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Patho > L3 > Flashcards

L3 Flashcards

1
Q

The morphologic hallmarks of all acute inflammatory reactions are: ?

A

➢ Dilation of small blood vessels
➢ Slowing of blood flow
➢ Accumulation of leukocytes and fluid in the extravascular tissue

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2
Q

Special morphologic patterns of Acute Inflammation:

A

➢ Catarrhal مخاطي
➢ SEROUS INFLAMMATION
➢FIBRINOUS INFLAMMATION
➢SUPPURATIVE OR PURULENT INFLAMMATION; ABSCESS
➢ULCERS
➢PSEUDOMEMBRANOUS INFLAMMATION
➢hemorrhagic
➢allergic
➢purulentصديدي

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3
Q

serous inflammation ?

A

marked by the accumulation
of serumlike protein-rich exudates sterile cell poor
fluid in body cavities lined by the peritoneum,
pleura, or pericardium or spaces created by tissue
injury.

Examples:
¢ The skin blister resulting from a burn.
¢ Viral infection represents a large accumulation of serous fluid.
¢ Inflammation of serous sacs.

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4
Q

In the serous inflammation the fluid derived from ?

A

the plasma or mesothelial cells

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5
Q

serous inflammation result from ?

A

burn, viral infection or local irritation
of mesothelial cells.

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6
Q

What is the effusion?

A

Accumulation of fluid in peritoneal, pleural, and
pericardial cavities is called an effusion.

clear, pale yellow appearance of the fluid. This is a serous effusion

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7
Q

Serous inflammation.
Across-section of a skin blister showing ?

A

the epidermis separated from the dermis by a focal collection of serous effusion.

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8
Q

FIBRINOUS INFLAMMATION • Characterized by?

A

the deposition of fibrin as a result
of the local activation of coagulation——-Larger molecules such as fibrinogen pass
the vascular barrier, and fibrin is formed
and deposited.

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9
Q

FIBRINOUS INFLAMMATION Associated with ?

A

increase vascular permeability resulting in passage of large molecules(fibrinogen) deposited in the extracellular space.——More severe injuries and greater vascular
permeability.

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10
Q

FIBRINOUS INFLAMMATION Occurs in: ?

A

Cancers as a resulting from leaks of procoagulant
molecules from cancer cells.

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11
Q

FIBRINOUS INFLAMMATION happend in ?

A

the lining of body cavities, such as
the meninges, pericardium and pleura.

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12
Q

Fibrinous exudates removed by ?

A

fibrinolysis and clearing of other debris by macrophages.

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13
Q

Persistence of fibrin ?

A

stimulate the ingrowth of fibroblasts and
blood vessels and thus lead to scarring ( organization)

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14
Q

Microscopically:
• fibrin appears as ? 2

A

an eosinophilic meshwork or an amorphous coagulum.——A pink meshwork of fibrin exudate

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15
Q

The Complications of FIBRINOUS INFLAMMATION?

A

• organization within the pericardial sac leads to impair cardiac function
• obliteration of the space eg pericardial space.

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16
Q

Abscess is ?

A

a localized collections of
(pus)purulent inflammatory tissue caused by suppuration buried in a tissue, an organ, or a confined space.

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17
Q

SUPPURATIVE OR PURULENT INFLAMMATION • Characterized by ?

A

the production of large amounts of purulent exudate (pus) consisting of neutrophils, liquefactive necrosis, and edema fluid.

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18
Q

SUPPURATIVE OR PURULENT INFLAMMATION Cause by ?

A

pyogenic (pus-producing) bacteria(e.g staphylococci)

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19
Q

A common example of an acute suppurative inflammation ?

A

is acute
appendicitis.

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20
Q

The yellowish fluid in this opened pericardial is ?

A

is a purulent exudate.

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21
Q

A thick yellow exudate coats the peritoneal surfaces that resulted from rupture of the colon is ?

A

SUPPURATIVE OR PURULENT INFLAMMATION

22
Q

Abscesses have a central region of…………and.

Surrounded by……., and outside this region…. and…… and……

A

necrotic leukocytes and tissue cells.

neutrophils, vascular dilation and parenchymal and fibroblastic proliferation

23
Q

ulcer is?

A

a local defect on the surface of an organ or tissue that is
produced by the shedding of inflamed necrotic tissue.

24
Q

Ulceration can occur only ?

A

when tissue necrosis and resultant
inflammation exist on or near a surface.

25
Q

Common sites of ulcers ? 2

A

• (1) the mucosa of the mouth, stomach, intestines, or genitourinary
tract
• (2) the skin and subcutaneous tissue of the lower extremities in
patients with atherosclerosis

26
Q

Pseudomembranous inflammation ?

A

Plaquelike adhesion formed of fibrinopurulent debris and mucus that attached to the damaged superficial mucosa.

27
Q

Causes of Pseudomembranous inflammation ? 2

A

Antibiotics that unbalance the normal bacterial flora resulting in overgrowth of
cytotoxin-producing Clostridium difficile strains lead pseudomembranous colitis

Bacterial toxins ( corynebacterium diphtheriae) damaging the mucosa lining producing
membrane composed of necrotic tissue

28
Q

Morphology of Pseudomembranous inflammation ?

A

Gross photograph showing plaques of yellow fibrin and inflammatory debris adherent to a reddened colonic mucosa.

29
Q

micrograph of Pseudomembranous inflammation ?

A

showing superficial mucosal erosion, an adherent pseudomembrane of fibrin, and inflammatory debris

30
Q

بداية من جديد شوي معلش
Several types of inflammation vary in their morphology and clinical correlates. Why?

A

1) Severity of the reaction
2) Specific cause
3) The particular tissue
4) The involved site

31
Q

Catarrhal inflammation

A

Mucous-rich exudate ž
Common in mucous membranes ž
Usually by virus infection (common cold, rhinitis, Infleunza) ž
Mild and disappears by resolution

32
Q

Hemorrhagic inflammation

A

The exudate is serosanguineous being rich in RBCs. ž
Caused by:
¡ Hemolytic streptococci
¡ Anthrax bacilli

33
Q

One consequence of acute inflammation is?

A

ulceration

34
Q

Membranous inflammation

A

An inflammation in which the mucosal epithelium is coated by a membrane formed of fibrin, desquamated cells and inflammatory cells. žExamples:
¡ Amaebic dysentery
¡ Diphtheria
¡ Infleunzal bronchitis

35
Q

Allergic inflammation?

A

-Caused by antigen antibody reaction. ž
-There is marked edema and excess eosinophils in both blood and tissue žExamples:
¡ Bronchial asthma
¡ Urticaria

36
Q

Purulent inflammation

A

-Characterized by the production of large amounts of pus or purulent exudate consisting of neutrophils (living and dead), necrotic cells(liquefactive necrosis), and edema fluid
-Certain bacteria (e.g., Staphylococcus aureus) produce this suppuration and are therefore referred to as pyogenic (pus-producing) bacteria.
-A common example of an acute suppurative inflammation is acute appendicitis

37
Q

Purulent inflammation types?

A

localized: Abscess-furuncle(boil)-carbuncle
Diffuse: cellulitis

38
Q

Abscess?

A

-Abscess is a localized collections of (pus)purulent. -inflammatory tissue caused by suppuration buried in a tissue, an organ, or a confined space.
ž Inflammatory exudate forces tissue apart.
-Liquefactive necrosis in the centre. ž
-Cause high pressure therefore PAIN. ž
-Cause tissue damage ž Squash adjacent structures.

39
Q

The abscess contains?

A

neutrophils, edema fluid, and cellular debris.

40
Q
A

Furuncle (Boil) ž:In hair follicles- žIn hairy parts on
the body-Tender and painful.

Carbuncle: Common in skin in upper back- In diabetics -Multiple sinuses discharging pus

41
Q

Cellulitis:?

A

Diffuse Purulent (suppurative) inflammation. ž
Due to streptococcal infection:
¡ Streptokinase— ¡ Hyaluronidase ž
Seen in areas with loose tissues:
¡ Orbit—- ¡ Extremities—- ¡ GIT

42
Q

Acute inflammation may have one of the four
outcomes:

A

1) Complete resolution.
2) Organization: Healing by connective tissue replacement (fibrosis).
3) Progression to chronic inflammation.
4) Suppuration and/or spread.

43
Q

Variables may modify the basic process of inflammation:?

A

➢the nature and intensity of the injury.
➢ the site and tissue affected.
➢the responsiveness of the host.

44
Q

One of the Acute inflammation outcomes, Complete resolution of Acute inflammation, when?

A

1) the injury is limited or short-lived.
2) there is no or little tissue destruction.
3) the damaged parenchymal cells can regenerate.

Note that if tissue architecture has been destroyed, complete resolution is not possible.

45
Q

One of the Acute inflammation outcomes,
Complete resolution Mechanism:

A

-Neutralization and removal of chemical mediators
-Normalization of vascular permeability
-Halting of leukocyte emigration
-Clearance of edema (lymphatic drainage) , inflammatory cells and necrotic debris (macrophages).

46
Q

One of the Acute inflammation outcomes,
Healing by connective tissue replacement (fibrosis):

A

This occurs after substantial tissue destruction.
-the inflammatory injury involves tissues that are incapable of regeneration.
-there is abundant fibrin exudation.
-The destroyed tissue is replaced by fibrosis.
-Serous cavities.

47
Q

Connective tissue grows into the area of damage or exudate, converting it into a mass of fibrous tissue—a process also called?

A

organization

48
Q

One of the Acute inflammation outcomes, Progression of the tissue response to chronic
inflammation:

A

Occurs when the acute inflammatory response cannot be resolved. WHY?
Due to:
1. The persistence of the injurious agent eg. TB
2. Some interference with the normal process of healing

49
Q

Local effects of acute information

A

-Swelling: Blockage of tubes, e.g. bile duct, gland duct, intestine.
-Exudate: Compression e.g. cardiac tamponade.
-Loss of fluid e.g. burns.
-Pain & loss of function especially if prolonged.
-Spread to adjacent tissues.
-Exaggerated response (hypersensitivity).

50
Q

Inflammation Systemic Effects

A

• Pyrexia
• Leukocytosis
WBC count climbs to 15,000 or 20,000 cells/μl
• Neutrophilia • Eosinophilia
• Monocytosis • Lymphocytosis

• Spread of micro-organisms and toxins
• Toxaemia • Pyaemia • Septicaemia

• Weight loss (in chronic inflammation)
• SHOCK

Patho (11 decks)

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