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Pathology Flashcards

1
Q

What is Lysozyme?

A

 antibacterial factor

 Enzyme present at mucosal surfaces

 Active in breaking down the Gram-positive cell wall

 reduces the chance of symptomatic gram-positive infections

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2
Q

What is Lactoferrin?

A

 antibacterial factor

 Protein found at mucosal surfaces

 Chelates iron and therefore reduces soluble iron in the GI/respiratory tract

 Inhibits the growth of bacteria as they do not have access to iron

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3
Q

What are the three different pathways of activating complement:

A

 Classical pathway: Ag-Ab complex can bind to and activate complement

 Alternative pathway: complement is activated directly by pathogen surfaces

 Mannose-binding Lectin pathway: activation of complement by specific sugar residues on pathogen surface

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4
Q

Roles of complement

A

 Killing of pathogens by membrane attack complex (direct lysis via MAC)

 Recruitment of inflammatory cells

 Opsonization of pathogens (makes them more palatable for phagocytosis)

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5
Q

Which WBC are important in the immune response to parasites?

A

Eosinophils

They are also involved in allergy responses

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6
Q

Functions of antibodies

A

1) Opsonise for phagocytosis
2) Activate Complement for lysis
3) Neutralise toxins and pathogen binding sites

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7
Q

What is Central tolerance?

A

process whereby immature T and B cells acquire tolerance to self-antigens during
maturation within the primary lymphoid organs.

It involves the elimination of cells with receptors for
self-antigens = NEGATIVE SELECTION

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8
Q

What is Clonal deletion?

A

mechanism that causes elimination of self-reactive lymphocytes on contact with self-antigens.

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9
Q

Explain positive and negative selection in relation to T cell development.

A

T cells expressing receptors with weak binding to MHC I and II antigens are permitted to survive –
they are POSITIVELY SELECTED

If the T cell receptor binds strongly to MHC alone or MHC carrying self peptide in the thymus, T cells are
induced to die by apoptosis – NEGATIVE SELECTION

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10
Q

What is Peripheral tolerance?

A

Peripheral T cells are made unresponsive (anergic) through the absence of the second signal,
which is essential for T cell activation

Peripheral B cells are made unresponsive by the absence of co-stimulatory signals from T cells

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11
Q

What do Th1 cells predominantly produce and what is their role?

A

IFN-gamma

Important in the defence against intracellular microbes

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12
Q

What do Th2 cells predominantly produce and what is their role?

A

IL-4 (IL-5, IL-13)

Important in the defence against parasites

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13
Q

What do Th17 cells predominantly produce and what is their role?

A

IL-17

Important in the defence against some bacteria

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14
Q

Hypersensitivity

A

a heightened immune response to an offending agent with subsequent clinical symptoms.

Tissue damaging reactions may occur to innocuous agents.

Classified into 4 types based on the mechanism leading to tissue damage

Hypersensitivity reactions are antigen specific, and occur after the immune system has already responded to an antigen (i.e. the immune system has been primed)

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15
Q

Type I Hypersensitivity

A

Immediate (2-30 minutes)
most common type
IgE mediated - result from antigen cross-linking to mast cell-bound IgE

can be systemic or localised, mild or life threatening

e.g. allergic dermatitis, asthma, eczema, hayfever

tends to increase in severity with repeated challenges

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16
Q

Type II Hypersensitivity

A

5-8 hours

Cytotoxic, antibody dependent

IgG or IgM mediated (reacts to cell-bound antigen)

induces lysis through complement activation

e.g. Rh disease of the newborn
blood transfusion reactions, AIHA, rheumatic heart disease

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17
Q

Type III Hypersensitivity

A

2-8 hours

Immune complex formation

IgG or IgM bound to soluble antigen

complexes aggregate in small blood vessels, causing occlusion, inflammation and complement activation

complement recruits PMNs, which release tissue-damaging enzymes

systemic complex deposition causes vasculitis

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18
Q

Type IV Hypersensitivity

A

delayed - 24-72 hours

Cell mediated 
T cells (CD4 + & CD8 + )

Can be granulomatous

e.g. TB, contact dermatitis

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19
Q

Type V Hypersensitivity

A

chronic subtype of type II hypersensitivity

“stimulatory hypersensitivity”. IgM or IgG bound to receptors.

results when stimulatory (rather than cytolytic) antibodies develop to self antigens

e.g. Graves’ disease

20
Q

Process of Type I hypersensitivity

A

1) person becomes sensitised to the antigen (involves IgE antibody production)
2) mast cells are primed with IgE formed on initial contact with antigen
3) person is re-exposed to the antigen
4) the antigen binds and crosslinks with IgE on mast cells
5) mast cells degranulate, releasing pro-inflammatory substances
6) eosinophils recruited to the site release mediators, causing a prolonged reaction

21
Q

Describe the early phase of type I hypersensitivity reactions

A

occurs within 20 minutes

largely mediated by histamine and prostaglandins

  • smooth muscle contraction
  • increased vascular permeability
22
Q

Describe the late phase of type I hypersensitivity reactions

A

Principally mediated by T cells

tissue remodelling - inflammation, fibrosis, oedema and necrosis

sustained muscle contraction/hypertrophy -> inflammatory cells release growth factors

23
Q

Autoimmune disease

A

harmful inflammatory response directed against ‘self’ tissue by the
adaptive immune response

24
Q

Which type of hypersensitivity reactions are involved in Type 1 Diabetes?

