Human Diseases > 2 Pathological processes II > Flashcards

2 Pathological processes II Flashcards

(40 cards)

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1
Q

What is inflammation?

A

An adaptive physiological response to tissue malfunction or homeostatic imbalance.
Involves many physiological and behavioural processes.

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2
Q

What are the 4 functions of inflammation?

A
  • Rapidly destroy or isolate a source of homeostatic disturbance
  • Remove damaged/necrotic tissue
  • Restore tissue homeostasis
  • Facilitate tissue healing/regeneration
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3
Q

Briefly outline the mechanism of inflammation (5 steps).

A

1) Recognition of infection or tissue damage (via receptors for specific molecular patterns- PAMPs or DAMPs)
2) Signal transduction
3) Inflammatory cytokine release (initiates response)
4) Cytokines attract effector cells (e.g. neutrophils and macrophages)
5) Resolution (return to tissue homeostasis)

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4
Q

What are PAMPs and DAMPs?

A
  • Pathogen associated molecular patterns
  • Damage associated molecular patterns
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5
Q

Where do cytokines exert their effects?

A

Cytokines have an effect on:
- Local circulation
- White blood cells
- Clot formation

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6
Q

How do cytokines affect local circulation?

A
  • Increase localised blood flow
  • Increased permeability and vasodilation
  • Plasma leakage
  • Leukocyte margination (adhesion to endothelium)
  • Increased blood viscosity
  • RBC sludging and platelet clumping
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7
Q

How do cytokines affect white blood cells?

A

Mobilisation, activation, adhesion and migration of neutrophils and macrophages to target tissues.

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8
Q

What is meant by the term acute inflammation?

A

Local inflammation

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9
Q

What are the 4 clinical signs of local inflammation?

A
  • Heat
  • Redness
  • Oedema
  • Pain
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10
Q

Describe how local inflammation is resolved.

A
  • Co-ordinated by tissue-resident and recruited macrophages
  • Switch from production of pro-inflammatory cytokines (prostaglandins and leukotrienes) to anti-inflammatory cytokines (lipoxins and resolvins)
  • Blocks neutrophil recruitment
  • Favours macrophage infiltration and wound healing
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11
Q

What are the 3 broad phases of skin wound healing?

A
  • Inflammation
  • Proliferation
  • Remodelling
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12
Q

Which cell type is important in the transition from inflammation to proliferation in wound healing?

A

M2 macrophages- synthesis of anti-inflammatory cytokines and ECM, and initiate angiogenesis and fibroblast prolfieration
(M1 macrophages are involved earlier for production of pro-inflammatory cytokines)

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13
Q

Describe angiogenesis in wound healing.

A

Triggered by platelet derived GFs, pro-inflammatory cytokines and macrophages.
Rich vascular network of initially fragile capillaries created, allows delivery of necessary nutrients and cells to aid in the wound healing process.

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14
Q

Which tissue first forms in the wound healing process?

A

Granulation tissue.

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15
Q

What is the role of growth factors in wound healing?

A

Stimulate fibroblast proliferation and production of ECM

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16
Q

Describe the ECM produced in wound healing.

A

ECM rich in glycoproteins, fibronectin and hyaluronic acid.

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17
Q

What is the role of fibroblasts in wound healing?

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A

Produce collagen and change phenotype to become myofibroblasts (mediate wound contraction to bring edges of wound back together).

18
Q

Where does the epidermis regenerate from in wound healing?

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A

Regenerates from:
- Wound margins
- Pilosebaceous units

19
Q

Which factors influence wound healing?

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A
  • Wound location and depth of injury
  • Age
  • Genetics e.g. defect in producing cytokines
  • Oxygen delivery/ cardiovascular function
  • Smoking and nutrition
  • Infection/ wound contamination
  • Immunosuppression
20
Q

What are the 2 forms of classification of wounds?

