis and degradation, ubiquitin-proteasome pathway
Metaplasia
reversible change in which one adult cell type is replaced by another adult cell type

most common: columnar epithelial cell to squamous epithelial cell in cigarette smokers

Connecive tissue metaplasia: formation of cartilage, bone, or adipose tissue

Mechanism: result of reprogramming of stem cells known to exist in normal tissues
Reversible injury
reversible if damaging stimulus removed

hallmarks: reduced oxidative phosphorylation, ATP depletion, cellular swelling
Irreversible injury and cell death
cells undergo morphologic changes that are recognized as cell death
Necrosis
damage to membranes is severe, lysosomal enzymes enter cytoplasm and digest cell
Apoptosis
damage to DNA, characterized by nuclear dissolution without complete loss of membrane integrity

causes of cell injury:
-oxygen deprivation
-physical agents
-chem agents and drugs
-infectious agents
-genetic derangements
-nutritional imbalances