6 - Immunity Inflammation and Wound Healing Flashcards

1
Q

Innate Immunity (+2 types)

A

Immunity we are born with.
First line of defece: Physical, mechanical and chemical barriers
Second line: Inflammation, (macrophages and neutophils)

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2
Q

Adaptive Immunity

A

Aquired immunity, third line of defence
-uses B-cells and T-cells

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3
Q

Dendritic cells

A

Connect innate and adaptive immune response, first cell to contact the pathogen

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3
Q

Prostaglandins

A

Overseer of events in immune resonse

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4
Q

Mast Cells

A

Important inflammation activator

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5
Q

Lymphokines

A

cytokines relased from lymph

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5
Q

Cytokines

A

Chemical molecules released that regulate innate and adaptive immunity, can be pro-inflammatory or anti-inflammitory

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6
Q

IL-1 produced by?

A

Macrophages

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6
Q

Monokines

A

Cytokines released from monocytes, change into macrophages

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7
Q

Interleukins

A

Released by macrophages and lymphocytes, simiar to cytokines but are self-limiting

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8
Q

IL-6 produced by?

A

macrophages, lymphocytes and fibroblasts

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9
Q

Cytokine storm syndrome

A

In covid 19, severe systemic inflammatory response where IL-6 –> excessive recruitment of lymphocytes
-treatment: IL-6 antibodies to counteract

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10
Q

Cachexia

A

Muscle wasting

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11
Q

Granuloma

A

A section of tissue walled off by the body (often to hold back an infection)

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12
Q

TNF-a (+ it’s effects)

A

cytokine, not an interleukinm, massive inflammatory effects
-released by macrophages and mast cells
Causes: fever, cachexia, fatal shock (gram - bacterial infections) , granulomas

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13
Q

IL-10

A

Lymphkine, anti-inflammitory

14
Q

5 Signs of Acute Local Inflammation

A

Heat, redness, swelling, tenderness, pain

15
Q

Inflammation

A

Cooridinated response to cell injury or death, can be acute or chronic

16
Q

Erythrocyte Sedimentation Rate (ESR)

A

Determination of the rate of RBC settling in saline solution
-Increase in infection –> RBCs bind to eachother and settle at a faster rate
-So, increased ESR = increased infection

17
Q

C-reactive protein

A

Caused by effect on liver, concentration in blood increases in response to inflammation
-non-specific, not unique to any disease

18
Q

WBC count

A

Measurement of increased neutrophils, increase in neutrophills in the bloodstream indicates infection is ongoing

19
Q

Acute inflammation (+3 systemic changes)

A

-Lasts less than two weeks, but can become chronic if not resolved
-swelling, pain, redness, heat
-localized
Three changes: fever, leukocytosis, increase in circulating protiens (used as building blocks to repair damage)

20
Q

Chronic Inflammation

A

Longer than 2 weeks, can be preceeded by acute or its own process
Cause resistant microrganisms (produce toxins, survive in a macrophage etc..)
-presents with dense infiltration of lymphocytes and macrophages
-creates granuloma

20
Q

Wound healing phases (3)

A

1.Inflammation
2.Proliferation
3.Remodeling and Maturation

21
Q

Tissue Repair Intentions (3)

A
  1. Primary –> clean incision, early suture, fine scar
  2. Secondary –> gaping wound, edges cannot be brought together, wound is left open to heal spontaneously
    3.Tertiary –> Delayed primary closure (allows for wound observation), leads to increased granulation, is eventually sutured but with wider scar
22
Q

Adhesions

A

Abnormal union of membranous surfaces, painful

23
Q

Strictures and Contractures

A

Excess wound contraction, leading to tight skin, common with burns

24
Q

Dehiscense

A

Incision separates following surgery, wound is considered “dishiced”

25
Q

Evisceration

A

Surgical complication, incision opens and abdomnial organs protrude

26
Q

Antineoplastic

A

Drugs used for cancer treatment to slow cell division, blocks formation of new neoplasms (abnormal cell growth). Has negative side effects.