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Pathology > Immuno 2 > Flashcards

Immuno 2 Flashcards

1
Q

Acute Rheumatic Fever/Heart Disease

  1. Type of hypersensitivity?
  2. Abs to?
  3. Pathology is characterized by?
  4. Inflammatory cells?
  5. What focal development in the heart? Other heart manifestations?
A
  1. Type II
  2. M. proteins of S. pyogenes that cross react with cardiac and other antigens
  3. Exudative and proliferative inflammatory lesions in CT of heart, joints, and subcutaneous tissue
  4. lymphocytes, plasma cells, and giant cells
  5. Perivascular inflammatory lesions (Aschoff’s nodules); pericarditis, myocarditis and/or endocarditis, residual rheumatic valvular disease with murmur
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2
Q

Acute Rheumatic fever/Heart disease cont.

  1. Paryarthritis involves?
  2. Can have symptoms of syndeham’s chorea: what are these symptoms? When do they occur?
  3. Highest occuring symptoms?
A
  1. Fibrinous exudate and effusion without erosions or pannus, disabeling arthritis
  2. Occurs after other symptoms have resolved - involuntary movement of limbs/face
  3. 75% polyarthritis, 50% carditis, 15% chorea
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3
Q

Type III Hypersensitivity

  1. What is this associated with?
  2. What is the arthus reaction?
  3. Difference in the way large vs. small ICs are dealt with?
  4. IC mediated acute necrotizing vasculitis often results in?
A
  1. Immune complexes that either form in tissue or deposit from the circulation: Ag may be endogenous or exogenous
  2. Ab is injected IV and diffuses to tissue, then the Ab specific Ag is injected into the skin and the Ag-Ab complex forms –> compliment is activated, inflammatory cells are recruited, mast cells degranulate and cause inflammation with increased vascular permeability –> vasculitis with erythema, edema, and hemorrhage
  3. Large ICs are removed by macrophages in the liver, small may circulate and have greater chance of depositing in tissue
  4. fibrinoid necrosis
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4
Q

Systemic IC diseases

  1. What is polyarteritis nodosa? Onset associated with?
  2. What is a characteristic of this? Common morphology?
  3. What causes serum sickness? Symptoms?
A
  1. systemic vasculitis of kidney, heart, GI, and CNS (lungs are spared); infection
  2. All stages of inflammation coexist at the same time; fibrinoid necrosis with occluded lumen
  3. Large doses of any high molecular weight compound (venom/abx); pruritic rash first followed by fever, arthritis, GN, lymphadenopathy, splenomegaly, and myalgia
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5
Q

IC glomerulonephritis

  1. Ags: Exogenous associated with? Endogenous?
  2. Common characteristic of all IC-GNs?
  3. 2 variations of pathogenesis?
  4. What determines location of deposit?
  5. 2 clinical similar syndromes associated with IC-GNs and differences?
  6. Difference between anti-GBM GN vs IC-GN?
A
  1. components of infectious agents/certain tumor Ags; Lupus
  2. Granular IC deposits
  3. In situe rxn of Ab with Ag: intrinsic or extrinsic Ag in GBM and Deposition of circulating ICs: deposit in areas of increased pressure and turbulence
  4. Charge and size also increased vas. perm
  5. Nephritic syndrome (mild proteinuria/edema/hypertension) Nephrotic syndrome (extensive proteinuria/edema/hypertension)
  6. Anti-GBM: Ag in BM only IC: larger in subendo.
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6
Q

Acute diffuse proliferative GN

  1. Post infectious associated with? Nonpostinfection associated with?
  2. Pathology? Deposit location? Type of deposits?
  3. Children post infection present with?
  4. Post-infectious adults causes?
  5. Most common cause of nephrotic syndrome?
A
  1. streptoccal pharyngitis or impetigo; lupus
  2. Diffuse hypercellularity with inflammatory cells; granular deposit in subepithelium
  3. Nephritic syndrome with edema, mild hypertension, hematuria, RBC casts, and hypocomplementemia
  4. Some will resolve, some develop chronic GN, others: RPGN
  5. membranous GN
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7
Q