A

Usually a combination of type II and type IV

25
Myasthenia Gravis
Syndrome of fatigable muscle weakness – Limbs – Respiratory – Head and neck * Caused by IgG against acetylcholine receptor * Antibody blocks receptor and prevents signal transduction
26
What is Rheumatoid Factor?
IgM and IgA directed against IgG Fc region – Forms large immune complexes: High concentration within synovial fluid Also found in other tissues • Not specific for rheumatoid arthritis
27
Briefly explain the Pathophysiology of RA
Inflammation leads to release of PAD enzymes from inflammatory cells PAD alters a variety of proteins by converting alanine to citrulline These are then recognized by the immune system as non-self anti-citrullinated protein/peptide antibodies are common o These build up within the joints Vicious cycle ensues: abnormal proteins generate inflammation, and inflammation generates the production of more abnormal proteins Further chemoatraction of inflammatory cells into synovium causes osteoclast activation and joint destruction systemic inflammation ensues
28
Risk factors for autoimmune disease
AI disease results from a complex interaction between genetic and environmental factors Genetic predisposition - HLA genes (MCH I/II) - cytokines and receptors Environmental factors: - infection and molecular mimicry - geographical - vitamin D levels - smoking
29
DEVELOPMENTAL ANOMALY
any congenital defect that occurs when normal growth & differentiation of the foetus is disturbed
30
How is developmental anomaly different from congenital anomaly?
Congenital anomalies exist at or before birth regardless of the cause. They may be either functional/metabolic or structural. Developmental anomaly is deformity, absence or excess body parts/tissues which occur when normal growth is disturbed. i.e. DEVELOPMENTAL ANOMALY = STRUCTURAL CONGENITAL ANOMALY
31
Acyanotic congenital heart defect
(aka a left-to-right shunt) o no signs of cyanosis in the early stage o uncorrected VSD can increase pulmonary resistance due to higher than usual pressure on the right side of the heart (blood passes from left to right, i.e. from high pressure to low pressure) o This increased pressure in the pulmonary circulation leads to the reversal of the shunt and corresponding cyanosis (with deoxygenated blood passing into the left side of the heart and thereby entering the systemic circulation)
32
HAMARTOMA
Malformation that may resemble a neoplasm that results from faulty growth in an organ Composed of a mixture of mature tissue elements which would normally be found at that site which develop and grow at the same rate at the surrounding tissue
33
CHONDROID HAMARTOMA
Lung lesion which may be seen as a ‘coin lesion’ on x-ray Composed of a mixture of epithelium, cartilage, fat, smooth muscle (i.e. tissue that should be at that site)
34
DIVERTICULUM
Circumscribed pouch/sac caused by herniation of lining mucosa of an organ through defect in muscular coat
35
METAPLASIA
Reversible change from one fully differentiated cell type into another
36
Neoplasia
An abnormal tissue mass of which the growth is excessive (ie not an adaptation to physiological demands) and uncoordinated compared to adjacent normal tissue
37
Carcinoma
Malignant tumour of epithelial origin
38
Sarcoma
Malignant tumour of messenchymal origin
39
Melanoma
Malignant tumour of melanocyte origin
40
Lymphoma
Malignant tumour of haemopoietic origin
41
tumours - Differentiation
extent to which the tumor cell resembles the original cell
42
Tumour stage
based on: 1) size of the primary tumor 2) extent of invasion into surrounding tissue 3) spread to regional lymph nodes 4) presence or absence of metastases
43
CARCINOMA IN-SITU
Full-thickness epithelial dysplasia extending from the basement membrane to the surface of the epithelium Applicable only to epithelial neoplasms
44
METASTASES
Tumor implants discontinuous from the primary tumor
45
Routes of tumour spread
1) haematogenous – typical of sarcomas. Arteries are more difficult for tumour to penetrate than veins. Blood-borne cells follow the venous flow draining the site of the tumor. Liver and lungs are frequently involved 2) lymphatic – most common pathway for dissemination of carcinomas. Follows natural route of drainage (Sentinel node involvement) 3) transcoelomic - occurs when a malignant neoplasm penetrates into a natural ‘open field’ such as peritoneal cavity, pleural space, pericardial cavity, etc. - ovarian carcinoma and gastric carcinoma

J3 (18 decks)

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