human pathology final cramming

necrosis

tissue death

necrosis is usually caused by?

ischemia, which leads to hypoxia

infart

dead tissue

types of necrotic tissue (4)

gangrenous

caseous

fibrinoid

liquefactive

gangrenous (wet and dry) necrotic tissue description

dry is known as coagulative necrosis (frostbite)

wet is a form of liquefactive necrosis

gas gangrene is caused by

saprophytic bacterium or blisters

caseous necrosis description

cheesy, doesn’t need microscope, linked to tb

fibrinoid necrosis description

always refers to an autoimmune disorder like rheumatoid arthritic nodules

liquefactive necrosis description

found in CNS due to lung/bacterial/fungal infection

tissue turns to liquid, caused by enzymes released by lysosomes

what dies first in a person?

neurons within 3-7 min

4 stages of death

1. algor mortis

2. livor mortis

3. rigor mortis

4. postmortem autolysis

algor mortis

stage 1: cooling of body temp to room temp

livor mortis

stage 2: blueish-purple discoloration of skin due to blood pooling bc of gravity (stage with ecchymosis)

ecchymosis

bruises caused by RBCs lysing. seen in livor mortis stage

rigor mortis

stage 3: stiffening of joints and muscles

postmortem autolysis

stage 4: body decomposition. maceration and putrefaction occur in this stage.

maceration

softening of tissues due to enzyme activity after death

putrefaction

skin of abdomen turns greenish color outlining the colon and the liver

skeletonization

occurs when the soft tissue is removed from the bones and gas escapes the body

pyrexia

fever

five cardinal signs of acute inflammation

1. rubor - redness

2. tumor - swelling/edema

3. calor - increased heat

4. dolor - pain

5. functio laesa - loss of function

normal body temp

98.6

four steps of a physical assessment

inspect, palpate, percuss, ausculate

local effects of inflammation

capillary dilation

increased blood flow

increased warmth and redness

swelling

attraction of neutrophils

hyperemia

increased blood flow

erythema

increased warmth and redness

tylenol is good for what symptoms and bad for what?

good for pain and fever

bad for inflammation

systemic effects of inflammation

pyrexia

acute inflammation is initiated by what white blood cell?

neutrophils

how does Tylenol reduce fever?

it’s a COX inhibitor

white blood cell types, mnemonic, and their percentages

never let my engine blow

neutrophils 60%

lymphocytes 30%

monocytes 5%

eosinophils 4%

basophils 0-1%

most abundant type of WBC

neutrophils

what WBC becomes macrophages?

monocytes

which WBC is the first to show up at infections?

neutrophils

3 events to know for inflammation

1. vasodilation

2. cellular PMNs (neutrophils) appear during acute inflammation

3. mediators (chemicals involved in inflammation)

acute inflammation is caused by?

immune reactions, penetrating injuries, necrosis, infections, burns, frostbite, and caustic chemicals

acute inflammation process sequence

1. congestion

2. exudation

3. suppuration

4. resolution

transudate

leakage of water

serous

primarily fluid, little protein (ex: blisters)

serosanguineous

clear, thin, and pink

sanguineous

thin, watery, and reddish

purulent

opaque, milky, and green (pus)

hemopurulent

purulent and red-tinged (bloody pus)

fibrinous

rich in fibrinogen; coagulates and forms fibrin; produces a stick film on surface of inflamed tissue

catarrhal

cloudy mucus (rhinorrhea)

how is exudate quantified clinically?

1. non-present

2. scant: wound is moist

3. small/minimal: covers less than 25% of bandage

4. moderate: covers 25-75% of bandage

5. large/copious: covers over 75%

inflammatory lesion types

abscess

ulcer

furuncle

carbuncle

cellulitis/phlegmon

pustule

vesical

abscess

circumscribed collection of pus surrounded by a wall of inflammatory tissue

ulcer

open sore or lesion of the skin accompanied by inflamed necrotic tissue

furuncle

abscess or pyogenic infection of a sweat gland or hair follicle

carbuncle

several communicating boils with the production and discharge of pus and dead tissue

cellulitis/phlegmon

diffused inflammatory infiltration of the tissues. infection is in all the tissues

pustule

small, circumscribed elevation of the skin containing pus; pimple

vesical

small, circumscribed elevation of the skin containing a thin, non-purulent fluid; blister

prostaglandin PGs (definition and what it can cause)

hormone-like substances found in almost every tissue of the body that can cause:

• vasodilation or vasoconstriction

• platelets to aggregate or disaggregrate (stick/not stick)

• induction of labor and delivery

• pyretic (fever producing)

• bronchodilation and bronchoconstriction

• hyperalgesic (increase pain)

mediators of acute inflammation and what they do

arachidonic acid (AA) released by phospholipid cell membranes by the cleaving of acids via phospholipase A2

AA is then acted upon by COX to produce a class of eicosanoids responsible for inflammatory response. (most important being prostaglandin E2)

most common prostraglandin that is responsible for most inflammation-response events

PGE2

WBC exit sequence

1. margination: WBCs get attracted to peripheral wall of vessel

2. rolling: WBCs roll, tumble, and heap on themselves

3. adhesion: WBCs adhere to vessel wall

4. transmigration: WBCs exit bloodstream into tissues to fight injury/infection

how does fever work?

macrophages release an endogenous pyrogen, Interleukin-I and TNF.

these stimulate the release of COX in hypothalamus, raising temp