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Human Diseases > 2 Pathological processes II > Flashcards

2 Pathological processes II Flashcards

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?

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?

A

Regenerates from:
- Wound margins
- Pilosebaceous units

19
Q

Which factors influence wound healing?

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?

A
  • Depth of injury
  • Type of healing
21
Q

How are wounds classified by depth of injury?

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?

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?

A

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

Keloid scar: genetic predisposition

24
Q

What is chronic inflammation?

A

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

25
Q

When/why may chronic inflammation occur?

A
  • Pressure ulcers in bed bound/immobile patients
  • Poor healing for other reasons
26
Q

What type of microenvironment exists in a chronic wound?

A

Unfavourable microenvironment for healing: persistent inflammation, hyperglycaemia, cytokine and growth factor deficiencies

27
Q

Describe fracture healing.

A

1) Haemostasis and inflammation
2) Proliferation of cells leads to hard callus formation
3) Callus remodelled, bone formed

28
Q

Describe the features of healing in palatal/gingival tissue.

A
  • 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
Q

What are the systemic effects of pro-inflammatory cytokines?

A

Acute phase response:
- Acute phase proteins produced (CRP, complement factors, coagulation factors)
- Fever

Sickness behaviours:
- Reduced food/water intake
- Fatigue
- Feeling drowsy

30
Q

What are the potential harmful inflammatory responses?

A
  • 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
Q

What is a cerebral infarction?

A

Also called an ischemic stroke.
- Disrupted blood flow to the brain
- Localised tissue damage/necrosis

32
Q

What type of processes are inflammation and wound healing?

A

Catabolic processes (energetically costly)

33
Q

What are the possible systemic complications of inflammation?

A
  • SIRS (systemic inflammatory response syndrome)
  • Multiple organ failure
  • Sepsis
34
Q

How can SIRS progress to MODS, MOF and death?

A

Increasing homeostatic dysfunction due to SIRS can cause multiple organ dysfunction sydrome, multiple organ failure and death.

35
Q

What are the SIRS criteria?

A

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
Q

Define sepsis.

A

Life threatening organ dysfunction caused by a dysregulated host response to infection.

37
Q

Which alternative 2 systems can be used to score illness/organ dysfunction (other than the SIRS criteria)?

A

Sequential organ dysfunction score.
National early warning score.

38
Q

What is the sequential organ dysfunction score (SOFA)?

A

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
Q

What is the national early warning score (NEWS)?

A

Measures physiological parameters, higher number= more ill.

40
Q

What are the signs of sepsis?

A
  • 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

Human Diseases (47 decks)

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