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Pathology > Immunopathology > Flashcards

Immunopathology Flashcards

1
Q

What is a Type I Hypersensitivity Reaction?

A

Immediate with rapid reaction within minutes. Characterized by shock, edema, and respiratory compromise

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2
Q

What is Type II Hypersensitivity Reaction?

A

Antibody-mediated, caused by Abs against cell surface or ECM antigens

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3
Q

What is Type III Hypersensitivity Reaction?

A

Immune complex-mediated, damaging inflammatory reaction to antigen-Ab complexes especially in blood or glomeruli

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4
Q

What is Type IV Hypersensitivity Reaction?

A

Cell-mediated, delayed, caused by sensitized CD4 T cells, producing granulomas

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5
Q

What does anti-CCP test for?

A

Rheumatoid Arthritis

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6
Q

Anti-centromere?

A

CREST syndrome (limited systemic sclerosis)

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7
Q

Anti-Jo-1

A

Polymyositis/dermatomyositis

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8
Q

Anti-Scl70 = Anti-DNA topoisomerase

A

Systemic Sclerosis (diffuse)

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9
Q

Anti-RNA Polymerase

A

Systemic Sclerosis, with renal crisis

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10
Q

Anti-U1 RNP

A

Mixed connective tissue disease

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11
Q

Anti-Sm

A

Lupus

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12
Q

Anti-ddDNA

A

Lupus

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13
Q

Anti-Nuclear (ANA)

A

Lupus and many other rheumatic disease

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14
Q

Anti-SSA

A

Sjogren’s Syndrome, Neonatal Lupus, Subcut, Lupus

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15
Q

Anti-SSB

A

Sjogren’s Syndrome, Neonatal Lupus, Subcu Lupus

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16
Q

Anti-Myeloperoxidase, P-ANCA

A

Microscopic Polyangiitis, Eosinophilic granulomatosis with polyangiitis

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17
Q

C-ANCA

A

Granulomatosis with polyangiitis

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18
Q

What are general types of therapy used?

A

Chemotherapy, corticosteroids, transplant rejection medicines

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19
Q

What are immunosuppressive chemotherapeutic drugs freqeuntly used?

A

Methotrexate and Cyclophosphamide

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20
Q

What effect to corticosteroids have?

A

Anti-inflammatory

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21
Q

What are two transplant rejection drugs?

A

Cyclosporine and Tracrolimus

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22
Q

What is the method of transplant rejection drugs?

A

They are calcineurin inhibitors. Bind intracytoplasmic receptor proteins called immunophilins, which inhibit calcineurin. Calcineurin normally dephosphorylates regulatory proteins, allowing them to pass into the nucleus of the lymphocyte, promoting T cell activation and secretion of TNF, IFN-GAMMA, IL2 AND IL4.

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23
Q

What is mycophonelate mofetil (cellcept)?

A

Reversible inhibitor of inosine monophosphate dehydrogenase in purine biosyn that inhibits DNA replication, inhibiting lymphocyte proliferation

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24
Q

What is mycophenolate mofetil used to treat?

A

SLE

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25
Q

What is azathioprine?

A

Messes up DNA replication, used in SLE, Rheumatoid Arthritis, and other AI diseases

26
Q

What is hydroxycholoroquine?

A

Anti-malarial antibiotic with anti-inflammatory activity used to treat SLE and Rheumatoid Arthritis

27
Q

What are gross pathologies of Systemic Lupus Erythematosus?

A

Non-erosive synovitis, pluritis, pericarditis, peritonitis, splenomegaly

28
Q

What are microscopic pathology of SLE?

A

Acute necrotizing vasculitis of arteries, nephritis, cerebritis

29
Q

What are signs of SLE?

A

Butterfly skin rash on face, edema, fatigue, weight loss, joint pain, fever, pleuritic chest pain

30
Q

What are symptoms of sjogren syndrome?

A

Dry ocular and oral mucosa, enlarged salivary and lacrimal glands, fatigue, joint pain, conjunctival and oral ulcers

31
Q

What is systemic sclerosis?

A

An abnormal accumulation of fibrous tissue in skin and organs. Widespread skin involvement

32
Q

What is the pathogenesis of systemic sclerosis?

A

Abnormal immune response + vascular damage = increased growth factors leading to fibrosis.

33
Q

What are symptoms of systemic sclerosis?

A

Joint pain, stiffness, digestive problems, edema of hands and feet, puffy fingers are first sign

later: hard or shiny skin over long bones of arms and lower legs

34
Q

What are microscopic manifestations of GVHD

A

erythematous rash and biopsy show lymphocytic infiltrate with apoptosis of epidermal cells, especially at dermal-epidermal junction. visible by a gap between the two layers. in liver, hepatocytes undergo apoptosis

35
Q

What is XLA?

