Pathology Flashcards

1
Q

What are the 4 stages of wound healing?

A

Haemostasis
Inflammation
Proliferation
Remodelling

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2
Q

Describe the haemostasis stage of wound healing

A
  1. Platelet adhesion, activation and aggregation
  2. Activation of coagulation cascade
  3. Waterproof layer of fibrin and fibronectin forms
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3
Q

Describe the inflammation stage of wound healing

A
  1. Infiltration by neutrophils
  2. Infiltration by macrophages on day 3
  3. Basal epithelial cells respond to epithelial growth factor to proliferation and migrate under the clot
  4. Platelets secrete platelet derived growth factor to stimulate fibroblasts
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4
Q

Describe the proliferation stage of wound healing

A
  1. VEGF stimulates new blood vessels to form
  2. Fibroblasts (on day 3-5) secrete type 3 collagen and fibronectin to plug the gap
  3. Myofibroblasts contract reducing the size of the wound
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5
Q

Describe the remodelling stage of wound healing

A
  1. Type 3 collagen is replaced by type 1 collagen (scar tissue) on day 5
  2. Blood vessels regress
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6
Q

Describe wound healing by secondary intention

A
  1. The defect fills with granulation tissue
  2. Epithelial regeneration occurs to cover the surface
  3. Myofibroblasts within granulation tissue contracts leading to scar formation
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7
Q

Describe the activation of a B-cell

A
  • Matures in the bone marrow
  • Circulates in the peripheral blood until they recognise an antigen (free or on antigen-presenting-cell)
  • Ingests the antigen and displays fragments to attract a T-helper Cell
  • Cytokines released by the T-cell helps the B-cell mature into plasma cells or memory cells
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8
Q

What are the 2 types of mature B-cell and describe them:

A

Plasma Cell
- found in the bone marrow and spleen
- live 1-2 weeks
- secrete large quantities of immunoglobulins

Memory Cell:
- needed in the secondary response of the adaptive immune system

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9
Q

Where does the maturation of T-cells happen?

A

In the thymus as they travel from the cortex to the medulla

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10
Q

What are the 2 types of mature T-cells?

A

CD4+ (helper)
CD8+ (cytotoxic)

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11
Q

How are CD4+ T cells activated and what is their response?

A

Recognise antigen in association with HLA II molecules found on antigen-presenting cells

Secrete cytokines to recruit and activate macrophages, cytotoxic T-cells, NK cells as well as activate B-cells to produce immunoglobulin

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12
Q

How are CD8+ T cells activated and what is their response?

A

Recognise antigen only on association with HLA I molecules found on endogenous antigens (found on cells infected by virus and bacteria)

Their response is the cytotoxic killing of target cells by inducing apoptosis

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13
Q

What are natural killer cells?

A

Cytotoxic CD8 cells that lack a T-cell receptor

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14
Q

What is the relation of HLA I molecules and the ability of a NK-cell to kill its target?

A

HLA I displayed on a target cell has an inhibitory effect on the NK-cell. Therefore when HLA molecules are absent (viral infections and malignancy) the NK-cell can kill its target

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15
Q

Name the causes of lymphocytosis

A

(Common in children vs neutrophil reaction in adults)

  • Viral and bacterial infections
  • CLL and ALL
  • Non-Hodgkin lymphoma
  • Thyrotoxicosis
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16
Q

What investigation results would you expect to see in Hodgkin Lymphoma?

A

Reed-Sternburg cells!

  • Normocytic, normochromic anaemia
  • Neutrophilia
  • Lymphopenia
  • Raised platelets (Early disease)
  • Low platelets (Late disease)
  • Raised ESR and CRP
  • Raised LDH
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17
Q

Describe the regenerative properties of labile cells and give examples

A

Constantly dividing and regenerating

  • Surface skin epithelium
  • GI tract
  • Blood cells
18
Q

Describe the regenerative properties of stable cells and give examples

A

Generally dormant or very slowly replicating however can rapidly regenerate if stimulated to do so

  • Liver
  • Renal tubular epithelium
  • Endocrine glands
19
Q

Describe the regenerative properties of permanent cells and give examples

A

Cells have left the cell cycle so are incapable of division

  • Skeletal muscle
  • Brain
  • Myocardium
20
Q

Describe the epidemiology of CML vs CLL

A

CML: 40-60 but can be any age
CLL: 60-80, males

21
Q

What investigation results would you expect to see in CML?