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A
  • Depth of injury
  • Type of healing
21
Q

How are wounds classified by depth of injury?

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A
  • Partial thickenss wounds: epidermis +/- part of dermis (will heal with intact appendages e.g. hair, nails, sweat glands)
  • Full thickness wounds: epidermins/dermis/deeper tissues (granulation tissue and re-epithelialisation occurs)
22
Q

How are wounds classified by how they heal?

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A
  • Primary intention: uninfected surgical sites or clean wounds with minimal tissue loss, wound is closed with sutures or cips
  • Secondary intention: wound left to heal by itelf by re-epithelialisation+/- contraction
  • Tertiary intention: complex wounds left open and sutured later
23
Q

What are the 2 main types of scars?

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A

Hypertrophic scar: a thick, raised scar caused by excess collagen production

Keloid scar: genetic predisposition

24
Q

What is chronic inflammation?

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A

Slow, long-term inflammation lasting for prolonged periods of several months to years.

25
When/why may chronic inflammation occur?
- Pressure ulcers in bed bound/immobile patients - Poor healing for other reasons
26
What type of microenvironment exists in a chronic wound?
Unfavourable microenvironment for healing: persistent inflammation, hyperglycaemia, cytokine and growth factor deficiencies
27
Describe fracture healing.
1) Haemostasis and inflammation 2) Proliferation of cells leads to hard callus formation 3) Callus remodelled, bone formed
28
Describe the features of healing in palatal/gingival tissue.
- More rapid healing - Early onset of inflammatory phase - Decreased levels of immune mediators - Fewer new blood vessels - Rapid epithelialisation - Rapid fibroblast proliferation - Minimal scarring
29
What are the systemic effects of pro-inflammatory cytokines?
Acute phase response: - Acute phase proteins produced (CRP, complement factors, coagulation factors) - Fever Sickness behaviours: - Reduced food/water intake - Fatigue - Feeling drowsy
30
What are the potential harmful inflammatory responses?
- Alarmins released from injured cells creates a procoagulant state in the local area - However, fibrin microthrombi can form at other sites - If this occurs in an area of end circulation e.g. brain, heart, kidneys- the blood supply is blocked and the organ downstream to the blockage becomes ischemic (risk of necrosis)
31
What is a cerebral infarction?
Also called an ischemic stroke. - Disrupted blood flow to the brain - Localised tissue damage/necrosis
32
What type of processes are inflammation and wound healing?
Catabolic processes (energetically costly)
33
What are the possible systemic complications of inflammation?
- SIRS (systemic inflammatory response syndrome) - Multiple organ failure - Sepsis
34
How can SIRS progress to MODS, MOF and death?
Increasing homeostatic dysfunction due to SIRS can cause multiple organ dysfunction sydrome, multiple organ failure and death.
35
What are the SIRS criteria?
At least 2 of the following: - Temperature above 38 degrees or lower than 36 degrees - Heart rate above 90bpm - Respiratory rate above 20 or PaCO2 less than 4.3kPa - White cell count above 12,000 cells/mm^3 or less than 4000cells/mm^3
36
Define sepsis.
Life threatening organ dysfunction caused by a dysregulated host response to infection.
37
Which alternative 2 systems can be used to score illness/organ dysfunction (other than the SIRS criteria)?
Sequential organ dysfunction score. National early warning score.
38
What is the sequential organ dysfunction score (SOFA)?
Based on PaO2, platelets, bilirubin, mean arterial BP, GCS, creatine and urine output. There is also a quick version: qSOFA (based on resprate, GCS, BP)
39
What is the national early warning score (NEWS)?
Measures physiological parameters, higher number= more ill.
40
What are the signs of sepsis?
- Fast respiratory rate or long pauses in breathing - Blotchy, blue or pale skin - Floppy - Rash that doesn't fade when pressed - Drowsy, confused, difficult to wake - Abmormally coldto touch - Fit or convulsion - A lot of pain or very restless
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