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140 Cards in this Set
- Front
- Back
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If we can't grow organism in a culture, what do we use to identify it? |
PCR, DNA sequence analysis |
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Which virus example can transform host cell into neoplastic ones? |
HPV |
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3 examples of atypical bacteria? |
Chlamydia, Rickettsia, mycoplasma |
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3 classifications of protozoa and examples of each? Are they unicellular or multicellular? |
Protozoa: bloodborne (plasmodium) Intestinal (toxoplasma, giardia) SEX (trichomonas) They are unicellular Helminths are multicellular |
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Ectoparasites attach and live on ______ on humans |
skin |
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Criteria of microorganism colonization (2) and proliferation? (3) What are the other 2 parts of virulence? |
Colonization criteria: -Size of inoculum -ability to adhere to host (viruses - receptors, bac - adhesion proteins and stuff) Prolif: -Local factors (pH, etc.) -Outcompete local flora -Ability to evade host defense Other 2 parts of virulence: tissue injury, transmission |
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Viral tropism definition |
the cells and tissues of a host that are infected by a bacteria or virus (i.e. these microorgs are tissue and cell-specific) |
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Endotoxins disrupt what? (1) Exotoxins disrupt what? (2) |
Endo: structural features Exo: PM integrity, host metabolism |
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Viral tissue injury methods: |
Viruses: inhibit host metabolism, affect integrity of host PM, lysis (direct injury?), host autoimmune destruction, induce cell prolif/transformation |
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Epithelial vs epidermal Which is mucosal and which is skin? |
Epithelial is mucosal, skin is epidermal |
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Opportunistic microorganisms have ______ virulence? (low or high?) Examples: bac (1), virus (2), fungus (2), protozoa (2) |
Low virulence Bac: pneumococcus Viruses: CMV, herpes Fungal: C. albicans, Aspergillus Protozoa: toxoplasma (intestinal), pneumocystis |
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5 types of inflammation? |
Suppurative (PMN) Mononuclear, granulomatous Cytopathic-cytoproliferative Necrotizing Chronic inflammation and scarring |
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For Suppurative and mononuclear,granulomatous: what immune cells come? What microorg is the cause? For Cytopathic-cytoproliferative: what microorg? |
Suppurative: neutrophils; bacteria M/G: lymphocytes; intracellular bac, viruses, parasites C/C: viruses |
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Granulomatous characterized by accum of what? 2 examples? |
Accum of epitheliod histocytes (altered macrophages) Examples: Fungal infections, TB |
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Clinical features of infection |
Leukocytosis, erythema, pain, swelling, fever, hypotension, shock |
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First barriers to infection? (2) |
Skin and mucous/mucosal secretions (e.g. IgA) |
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Is wet or dry skin more permeable to infections? |
Wet skin (e.g. sexytime = bad microorgs like) |
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4 outcomes of infection? Which one leads to chronic infection? Fun fact; most chronic infections caused by viruses! |
-Organism dies -> no infxn -Host successful immune system -> no or mild symptoms -> subsequent immunity to prevent further disease -Host defenses contain, but don't kill org (Chronic infection) -Host defenses unsuccessful -> u die |
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60% of person’s body weight is water -> what is the breakdown of this60%? |
40% intracellular 15% interstitial (extracellular) 5% plasma |
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Pressure in mmHg of Hstatic, oncotic (COP) and interstitial fluid pressure?(Int fluid osmotic pressure is very low) |
Hstatic: 32 @ arterial end; 12 @ venous Oncotic (COP): 26 Interstitial fluid: 3-4 |
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4 causes of edema and examples of each? |
1. Incr hstatic pressure (congestive heart failure, deep venous thrombosis of legs) 2. Decrease COP (renal failure, liver cirrhosis, malnutrition) 3. Lymphatic obstruction (cancer, inflammation, postsurgical lymphedema) -> incr int fluid osmotic pressure 4. Sodium retention (kidney failure) |
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Which cause of edema is associated with hypoproteinemia? |
Decreased COP (less albumin) |
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For lymphatic obstruction: what are the 2 effects? Which effect causesincreased oncotic fluid pressure in int space? |
1. Less reabsorption 2. Less protein removal The latter associated with increased oncotic pressure |