RPGN

  1. Causes? If IC where?
  2. What forms from proliferation of epithelial cells and inflammatory infiltrate? What does this cause?
  3. What occurs to the GBM? This allows what?
  4. What GNs are supepithelial? Subendothelial?
A
  1. immune mediated: either IC or Anti-GBM; subepith
  2. crescents form causing compression of the glomerular tuft
  3. thickens and ruptures - allows cells, inflammatory mediators, and protein into urinary space
  4. RPGN, Acute diffuse proliferative GN, Membranous GN; primary MPGN type I and secondary MPGN
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8
Q

Membranous GN

  1. Where does IC deposit? What does this cause?
  2. Idiopathis vs secondary form?
  3. What eventually happens to the GBM? Classic tell?
  4. Inflammatory infiltrate? GBM damage associated with?
  5. Clinical: 85% present with? 25% present with?
A
  1. subepithelial - GBM spikes and effacement of epithelial foot processes
  2. I: autoimmune Abs to renal Ags S: drugs, tumor Ags, lupus, other autoimmune diseases
  3. Grows over the deposit –> universal thickening with “wire loop” lesions
  4. not much; complement activation and activation of mesangial cells
  5. nephrotic syndrome with mild edema; end stage renal failure
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9
Q

Membranoproliferative GN (MPGN)

  1. Primary MPGN Type I location? TYpe II? (deposits where)
  2. Secondary MPGN presentation? Association?
  3. Immune pathogenesis?
  4. ____ from inflammatory infiltrate, mesangial, and ___ proliferation. The GBM is thickened often showing a “___ ___” especially in ____.
  5. Clinical manifestation? 50% progress to?
A
  1. subendothelial (and some mesangial IC); intramembranous
  2. like Type I; various infections, neoplasms, lupus, and other autoimmune diseases
  3. Pre-formed IC deposit or In situ formation
  4. Hypercellularity; endothelial; double contour; Type I (because of extra GBM synthesis)
  5. nephritic or nephrotic syndrome with edema, hypertension, and hematuria; end stage renal failure
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10
Q

Type IV hypersensitivity

  1. DTH: role of TH1?
  2. DTH: role of TH17?
  3. CMI: role of TH1?
A
  1. secrete IFN gamma that activates macrophages to kill microbes in phagolysosomes
  2. secreted IL-17/22: recruits/prolongs survival of neutrophils and induces activation/proliferation of fibroblasts and keratinocytes
  3. Secrete IFNgamma and IL-2 that activates Tc to lyse targets with intracellular microbes (viruses) and tumor cells. Also activates NK cells via cytokines
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11
Q

DTH

  1. Ultimate effector? What does DTH hypersensitivity occur?
  2. The model is Tuberculin-type hypersensitivity rxn to purified protein derivative (PPD) from M. tuberculosis: Steps?
  3. If macrophage fails to eliminate the stimulus, ____ inflamation occurs and may involve?
A
  1. Activated macrophage; when Ag is not a microbe (eg. plant catechols)
  2. initial recognition of PPD –> sentitization –> TH1 memory cells…. 2nd encounter –> elicitation phase –> inflammation and induration (hardening) [increased vas perm allows leakage of fibrinogen to tissue and converted to fibrin and mononuclear infiltrate = induration)…. followed by resolution/healing
  3. chronic; Granuloma (epithelial most common) and fibrosis
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12
Q

DTH: Allergic Contact dermatitis

  1. Ags? What is sensitization?
  2. What is elicitation? Infiltrate?
  3. What is down-regulation?
  4. Acute symptoms?
  5. Chronic symptoms?
  6. Treatment?
A
  1. chemicals (drugs/plat catechols); Ag-tissue protein processed by langerhans cells –> presented to TH1/TH17 (become memory cells)
  2. Ag contact –> activated TH1/TH17 –> secretion of cytokines –> activation of endothelial cells and keratinocytes; basophils, eosinophils, and monocytes
  3. PGs from keratinocytes/APCs block TH1 cytokine release
  4. pruritic vesicular rash
  5. pruritic crusty lesions
  6. corticosteroids
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13
Q

CMI: Role of Tc

  1. What are Tc important for eliminating?
  2. Tc released from the ___ must bind Ag via class __ proteins and activated by ___ and ___ (from TH1) to become cytolytic.
  3. ___ from APCs stimulates IFNgamma production from ___ cells, ___, and ___.
  4. Tc degranulates what? Mechanism?
  5. 2 alternative mechanisms?
A
  1. viruses, bacteria, fungi, allogenic transplants, and tumors
  2. thymus, I, IL-2 and IFNgamma
  3. IL-12; NK; Tc and TH1
  4. Perforin and granzyme - induces apoptosis/lysis
  5. FasL on Tc to Fas on target cell; TNFbeta from Tc–<both></both>

</both>

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14
Q
  1. Tissue derivation for: Autograft? Syngraft? Allograft? Xenograft?
  2. Graft rejection depends on?
  3. Rejection mediated by Ab =? By T cells =?
  4. Direct vs. indirect pathway of rejection?
A
  1. same person; genetically similar person; genetically different person; different species
  2. Recognition of foreign MHC Ags by host immune system
  3. humoral rejection; cellular rejection
  4. D: recipient T cells react to donot MHC (dendritic cells) NO ANTIGEN I: donor Ag processing and presentation occurs by recipients dendritic cells
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15
Q

Rejection mechanisms

  1. Hyperacute: time? Occurs from? Induces?
  2. Acute humoral: Time? What occurs?
  3. Acute cellular: Infiltrate? what occurs in kidney? Endothelium?
  4. Chronic: Time? What occurs in kidneys? Vasculature?
A
  1. min/hrs; from preexisting Abs to MHC or mismatched blood type; damage endothelium –> inflammation, thrombosis, and infarction
  2. days/weeks; Ab to endothelial Ags –> necrotising vasculitis, lumen narrows, infarction
  3. Extensive T cells; invasion of tubules –> necrosis; injury
  4. months/years; intersitial fibrosis, tubular atrophy, loss of renal parenchyma from ischemia; intimal fibrosis and smooth muscle proliferation
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16
Q
  1. What is graft vs. host disease? Most common? how can it be controlled?
  2. Acute GVH involves what organs? Chronic?
  3. What is prolong immunodeficiency associated with? Results in?
  4. What occurs in Host vs. Graft disease?
  5. Kidney transplant: rare rejection? most common?
  6. Heart: what occurs with chronic rejection? Most common recurrent disease?
A
  1. Donor cells mount a response; allogenic bone marros; corticosteroids and cyclosporin
  2. skin, liver, GI; same but more severe
  3. Chemo or delay in repopulating lymphatic organs; Increased risk of infection
  4. NK and T cells of recipient attack transplant
  5. hyperacute; chronic
  6. Arteriopathy in distal epicardial and intramiocardial branches; atherosclerosis
17
Q
  1. Liver transplant: rare rejection? What does acute cellular rejection involve? Chronic? Most common recurrent disease?
  2. Long term complications in transplantation
  3. What is central tolerance? Reculator of +/- selection?
  4. Peripheral tolerance: when are self reactive cells induced to be anergic (unresponsive)?
  5. How are self reactive cells suppressed?
  6. When do self reactive cells undergo apoptosis?
A
  1. Hyperacute/acute humoral; portal inflammation, bile duct injury, and endothelial venous inflammation; arteriopathy; HBV and HCV
  2. post-transplantation lymphoproliferative disorder
  3. self reactive B and T cells induced to undergo Apoptosis; AIRE
  4. when Ag is presented without costimulatory molecule
  5. by Tregs through secretion of TGFbeta and IL-10
  6. by repeated and persistant activation via Fas
18
Q

Systemic Lupus Erythematosus

  1. Characterized by? Hallmark of active diesease?
  2. Criteria for diagnosis? (must have 4+)
  3. Most common manifestations and %?
  4. Kidney manifestations? Highest %?
  5. Symptoms of active disease?
  6. What is CREST? Occurs with positive ___ test.
A
  1. Formation of auto-Ab reactive to numerous cellular Ags; Anti-dsDNA Ab
  2. malar rash, discoid rash, photosensitivity, oral ulcers, arthritis, serositis, renal disorder, neurologic disorder (w/ seizures), hematologic disorder (HA), immune disorder, Anti-nuclear Ab/Anti-dsDNA
  3. 100%: HA, 90% arthritis, 85% photosensitivity, 50% GN, 50% pneumonitis, 50% depression/seizures
  4. Mesangial, focal proliferative, diffuse proliferative, and membranous GN
  5. fever, fatigue, anorexia, joint pain, and nephritic s.
  6. Calcinosis - raynauds - esophageal dismotility - sclerodactyly - telangeictasia; ANA
19
Q