A

Congential immunodeficiency with failure of B cells to produce Abs due to faulty Bruton’s Tyrosine Kinase

36
Q

What is amyloidosis?

A

Progressive organ dysfunction that can be systemic or localized.

37
Q

What are symptoms of amyloidosis?

A

Nonspecific complaint such as weakness, fatigue, weight loss. Later, renal disease (gaining water weight), hepatomegaly, splenomegaly, or cardiac abnormalities

38
Q

A man gets a platelet transfusion and gets growing areas of itchy skin edema. What’s the mechanism?

A

Mast cells, IgE, and leukotriene

39
Q

What do mast cells release?

A

Histamine

40
Q

What is the major prostaglandin that mast cells release

A

PGD2

41
Q

What are mast cell products?

A

Histamine chemokines, kallkrein generating factors, granule-associated proteases, peroxidase, proteoglycans

42
Q

What is urticaria?

A

Hives, type I immediate hypersensitivity reaction caused by antigen reaction with preformed IgE on surface of mast cells.

43
Q

What plus what plus…. = type I immediate hypersensitivity?

A

Mast cells + IgE + histamine + leukotrienes + PGD2

44
Q

A 5 yo gets a sore throat, week later onset of malaise, nausea and slight fever. Her urine is smoky brown and decreased. What is mechanism of her disease?

A

Antigen-Xs immune complexes. Ab-antigen complexes accumulate in the kidneys. Poststreptococcal acute glomerulonephritis

45
Q

What is Goodpasture’s Syndrome?

A

Affects lungs and kidneys, Abs to alveolar and glomerular basement membranes. Hemoptysis and hematuria. Usually in 20-40 yo. Kidneys - rapidly progressive glomerulonephritis with glomerular crescent formation. Lungs - heavy, areas of red-brown consolidation from bleeding and hemosidering deposition. LINEAR deposits of IgG

46
Q

What kind of IgG deposits are present in SLE?

A

Granular subendothelial deposits of IgG thickening capillaries circumferentially.

47
Q

What is poststreptococcal acute glomerulonephritis?

A

Most common in 6-10 yo. Fever, malaise, nausea, smoky urine. Hematuria, edema, proteinuria, hypertension. Increased IgG, decreased C3 complement. Granular deposits of IgG and C3. Swelling periorbital region due to edema

48
Q

What are symptoms of AIDS?

A

Acute phase - sore throat, myalgia, fever, rash and sometimes aseptic meningitis

Crisis phase - fever of more than one month, fatigue, weight loss, and diarrhea

49
Q

What are symptoms of amyloidosis?

A

nonspecific complaints such as weakness, fatigue, weight loss, Later, renal disease (severe edema), hepato,splenomegalies, cardiac abnormalities

50
Q

What are symptoms of heart failure?

A

Dyspnea, orthopnea, paroxysmal noctural dyspnea (waking up short of breath),

51
Q

Hepatic Failure symptoms

A

jaundice, bleeding (decreased clotting factors), edema, hepatic encephalopathy (confusion progressing to coma)

52
Q

What are symptoms of SLE?

A

Weight loss, fatigue, joint pain, fever, butterfly rash, pleuritic chest pain

53
Q

What is the time course of HIV viral load?

A

Acute phase - increases to peak of 10 million/ml plasma at about 6 weeks

Clinical latency - decreases to about 10,000/ml plamsa

Final crisis stage - 11 years and back up to 10 million

54
Q

What is the course of CD4 load in HIV?

A

Acute phase - initial normal of 1000 to around 500 at six weeks

Clinical latency - gradual decline to around 50/cu mm at about 9 years

Final crisis stage - down to around 5/cu mm

55
Q

At what CD4 load count to symptoms begin? At what count to opportunistic infxns begin?

A

200/cu mm

100/cu mm

56
Q

What is primary amyloidosis?

A

Deposition of Amyloid-Light chains. Associated with multiple myeloma

57
Q

What is secondary amyloidosis?

A

Amyloid-Associated. Associated with chronic inflammation

58
Q

What is localized amyloidosis?

A

Deposition in a single organ. associated with alzheimers. Most common form of dementia. Alpha-Beta chains

59
Q

What is the common patient for systemic sclerosis (scleroderma)?

A

Women of childbearing age

60
Q

What is the classic patient for SLE?

A

Women of childbearing age

61
Q

What is induced amyloidosis?

A

It’s frequently dialysis patients because they cannot get rid of the HLA,so you accumulate MHC Class I.

62
Q

What is scleroderma?

A

Scleroderma excess fibrous deposition and tissue. Typically associated with CREST. Due to xs inflammation an tissue destruction. IgG-mediated with rheumatoid factor. Assocaited with Scl-70. Results in contracture. Mask face, claw hand! No treatment. Vasculature and smooth muscle replaced by collagen.

Pathology (8 decks)

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