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Unit 2 > Acute Inflammation (10/8a) [Biomedical] > Flashcards

Acute Inflammation (10/8a) [Biomedical] Flashcards

1
Q

Inflammation

A

Response of vascularized tissues to infection and damage

Brings cells and molecules of host defense from the circulation to affected sites

Eliminate offending agents

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2
Q

Goals of Inflammation

A

Rid the host of the initial cause of injury

Remove necrotic cells and tissues

Initiate the process of tissue repair (Inflammation → Proliferation → Maturation)

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3
Q

The Five R’s of Inflammation

A

RECOGNITION of injury (turn on)

RECRUITMENT of white blood cells to area of injury (turn on)

REMOVAL of injurious agent and damaged tissue (turn on)

REGULATION of response (turn off)

RESOLUTION (turn off)

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4
Q

Cardinal Signs of Inflammation

A

Rubor = redness

Calor = heat

Tumor = swelling

Dolor = pain

Functio laesa = loss of function

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5
Q

___ ___ sensitizes specialized nerve endings to effects of Bradykinin and other pain mediators

A

Prostaglandin E2

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6
Q

Inflammation - Cells in the Blood

A

Platelets (thrombocytes)

White blood cells (leukocytes)

  • Neutrophils: most common
  • Monocytes: become macrophages in tissue
  • Lymphocytes: can be B or T lymphocytes
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7
Q

Inflammation - Cells in the Tissues

A

Sentinel cells - immune cells that reside in tissue, sense microbes/tissue damage and can respond on their own

3 Types: Resident macrophages, Dendritic cells, Mast cells

3 Key Features

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8
Q

3 Key Features of Sentinel Cells

A

Surface/cytosolic receptors recognize invading microbes/substances released by necrotic tissue

Bind, ingest, and phagocytize microbes and necrotic tissue

Release cytokines and other inflammatory mediators as signals to recruit help

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9
Q

Substances and Inflammatory Mediators

A

Cytokines

Histamine

Prostaglandins and leukotrienes

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10
Q

Cytokines

A

signaling molecules secreted by immune cells in response to injury/infection that induce and modulate immune response

Include interleukins, interferon, TGF-beta, TNF

Pro-inflammatory vs Anti-inflammatory

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11
Q

Pro-inflammatory vs Anti-inflammatory

A

Pro-inflammatory induce fever, inflammation, tissue destruction in response to injury

Anti-inflammatory suppress actions of pro-inflammatory

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12
Q

Histamine

A

released by mast cells

Causes vasodilation and increased capillary permeability

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13
Q

Prostaglandins and Leukotrienes

A

produced in response to cytokines

Contribute to vasodilation, pain, and platelet activation

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14
Q

Parts of Turning ON Inflammation

A

Hemostasis

Recognition of injury

Recruitment of WBCs

Removal of damaged tissues

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15
Q

Hemostasis

A

Immediate response to traumatic injury to prevent blood loss

Damaged endothelial cells release mediators that cause
-Vasoconstriction — decrease blood flow to the area

  • Platelet activation — adhere to lesion/each other, attract other platelets, initiate coagulation cascade → fibrin production
  • Fibrin clot formation — fibrin stabilizes the clot, fibronectin provides initial scaffolding for infiltrating cells and ECM components
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16
Q

Injury

A

trauma

necrotic tissue

infection by pathogens or foreign bodies

maladaptive immune response

17
Q

Recognition of Injury

A

Injury recognized by immune cells - sentinel cells in tissue, leukocytes in blood stream

Receptors on cell surface/interior recognize molecules

  • On surface of invading microbes
  • Released by damaged tissue (ATP, DNA, low K+)

Leukocytes ingest and phagocytize microbes and necrotic tissue

Recognition causes release of mediators that trigger recruitment

18
Q

Mediators that Trigger WBC Recruitment

A 
cytokines
histamines
prostaglandins
bradykinins
leukotrienes
19
Q

Recruitment of White Blood Cells

A

Cytokines and inflammatory mediators act on endothelial cells of local blood vessels

Vasodilation — increase blood flow

  • Histamine/mediators released by mast cells cause vessel relaxation
  • Decreases velocity of blood flow

Increase vessel permeability

  • Endothelial cell retraction creates holes in the vessel wall
  • Plasma and proteins leak into tissue, causing edema

Vascular stasis

  • Results from increased blood flow, decreased velocity, and hemoconcentration
  • Accounts for redness and warmth of inflamed tissue
  • Facilitates extravasation of leukocytes into tissues
20
Q

Hemoconcentration

A

increased concentration of RBCs due to decreased plasma/fluid volume

21
Q

Extravasation

A

movement of white blood cells from the capillaries to the tissues surrounding them

also known as diapedesis

22
Q

How are leukocytes recruited into tissues?