Rheumatoid Arthritis

  1. Begins as? Turns into? Most common cutaneous manifestation? Systemic?
  2. What does the Ag activate? This causes what?
  3. Role of ICs?
  4. Role of TH17? TH1?
A
  1. small joins of hands/feet as synovitis; collagen destruction, cartilage erosion, bone resorption, and loss of function; rheumatoid nodule; vasculitis that resembles polyarteritis nodosa as well as fatigue, weight loss, and fever
  2. CD4 T helper cells –> activate B cells –> production of RF –> initiates ICs
  3. activate compliment –> inflammatio and neutrophil recruitment
  4. Neutrophil recruitment and survival; activate macrophages
20
Q

RA cont:

  1. What do macrophages release?
  2. What do TNF and IL1 stimulate?
  3. What happens to the synovium?
  4. End result?
  5. Non-articular manifestations?
A
  1. Proinflammatory cytokines: TNFalpha, IL-1/6/8
  2. Synovial cells to proliferate –> produce PG and metalloproteinases
  3. Thickens –> CT replaces cartilage and bone forming a pannus (granulation tissue)
  4. Bone/cartilage destruction, bone erosion/resorption
  5. Rheumatoid nodules, lung - pleurisy/pneumonitis, pericarditis, vasculitis
21
Q

Sjogrens Syndrome

  1. Characterized by? Due to?
  2. Hallmark? Infiltrate?
  3. What happens to the ducts? Rest of the gland?
  4. Tested findings?
  5. Symptoms?
  6. Increased risk of what malignancy?
A
  1. Dry eyes and mouth; auto-Ab destruction of lacrimal and salivary glands
  2. lymphocytic infiltrate; CD4, B, and plasma cells
  3. hyperplasia (occusion); fibrosis, atrophy of acini, fat deposition
  4. Antiribonuclear protein Abs
  5. Blurred vision, ulcerated cornea, difficulty swallowing, mouth ulcers/fissures, dental caries, enlargement of salivary glands, dry nose, dysuria
  6. lymphoid
22
Q

Mixed CT disease

  1. Describes the coexistance of what diseases?
  2. Abs to? Therapy?

Progressive systemic sclerosis

  1. Type of disease? Characterized by?
  2. Immunopathogenesis?
  3. Localized vs. limited vs. diffuse?
A
  1. SLE, polymyositis, RA, and systemic sclerosis
  2. Ribonuclear proteins; corticosteroids
  3. collagen-vascular; fibrosis in skin and other organs
  4. abnormal BV physiology, dysfunctional endothelium, immune activation
  5. Local - isolated in skin (kids) limited- skin confined to face, neck, and areas distal to elbows/knees with slow visceral involvement diffuse - widespread skin and rapid progression to viscera
23
Q

Progessive systemic sclerosis (Scleroderma)

  1. First clinical manifestation? Progression?
  2. Diffuse clinical manifestation?
  3. Some also develop what syndrome?
A
  1. Raynauds; cutaneous fibrosis (begins with soft tissue edema)
  2. CT infiltration of small arteries, lung, heart, kidney, muscles, bon, joints, and GI –> arthralgia, pulmonary fibrosis, cardiac arrhythmia, and diarrhea
  3. CREST
24
Q

Polymyositis Dermatomyocitis

  1. Disease of?
  2. CMI directed at? This causes?
  3. Presents with?
  4. Describe rash?
  5. What is found in blood? Urine? Disease course characterized by?
A
  1. skeletal muscle with or without a rash (acute/chronic)
  2. Skeletal muscle Ags –> muscle cell atrophy and necrosis
  3. symmetric proximal muscle weakness and pain
  4. photosensitive on face, hands, and chest
  5. muscle enzymes; creatinine; remissions and exacerbations
25
Q

Primary Immunodeficincies

  1. How are they determined?
  2. Manifestations?
  3. B cell IDs: infection with?
  4. T cell IDs: infection with?
  5. Complement IDs? MAC deficiencies?
  6. Clinical evaluation?
A
  1. genetically
  2. skin lesions, chronic diarrhea, impaired growth, and failure to thrive
  3. H influenzae, strep pneumonia, staph aureus, echovirus, and giardia
  4. herpes, myco. tb, candida, pneumocystitis, cryptococcus, fungi
  5. bacteria like B cell IDs; Nisseria
  6. measure cell # and Ab levels, DTH skin test, measure chemotaxis, adhesion O2 metabolism, and microbial killing of phagocytes
26
Q

X linked Agammablobulinemia

  1. Age? Presentation
  2. Hypoplasia of? Results in?
  3. Defect and Result? Treat?

Common Variable ID

  1. Age? Presentation?
  2. Occurs due to? Lymph node size? Treat?
A
  1. 5/6 months; chronic/recurrent infections: otitis, conjunctivitis, rash, dental deday
  2. Nodes with lack of follicles (NO B CELLS) but normal T cells
  3. Tyrosine Kinase results in failure of Pre-B to mature; IvIg
  4. 13-35yr; chronic sinopulmonary infection and increased risk of autoimmune disease
  5. B cells dont differentiate to plasma cells; normal; IvIg
27
Q
  1. Selective IgA deficiency: most common: presents with?
  2. Selective IgA deficiency: deficiency results from? Results in?
  3. Hyper-IgM syndrome: defect in what cells? Results in deficiency of?
  4. Hyper-IgM syndrome: main problem? presentation?
A
  1. recurrent infections (especially sinopulmonary and GI) and an increased risk for allergies/autoimmune d.
  2. Isotype switch failure or a secretion failure; no IgA
  3. TH1 and TH2; Ab and CMI deficiency
  4. Failure of T cells to produce cytokins for IgM class switching; excess IgM, recurrent pyogenic infections and infections caused by intracellular microbes
28
Q

Congenital Thymic Aplasia (DiGeorge)

  1. What is this?
  2. Early presentation? Time? what occurs?
  3. Treatment?
  4. Primary combined immunodeficiencies: characterized by?
  5. What occurs in X-linked SCID?
  6. Most common deficiencies of autosomal recessive SCID? Result?
A
  1. incomplete development of thymus and parathyroid gland
  2. 24hrs: hypoparathyroidism resulting in hypocalcemia; chronic infections
  3. marrow or stem cell transplants
  4. total absence of immune function with thymus and/or node hypoplasia
  5. defective cytokine receptors especially IL-1 needed for T cell maturation
  6. Adenosine deaminase and purine nucleoside phosphorylase; impaired lymphoid stemm cell development bc ribonucleotide reductase is inhibited and toxic metabolites accumulate
29
Q

Primary Phagocyte Deficiencies

Chronic Granulomatous disease

  1. Defects in?
  2. Presentation? Treatment?

Leukocyte adhesion deficiency

  1. No expression of? Results in?
  2. Presentation?
A
  1. NADPH oxidase
  2. recurrent infection with lymphadenopathy, skin lesions, and sinopulmonary infection; IFNgamma
  3. LFA-1 and MAC1; defective chemotaxis and cytotoxic activity
  4. Recurrent skin, vaginal, and sinopulmonary infection
30
Q

Primary complement deficiencies

  1. Cause?
  2. What is Proxysmal nocturnal hemoglobinuria?
  3. What causes hereditary angioedema?
  4. Defects in MAC from infection of what?
A
  1. Decreased phagocytosis and chemotaxis –> recurrent infections and increased risk of auto-IDs
  2. Deficiency in DAF and CD59 (MAC inhibitor) –> pancytopenia
  3. C11NH deficiency
  4. Nisseria
31
Q

Secondary IDs

AIDS

  1. General retroviral characteristics: enveloped? Genetic material? Replication?
  2. HIV initially infects what cells? Where do these migrate?
  3. What occurs in the node?
  4. Eventually what occurs?
  5. What binds CD4? Induces HIV-host fusion?
A
  1. enveloped; 2 + polarity ssRNA; reverse transcriptase
  2. mucosal CD4 T cells and macrophages; draining lymph node
  3. viral replication –> viremia –> controlled and thus a latent infection is promoted
  4. CD4 declines and allows opportunistic infection
  5. GP120; GP41
32
Q

