Unit 2 Flashcards
lines of defence in the body
1st line: mechanical barrier, skin or mucous membrane, nonspecific
blocks bacteria and harmful substances
saliva and tear enzymes destroy potential harmful substances
2nd line: phagocytosis and inflammation
Phagocytosis: neutrophils and macrophages engulf and destroy bacteria, debris
inflammation: limit injury or dangerous material effects
interferons: nonspecific agents protecting uninfected cells
3rd line: specific defence machanism, stimulated production of antibodies
lymphocytes
capillary exchange
all capillaries arent open : regulated by precapillary sphincters
hydrostatic pressure: determines if material (oxygen, fluid, electrolytes, nutrients) will flow out of capillary, based on the difference between capillary and interstital hydrostatic pressure
diffusion of materials is dependant on concentration in the blood
excess fluid and proteins picked up by the lymphatic system
inflammatory response
- nonspecific response to tissue injury
causes: direct cuts and sprains, chemical acids, ischemia and infarction, allergic reactions, physical reactions to heat (burns) and radiation, foreign bodies (splinters and dust), infection from viruses, bacteria, fungi
- itis
inflammation of the root proceding this suffic
acute inflammation response
early response to injury
- vascular response: vasodilation for redness and heat, increased capillary exchange and capillary permeability for swelling and deem
- cellular response: diapedesis: pavementing and emigration of neutrophils out of the blood vessel, chemotaxis, phagocytosis
mast cell: primary activator of inflammation, in tissues, stim by injury,
- degranulation: responds by spilling out contents like histamine
- synthesis: produces chemicals like leukotrienes and prostaglandins
5 cardinal signs of acute inflammation
heat, redness, swelling, pain, loss of funtion
mast cell effects
release histamine: dilation and increased permeability of capillaries
chemotaxis factors of histamine: attracts leukocytes, to the site of inflammation
produce leukotrienes and prostoglandins:
similar effect to histamine
function and activity of leukocytes and lymphocytes in inflammation
leukocytes:
neutrophils: phagocytosis of microorganisms
basophils: release histaimne leading to inflammation
eosinophils: numbers increase in allergic responses
Lymphocytes:
T lymphocytes: active in cell-mediated immune responce
B lymphocytes: produce antibodies
monocytes: phagocytosis
Macrophages: active in phagocytosis (mature monocytes)
chronic inflammation
inflammation lasting longer periods
due to unsuccessful acute response
macrophage role
engulf bacteria, results in pus
fibroblast role
produce scar tissue, tissue repair
compare nonspecific chronic inflammation and granulomatous inflammation
G: body cannot get rid of problem easily, body then walls ofd the problem
- eg/ splinters, asbestos
N: macrophaes engulf bacteria and fibroblasts produce scar tissue
local manifestations of inflammation
- serous exudate: watery fluid in the tissues from the plasma
- hemorrhagic exudate: dammaged vessels leak blood into tissue
- fibrinous exudate: increased fibrinogen creating a thcik and sticky meshwork
- membraneous exudate: fibropurulent material in mucous membranes
- purulent or suppurative exudate: pus, tissue debris, old WBC, proteins
- abscess formation: pus core surrounded by neutrophils and walled off
- ulcers: site of inflammation where epithelial tissue eroded (eg/ stomach ulcer)
abscess
pus core surrounded by neutrophils and walled off
ulcer
ulcers: site of inflammation where epithelial tissue eroded (eg/ stomach ulcer)
systemic and general manifestatuons of inflammation
malaise, fatigue, headaches, anorexia, fever (pyrexia), increased WBCs
leukocytosis and leukopenia
Leukocytosis: increased WBC, neutrophils due to infection
leukopenia: decrease in WBCs because infection overwhelms immune system
A shift to the left
blood test shows immature neutrophils in blood because WBC production cannot meet the demands and immature WBC are released from bone marrow
abnormal lab values during inflammation
differential counts: increased neutrophils from bacterial infection, decreased neutrophils from viral infection, increased eosinophils from allergic or parasitic response
Increased cell enzymes:
increased AST or SGOT: necrosis in the liver
increased ALT/SGPT: liver
lymphadenitis
swollen and painful nodes, reaction of lymph nodes to inflammation
non painful: indicate neoplasms (tumours)
drugs to treat inflammation
- ASA:
Anti -inflammatory analgesic for pain and antipyretic (fever)
delays blood clotting and causes nausea, stomach ulcers and bleeding
- Acetaminophen:
analgesic or antipyretic
in high doses, causes kidney or liver damage
- NSAIDs:
anti-inflammatory, analgesic, antipyretic
may cause allargy, delay blood clotting, nausea, stomach ulcers and bleeding
- Prednisone (steroid glucocorticioid):
anti-inflammaotry, decreases immune respone, increases risk of infection
can increase blood pressure and edema, osteoporosis and skeletal muscle weakness
types of healing
resolution, regeneration, replacement
resolution and its outcome
Resolution: minimal tissue damage, tissue returns to normal in short period
eg/ mild sunburn
labile cells - regeneration and replacement
continued replication throughout life
- little or no evidence of injury (skin and oral cavity)