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What causes for: Localized (2) vs. generalized (3) edema? |
Localized: 1. Incr hstatic pressure (vascular obstruction) 2. Lymphatic obstruction Generalized: 1. Incr hstatic pressure (heart failure) 2. Decreased COP (loss of albumin) 3. Sodium retention |
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Hyperaemia and congestion causes? Which one is an active and which is passive process? |
Hyperaemia: incr arterial inflow (active) Congestion: decr venous outflow (passive) |
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Hyperaemia shows a red tissue pattern - what colour does congestion show? |
Blue-red |
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What is Virchow's triad? What disease/effect is it related to? |
Represents causes of thrombosis 1. Vessel damage 2. Blood flow ∆ [stasis] (Decr CO, higher viscosity) 3. Blood composition ∆ (incr platelet conc.) |
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Possible outcomes/prognosis of a thrombus? |
Propagation: enlarge Break into emboli -> If newer thrombus: dissolve -> If older thrombus: may recanalize |
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Examples of emboli? (5) |
Thromboemboli (most common) Gas (e.g. air) Fat Tumour Others e.g. foreign bodies |
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What blood vessels can thromboemboli occlude? |
Arteries OR veins |
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2 causes of ischemia? How does the degree of ischemia affect disease results? |
1. Occlusion 2. Decreased CO Low degree: i.e. you get enough blood -> no disease High degree: not enough blood -> TISSUE INJURY AND STUFF |
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Infarction: is it reversible or irreversible? Healing occurs through what process? Infarct area is in what shape? |
Irreversible Healing through fibrosis Wedge shape |
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White vs. Red infarct: -Occlusion in what vessel? What type of tissue/organs? -Which one associated with leg gangrene? -Which one associated with hemorrhage? |
White: Arterial occlusion, in solid organs (heart, kidney, spleen), associated with leg gangrene Red: Arterial OR venous occlusion, in loose tissues (intestine, lung, brain [need dual blood supply]), assoc with hemorrhage |
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Hemorrhage: escape of blood from _________ into surrounding tissues or body cavities or outside body |
Blood vessels |
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Some causes of hemorrhage? |
1. Trauma to large blood vessels 2. Weakened artery (atherosclerosis) 3. Infections (Pulmonary TB) 4. Invasive tumours 5. Hypertension 6. Hemorrhages diastheses (affecting capillaries, including Thrombocytopenia) |
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Thrombocytopenia: Deficiency in what? (2) |
1. # of platelets 2. Coag/clotting factors |
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Bleeding into where? Hematoma Purpura Ecchymosis Petechia Hemothorax Hemocardium Hemoperitoneum Hemoarthrosis |
Hematoma: soft tissue Purpura: skin Ecchymosis: skin, assoc with discolouration Petechia: Skin, mucosal, serosal surfaces Hemothorax: Pleural cavities Hemocardium: Pericardium Hemoperitoneum: Ab cavities Hemoarthrosis: joints |
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Due to trauma/rupture of what? Hemothorax Hemocardium Hemoperitoneum |
Hemothorax: aorta Hemocardium: heart or aorta Hemoperitoneum: aorta, liver, spleen |
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Rank from largest to smallest: Purpura Ecchymosis Petechia |
Ecchymosis > Purpura > Petechia (pinpoint) |
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Shock: failure of circ system to maintain appropriate blood supply to ________? (i.e. macro or micro circ?) Inadequate _______ of all organs |
microcirculation Perfusion |
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3 general causes of shock? |
1. Decreased BV 2. Decreased CO 3. Redistribution of blood |
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Types of shock (4) |
1. Hemorrhagic/hypovolemic (loss of FLUID from vascular component) - i.e. can be loss of plasma (water) 2. Cardiogenic 3. Septic 4. Anaphylactic/Neurogenic |
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2 causes of cardiogenic shock and examples |
1. Heart can't pump blood (myocardial infarction, pericardial tamponade) 2. Decr CO (pulm embolism) |
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Neurogenic shock caused by (2) |
Anaesthesia, spinal cord injury |
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What 3 shock types associated with peripheral vasodilation? |
Anaphylatic, neurogenic, septic shock |
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Examples of autosomal recessive diseases? (7) |
CF Phenylketonuria Galactosemia Tay-sachs Mucopolysaccharidoses Lysosomal storage diseases Niemann-pick |
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Examples of autosomal dominant diseases? (5)* |
Familial hypercholesterolemia Marfan Ehler-Danlos Acute intermittent poryphria (AIP) *Huntington's |
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Examples of X-linked recessive diseases? (4)* -> Note: affects mainly males |
