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29 Cards in this Set

  • Front
  • Back
Homeostasis
body's way of maintaining a stable internal environment.
Factors that interfere with homeostasis include infection, genetic defects, trauma, and organ systems under stress.
Negative Feedback
Body sends signals to stop a given reaction and results in the discontinuation of the reaction
Positive Feedback
Sends signals to continue a given action. Reinforces reaction
Cellular Injury
ATP depletion-loss of mitochondrial ATP and decreased ATP synthesis results in cellular swelling, decreased protein synthesis, decreased membrane transport and lipogenesis. Changes contribute to loss of integrity of plasma membrane.
Cellular Injury
Free radicals-lack of oxygen key to progression of cell injury. Activated free radicals cause destruction of cell mmbrane and cell structure. Intracellular Ca normally low, changes cause increase which leads to damage of plasma membrane and intracellular damage.
Cellular Damage
Cellular strain lead to injury or adaptation. Injury can be reversible or irreversible (necrosis or apoptosis).
Atrophy
This is a decrease or shrinking in cell size. Most common in skeletal muscle, heart, secondary sex organs, and brain.
Physiological-early development
Pathological-result due to decrease in workload, use, pressure, bloodsupply, nutrition, hormone stimulation, and nervous stimulation.
hypoxia
low oxygen
Hypoxemia
lack of oxygen in blood
Ischemia
Lack of oxygen in tissue
Hypertrophy
The increase in cell size and size of affected organ. Heart, kidneys
-increase in protein of cellular components
-caused by hormone stimulation or increase in functional demand.
Physiological-skelatal-response to heavy work, diminishes when excessive work diminishes.
Pathological-heart-secondary to HTN or problem with valves. BPH, neoplasms, Cardiomyopathy
Hyperplasia
Increase int he number of cells resulting from increase rate of cellular division.
Compensatory-adaptive mechanism that enables certain organs to regenerate. eg. skin and liver...nerve, skelatal, heart, and eye do not regenerate.
Hormonal-uterus-in preparation to accept ovum
Pathological-abnormal proliferation of normal cells. respond to excessive hormonal stimulation or growth factors on target cells. eg..gynomastia, acromegaly, goiter, pathologic endometrial hyperplasia
Metaplasia
Reversible replacement of mature cell by another less differentiated cell type.
Bronchial metaplasia-replacemnt of columnar ciliated epithelial cells with stratified squamous cells-thse do not secrete mucus or have cilia, causing loss of protective mechanism
Barrett's esophagus-precursor to esophageal Ca.
Dysplasia
Abnormal change in size, shape, and organization of mature cells. Type of atypical hyperplasia. Found in cervix and resp tract. Commonly associated with neoplastic growths and often adjacent to cancerous cells. Considered mild, moderate and severe.
Strong predictor of Ca, if stimulus is removed, dyplastic changes often reversible.
Intracellular Accumulations
Pathological......
Lipids-Liver Disease
Iron-Hemochromatosis
Copper-Wilson's Disease
Uric Acid-Gout
Beta-Amyloids-Alzheimer's
Bilirubin-Liver, GB, Pancreas
Melanin-Addison's
Dystrophic Calcification-Atherosclerosis
malignant Calcification-Hyperparathyroidism, malignancy
Hemochromatosis
Increased iron absorption and storage
Primary-Genetic-Autosomal Recessive
Secondary-alcoholism
SX: fatigue, arthritis, deposits in liver, pancreas, heart, gray or bronze skin tone
TESTING: increased FE, transferrin sats > 45%. decreased TIBC, DNA testing EKG
MANAGEMENT: therapeutic phlebotomy.
DO NOT give Vit C-increases absorption of iron
Necrosis
The sum of cellular changes after local cell death and the process of cellular lysis. It provokes an inflammatory reaction in surrounding tissue.
Types of Necrosis
Coagulative-occurs in kidney, heart, adrenal glands. Caused by hypoxia, cardiac ischemia.
Liquefactive-ischemic injury to brain. Infectious
Caseous-combination of above found in lungs-TB, histoplasmosis
Fat-breast, pancreas, abdomen-cellular dissolution by lipases.
Gangrenous-death of tissue
dry-ischemia
wet-bacteria
Cells involved in inflammation
Neutrophils-1st responders
Basophils-histamine
Eosinophils-parasyte, allergies
macrophage-clean up debris
Lymphocyte-B cells-antibodies and immunity
Platelets-help with clotting. could be increased on count
Genetics
Dominant-Received from one parent-seen in midlife of older
Recessive-both parents have gene-do not have themselves.
Chromosomal
Sex-linked-XY linked
Autosomal-everything outside of x-linked
Multifactorial-combination of environmental and genetic
Down Syndrome
Chromosomal-trisomy 21
physical and mental disorders which increase with maternal age.
S/SX: small head with flat facial features, slanted eyes, single crease in palm, heart defects, leukemia, dementia, may have decreased IQ and speech difficulties.
TESTING: prenatal care, US or amnio
Klinefelter Syndrome
Chromosomal-XXY
S/SX:bth male andd femal sex characteristics. Decreased testosterone, less body and facial hair, gynecomastia (? breast Ca), weak muscles andd bones (osteoporosis), shy, infertility
TESTING: clinical exam, chromosomal testing, hormones
Turner Syndrome
Chromosomal-XO(X only)
S/SX: short stature, no or irregular menstrual periods, ovarian failure, no breast development, infertility, Aortic stenosis, COA, webbing of neck
TESTING: clinical, chromosomal, echo, reproductive hormones
TX:estrogen, HGH
Huntington's Chorea
Autosomal Dominant
progressive degeneration of nerve cells
Causes:genetic, fhx, middle age onset
S/SX: chorea-flailiing movement, problems include speech, balance, swallowing, cognitive impairment, behavioral personality changes
TESTING: CT/MRI, genetic testing
Cystic Fibrosis
Autosomal Recessive
decreased chloride metabolism which increases sodium and water reabsorption...sticky mucus
S/SX: Resp-cough, wheezing, freq inf (pseudomonous)clubbing, bronchiectasis
GI:meconium ileus, abnormal fat metabolism, steatorrhea, fecal impaction. panccreas, liver, growth, reproductive delay.
TESTING: sweat test, genetic
Dwarfism
Achondroplasia-Autosomal Dominant-most common typre of dwarfism-problem from hip down. no cartilage or bone production. caused by decreased GH
Primordial Dwarfism-Autosomal Recessive-both parents carry disease
S/SX:hip deformitie, club foot, scoliosis/lordosis
TESTING:clinical exam, hormones, xray/ct, genetic testing
Muscular Dystrophy
X-linked Recessive
skeletal muscle degeneration
CAUSE: Duchenne MD-early onset, make children, weakness in proximal musces-necrosis of muscle fibers-replacement of fatty tissue-pseudohypertrophy, pneumonia, decreased IQ, cardiomyopathy, incr intestinal transit time
Becker MD-less severe
TESTING:increased CK, EMG, genetic, Biopsy
Osteoporosis
Osteopenia-weakening of bone
-estrogen promotes building of bone.
Estrogen deficiency-post-menopausal, CA def, inactivity, hyperthyroid (malabsorption), parathyroid hormone job is to inrease CA levels in blood, bound to Vit D
CAUSES:multiple myeloma, Vit D def, renal
S/SX: kyposis, comp fx's, radiolucency
TESTING: dexa scan T-score < -2.5
Alzheimers
Progressive destruction of the brain. 7th leading cause of death.
CAUSES:genetics, FHX, Down's, Age
S/SX:amyloid plaques-cortical atrophy. Accumulation of tau protein-neurofibrillary tangles, decreased acetylcholine
PROBLEMS:memory, judgement, behavior reasoning
TESTING: cognitive, ct/mri, R/O organic disorders ie: STD, drugs, anemia, hyperthyroid