6 - Immunity Inflammation and Wound Healing Flashcards
Innate Immunity (+2 types)
Immunity we are born with.
First line of defece: Physical, mechanical and chemical barriers
Second line: Inflammation, (macrophages and neutophils)
Adaptive Immunity
Aquired immunity, third line of defence
-uses B-cells and T-cells
Dendritic cells
Connect innate and adaptive immune response, first cell to contact the pathogen
Prostaglandins
Overseer of events in immune resonse
Mast Cells
Important inflammation activator
Lymphokines
cytokines relased from lymph
Cytokines
Chemical molecules released that regulate innate and adaptive immunity, can be pro-inflammatory or anti-inflammitory
IL-1 produced by?
Macrophages
Monokines
Cytokines released from monocytes, change into macrophages
Interleukins
Released by macrophages and lymphocytes, simiar to cytokines but are self-limiting
IL-6 produced by?
macrophages, lymphocytes and fibroblasts
Cytokine storm syndrome
In covid 19, severe systemic inflammatory response where IL-6 –> excessive recruitment of lymphocytes
-treatment: IL-6 antibodies to counteract
Cachexia
Muscle wasting
Granuloma
A section of tissue walled off by the body (often to hold back an infection)
TNF-a (+ it’s effects)
cytokine, not an interleukinm, massive inflammatory effects
-released by macrophages and mast cells
Causes: fever, cachexia, fatal shock (gram - bacterial infections) , granulomas
IL-10
Lymphkine, anti-inflammitory
5 Signs of Acute Local Inflammation
Heat, redness, swelling, tenderness, pain
Inflammation
Cooridinated response to cell injury or death, can be acute or chronic
Erythrocyte Sedimentation Rate (ESR)
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
C-reactive protein
Caused by effect on liver, concentration in blood increases in response to inflammation
-non-specific, not unique to any disease
WBC count
Measurement of increased neutrophils, increase in neutrophills in the bloodstream indicates infection is ongoing
Acute inflammation (+3 systemic changes)
-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)
Chronic Inflammation
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
Wound healing phases (3)
1.Inflammation
2.Proliferation
3.Remodeling and Maturation
Tissue Repair Intentions (3)
- Primary –> clean incision, early suture, fine scar
- 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
Adhesions
Abnormal union of membranous surfaces, painful
Strictures and Contractures
Excess wound contraction, leading to tight skin, common with burns
Dehiscense
Incision separates following surgery, wound is considered “dishiced”
Evisceration
Surgical complication, incision opens and abdomnial organs protrude
Antineoplastic
Drugs used for cancer treatment to slow cell division, blocks formation of new neoplasms (abnormal cell growth). Has negative side effects.
