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91 Cards in this Set
- Front
- Back
what are the FOUR major aspects of Pathology
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1. Etiology: cause
2. Pathogenesis: mechanism 3. Morphologic changes: structural alteration in cells and organs 4. Clinical Sig: functional consequences (S/S, Course, Dx, Complications, Px) |
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what is the most common cause of cell injury in Clinical Medicine...THREE CAUSES??
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HYPOXIA: due to insufficient blood supply to tissues (ischemia)
1. obstruction of arterial flow or venous drainage 2. inadequate oxygenation of blood owing to cardio-respiratory failure 3. loss of oxygen carrying capacity of blood (anemia) |
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lipofuscin...more prevalent in who??
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yellow/brown wear and tear pigment caused by physical, chemical, or other injurious agents causing somatic mutation and changes in cell constituents
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how does the body protect against oxidation
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body produces superoxide dismutase (SODs), glutathione peroxidase and catalase
taking antioxidants (vit A, C, E) also helps |
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ubiquitin-proteasome system?
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perform selective protein elimination to prevent cell injury and disease...operates under physiological and pathological processes
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what are THREE nuclear changes in NECROSIS
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1. pykosis: nucleus condenses into solid, shrunken basophilic masses
2. karyorrhexis: nucleus undergoes fragmentation 3. karyolysis: basophilia of chromatin fades and nucleus totally disappears IRREVERSIBLE |
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what are the FIVE types of NECROSIS
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1. Coagulative: happens everywhere except the brain
2. Liquefactive: primarily in the brain due to breakdown of myelin 3. Caseous: white, milky, amorphous material in tuberculous lesion 4. Enzymatic Fat: occurs when fats are digested by lipases and pooled 5. Gangrenous: dry and wet, also a type of coagulative necrosis |
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apoptosis
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a distinct pattern of death of a single cells (distinct from necrosis)
suppression may be a determinant of growth of cancer |
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THREE causes of intracellular accumulation
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1. excessive amounts of normal metabolites
2. abnormal nonmetabolizable substances 3. excessive intracellular synthesis of some products REVERSIBLE!! |
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difference between:
1. dystrophic calcification 2. metastatic calcification |
1. dystrophic:
calcium deposition in dead and dying tissues normal calcium metabolism normal serum level 2. metastatic: calcium deposition in normal tissues due to hypercalcemia abnormal calcium metabolism |
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SIX causes for HYPERCALCEMIA
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M.I.S.H.A.P
1. Malignancy 2. Immobilization 3. Sarcoidosis 4. Hyperparathyroidism/Hypervitaminosis D 5. Alkalidosis/Addison Syndrome 6. Paget |
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what are SEVEN types of ATROPHY
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1. Disuse: decreased workload
2. Denervation: muscle paralysis 3. Vascular: diminished blood supply 4. Nutritional: starvation 5. Endocrine: trophic hormones 6. Pressure: prolonged pressure 7. Senile: morphological changes of aging |
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what is the difference between hypertrophy and hyperplasia
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1. Hyperplasia: increase in # of cells in a tissure w/ increase in size of organ
2. Hypertrophy: increase in size of tissue or organ due to increase in size of its component cells |
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FIVE characteristics of dysplasia
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abnormality in maturation with variation in size, shape, orientation and organization of epithelial cells
1. increase in size of nucleus relative to that of cytoplasm (N:C ratio) 2. hyperchromasia 3. abnormal chromatin forming coarse clumping and irregular and thickened nuclear membrane 4. presence of NORMAL and ABUNDANT mitotic figures 5. disorderly maturation of cells REVERSIBLE |
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what is the difference between benign and malignant tumors
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benign
1. high degree of differentiation, resembles tissue of origin 2. expansile growth, compression of adjacent tissue and forms CAPSULE 3. slow rate of growth and it MAY stop 4. NEVER METASTASIZE malignant: 1. varying degrees of undifferentiation and anaplasia 2. invade adjacent tissues, NO CAPSULE 3. rapid AND continual growth 4. spread via METASTASES |
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what is the difference between ANAPLASIA and DYSPLASIA
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anaplasia shows all features of dysplasia
ANAPLASIA is a major microscopic characteristic of malignancy...DYSPLASIA is reversible |
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what are malignant tumors of the epithelium called...mesenchymal tissue
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epithelium: CARCINOMA
mesenchymal: SARCOMA |
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what are the FOUR pathways of spread of MALIGNANT TUMORS