A
  • Leucocytosis (predominantly neutrophils, and myelocytes)
  • Raised basophils
  • Normochromic, normocytic anaemia

Philadelphia chromosome in 98% of cases

22
Q

What is the treatment of CML?

A

Tyrosine kinase inhibitors

23
Q

How does the presentation of CML vs CLL differ?

A

Both are normally picked up on routine bloods

CML: massive splenomegaly
CLL: enlarged lymph nodes

24
Q

What investigation results would you expect to see in CLL?

A
  • Lymphocytosis
  • Normochromic, normocytic anaemia
  • Thrombocytopenia
25
Q

Describe a type 2 hypersensitivity reaction and give some examples

A

Antibody mediated (IgG or IgM)

  • Haemolytic diseases
  • Blood transfusion reactions
  • Goodpastures
  • Bullous pemphigoid
  • Rheumatic heart disuease
26
Q

Describe a type 3 hypersensitivity reaction and give some examples

A

Immune complex mediated (IgG)

  • Extrinsic allergic alveolitis
  • SLE
  • Post-streptococcal glomerulonephritis
  • Reactive and rheumatoid arthritis
27
Q

Describe a type 4 hypersensitivity reaction and give some examples

A

T-cell mediated

  • Crohns
  • Hashimotos
  • Primary biliary cholangitis
  • Sarcoidosis
  • Chronic transplant rejection
  • Contact dermatitis
28
Q

A deficiency in which coagulation factors leads to a prolonged PT? Which disease processes does this happen in?

A

EXTRINSIC AND COMMON PATHWAY
- 7
- 10, 5, 2, fibrinogen

  • Liver disease
  • Warfarin
  • DIC
29
Q

A deficiency in which coagulation factors leads to a prolonged APTT? Which disease processes does this happen in?

A

INTRINSIC AND COMMON PATHWAY
- 12, 11, 9, 8
- 10, 5, 2, fibrinogen

  • Liver disease
  • Warfarin
  • DIC
  • Heparin
  • Haemophilia
  • Christmas disease
30
Q

Haemophilia A is due to a deficiency in which clotting factor?

A

8

31
Q

What is the inheritance pattern of haemophilia A?

A

X-linked recessive

32
Q

What laboratory findings would you expect in haemophilia A and B?

A

Prolonged APTT
Normal PT
Low factor 8

33
Q

Haemophilia B is due to a deficiency in which clotting factor?

A

9

34
Q

What is the role of Von Willebrand factor?

A

Promotes platelet adhesion

Carrier molecule of factor 8

35
Q

What is the inheritance pattern of Von Willebrand disease?

A

Autosomal dominant

36
Q

What laboratory results would you find in Von Willebrand disease?

A

Prolonged APTT
Normal PT
Low factor 8
Normal platelet count but defective aggregation

37
Q

What is the definition of an acute leukaemia?

A

Over 20% blast cells in the bone marrow

38
Q

Which age groups are affected by AML vs ALL?

A

AML: adults (65)
ALL: kids (3-7) and second peak at 40

39
Q

What haematological investigation results would you expect to see in AML?

A
  • Normochromic, normocytic anaemia
  • Thrombocytopenia
  • Increased WCC
  • Blast cells on blood film
40
Q

What haematological investigation results would you expect to see in ALL?

A
  • Normochromic, normocytic anaemia
  • Thrombocytopenia
  • Variable WCC
  • Blast cells on blood film
  • Raised uric acid
  • Raised LDH
41
Q

Define virulence

A

The ability of a pathogen to cause severe disease