A

ACTIVATION
- Cytokines produced by mast cells and activated platelets “turn on” leukocytes

EXTRAVASATION
- Vascular endothelial cells express surface proteins that grab leukocytes, causing them to roll, adhere, and migrate through endothelium into tissue

CHEMOSTASIS
- Once in tissue, leukocytes migrate to the area of damage

23
Q

Removal of Damaged Tissue - 1st Wave

A

1ST WAVE — NEUTROPHILS

Ingest and destroy microbes and damaged tissues through phagocytosis

Die quickly via apoptosis, half life of only a few hours

24
Q

Removal of Damaged Tissue - 2nd Wave

A

2ND WAVE — MACROPHAGES

Phagocytize remaining microbes, necrotic tissue, and dead neutrophils

Clean up the mess made by damage and neutrophils

Produce anti-inflammatory cytokines that begin to downregulate inflammation

25
Q

Parts of Turning OFF Inflammation

A

Regulation of response

Resolution

26
Q

Regulation of Inflammatory Response

A

Once activated, leukocytes have short half lives

Anti-inflammatory signals activated to downregulate inflammation (EX: lymphocytes)

27
Q

Resolution of Inflammation

A

Leukocyte activation triggers proliferation and migration of fibroblasts

Produce collagen and extracellular matrix components

Main cell of proliferative phase

28
Q

Some sources of injury

A 
chronic inflammation
persistent injury
autoimmune disease
viral/bacterial infections
infarction
toxins
trauma
29
Q

What can go wrong with inflammation?

A

Too little inflammation
- Infections go unchecked, wounds/tissues don’t heal

Misdirected inflammation
- Against self/healthy tissues in autoimmune diseases (EX: rheumatoid arthritis)

Inflammation in response to normally harmless stimuli
- Hypersensitivity and allergies

Inflammation is excessively prolonged or repetitive
- Becomes chronic inflammation → more damage and scar tissue, fibrosis

30
Q

Inflammation - PT Key Observations

A

Look for cardinal signs and how exaggerated they are

Impact on movement and gait

31
Q

Inflammation - PT History Questions

A

When and how did this happen?

  • When: to understand how long it’s been an issue
  • How: to understand the mechanism of injury and parts of body involved (traumatic vs nontraumatic)

Ask if this repeated injury (acute vs chronic)

Pain - location, type/quality, severity, aggravating/relieving factors
- Scale of 0-10 (0 = no pain, 10 = worst pain you can imagine)

32
Q

Inflammation - PT Tests and Measures

A

Assessment of function (if region is stable) - ROM, strength, gait, standing, etc

Edema assessment

Joint stability - joint play assessment

Test a joint above and below

33
Q

Inflammation - PT Prognosis

A

How long should acute inflammation last?

If no change in signs and symptoms in 1-2 weeks, consider:

  • Repeated injury?
  • Another source of inflammation?
34
Q

Edema - Overview

A

Excess fluid in the interstitial space

Increased girth of body part

May also see:

  • tight, shiny skin
  • indentation of skin under clothing
  • weeping, leaking
35
Q

Edema - Why is it a problem?

A

Interferes with movement

Decreased neuromuscular control and ROM, painful

May indicate health problem
- Tissue injury, DVT, heart failure, liver/kidney failure

36
Q

Edema - Types

A

Inflammatory

  • Red, hot, painful
  • Due to trauma, infection, or inflammatory reaction

Non Inflammatory

  • Pitting = indentation in skin after applying pressure
  • Variety of causes
37
Q

Edema - Describing It

A

LOCATION

  • Limb/tissue
  • Unilateral vs bilateral

DURATION

  • Acute = days to weeks
  • Chronic = weeks to months/years

INFLAMMATORY/NONINFLAMMATORY

  • Are other signs of inflammation present?
  • Is there pitting?

MEASUREMENT
- girth measurements, volumetric

38
Q

Pitting Scale

A

press firmly into skin for 5 sec

1+ — indentation barely detectable

2+ — slight, returns to normal in 15 sec

3+ — deeper, returns to normal in 30 sec

4+ — indentation lasts > 30 sec

Unit 2 (27 decks)

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