Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 5 Pathology > Immunology > Flashcards

Immunology Flashcards

1
Q

The main cause of renal allograft loss (excluding patient death with a functioning graft) is…

A

Graft rejection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

The most commonly transplanted solid organ is…

A

Kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Target of tacrolimus

A

Calcineurin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Drugs targeting calcineurin

A

Cyclosporine Tacrolimus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Immunosupressive drugs targeting the cell cycle

A

Azathioprine MMF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Anti-CD20 drug

A

Rituximab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Signs and symptoms of GVHD

A

Skin: Rash Gut: Nausea, vomiting, abdominal pain, diarrhoea, bloody stool Liver: Jaundice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Treatment of GVHD

A

Corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Clinical features suggesting primary immune deficiency

A

Two major or one major and recurrent minor infections in one year Unusual organisms Unusual sites Unresponsive to oral antibiotics Chronic infections Early structural damage Family history Failure to thrive Skin rash (eczema) Mouth ulceration Chronic diarrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

List constitutive barriers to infection provided by skin

A

Keratin cells: tightly packed. Limit colonisation

Low oxygen tension

Low pH: due to secretions

Sebaceous glands: Produce hydrophobic oils to repel water and microorganisms

Produce lysozyme which destroys srtructural integrity of cell walls

Produce defensins: small cationic proteins that form pore like microbial membrane defects

Sweat glands: produce a watery fluid containing ammonia, and lactic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

List constitive barriers to infection provided by mucosal surfaces

A

Secreted mucous:

Physical barrier to trap invading pathogens

Secretory IgA prevents bacteria and viruses attaching to and penetrating epithelial cells.

Lysozyme and antimicrobial peptides directly kill invading pathogens.

Lactoferrin acts to starve invading bacteria of iron (and has a direct antimicrobial effect)

Cilia: Cilia directly trap pathogens and contribute to removal of mucous, assisted by physical manoeuvres such as sneezing and coughing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

List the cells and soluble components of the innate immune system

A

Cells Polymorphonuclear cells – neutrophils, eosinophils, basophils Monocytes and macrophages Natural killer cells Dendritic cells Soluble components Complement Acute phase proteins Cytokines and chemokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Names of specialised macrophages in different tissues: Liver Kidney Bone Spleen Lung Neural tissue Connective tissue Skin Joints

A

Liver Kupffer cell Kidney Mesangial cell Bone Osteoclast Spleen Sinusoidal lining cell Lung Alveolar macrophage Neural tissue Microglia Connective tissue Histiocyte Skin Langerhans cell Joints Macrophage like synoviocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Examples of opsonins

A

Antibodies Complement components Acute phase proteins such as CRP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Reactive oxygen species used in oxidative killing

A

Hydrogen peroxide Superoxide (O2-)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Enzyme that produces reactive oxygen species used for oxidative killing

A

NADPH oxidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Types of recurrent infections caused by phagocyte defiencies

A

SKIN AND MOUTH Recurrent deep bacterial infections: Staphylococcus aureus

Enteric bacteria

Mycobacteria: MTB and atypical

Recurrent fungal infections: Candida albicans Aspergillus fumigatus and flavus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Primary immune deficiencies characterised by failure to produce neutrophils (Name and mutation/protein affected)

A

Failure of stem cells to differentiate along myeloid or lymphoid lineage Reticular dysgenesis – autosomal recessive severe SCID: mutation in mitochondrial energy metabolism enzyme adenylate kinase 2 (AK2)

Specific failure of neutrophil maturation Kostmann syndrome - autosomal recessive severe congenital neutropenia: classical form due to mutation in HCLS1-associated protein X-1 (HAX1)

Cyclic neutropenia - autosomal dominant episodic neutropenia every 4-6 weeks: mutation in neutrophil elastase (ELA-2) NOTE: ELA-2 now known as ELANE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Primary immune deficiencies characterised by failure of leukocyte migration (Name and mutation/protein affected)

A

Leukocyte adhesion deficiency: Deficiency in CD11a/CD18 and CD11b/CD1. In LAD1 (the more common variant) the defiency is in the Beta-2 integrin subunit (CD18) In LAD2 fucosylated carbohydrate ligands for selectins are absent. This is rarer and causes severe growth restriction and mental retardation In LAD 3 activation of all beta integrins (1, 2, and 3) is defective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Primary immune deficiencies characterised by failure of oxidative killing (Name and mutation/protein affected)

A

Chronic granulomatous disease Deficiency in one of the components of NADPH oxidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Nitroblue tetrazolium (NBT) test and Dihydrorhodamine (DHR) flow cytometry test, test for the presence of… and therefore assess….