Diabetes insipidus Lesch-Nyhan Megaloblastic anemia *Fragile X |
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Top 2 leading GENETIC causes of mental retardation? |
1. Down Syndrome 2. Fragile X |
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Triplet repeat expansions: Fragile X vs Huntington's -Location? (which area of chromosome/genome) -Triplet repeat codon? -Loss or gain of protein function? -Premutations expand to full mutations during? (Oogenesis or spermatogenesis?) |
Fragile X: -X chromosome @ q27.3 -CGG -Loss of fxn -Oogenesis Huntington's -Huntingtin gene? -CAG -Gain of toxic protein fxn -Spermatogenesis |
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Mitochondrial inheritance is maternally or paternally derived? 2 disease examples |
Maternally LHON, MERRF |
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Genomic imprinting is reset during ________ 2 disease examples? and result from disruption on paternally or maternally derived genes? -> Which of paternally or maternally derived genes is silenced/imprinted? |
gametogenesis -PWS -> paternally derived (maternal silenced) -AS -> maternally derived (paternal silenced) |
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Kuru related to what type of infectious agent? |
Prions |
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Haplotypes associated with what kind of analysis? |
Linkage analysis/Genome-wide association studies |
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Phenylketonuria: clinical results? Accum of what? Assay/test? |
Severe mental retardation, seizures, hyperactivity, less hair/skin pigmentations Accum Phenylalanine (amino acid) Gluthrie test |
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Galactosemia: clinical results? Accum of what? Assay/test? |
Jaundice, liver damage (fatty change -> hepatomegaly), cataracts, neural damage Accum of galactose -> impair AA transport (aminoaciduria) Assay for transferase in WBC/RBC |
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What metabolic disease (auto recessive) has many variants, sometimes a milder form in adult onset? What accumulates in that disease? |
lysosomal storage diseases Accum insoluble metabolite (lysosome can't fully degrade) |
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What auto recessive disease is a type of GM2 Gangliosidosis? Most common in what type of people? Accum of what and where? What appearance in glial cells in CNS? |
Tay-Sachs -Ashkenazi Jews -Ganglioside accum in brain -Glial cells appear swollen/foamy, with lipid vacuolation appearance |
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Niemann-Pick A and B -DIfferences in clinical manifestations? -Accum of what? |
Both have organolegaly (spleen, bone marrow, liver, lymph nodes, lungs) -> SB, LLL. But type A also has neurological symptoms while B does not Accum sphingomyelin |
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What is impaired to cause these auto dominant diseases?? Familial hypercholesterolemia AIP |
Familial hypercholesterolemia: LDL receptor AIP: Heme synth impaired -> accumulate porphyrin intermediate |
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What is impaired to cause these auto dominant diseases?? Lesch Nyhan Megaloblastic anemia |
Lesch Nyhan: HPRT enz impaired -> accum uric acid Megaloblastic anemia: HPRT enz lack -> poorly use B12 |
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What disease associated with pour gout? What is the 'striking feature' of that disease? |
Lesch Nyhan Self-mutilating behaviours (lip biting, finger biting) |
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Acquired metabolic disorders are most commonly associated with what? (2) |
Hypoxia, ischemia (Usually related to atherosclerosis in large-medium sized arteries) |
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Athlerosclerosis begins when in life? Earliest path lesion and progression? Modifiable risk factors? (4) Non-modifiable risk factors? (2) Other risk factors? |
Early in life, clinically silent until progression to disease point Fatty streak -> fibro-fatty plaque Mod: Hypertension, hyperlipidemia, smoking, diabetes mellitus Non-mod: sex (Male more likely), family history Other: Type A personality, etc. |
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Prominent symptoms of Type 1 diabetes? (2) |
polyuria (gotta pee) polydipsia (thirstayyyyyyyy) |
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Type 1 vs type 2 diabetes -Onset? -Weight -Blood insulin lvls (ins dependent or not?) -Antibody to islet cells? -Ketoacidosis? -Twin concordance, which linked to MHC II HLA? -Insulitis? -Atrophy -Beta cell depletion |
Type 1 ; 2 respectively: -Onset: <20 yrs (develop in childhood, peak in puberty); >30 yrs -Weight: normal; obese -Blood insulin: decreased; incr early then normal to moderate decreased dependent; independent -Ab to islet: Yes; no -Ketoacidosis: common; rare -> nonketotic hyperosmolar coma -Twins: lower concordance (link to MHC II HLA); higher concordance -Insulitis: early; none -Atrophy: atrophy and fibrosis; focal atrophy and amyloid deposition -Beta cell depletion: yes; mild |
