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
Tissue Repair Intentions (3)
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
Adhesions
Abnormal union of membranous surfaces, painful
23
Strictures and Contractures
Excess wound contraction, leading to tight skin, common with burns
24
Dehiscense
Incision separates following surgery, wound is considered "dishiced"
25
Evisceration
Surgical complication, incision opens and abdomnial organs protrude
26
Antineoplastic
Drugs used for cancer treatment to slow cell division, blocks formation of new neoplasms (abnormal cell growth). Has negative side effects.