immunology - acute inflammatory response 1

what is the goal of the inflammatory response

eliminate cause of cellular injury and rid necrotic debris

what types of inflammation are capable of harming normal tissues

hypersensitivities

autoimmune disease

acute inflammation

rapid onset, short duration, fluid and plasma protein exudation, mainly neutrophil response

chronic inflammation

insidious, longer duration, lymphocytes and macrophages, vascular proliferation and scarring (fibrosis)

inflammatory response is usually controlled and self limiting, if not what happens?!

chronic inflammation

patient with diabetes mellitus may have these on retina

exudation (macular edema), retinal hemorrhages, cotton wool spots

what are the 5 cardinal sings of the inflammatory response

calor (heat)

rubor (redness)

tumor (swelling)

dolor (pain)

loss of function (functio laesa)

what does recognition of stimuli

toll-like receptors

- on phagocytes, dendritic cells

inflammasome

what vascular changes occur with acute inflammation

vasodilation (increased blood flow)

increased vascular permeability

what happens with increased vascular permeability

blood vessel wall alterations, plasma proteins leave circulation and move into extravascular tissues, activation of endothelial cells with WBC adherence and their leakage

what is conjunctival hyperemia

dilated vessels in conjunctiva

exudate occurs because of ???

transudate occurs because of ???

exudate: due to endothelium separating, more protein

transudate: interstitial fluid accumulations, increased HYDROSTATIC pressure, low protein amt

what is exudate

endothelium separates, protein rich fluid leaks out and accumulates into extravascular tissues

may lead to tissue edema

conjunctival chemosis is due to ?

allergic hypersensitivity (usually)

hyperactive immune and inflammatory response

function of leukocytes in inflammatory response

"called" there, leak out of BV to site of inflammation

activate and eliminate

- ingest, kill, eliminate the injurious source and necrotic debris

neutrophil response

margination --> neutrophils accumulate along endothelial cell surfaces and ultimately move into interstitial tissue

leukocyte recruitment

selectins:

margination and rolling along BV wall, mediate initial weak interactions

leukocyte recruitment

integrins:

firm adhesion to the endothelium

leukocyte surface proteins

leukocyte recruitment

diapedesis

transmigration betwee endothelial cells, leukocytes leave BV

leukocyte recruitment

cytokines

migration to the interstitial tissues toward chemotactic stimulus

neutrophil characteristics and fun facts ;)

most common type

first to arrive

replaced by monocytes in 24-48 hours

present in BACTERIAL infections

monocyte fun facts

replace neutrophils after 24-48 hours

which leukocyte deals with viral infections

lymphocytes

what leukocyte deals wtih hypersensitivity reactions (allergy)

eosinophils

leukocyte activation

phagocytosis & CLEAN UP

intracellular destruction of phagocytosed microbes and dead cells

liberation of substances that destroy extracellular microbes and dead tissues

production of mediators

leukocyte-induced tissue injury

can secrete _____ and _____, thus can cause _____

reactive oxygen species and enzymes

injury in normal cells and tissues

examples of leukocyte-induced tissue injury

tuberculosis, post myocardial infarction (MI), autoimmune diseases, hypersensitivity

lymphangitis

inflammation of lymphatic vessels

lymphadenitis

enlarged, inflamed lymph nodes

PAL-preauricular lymphadenopathy

swelling in front of ear - eye drains here

3 outcomes of acute inflammation

resolution

chronic inflammation

scarring

resolution of acute inflammation

regeneration and repair

removal of exudate

restoration of the normal tissue architecture

inflammatory response is STOPPED

phagocyte clearing and lymphatic drainage

chronic inflammation can occur from 2 things

1. offending agent is not removed (acute didnt resolve)

2. chronic inducing stimulus from the start

- autoimmunity, some viral infections

scarring

repair type, after significant tissue destruction, in tissues that cant regenerate--> connective tissues fills in and fibrosis

5 steps of the inflammatory response (5 Rs)

1. recognition of the injurious agent (toll-like, inflammasomes)

2. recruitment of leukocytes (neutrophils, WBCs)

3. removal of the agent (phagocytosis)

4. regulation (termination)

5. repair

acute vs chronic

duration

a: short (days)

c: long (weeks to months)

acute vs chronic

inflammatory cells

a: neutrophils

c: lymphocytes, plasma cells

acute vs chronic

vascular changes

a: active vasodilation, increased permeability

c: neovascularization

acute vs chronic

edema

a: present

c: not usually ? idk

acute vs chronic

fibrosis

a: not usually

c: yes

acute vs chronic

systemic manifestations

a: fever, leukocytosis

c: low grade fever, weight loss, anemia

morphologic patters of acute inflammation

1. serous inflammation (watery, protein poor fluid)

2. suppurative inflammation (pus, necrotic cells, edema fluid)

3. ulcer (defect of excavation on surface of tissue)

types of suppurative inflammation

pyogenic: bacteria

abscess: pus + bacteria + necrotic cells

how to detect corneal ulcer

sodium fluorescein dye, epithelial defect light sup with cobalt blue filter

optometric clinical correlates

red eye testing

discharge either serous, mucous or mucopurulent

conjunctival scraping determines type of WBC

tests may indicate viral, allergic, bacterial conjunctivitis

what accompanies corneal ulcers?

uveitis, anterior chamber inflammation