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Diabetic complications: long term in where? |
Kidneys, eyes, nerves, blood vessels in both diabetes |
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-Explain Sorbitol and AGE effects |
Glucoses binds to many diff proteins -> form AGE -> inac fxn of protein or crosslink to others Intracellular hyperglycemia can activate many pathways incr glucose flux -> metabolism by polyol pathways -> form sorbitol in tissues Sorbitol can be directly toxic, or can cause osmotic gradient -> swelling Polyol pathway may cause eye damage |
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Hallmark of diabetic macrovascular disease Most common death cause in diabetics? Renal artery also can be affected, but most damaging effects exerted at level of what?? What else is more common diabetics than general population? (lower areas) |
Accelerated atherosclerosis affecting aorta, large/med-sized arteries Myocardial infarction due to atherosclerosis of coronary arteries glomeruli, microcirculation Gangrene of lower areas |
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Long-standing diabetes can lead to visual impairment: lesion in retina takes what two forms? Major way to minimize these complications? |
Non-proliferative retinopathy Proliferative retinopathy (make new blood vessels, fibrosis, vitreous hemorrhages) Endogenously administered insulin |
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Group of disorders -> leading cause of death in children <5 in developing world? What are its 3 types? (technically 4) |
PEM: Marasmus, Kwashiorkor, Anorexia nervosa, bulimia |
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Difference of Kwashiorkor to Marasmus? |
-Only protein deficiency vs. all nutrients -Normal subcutaneous fat, severe edema, hepatomegaly, fatty liver present |
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Leading cause of blindness in world? |
Vit A deficiency |
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Vit A deficiency results in: (3) |
Xerophthalmia, Bitot spots -> keratomalacia |
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Vit C deficiency: -Is ascorbic acid water soluble? -Crosslinking of what? -Collagen with large conc. of what is mostly affected? -Vit C can also act as what? |
-Yes, cuz ADEK are the fat-soluble ones so C is water soluble -Proline-lysine crosslinking -Large conc of hydroxy-proline -Antioxidant - can scavenge free radicals -> vit E is also powerful antioxidant |
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Vitamin toxicities due to fat-soluble or water-soluble vitamins? |
fat |
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Which vitamin is a teratogen when ingested in excess? |
Vit A |
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Innate vs. adaptive immunity -Which one is non-specific? -Which one has lag time between exposure and maximal response? |
Non-spec: innate Lag: adaptive |
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2 humoral and chemical barriers? |
Inflammation, complement system |
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Cellular components of inflammation (6) |
neutrophils Eosinophils/basophils Monocytes/macrophages Mast cells Dendritic cells NK cells |
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Complement systems are normally inactive while circulating in blood. Can be activated by (3): |
-Proteases -Binding of complement to Abs on microbes -Binding of complement to carbs on microbes |
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What kind of receptors to phagocytes use to recognize microbes |
Toll-like receptors |
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NK cells recognize what MHC class? Is the signal inhibitory or stimulatory? |
MHC I Inhibitory signal to NK -> i.e. if MHC I is present on cell, NK will not attack; if MHC I is damaged, NK will attack |
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NK cells can also be a part of adaptive immunity by recognizing ______ NK cells can also produce the cytokine ________ |
Ab-coated cells (opsonized) -> kill (antibody-mediated cytotoxicity) IFN-gamma -> activate macrophages |
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Besides NK cells, what else can make IFN-gamma? |
TH1 (CD4-mediated immunity) aka humoral |
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T lymphocytes vs. B lymphocytes: -Where do they mature? -Make up what % of peripheral blood lymphocytes? |
T: thymus; 60-70% B: bone marrow; 10-20% |
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Does CD3 bind antigen? |
No, linked to TCRs and involved in signal transduction of signals into T cell after it has bound antigen (activation) |
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Macrophages are involved in adaptive immunity: how? (4) |
-it is an APC -Involved in delayed hypersensitivity rxn (cell-mediated immunity) -Involved in effector phase of humoral immunity (phagocytose opsonized things) -Secrete cytokines |
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APCs have Fc receptors for molecule? |
IgG (opsonization) |
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What does a B cell have on its surface? |