AIDS cont

  1. What activates transcription of HIV genes? Where?
  2. Most important effect? What occurs to macrophages?
  3. What happens to B-cells?
  4. Acute infection: stage? incubation? Acute retroviral syndrome with what symptoms? What occurs after?
  5. Chronic phase (stage 2): persistant symptoms?
  6. Crisis phase (stage 3): As immune system declines there is onset of?
A
  1. NF-kB binding LTR; memory T cells
  2. CD4 T cell death; Decreased Ag presentation and cytokine production
  3. Polyclonal activation causing hypergammaglobulinemia, ICs, and inability to mount response to new Ags
  4. 1; 1-6 weeks; fever, lymphadenopathy, pharyngitis, rash, myalgia, and decrease CD4; latency
  5. lymphadenopathy, splenomegaly, fatigue, fever, wt loss, oral diseases (hairy oral leukoplakia)
  6. opportunistic infection of GI, skin, genital tract, renal, respiratory, and CNS
33
Q

Amyloidosis

  1. This is a group of diseases with what in common?
  2. What is amyloid? how is it visualized?
  3. What occurs as it collects? conformation?

Proteins involved:

  1. Ig light chains from what cells? Called what in tissue? condition?
  2. Serum amyloid associated protein A condition?
  3. Transthyretin: normal protein? ‘mutant’ in what type of amyloidosis?
A
  1. deposition of fibril proteins in intersitial tissue tissue
  2. proteinaceous substance btwn cells; H/E or congo
  3. Pressure atrophy of adjacent cells; Beta pleated sheet
  4. neoplastic plasma cells; amyloid light chains; Primary amyloidosis (AL)
  5. secondary amyloidosis (AA)
  6. thyroxine and retinol transport protein; hereditary amyloidosis
34
Q

Amyloidosis cont

  1. What is senile amyloidosis?
  2. Who accumulates beta2-microglobulin? why?
  3. 2 other main proteins?
  4. Amyloidosis is a combination of what?
A
  1. Normal transthyretin (TTR) deposited in a number of organs
  2. patients on long term hemodialysis bc cant pass through the dialysis membrane
  3. Alzheimer disease beta-amyloid and prion proteins
  4. abnormal protein folding and abnormal proteolytic activity that normally degrades misfolded proteins
35
Q

Primary amyloidosis

  1. Associated with ___ cell dyscrasias, often ___ __. The amyloid protein (AL) is usually an __ chain. Not all patient with ___ chain multiple myeloma develop ___.
  2. Most patients with AL amyloid dont have what symptoms? But have detectable ___ protein. Where?
  3. Secondary: protein? deposits where?
  4. Secondary: associated with? most frequent association?
A
  1. plasma; multiple myeloma; L; L; amyloidosis
  2. systemic symptoms; M proteins; serum or urine
  3. AA protein (from serum amyloid-associated protein); multiple organs
  4. Chronic inflammatory diseases or disease resulting in necrosis; rheumatoid arthritis
36
Q

Heredofamilial amyloidosis

  1. Familal mediterrenian fever: protein? presentation?
  2. Familial amyloid polyneruopathy: amyloid protein? Deposits where? results in?
A
  1. AA protein; fever and serosal inflammation mostly involving the pleura, peritoneum, and synovial membranes
  2. Mutant tranthyretin that deposits in nerves resulting in progressive peripheral and autonomic neuropathy
37
Q

Localized Amyloidosis

  1. Infiltrate? responsible for?
  2. associated with what tissue? frequently seen in what cancer?
  3. May also occur in what other disease?
A
  1. mononuclear infiltrate; M protein secretion
  2. endocrine tissue; medullary carcinoma of the thyroid
  3. Type II diabetes
38
Q

Generalized amyloidosis

  1. Most common organ? What can develop?
  2. Spleen deposition pattern?
  3. Deposits in the liver cause?
  4. GI involvement?
A
  1. kidney; nephrotic syndrome and renal failure
  2. splenic follicles or walls of sinuses
  3. hepatomegaly and loss of hepatocytes by pressure atrophy
  4. Any part; involvement of the tongue may hamper speech/swallowing
39
Q
  1. Major organ of senile amyloidosis? What occurs?
  2. Prognosis of patients with generalized amyloidosis?
A
  1. heart; interrupts contractile function/electrical conduction, CHF, monocyte necrosis ==> systolic ventricular dysfunction, valvular insufficiency, myocardial ischemia from infiltration of vessels
  2. poor prognosis

Pathology (11 decks)

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