A

Hydrogen peroxide Ability of a cell to produce reactive oxygen species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

a) Cytokines important in oxidative killing of mycobacteria b) Briefly describe the pathway

A

a) IFN gamma and IL12 b) Infected macrophages stimulated to produce IL12 IL12 induces T cells to secrete IFNg IFNg feeds back to macrophages & neutrophils Stimulates production of TNF Activates NADPH oxidase Stimulates oxidative pathways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Investigation of Kostmann syndrome Neutrophil count: Leukocyte adhesion markers: Nitroblue test: Pus: Deficiency: Problem:

A

Neutrophil count: Absent Leukocyte adhesion markers: Normal Nitroblue test: Absent Pus: No Deficiency: HCLS1-associated protein X-1 (HAX1) Problem: Maturation of neutrophils leading to congenital neutropenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Investigation of Leukocyte adhesion deficiency Neutrophil count: Leukocyte adhesion markers: Nitroblue test: Pus: Deficiency: Problem:

A

Neutrophil count: Increased during infection Leukocyte adhesion markers: Absent Nitroblue test: Normal Pus: No Deficiency: deficiency in CD11a/CD18 and CD11b/CD18 Problem: Inability of leukocytes to leave the bloodstream due to lack of adhesion molecules.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Investigation of chronic granulomatous disease Neutrophil count: Leukocyte adhesion markers: Nitroblue test: Pus: Deficiency: Problem:

A

Neutrophil count: Normal Leukocyte adhesion markers: Normal Nitroblue test: abnormal Pus: Yes Deficiency: Any of the components that make up NADPH oxidase Problem: Absent respiratory burst leading to failure of oxidative killing. Persistent infection and inflammation. Granuloma formation. Lyumphadenopathy and hepatosplenomegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Treatment of Kostmann syndrome

A

G-CSF, prophylactic antibiotics. BMT if G-CSF if ineffective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Treatment of leukocyte adhesion deficiency

A

Depends on severity. LAD1: good hygiene especially oral hygiene. Systemic antibiotics guided by culture and sensitivity for acute infections. BMT used for severe phenotype. LAD2: antibiotic treatment usually effective for acute infections. Can use prophylaxis if infections recurrent. (Children afflicted with multiple other issues). LAD3: BMT, needs to be in early infancy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Treatment of chronic granulomatous disease

A

Antibiotic prophylaxis: Septrin Antifungal prophylaxis: itraconazole Interferon gamma prophylaxis Aggressive treatment of infections Treat inflammatory manifestations e.g. glucocorticoids

29
Q

Natural killer cells are…

A

Lymphocytes that express inhibitory receptors capable of recognising HLA class I molecules and have cytotoxic capacity

30
Q

Complement proteins are produced by..

A

Liver

31
Q

Formation of antigen-antibody complexes activates which complement pathway? Starts with which protein?

A

Classical C1 (conformational change)

32
Q

Describe initiation of the MBL complement pathway

A

MBL: mannose binding lectin. Produced by the liver in response to infection. Binds to carbohydrates found on many pathogens including multiple bacteria, viruses and yeasts. In blood MBL is complexed with another protein (MASP). MASP has enzymatic activity and cleaves C4 into C4a and C4b. C4b binds to the pathogen and starts the process forming C3 convertase.

33
Q

Roles of fragments released during complement activation pathway

A

Punch holes in bacterial membrabes Increases vascular permeability and cell trafficking to site of inflammation Solubilise and clear immune complexes Promotes mast cell/basophil degranulation Activates phagocytes Opsonisation of pathogens to promote phagocytosis

34
Q

Complement deficiency increases risk of which type of infection

A

Neisseria meningitides (Meningococcus) Streptococcus pneumoniae (Pneumococcus) Group B streptococcus Haemophilus influenza Specifically if alternative/terminal pathway are involved.

35
Q

Deficiency in components of classical complement pathway increases risk of… Why?

A

SLE: The classical pathway clears necrotic and apoptotic cells. Failure leads to build up of self antigens especially nuclear components. This leads to increased risk of autoimmunity Also complement activation increases clearance of immune complexes by erythrocytes. Deficiency leads to build up in joints, skin and kidneys and resulting local inflammation. Infection: Immune complexes fail to trigger complement

36
Q

Most common complement deficiency seen in SLE

A

C2 deficiency

37
Q

MBL deficiency leads to…

A

Increased infection in patients who have another cause of immune impairment Premature infants Chemotherapy HIV infection Antibody deficiency

38
Q

Deficiency in alternative complement pathway factors leads to…

A

Increased risk of infection with encapsulated bacteria

39
Q

Factors involved in alternative complement pathway

A

Factor B Factor I Factor P

40
Q

Consequences of C3 deficiency

A

Severe susceptibility to bacterial infections Especially encapsulated bacteria as unable to lyse encapsulated bacteria Increased risk of development of connective tissue disease

