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inflammation Flashcards

1
Q

Inflammation

A

unspecific response in living tissue. multistaged responce that can last from minutes to years. Protective role but may be more harmful than good.

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2
Q

neutrophils are

A

Pus due to infections

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3
Q

Anthracosis macrophages

A

move carbon around lungs

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4
Q

5 signs of inflammation

A

Calor, Rubor (redness), tumor (swelling), Dolor, functio laesa

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5
Q

Inflammation: Circulatory changes

A

Nerves: smooth muscle to precapillary arterioles to constrict then relax = dilation = rush of new blood.
redness, swelling, warmth

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6
Q

capillary made of

A

only 1 layer of endothelium and the basement membrane, poor regulation of blood. Increase blood = increased pressure = edema and blood slows in the capillarys due to hemoconcetration.

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7
Q

Blister

A

clear plasma w/o RBC, WBC, platelets

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8
Q

If plasma is pulled out of the blood…

A

Blood in capillaries has less plasma = hemoconcentration and slow flow. RBC aggregate (ruleaux formation = stack on top of each other)

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9
Q

what is Rouleaux formation

A

Sludge RBC stack and slow circulation. This allows the WBCs to attached to the endothelium = Pavementing to attatche to capillary and venules walls.

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10
Q

Pavementing

A

adhesions on WBC endothelial cells normally inactivated are activated by ILs

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11
Q

ILs

A

activate pavementing and are found mostly at inflammation site to trigger inflammation. platelets initiat clot = fibrin strands to anchor leukocyte to vessel walls to slow movement.

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12
Q

Emigrating leukocytes

A

Increases permeability into damaged area from cepillaries & venules.

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13
Q

Acute inflammation

A

Neutrophils

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14
Q

Chronic inflammation

A

monoctes, lymphocytes, macrophages, plasma cells.

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15
Q

Emigration of Leukocytes steps (4)

A

1) Adhered neutrphils to endothelium
2) Insertion of cytoplasmic pseudopodes btween junctions of endothelium
3) pass though basement membrane
4) Ameboid movement to inflammation.

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16
Q

Chemotaxis

A

neutrophil movment along concentration gradient. chemo-attraction also due to destroyed cell debris and cmplement

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17
Q

Cells that phagocytize

A

macrophages, monocytes, neutrophils

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18
Q

Opsonins

A

Complement (C3) or Ig (Fc) can make antigen to be destroyed.

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19
Q

Pus

A

dead neutrophils with debris make a yellow viscous fluid. Inflammation dominated by pus formation are called purulent or suppurative inflammation.

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20
Q

Inflammatation produces what 2 clincal findings?

How?

A

Fever over 37 degrees by endogenous pyogens. IL1 and TNF act on Hypothalamus, which releases pyogens that act on prostoglandins. PMN and Macrophases also release pyogens during inflammation.

Leukocytosis: normal is 10,000. Bone marrow releases 12-15,000 leukocytes (PMNs). clinical symptoms = weakness, depression, pain, exhaustion, no appetite

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21
Q

Where are gross signs of inflammation

A

skin, eyes, mouth, genitals, internal organs.

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22
Q

Serous inflammation, what is it, example,

A

Mildest form, clear serum = early stages of inflammation. Viral (HSV), Lupus, pericarditis, pleuritis, peritonitis, 2nd degree burns

23
Q

Cytopathic effect of serous inflammation

A

intranuclear vesicle is where the HSV is.

24
Q

Fibrinous inflammation and example

A

Fibrin replaces serous fluid in pericardial sac. Fibrin exudate, Strep pneumo. Inflammation in pericardial sac of epicardium and pericardium (bread and butter).