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1. DIRECT LOCAL INVASION: tumor becomes fixed to the adjacent structure
2. TRANSCOELOMIC SPREAD: peritoneal cavity commonly involved (Krukenberg tumor from stomach to overies) 3. LYMPHATIC SPEAD 4. HEMATOGENOUS SPREAD: if systemic (if vena cava is involved then lungs are most common site), if portal venous system (liver, most common site), if arterial (brain, liver and bone |
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what is the difference between grading and staging of cancer
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1. grading: based on degree of differentiation of tumor cells and number of mitoses present (1-4 with increasing anaplasia)
2. staging: based on size of tumor, extent of spread to regional lymph nodes, and the presence or absence of metastases. MORE CLINICALLY RELEVANT |
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what are the FOUR major viral oncogenic agents
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1. hepatitis B group, HBV (liver)
2. HPV (papilloma in skin, larynx, genitalia) (carcinoma of uterine cervix and vulva) 3. Epstein-Barr (Burkitt lymphoma, Immunoblastic lymphoma, nasopharyngeal carcinoma) 4. Human T-cell Leukemia (Adult T-Cell Leukemia/lymphoma) 1-3 are DNA, 4 is RNA |
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what are the FOUR antioncogenes
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1. Rb genes: normal genes product prevents cells from entering S phase of cell cycle
2. p53 gene: repair damaged DNA and induces apoptosis 3. BRCA 1&2: DNA repair 4. APC gene: A cell regulator gene |
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what are the NINE effects of tumor on host
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A.C.H.O.I.S.E.P.U.T
1. Anemia 2. Cachexia 3. Hormonal effects 4. Obstruction 5. Irritation of serous membrane 6. SEcondary Infection 7. Produce a Lesion: SOL 8. Ulceration and bleeding 9. Torsion |
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what is the most important method of cancer diagnosis
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HISTOLOGICAL EXAMINATION
still subjective though |
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what are the TWO most important tumor markers
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1. alpha-fetoprotein (liver and testes)
2. carcinoembryonic antigen (colon, pancreas, lungs, stomach, breast) NOT GOOD FOR Dx important for monitoring to see if treatment is working or not |
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what is edema? what is the difference between transudate and exudate?
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accumulation of abnormal amounts of fluids in intercellular tissues spaces or body cavities
transduate: NONINFLAMMATORY EDEMA fluid, LOW protein and colloids LOW specific gravity, FEW cells exudate: INFLAMMATION, HIGH protein, HIGH specific gravity, MANY cells |
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THREE causes of EDEMA
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1. increase in intravenous hydrostatic pressure
2. fall in osmotic pressure of plasma 3. impairment or obstruction of the flow of lymph |
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what happens when the pressure of the venous end is INCREASED (>12mmHg)
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EDEMA
fluid will not return to the capillary |
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how does heart failure cause edema
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INCREASE in hydrostatic pressure causing EDEMA
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how does HYPOPROTEINEMIA cause EDEMA
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hypoproteinemia will cause a DECREASE in osmotic pressure of plasma protein.
lower than 25mmHg, fluid can NOT enter back to the capillaries |
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what are FOUR clinical types (morphological) of edema
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cardiac, renal, pulmonary, cerebral
1. cardiac: subcutaneous edema most prominent in lower extremities...pitting edema(NOT HEART) 2. renal: generalized, manifested initially in loose tissues such as eyelids, pitting edema 3. pulmonary: seen in LV FAILURE, renal failure and lung disease 4. cerebral |
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what is active hyperemia
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1. increased arterial flow due to arteriolar dilation
2. seen in skin and muscles during exercise and at site of inflammation |
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what causes PULMONARY edema? what are the effects
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causes:
1. LEFT VENTRICLE FAILURE 2. Rheumatic heart disease 3. floppy MV with regurgitation effects: 1. HEART FAILURE CELLS (present in LUNGS not HEART)!! 2. pigmentation, brown induration of lungs |
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what causes LIVER edema? what are the effects
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causes
1. RIGHT VENTRICLE FAILURE can be ACUTE or CHRONIC effects: 1.pigmentation, NUTMEG LIVER |
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what causes SPLEEN edema? what are the effects
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causes:
PORTAL VEIN OBSTRUCTION effects: pigmentation, Gamma Gandi Bodies |
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what is Virchow's Triad
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1. endothelial injury releases thrombotic/antithrombotic factors result in clotting (important disease is Atherosclerosis)
2. changes in Blood Flow 3. hyper-coagulability of Blood |
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what causes hyper-coagulability of blood
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D.O.N.T.M.I.S.S.
1. Deficiency of antithrombin III or protein C 2. Oral Contraceptives 3. Nephrotic Syndrome 4. Trauma 5. Malignant cells secrete procoagulants 6. Increased # and Stickiness of platelets |
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what are the FIVE fates of thrombus
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I.ROPE
1. Infection: thrombus may become infected 2. Removal: via fibrinolytic action 3. Organization and recanalization 4. Propagation: may cause obstruction 5. Embolization: whole or part of thrombus may break off PROPAGATION and EMBOLIZATION is the WORST |
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what are the SIX clinical settings when a thrombus can occur
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1. advanced age
2. bed rest and immobilization 3. heart disease 4. tissue injury 5. cancer 6. late pregnancy and delivery |
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what is usual impact for emboli arising from the veins? arteries
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1. veins->lungs
2. arteries->legs, brain, systemic 99% of emboli are thrombi |
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what is significant about pulmonary embolism
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MOST IMPORTANT
1. large embolus may block MPA or become saddle embolus (immediate death or right heart failure) 2. >95% of pulmonary emboli arises from DVT |
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what is the clinical significance of infarction
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common cause of clinical illness and myocardial, cerebral and pulmonary infarctions are responsible for over HALF of all deaths
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what are the four major causes of SHOCK
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V.O.C.H.
1. Vasogenic 2. Obstructive 3. Cardiogenic 4. Hypovolemic |
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what are causes of hypovolemic shock
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inadequate blood volume
1. hemorrhage 2. trauma 3. surgery 4. burns 5. fluid loss (vomitting/diarrhea) particularly important in children |
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what are the causes of vasogenic shock (distributive)
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increase size of vascular shock (vasodilation, NORMAL blood volume)
1. fainting (neurogenic shock) 2. anaphylaxis (allergies) 3. sepsis (vasodilation and increase capillary permeability) peripheral pooling NO BLOOD LOSS blood not available for circulation |
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what are the causes of cardiogenic shock
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decrease cardiac output
1. myocardial infarction (MI) 2. congestive heart failure (CHF) 3. arrhythmias (ventricular arrhythmia) |
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what are the causes of obstructive shock
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obstructive blood flow
1. pulmonary embolism 2. cardiac tamponade 3. cardiac tumor 4. tension pneumothorax |
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what is the most common cause of death in the ICU
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SEPTIC SHOCK (Vasogenic)
vasodilation and myocardial depression |
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what happens during an allergic reaction
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ANAPHYLACTIC SHOCK
allergic reaction leads to a release in histamine causing vasodilation DECREASE BLOOD PRESSURE |
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what are the THREE forms of SEPSIS
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1. sepsis
tachycardia, tachypnea, inc/dec Temp, inc/dec WBC count 2. sepsis syndrome (sever sepsis): sepsis w/ decreased perfusion, peripheral dilation, hypoxemia. (also low lactate, low urine output, and low mental status) 3. septic shock: SS with hypotension despite fluid administration |
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what are the THREE important autosomal DOMINANT conditions
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1. Marfan's Syndrome
2. Familial Hypercholesterolemia 3. Neurofibromatosis |
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what are the SIX important autosomal RECESSIVE conditions
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GGCLAP
1. galactosemia 2. glycogenoses 3. cystic fibrosis 4. lysosomal storage diseases 5. albinism 6. phenylketonuria |
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Marfan Syndrome
1. type of disorder 2. what happens 3. clinical features |
1. autosomal DOMINANT disorder
2. qualitative and quantitative defects in fibrillin 3. affect skeleton, eyes, cardiovascular sys. high arched palate, bilateral dislocation of lens, retinal detachment, MV prolapse |
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Familial Hypercholesterolemia
1. type of disorder 2. what happens in homozygotes and heterozygotes conditions |
1. autosomal DOMINANT disorder
2. LDL receptor id deficient 1. Homozygotes: develop Xanthomas in childhood and soon death via MI 2. Heterozygotes: cholesterol deposit along tendon shealths and premature atherosclerosis |
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Neurofibromatosis
1. type of disorder 2. what are the 3 major features of type 1. |
autosomal DOMINANT disorder
1. multiple neurofibroma 2. pigmented skin lesions 3. pigmented iris hamartomas type 2 (acoustic): rare, characterized by skin pigmentation |
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cystic fibrosis
1. type of disorder 2. what happens |
autosomal RECESSIVE disorder
widespread defect in exocrine glands. clinically manifested by recurrent pulmonary infections and pancreatic insufficiency REVIEW: exocrine glands secrete sweat, digestive juices and mucus |
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phenylketonuria
1. type of disorder 2. what happens |
autosomal RECESSIVE disorder
1. deficiency or absent of hepatic enzyme, phenylalanine hydrooxylase (PAH) 2. result in failure conversion of dietary phenylalanine to tyrosine PA levels in blood NORMAL at birth, but very high after 2nd week. |
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what are the FIVE main infectious causes of newborn morbidity
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T.O.R.C.H.
1. toxoplasma 2. other 3. rubella 4. cytomegalovirus 5. herpes simplex |
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what are the THREE main causes of cytogenetic chromosomal disorders
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1. increasing maternal age
2. ionizing radiation 3. drugs (anticancer agents, thalidomide, especially in early stage of pregnancy) |
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Klinefelter Syndrome
1. type of disorder 2. what happens |
sex chromosome disorder
1. male hypogonadism 2. most patients with 47 XXY small balls, ball atrophy, mild retardation, etc. |
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turner syndrome
1. type of disorder 2. what happens |
sex chromosome disorder
1. female hypogonadism 2. 55% monosomy (45X) or 45% mixture 45X/46XX |
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what is the difference between cell mediated immunity and humoral immunity
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1. cell mediated: defense against intracellular microbes
2. humoral: defense against extracellular microbes and their toxins |
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1. CD4+ T Cells associate with...
2. CD8+ T Cells associate with... |
1. CD4+T cells associate with Class II MHC presentations
2. CD8+ T cells associate with Class I MHC presentations |
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where are the MHC clustered
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clustered and produced on a small segment of CHROMOSOME 6
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what tells the lymphocytes to activate, grow and differentiate
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interleukin 2 and 4
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what is an important ability of the natural killer cells
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1. ability to lyse variety of tumor cells, virally infected cells, and some normal cells w/o activation
2. first line of defense against neoplasm or viral infections 3. can lyse IgG coated targets and MHC expressions |
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what are the TWO phase of type 1 hypersensitivity
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1. initial: vasodilation and vascular leakage (happens within 5-30min)
2. late: tissue destruction, infiltration of WBC (eosinophils, neutrophils, basophils, monocytes) and CD4+ (2-8hrs) |
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in type 1 hypersensitivity what Ig does the antigen bind to and what does it cause
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Asthma
1. antigen binds to IgE 2. signals leads to mast cell degranulation |
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what are the three categories of type 2 hypersensitivity
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1. complement-dependent reaction: direct lysis and opsonization (blood allergy)
2. antibody-dependent cell mediated cytoxicity: cell lysis proceeds w.o. phagocytosis (tumor) 3. antibody-mediated cellular dysfunction (myasthenia gravis and graves disease) |
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what is the principle behind type 2 hypersensitivity
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mediated by antibodies (IgG and IgM) directed towards antigens present on the surface of the cells or other tissue components
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what happens in type 3 hypersensitivity
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1. antigen-antibody complex formation
2. complement activation 3. phagocytosis 4. lysosomal enzyme release 5. tissue damage or systemic damage |
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what happens in type 4 hypersensitivity and what is a common procedure that involves this type of rxn
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1. cell mediated hypersensitivity is initiated by specifically sensitized CD4+
2.involves direct cell cytotoxicity mediated by CD8+ TB SKIN TEST |
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what are the two mechanisms of host vs graft disease
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1. T-cell mediated reactions: direct (tcell of recipient recognizes MHC of donor) and indirect (classic model)
2. Antibody-Mediated reactions: hyperacute (antidonor antibodies are already present in body of recipient) |
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what is the pathogenesis of SLE
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1. generate antibodies against cell membrane (PhosphoLipid Bilayer)
2. Lupus anticoagulant prolongs PTT 3. causes false positive test result for Syphilis |
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how does SLE relate to Syphilis? Why?
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1. FALSE POSITIVE FOR SYPHILIS
2. antibodies against the phospholipid-beta2-glycoprotein complex also bind to CARDIOLIPIN antigen |
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what is used a clinically diagnosis for SLE
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presence of antibodies to dsDNA and the Smith antigen
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what is Sjogren Syndrome
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1. autoimmune disease
2. dry eye/dry mouth (sicca syndrome) 3. destruction/fibrosis of the lacrimal and salivary glands |
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what does the infiltrate activate in Sjogren Syndrome
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CD4+ helper T Cells and some B cells
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what is a clinically diagnosis for Sjogren
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present of two ribonucleoproteins
1. SS-A (Ro) 2. SS-B (La) detected in 90% of patients by highly sensitive techniques Biopsy of the LIP!!! |
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what is systemic sclerosis and what are the TWO types??
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autoimmune disease characterized by abnormal accumulation of fibrous tissue in the skin and multiple organs
1. diffuse: widespread, rapid progression and early visceral involvement 2. limited: limited to face, fingers, and forearm. visceral later... |
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what is C.R.E.S.T.?? what is it associated with??
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LIMITED SCLERODERMA
Calcinosis Raynaud phenomenon Esophageal dysmotility Sclerodactyly Telangiectasia |
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what are the clinical diagnosis of systemic sclerosis
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1. DNA topoisomerase I: highly specific, present in 28-70% of patients with DIFFUSE sys. sclerosis
2. Anticentromere antibody: is found in 22-36% of patients with LIMITED sys. sclerosis |
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what is X-linked Agammaglobulinemia of Bruton
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1. failure of B-cell precursors to differentiate to B cells
2. block maturation due to mutation in cytoplasmic tyrosine kinase 3. apparent after 6 months, antibodies are depleted 4. H.influenzae, Strep.pneumoniae, Staph. aureus |
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what is thymic hypoplasia
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DIGEORGE SYNDROME
1. T cell activation absent 2. infants are vulnerable to viral, fungal and protozoal infection 3. NO CD8 or CD4 NOTE: B CELL FUNCTION NORMAL |
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what is common variable immunodeficiency
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1. hypogammaglobulinemia (very low levels of antibodies)
2. block in Bcell maturation to plasma cells 3. NORMAL NUMBER OF B CELLS 4. NO PLASMA CELLS |
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what is the most common immunodeficiency disease
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isolated IgA deficiency
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what is isolated IgA deficiency
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1. block in terminal differentiation of IgA-secreting B cells to plasma cells
IgA is important in respiratory, and GI...so obviously block of IgA will cause these systems to malfunction |
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what is severe combined immunodeficiency diseases
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1. defect in BOTH humoral and cell-mediated immune response
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what is HIV envelope studded with?
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viral glycoproteins
1. gp120 2. gp41 |
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how does HIV enter the cells
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viral glycoproteins (gp120 & gp41) interaction with CD4 receptor and chemokine receptors
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what are the THREE phases of HIV infection
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1. acute: 3-6 weeks, CD4 reduction, cold like symptoms
2. chronic: lymphadenopathy develops, CD4 declines further, thrush 3. crisis: you're screwed |
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what are the THREE diagnostic processes for HIV
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1. ELISA: 99% sensitive (detect p24)
2. Western Blot: 2 bands (p24 & p41) (gp120 & gp160) 3. Viral Load: CD4 count |