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pathology > inflammation > Flashcards

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
Q

Purulent inflammation, examples.

A

Pus forming bacteria (Staph and Strep) with PMNs and necrotic debris.
Bacterial meningitis, Acute lobar pneumonia.

26
Q

What is an abscess, what is the capsule made of. what does the capsule prevent?

A

Localized pus = abscess that is walled off.
capsule made from fibrotic granulation tissue = does not heal.
Capsule prevents septic shock

27
Q

Large abscesses

A

May rupture and form a sinus.

May form fistula (bowels), channels between 2 pre-existing cavities

28
Q

Ulcerative Inflammation, examples

A

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
Q

what is an ulcer

A

defect of epithelium or connective tissue

30
Q

Peptic Ulcer causes

A

ulceration inflammation. Hx: smoking, alcohol, spicy food, loss of mucus, high acidity burns through 3 muscle layers.

31
Q

Pseudomembranous inflammation, how does it happen

A

C. Diff
ulcerative inflammation and fibrinopurulent exudation. Bleeds if you scrap it off.
Broad spec kills bacteria and leaves C diff.

32
Q

Granulomatous inflammation

A

Chronic inflammation not by acute mediated inflammation (PMNs). cell mediated hypersensitivity. TB = granulomas block spread.

33
Q

Miliary TB

A

TB that moves

34
Q

Can we kill TB? If not what can we do

A

No, collagen and giant cells block off TB. 6-9 months to kill TB with Meds

35
Q

Wound healing with inflammation

A

may or may not fully heal due to infection, dirty, immuncomp, diabetes.

36
Q

Libial/Stem cells do what in what tissues. How do we use this to kill cancer

A

quick mitosis in Skin, Hair, GI, Endometrium, RBC. Cancer reproduces 15x, we use chemotherapy drugs to kill fast reproducing cells.

37
Q

What cells never reproduce

A

Heart and brain

38
Q

Quiescent Cells, examples, and how?

What happens in a partial hepatoctomy

A

Stable Cells. do not divide unless they need to. Parenchymal organs (liver, kidney). Partial hepatoctomy stimulares the remaining liver to divide and regenerate

39
Q

Permanent Cells

A

Never divide. Neural, myocardial. repair by fibrous scarring. Fibro-scarring. Gliosis or astrogliosis

40
Q

Problems with Myofibrosis

A

conduction issues due to lack of conductivity

41
Q

Wound healing cells

A

Leukocytes, Macrophages, connective tissue cells, Epithelial cells.

42
Q

PMNs role in wound healing.

A

Kill bacterial while macrophages remove debris and attract 3 cells types to repair.

43
Q

Cell that are attracted by macrophages

A

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
Q

Collagen types

A

Type 3 = immature

Type 1 = strong, mature with meshwork.

45
Q

Granulation tissue is made of

A

Collagen and angioblasts (angiogenesis)

46
Q

Clinical wound healing

A

1st Intention and 2nd Intention

47
Q

Scabs and PMNs

A

Scabs are coagulated blood and PMNs scavange debris. Macrophages come later and call in myofibroblasts, angioblasts, and fibroblasts.

48
Q

1st Intention

A

PMN need to clean wound and Suturing helps to approximate. Prone to Dehiss

49
Q

Granulation Tissue

A

connective tissues rish in macrophages and 3 cells that are called

50
Q

Clinical wound healing

A

from Fibronectin and Collagen type 3 to Type 1
Also called a scar.
Scar forms between 3-6 weeks.

51
Q

2nd Intention

A

Large defects cant be bridged and no wound contraction my myofibroblasts.
Infected wound healing.

52
Q

Delayed wound healing

6 factors

A

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
Q

Complication of wound healing

A

1) Deficient Scar formation. diabetes, ischemia, corticosteroid hormones (poor collagen production).
2) Excess scaring formation. Keloids = Type 3 collagen, no epithelium (immature scar)

54
Q

Keloid

A

Excess dermal collagen Type 3

pathology (5 decks)

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