25
Purulent inflammation, examples.
Pus forming bacteria (Staph and Strep) with PMNs and necrotic debris. Bacterial meningitis, Acute lobar pneumonia.
26
What is an abscess, what is the capsule made of. what does the capsule prevent?
Localized pus = abscess that is walled off. capsule made from fibrotic granulation tissue = does not heal. Capsule prevents septic shock
27
Large abscesses
May rupture and form a sinus. | May form fistula (bowels), channels between 2 pre-existing cavities
28
Ulcerative Inflammation, examples
Inflammed body surface or hollow organ (stomach, intestines) that results in ulceration or loss of epithelial lining. Gastric peptic ulcer. Then duodenal peptic ulcer
29
what is an ulcer
defect of epithelium or connective tissue
30
Peptic Ulcer causes
ulceration inflammation. Hx: smoking, alcohol, spicy food, loss of mucus, high acidity burns through 3 muscle layers.
31
Pseudomembranous inflammation, how does it happen
C. Diff ulcerative inflammation and fibrinopurulent exudation. Bleeds if you scrap it off. Broad spec kills bacteria and leaves C diff.
32
Granulomatous inflammation
Chronic inflammation not by acute mediated inflammation (PMNs). cell mediated hypersensitivity. TB = granulomas block spread.
33
Miliary TB
TB that moves
34
Can we kill TB? If not what can we do
No, collagen and giant cells block off TB. 6-9 months to kill TB with Meds
35
Wound healing with inflammation
may or may not fully heal due to infection, dirty, immuncomp, diabetes.
36
Libial/Stem cells do what in what tissues. How do we use this to kill cancer
quick mitosis in Skin, Hair, GI, Endometrium, RBC. Cancer reproduces 15x, we use chemotherapy drugs to kill fast reproducing cells.
37
What cells never reproduce
Heart and brain
38
Quiescent Cells, examples, and how? | What happens in a partial hepatoctomy
Stable Cells. do not divide unless they need to. Parenchymal organs (liver, kidney). Partial hepatoctomy stimulares the remaining liver to divide and regenerate
39
Permanent Cells
Never divide. Neural, myocardial. repair by fibrous scarring. Fibro-scarring. Gliosis or astrogliosis
40
Problems with Myofibrosis
conduction issues due to lack of conductivity
41
Wound healing cells
Leukocytes, Macrophages, connective tissue cells, Epithelial cells.
42
PMNs role in wound healing.
Kill bacterial while macrophages remove debris and attract 3 cells types to repair.
43
Cell that are attracted by macrophages
Myofibroblasts: smooth muscle and fibroblast. Hold and pull margins to approximate. Enables epithelial proliferation. Firboblasts: produces most ECM and Fibronectin (glue) and COllagen (type 3 young and type 1 mature with meshwork). Angioblasts: precurser to blood vessels. appears 2-3 days after incision.
44
Collagen types
Type 3 = immature | Type 1 = strong, mature with meshwork.
45
Granulation tissue is made of
Collagen and angioblasts (angiogenesis)
46
Clinical wound healing
1st Intention and 2nd Intention
47
Scabs and PMNs
Scabs are coagulated blood and PMNs scavange debris. Macrophages come later and call in myofibroblasts, angioblasts, and fibroblasts.
48
1st Intention
PMN need to clean wound and Suturing helps to approximate. Prone to Dehiss
49
Granulation Tissue
connective tissues rish in macrophages and 3 cells that are called
50
Clinical wound healing
from Fibronectin and Collagen type 3 to Type 1 Also called a scar. Scar forms between 3-6 weeks.
51
2nd Intention
Large defects cant be bridged and no wound contraction my myofibroblasts. Infected wound healing.
52
Delayed wound healing | 6 factors
Local or systemic influences. 1) Site of wound: skin heals well, brain does not heal. 2) Infection: steril wounds heal faster. Approx 5% of hospitalizations = infection post-operatively 3) Mechanical: approximation of edges and kept immobile, FB retard healing. 4) Age, kids heal faster. 5) Circulatory: ischemia wounds heal slower (diabetes, high sugar stops PMNs) 6) Nutrition; Vitamin C and proteins
53
Complication of wound healing
1) Deficient Scar formation. diabetes, ischemia, corticosteroid hormones (poor collagen production). 2) Excess scaring formation. Keloids = Type 3 collagen, no epithelium (immature scar)
54
Keloid
Excess dermal collagen Type 3

pathology (5 decks)

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