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Microbiology & Pathology > Pathology > Flashcards

Pathology Flashcards

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1
Q

What are the different types of healing? What are examples of these

A

-Primary: Typically surgery
-Delayed primary: Wound initially left open then closed at day 2-3
- Secondary Intention: Tissue loss, granulation fills cavity, wound contraction with myofibroblasts

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2
Q

What are the 4 phases of wound healing?

A

1) Haemostasis
2) Inflammatory
3) Proliferative
4) Remodelling

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3
Q

What happens in haemostasis?

A

Tissue injury induces clotting cascade.
Platelet aggregation = clot formation
Platelet granules release growth factors initiating wound healing

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4
Q

What are the main inflammatory mediators?

A

Histamine
Serotonin
Bradykinin
Complement proteins

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5
Q

What happens in the inflammatory phase of wound healing?

A

Complement cascade activated
Polymorphs migrate to wound after a few hours & act up to 4 days
Monocytes migrate to the wound site & transform to macrophages

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6
Q

What happens in the proliferative phase of healing?

A

Fibroblasts move into the wound & lay down new extra-cellular matrix
Granulation tissue formation
Angiogensis
Epithelialisation

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7
Q

What happens in remodelling?

A

2weeks or more after injury can last >1year
Myofibroblasts promote wound contraction
Final product is avascular, acellular scar

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8
Q

What are the phases of fracture healing?

A

1) Reactive phase
2) Soft callus phase
3) Hard callus phase
4) Remodelling phase

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9
Q

What happens in the reactive phase of fracture healing?

A

0-7days
Platelet migration & haematoma formation
Acute inflammation
Fibroblast migration
Granulation tissue formation between bony ends

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10
Q

What happens in the soft callus phase of fracture healing?

A

4days- 3/52
Chondroblasts & fibroblasts migrate into granulation tissue
Lay down hyaline cartilage
Osteoblasts begin to lay down weak form of bone = Woven bone
Hyaline cartilage & woven bone form initial fracture callus which loosely unites bone ends

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11
Q

What happens in the hard callus phase of fracture healing?

A

1-3months
Osteoblasts differentiate from periosteum cells
Lay down woven & trabecular bone = Hard callus

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12
Q

When can callus be seen on xray

A

6 weeks

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13
Q

What happens in the remodelling phase of fracture healing?

A

Up to years
Osteoclasts & Osteoblasts slowly remodel bone to close it to its original shape
Trabecular bone replaced with stronger compact bone

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14
Q

Desceibe tendon healing

A

Fibroblasts produce type 3 collagen
Large amounts of disorganized collagen produced over weeks
Gradually remodelled over 18months to type 1 collagen

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15
Q

Describe nerve healing

A

Neuropraxia: Pressure on nerve self resolving over minutes-hours
Axonotmesis: Traction on a nerve, axon degenerates but surrounding tissue intact. Nerve regenerates up to 2cm/month
Neurotmesis: Connective tissue is lost. Neural integrity lost. Recovery limited but can improve with surgical repair

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16
Q

Describe cardiac healing

A

Necrotic muscle invaded by granulation tissue & fibroblasts- replaced by scar
Impairs ventricular function e.g no longer contractile

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17
Q

Describe brain healing

A

No fibroblasts in the brain
Necrotic area removed by gliosis leading to volume loss
Neuroplasticity allows some regain of function

18
Q

What factors lead to chronic wounds?

A

Infection
Ischaemia
Oedema
Under perfusion
Hypoxia
Further tissue damage
Lack of nutrients

19
Q

What is the purpose of inflammation?

A
  • Deal with cause
  • Remove damage
  • Initiate healing
20
Q

What are the 4 mechanisms of inflammation?

A
  • Acute phase response
  • Complement cascade
  • Kinin: Kallikrein system
  • Prostaglandins & eicosanoids
21
Q

What substances are released by cells in response to inflammation?

A

Macrophages: TNFa
Mast cell: Histamine

22
Q

How do endothelial cells take part in the inflammatory process?

A

Endothelial cells stimulate release of NO & Prostacyclin causing vasodilation

23
Q

What effect does vasodilation have on neutrophils?

A

Migrate towards endothelial surface. Roll along the surface and then stick to it
Endothelial cells contract and full apart allowing neutrophils to move between them and out of the vessel into the tissues

24
Q

How are monocytes attracted to an area of inflammation?

A

Stimulate by release of cytokines

25
Q

What happens in the acute phase response?

A

1) Tissue damage attracts neutrophil & macrophage release
2) These release Cytokines causing:
-Act on adrenal/pituitary axis releasing ACTH + glucocorticoids release
-Induce PG, acts on hypothalamus leading to febrile response
-Increases liver biosynthesis & acute phase proteins (CRP, Amyloid)

26
Q

What are the main acute phase cytokines?

A

IL-1
IL-6
TNF-a

27
Q

How is the complement pathway activated?

A

Classic: Antigen-antibody complexes
Alternate: C3b binds to pathogen surface
Lectin pathway

28
Q

What are the roles of the complement pathway?

A

Lysis of bacteria
Chemotactic for leucocytes
Opsonisation
Inflammation

29
Q

What receptors does bradykinin act on? What do these receptors do?

A

B1 receptors: Pain, stimulates mitogenesis
B2 receptors: VasoD, Inc capillary permeability

30
Q

What do prostaglandins do?

A

Produce COX-1 & COX-2

31
Q

Where are leukotrienes produced?

A

Arachidonic acid

32
Q

Which leukotriene is involved with smooth muscle contraction?

A

LTD4

33
Q

What do thromboxane do?

A

Produced by activated platelets
Promote platelet aggregation & VasoC

34
Q

What do prostacyclins do?

A

Released by vascular endothelium
VasoD
Inhibit platelet aggregation

35
Q

What are the 4 types of hypersensitivity?

A

Type 1: Anaphylaxis, atopic disease
Type 2: Transfusion reactions, SLE, Myasthenia, RA
Type 3: Serum sickness, Farmers lung
Type 4: Contact dermatitis, Late graft rejection, Tuberculin skin reaction

36
Q

What is the process in Type 1 hypersensitivity reactions?

A

Antigen reacts with IgE antibody on sensitised mast cell
Massive release of histamine & Vasoactive substances (vasodilation, bronchospasm)

37
Q

What is the process in Type 2 hypersensitivity reactions?

A

Antibody mediated
Circulating IgM/IgG reacts with antigen on cell surface
Complement activated & phagocytosis kills the cell

38
Q

What is the process in Type 3 hypersensitivity reactions?

A

Circulating antigen & antibody combine & precipitate out as immune complexes causing small vessel damage

39
Q

What is the process in Type 4 hypersensitivity reactions?

A

Cell mediated >12hours
Antigen stimulates sensitised T-lymphocytes causing release of lymphokines & inflammatory mediators
No antibody response

40
Q

What are the types of shock?

A

Cardiogenic: Pump failure
Hypovolaemia: Haemorrhage
Distributive: Sepsis, Anaphylaxis
Obstructive: PE, Tamponade

41
Q

What are the signs of compensated shock?

A

Lactic acid production
Catecholamine release
Agitation

42
Q

What are the signs of decompensated shock?

A

Capillary leakage & smudging
Hyperkalaemia
Metabolic acidosis

Microbiology & Pathology (6 decks)

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