-Non-activated: have Igs -Fc receptors -CD40 -Complement receptors |
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Do NK cells need previous sensitization to lyse tumour cells, viral-infected cells and some normal cells? |
No, can lyse IgG-coated target cells (as long as they're coated) |
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HLC genes encode what? |
MHC |
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MHC class I and II -On what cells? -Recognized by what cells? |
I: On all cells, recog by CD8, NK II: On APCs, recog by CD4 |
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Antigen presentation: -MHC I vs. II: which one presents extracellular derived and which one presents intracellularly-derived antigens? |
MHC I: Intra MHC II: Extra |
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CD4 functions? (3) |
-Secrete IL-2 -> T proliferation -Cytokine -CD40L binds CD40 on macrophages (activation) and B-cells (Ig production) |
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T proliferation by IL-2 into what types? What do those T-cell subtypes do? |
-TH1 -> make IFN gamma -> activate macrophages, B cells -TH2 -> eosinophils, mast cells -TH17 -> neutrophils |
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CD8 killing mechanism? What enzymes and what do they do? |
-Perforin makes hole in membrane, Granzyme triggers apoptosis |
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B cell activation can be T-cell independent and T-cell dependent: what types of antigens? -Which one requires CD40L from T-cell? -Which one requires coactivation? |
Independent: polysacc or lipid antigens (may bind many B-cell antigen receptors) Dependent: protein (need CD40L) -> coactivation |
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IgG is the only Ab involved in ___________ and can cross the __________ |
opsonization placenta |
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Which 2 Abs can activate the complement system? |
IgM, IgG |
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Which cells (3) have Fc receptors? (i.e. involved in ADCC - can destroy opsonized cells) |
Neutrophils, macrophages, NK -Non-specific killing |
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Hypofxn -> 2 main forms of disease: what are they and what results? |
1. Defense disorders -> more susceptible to infections 2. Surveillance -> higher frequency of malignant disease |
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Hyperfxn is often what kind of disease state? (acute chronic or latent?) |
Chronic |
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Type I: Anaphylatic -What Ab involved, attaches to what? -"Allergic" or "_______" reactions -Results? |
-IgE attaches to mast cells -Atopic -Vascular permeability increases, smooth muscle contraction (due to VAPE) |
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Type II: Ab mediated -What 2 antibodies? -Bind antigens where? -Mechanism? -Examples (3) |
-IgG, IgM (cuz they can activate complement) -Cell surfaces/tissue components -Opsonizes circulating cells, cells with Fc receptors come to kill (neutrophils, macrophages, NK) -Transfusion mismatch, ITP, goodpasture |
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Type III: Immune complexes -Ab against what antigens? -Mechanism? -Examples (2) |
-Circulating antigens -Form immune complexes -> trapped in tissues -> complement system come to kill. Can also be deposited into blood vessels -> necrotizing vasculitis -> ischemic necrosis, acute inflammation in surrounding tissue -Lupus, post-strep glomerulonephritis |
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Type IV: Cell-mediated 1. Delayed type hypersensitivity if persistent: -> granulomas -> giant multinucleated 2. T-cell mediated cytotoxicity -Examples of both? (3 each) |
-Delayed type: poison ivy, tuberculin rxn, granulomatous inflammation -T cytotoxicity: viral hepatitis, type I diabetes, solid-organ transplant rejection |
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2 main factors of autoimmune disease self/non-self stuff |
1. Discrimination of self and non-self by T 2. Suppression of immune response to self by T suppressor |
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1˚ Immunodeficiency disease examples (6) Pure ___-cell dysfunction unlikely |
Bruton (x-linked agammaglobulinemia) -> pure B-cell dysfunction Common variable deficiency Isolated IgA Hyper-IgM DiGeorge SCID T |
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Which 1˚ immunodeficiency disease is a 70% X-linked mutation in CD40L on T-cells? |
Hyper-IgM |
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Immunodeficiency disorders affecting innate immunity (3) |
1. Deficiency of complement proteins 2. Chronic granulomatous disease 3. Rare mutations in Toll-like receptors |
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2˚ immunodeficiency diseases can be caused by many things: (6) |
1. Infections 2. Immunosuppressive therapy 3. Malignancy 4. Chronic illness 5. Malnutrition 6. Aging |
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What 3 infections can cause temporary immunodeficiency? |
Mycoplasma, rubella, measles |
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Which malignant tumour especially can cause 2˚ immunodeficiency? |
lymphoma |
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Malformations examples (3) |
Polydactyly, spina bifida, congenital heart disease |
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Potter syndrome clinical features |
Abnormal lung development -> death Weird facies and weird feet/hand positioning |
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Congenital infections (3) |
Rubella, CMV, varicella zoster (chicken pox) |
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congenital rubella mechanism and clinical results |
-Cross placenta (TORCH) -> replicates in fetal cells and prevent proper division (host has no immune system yet) -> growth retardation, cataracts, deafness, congenital HD |
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Rubella has highest risk if the infection occurs in the first ____ weeks |
8 |
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What substance can cause phocomelia? |
Thalidomide Phocomelia = seal limbs |
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What substance's harmful effects extends through gestation? (Not restricted to period of early pregnancy) |
Alcohol in mama -> fetal alcohol syndrome |
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Maternal disorder: What is a huge risk factor? -What type gives highest risk? -Severity of malformations depends on? |
Diabetes Mellitus -> type I (insulin-dependent) Severity depends on maternal diabetes control during pregnancy (e.g. can supplement with endogenous insulin) |
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Down syndrome -What is a significant risk factor? |
-Maternal age -> older = much more likely |
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Chromosome abnormalities XO disease is called: XXY disease is called: |
XO: Turner XXY: Klinefelter |
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Cri-du-chat results from ______ ______ in short arm of chromosome 5 |
partial deletions |
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Marfan is a ________ tissue disorder -clinical features? |
connective long limbs, dislocation of lens, abnormal aorta dilation |
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CF is most common recessive disease in what race of children? Causes abnormalities to lung and _______ |
Caucasian pancreas -> intestinal malabsorption |
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What chromosome is Hemophilia A on? |
X |
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Multifactorial (polygenic) disorders? (3) |
-congenital heart disease -Cleft palate -Spina bifida |
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Perinatal infections can be acquired two ways: -> What microorganisms can cause each? |
1. Transcervically herpes, beta-hemolytic strep 2. Transplacentally TORCH (toxoplasma, other, rubella, CMV, herpes) |
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Main risk factor of respiratory distress syndrome? Treatment? |
prematurity (before 36 weeks gestations) Add corticosteroids for mom if early delivery unavoidable, supportive ventilation, natural/recomb surfactant |
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RDS mechanism RDS is also called: |
Type 2 pneumocytes can't make enough surfactant -> alveolar collapse -> atelectasis (infant tires from breathing) -> hypoxia -> damage -> hyaline membrane formation hyaline membrane disease |
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Hamartoma vs. Hematoma vs. Hemangioma |
Hamartoma: excess growth of tissue/cells in correct location Hematoma: Hemorrhage into soft tissues Hemangioma: benign tumour |
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Most common tumour of infancy? Where is it found? |
Hemangioma Capillary or cavernous areas -> skin and within internal organs |
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Most common malignant neoplasms in infancy found in? (3) -> contrast to adults? Often look primitive histologically -> what are they called? |
Found in hematopoietic system (bone marrow), neural tissue, soft tissues whereas adult tumours usually in epithelial things (lung, prostate, breast, colon) "small blue round cell tumours" |
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Neuroblastoma most commonly arise in |
Adrenal gland (adrenal medulla) |
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Retinoblastoma -recessive or dominant? -Increased risk of what sarcoma? Familial vs sporadic |
-Recessive -Osteosarcoma -Familial: multiple tumours, bilateral -Sporadic: one tumour, unilateral |
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Wilms tumour is often in the form of |
Abdominal mass |
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Which type of malignant babby tumour can undergo spontaneous regression? |
Retinoblastoma |
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Which chromosomes are these things found on? -Marfan -CF -MHC genes (HLA) -Cri-du-chat -familial hypercholesterolemia -Diabetes mellitus -Retinoblastoma -Neuroblastoma |
-Marfan: 15 -CF: 7 MHC genes: 6 Cri-du-chat: 5 -Familial hypercholesterolemia: 19 -Diabetes mellitus: 6 -Retinoblastoma: 13 -Neuroblastoma: 1 |