41
Q

List secondary causes of complement deficiency

A

Active lupus: persistent production of immune complexes leading complement consumption Nephritic factors: autoantibodies targeted at complement components. Stabilise C3 convertase leading to consumption of C3

42
Q

Two types of functional complement tests

A

CH50 classical pathway AP50 alternative pathway

43
Q

Management of complement deficiencies

A

Vaccination Boost protection mediated by other arms of the immune system Meningovax, Pneumovax and HIB vaccines Prophylactic antibiotics Treat infection aggressively Screening of family members

44
Q

Role of CCR7

A

Found in lymphatic tissue. Important role in directing dendritic cells to lymph nodes. CCL19 and CCL21 are ligands for CCR7

45
Q

Ligands for CCR7

A

CCL19, CCL21

46
Q

Brief pathogenesis of coeliac disease

A

Peptides from gliadin are deamidated by tissue transglutaminase (enzyme) and presented by APC CD4 T cells recognise these deamidated peptides presented by HLA DQ2 or DQ8 (possibly after an innate immune system trigger) CD4 T cell activation results in secretion of IFN-gamma and may indirectly lead to increased IL-15 secretion IL-15 promotes activation of the intra-epithelial lymphocytes (IEL) (Cells within the gut) Intra-epithelial lymphocytes kill epithelial cells in an NKG2D (expressed on NK cells) dependent manner The activation and function of the intra-epithelial lymphocytes appears to be independent of engagement of their T cell receptor B cell with surface receptors for gliadin interact with the T cells. B cells mature and start producing Abs against gliadin. T cells specific for gliadin provide help for B cells whose surface receptors recognise the transglutaminase part of the transglutaminase / gliadin complex. These mature and produce Abs against transglutaminase. (antibodies also produced against endomysial cells)

47
Q

First line immunological test for coeliac in most labs

A

Anti-transglutaminase antibodies (IgA) (but disappears within several months of gluten free diet, IgG anti-gliadin persists for upto 12 months).

48
Q

Gold standard test for coeliac

A

Duodenal histology remains the “gold standard”

49
Q

Coeliac histology

A

Villous atrophy and crypt hyperplasia Increased lymphocytes in villi

50
Q

Type of reaction caused by transfusion of incompatible blood (not ABO incompatibility)

A

EXTRAVASCULAR HAEMOLYSIS in the spleen – a delayed haemolytic transfusion reaction

51
Q

Cause of an immediate transfusion reaction

A

ABO incompatibility

52
Q

Plasma from the lab takes… minutes to thaw

A

20-30

53
Q

Compatibility required for plasma transfusion

A

Give ABO compatible but D group doesn’t matter AB plasma can be given to all groups as it has no RBC antibodies but it is in short supply No need to cross match

54
Q

Compatibility required for blood transfusion

A

Give ABO/D compatible Consider special requirements

55
Q

Compatibility required for platelet transfusion

A

ABO/D antigens weakly expressed Should be D compatible No need to cross match If group O given to A, B or AB patients select ‘high-titre’ negative

56
Q

Blood transfusion (red cells): …will typically give a Hb increment of…

A

4mL/kg 10g/L

57
Q

In acute blood loss, transfusion is indicated if patient has lost more than…% of blood volume

A

30%

58
Q

Irradiated blood is required for…

A

highly immunosupressed patients at risk of engraftment of donor lymphocytes to prevent transfusion associated graft versus host disease (TA-GvHD)

59
Q

CMV negative blood is only required for….

A

intra-uterine and neonatal transfusions (new guidance 2012). Also for elective transfusion in pregnant women (baby in-utero is exposed to maternal transfusion)

60
Q

Auto-inflammatory diseases are caused by…

A

Genetic abnormality affecting the innate immune system, often in a site-specific manner

61
Q

Immunopathology is caused by

A

May describe damage resulting from the immune response to ongoing infection

62
Q

Autoimmune disease is caused by…

A

Genetic abnormality affecting the adaptive immune system and is often associated with presence of auto-antibodies

63
Q

Monogenic auto-inflammatory diseases commonly affect which cytokines?

A

IL1 and/or TNF

64
Q

Name 2 monogenic autoinflammatory disorders

A

TRAPS (TNF receptor associated periodic syndrome) Familial mediterranean fever

65
Q

Draw the inflammasome complex

A
66
Q
A
67
Q

Describe pathway affected by calcineurin inhibitors

A
68
Q

Outline the the classification of vasculitis and give examples from each class

A
69
Q

Examples of infections seen in different types of immunodeficiency

B cell

T cell

Neutrophil defect

Complement

A

Year 5 Pathology (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions