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74 Cards in this Set
- Front
- Back
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Disease |
any deviation or interruption from the normal cessation of function or disorder manifestation of certain signs and symptoms |
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Aspects of a Disease |
etiology pathogenesis morphology clinical manifestations diagnosis clinical course |
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Etiology |
cause of the disease most multifactoral |
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Examples of etiology |
biological agents physical forces chemical agents nutritional imbalance congenital disease |
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Pathogenesis
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sequence of cellular &tissue events you see over time from initial exposure to time disease is expressed evolution of mechanism |
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morphology |
fundamental structure of cells/ tissues see morphological changes gross and histological |
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Clinical Manifestations |
evidence a disease is present noted by an observer signs and symptoms |
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signs |
noted by a clinician or outside observer
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symptoms |
effected individual presents or complains objective |
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syndrome |
compilation of multiple signs and symptoms |
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diagnosis |
nature or cause of health problem based on signs and symptoms |
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clinical course |
acute- rapid onset subacute- somewhat fast chronic-slow onset and change |
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cellular adaptation |
-cells adapt to internal environment -size, number, or type can change -single change or combination |
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Why alteration in gene function? |
housekeeping/functional genes differentiation genes- make cell unique stressors- produce signals to cause change |
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Types of Cellular adaptation |
-atrophy -hypertrophy -hyperplasia -intracellular accumulations -metaplasia dysplasia |
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Atrophy |
reduction in size of cell general causes - reduced workload - adverse conditions |
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Specific causes of Atrophy |
-disuse -denervation -loss of endocrine function -inadequate nutrition -loss of bold flow |
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Hypertrophy |
-increasing size of the cell -increase in tissue mass - due to increase in workload -increase in: organelles enzymes ATP and functional components Common in cardiac and skeletal muscle |
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Types of Hypertrophy |
1. Normal physiological condition -exercise 2. Abnormal pathological condition - adaptive or compensatory
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Specific cause of Hypertrophy |
-cells eventually reach limit -tissue enlargement can not compensate for increased demands -signaling molecules alter gene expression cell becomes larger
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examples of Hypertrophy (abnormal) |
kidneys, ovaries, testies -blockage causes thickening or urinary bladder -myocardial hypertrophy -valvular heart disease |
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Signaling molecules for hypertrophy |
atp depletion mechanical forces activation of cell degradation products chemical factors - cytokines, chemokines, growth factors, hormones |
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hyperplasia |
increase in the number of cells in an organ or tissue occurs in epithelium is common undergo mitotic division activation of genes by signals caused by growth intracellular messengers |
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myostatin |
deficiency results in increase in # of muscle cells -double muscling |
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stimuli for hyperplasia |
1. physiological - hormonal: breast and uterine for pregnant -compensatory: liver enlargement after hepatectomy, wound healing, angiogenesis 2. non-physiological -BPH -excessive GH stim or hormonal -skin warts |
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metaplasia |
replacing one somatic cell by another type |
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how does metaplasia occur |
reprogramming of undifferentiated cells to produce new ones - response to chronic irritation and inflammation - new cells better equipped to survive never oversteps primary tissue group |
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dysplasia |
deranged cell growth of a specific tissue variation in size shape and appearance |
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Frequent Dysplasia |
metaplasmic squamous epithelium - respiratory tract and cervix continued exposure is precursor for cancer |
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Intracellular accumulations |
buildup of substances that the cell can not immediately dispose of |
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Reasons for accumulations |
1. rate of production exceeds metabolism or removal 2. genetic disorders 3. pigment accumulations 4. pathologic calcifications |
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Rate of production exceed metabolism |
normal or abnormal endogenous or exogenous - FLD - steatosis |
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Fatty Liver Disease |
triglyceride accumulation in liver - delivery of free fatty acids from adipose to liver - starvation/ diabetes mellitus (1) - excess dietary lipids |
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Steatosis |
fatty liver
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Genetic Disorders (accumulations) |
degradation or transport of enzymes altered - Von Gierke - Tay-Sachs |
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Von Gierke Disease |
glucose 6 phosphate deficiency glycogen accumulation in liver and kidney
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Tay-Sachs disease |
mutation of HEXA gene on chromosome 15 lysosomal enzyme beta-N-acetylhexosaminidase -lipid buildup in brain -mental deterioration and death by age 3 |
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Pigment accumulation endogenous |
-jaundice retention of bilirubin excess RBC destruction obstruction of bile passages -lipfuscin indigestible residue of cell turnover wear and tear to heart nerves and liver cells |
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pigment accumulations exogenous |
-coal dust carbon accumulation= black lung disease - lead poisoning ALAD gene and ALAD 2 enzyme high affinity for lead -tattoos ink engulfed by macrophages |
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Pathologic calcifications |
abnormal tissue deposition of calcium salts and other minerals
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Types of pathologic calcifications |
dystrophic -injured tissue intra or extra cellular crystaline calcium phosphate deposits -not caused by hypercalcemia Metastatic -normal tissue -hypercalcemia -calcification in inappropriate areas
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Causes of cell injuries |
-physical agents -radiation -chemical injury -biological agents -nutritional imbalances |
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Physical agents of cell injury |
-mechanical forces impact, splitting, tearing, disrupt bold flow -temperature heat: low intensity -> heat stroke & 1 burns high intensity -> bld coagulation, protein denature cold: frostbite -> increase bld viscosity & pressure, capillary bld flow ends, clotting -Electrical |
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Electrical agents of cell injury |
damage depends on: -Voltage -Type of current (AC is bad) - Amperage -Pathway of Current -Resistance of tissue -duration of exposure |
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Radiation |
-ionizing produces free radicals that alter critical cell function mitotic cells more sensitive genetic mutations -ultraviolet disrupts intracellular bonds and DNA damage UVA &UVB (UVA = bad ) |
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Chemical Injury |
air/water pollution processed foods CO2 pesticides trace metals -injury to membranes -block enzymatic pathways -coagulated cell proteins -disrupt osmotic stuff |
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Biological agents
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-bacteria, viruses, and parasites -able to replicate & continue to harm |
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Nutritional imbalances |
-obesity leads to predispose for other diseases -Starvation nutrient, vitamine deficiencies
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Mechanisms of Cell injury |
-free radical formation -hypoxic tissue damage -apoptosis -necrosis |
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Free Radical Formation |
common pathway for tissue damage Causes: UV light ionizing radiation smoking chronic inflammation |
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-lipids -proteins -enzyme -DNA |
-peroxidation -degeneration -disactivation -damage and mutation |
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Reactive Oxygen Species |
oxygen containing molecule normal product of cellular respiration removed by cellular defense mechanisms may serve as signaling molecule used by healthy cells |
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Oxidative Stress |
-ROS production exceeds ability to neutralize -oxidizes cell components -activation of signal transduction pathways -DNA damage changes in gene expression |
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Pathways of oxidative stress
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1. cell damage and lung injury -> necrosis or apoptosis 2. Signal transduction -> transcription factors->gene expression -> apoptosis or necrosis or adaptation |
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Antioxidants |
neutralize free radicals by donating electrons |
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Natural enzyme antioxidants |
-superoxide dismutase -catalase -glutathione peroxidase -thioreductase |
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Non-enzyme antioxidants |
-carotene -tocopherols (vit E) - Ascorbate (Vit C) -glutathione -flavenoids -selenium -Zinc |
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Hypoxic Tissue Damage |
Deprives cell of oxygen interrupts oxidative metabolism reverts to anaerobic metabolism uses stored glycogen Lactic acid accumulates
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Results of hypoxic damage
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-chromatin clumping and cell shrinkage -reduced ammnt of ATP -effects ATP pumps -Na and water excess in the cell -alters pH -dilation of endoplasmic reticulum -increased membrane permeability |
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Causes of hypoxic damage |
-inadequate air -respiratory disease -ischemia -amenia -edema -cell inability to use O2
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Apoptosis
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controlled autodigestion highly selective process eliminated injured and aged cells pyknotic nuclei |
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Steps of apoptosis
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cell shrinkage and organelle clumping clumping of DNA wrinkling of cell membrane cell forms small fragments |
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Necrosis |
cell death of an organ or tissue that is still part of a living organism unregulated loss of cell integrity |
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paths of necrosis |
liquefaction coagulation caseous
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liquefaction |
cells die but enzymes still functional softening in center of access w/ discharge |
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coagulation |
denaturing of enzymes and structural proteins due to acidosis hypoxic injury seen in infarcted areas |
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caseous |
cheesy type of coagulative dead cells persist as soft cheesy like substance thought to be response of immune mech. tuberculosis lesions assoc. |
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Gangrene |
considerable mass of necrotic tissue types 1.dry 2.wet 3.gas |
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Dry Gangrene |
arterial blood supply interference line of demarcation areas shrink skin wrinkles and color changes spread is slow symptoms not as noticeable frostbite** |
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Wet Gangrene |
interfere with venous blood flow no line of demarcation skin is moist, black, under tension, cold, swollen, and pulseless blebs form on surface, liquefaction occus read is rapid |
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Sepsis |
caused by bacteria in the bld stream toxins fever chills, rapid breathing and HB, confusion and delerium, decrease BP, and Shock!
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Septic Shock |
no clotting mech internal bleeding vital organs shut down liver kidney and lungs Treatment: ICU, ASAP, oxygen, IV fluids, BP meds, dialysis, respirator, antibiotics |
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Gas Gangrene |
clostridium bacteria dirt and debree embedded in muscle bacterial toxins produce bubbles Results: death of muscle cell, hemolysis of RBC, edema, hemolytic anemia, hemoglobin in urea, renal toxicity |
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