What is the immune response?

It's a complex of protective reactions, which helps organisms to maintain antigenic peculiarities and
cellular homeostasis during contacts with the external environment

Indicate the factors, phenomena, and structures of the immune response system which prevent
the antigen getting into the internal environment of the organism.

Skin

Mucous membrane → such as gastrointestinal (begins in mouth), urogenital and respiratory.

How are cells of the immune organs classified?

Non specific (innate immunity) → acts against various antigens and genetically determined and is
characteristic for species

Specific (adaptive immunity) → Reactions are specific against antigen and immune response is
acquired by individuals during its contact with various antigens. It can be humoral or cellular.

Which immunity does determine non-specific immune response?

Non-specific (innate immunity) is the defense system with which you were born. It protects you
against all antigens. Innate immunity involves barriers that keep harmful materials from entering
your body.

What is inflammation? (a non specific immune response)

A complex of vascular reactions in the CT to the exogenous and endogenous injurious agents. injury
can be caused by → biological factors (microorganism), chemical and physical factors and necrosis.

What is the main protective mechanism of inflammation?

Mechanical →

- not damaged epithelial cells on skin

- cilia of epithelial cells
- mucos
- peristalsis

Chemical → Acid in gastric juice, lysozyme in tears, acidic environment on skin

Microbial → Competition between normal flora and pathogens for nutrients

Indicate the main phases of phagocytosis.

- Recognition and attachment (opsonization by C3b and igG)

- Engulfment and formation of phagosome and phagolysosome
- Killing or degradation by toxic oxygen and nitrogen products, lysozyme and proteases

What is the role of labrocytes in inflammation?

What is the role of granulocytes in inflammation?

Indicate the main groups of mediators of inflammation
Vasoactive amines → Histamine: mast cells, platelets and basophils. Serotonin (platelets) cause
dilatations of arterioles and increase permeability of venules.

Plasma factors (produced by liver) → Acute phase proteins, complement system, kinin system,
coagulation factors

Arachidonic acid metabolites → prostaglandins, thromboxane and leukotriene

Cytokines → its produced by macrophages ex) TNF - alpha and IL1,6,8,12

What are the stages of inflammation?

Rubor: Redness

Tumor: Swelling

Calor: hot or the place is warm

Dolor: Pain

Virchow added Functio laesa: Loss of function

What is the structure of inflammatory infiltration?

Indicate the main clinical-morphological features of inflammation; what do determine these

features?

What are the possible outcomes of inflammation? osäker!

Symptoms →

Rubor: Redness

Tumor: Swelling

Calor: hot or the place is warm

Dolor: Pain

Virchow added Functio laesa: Loss of function

What is chronic inflammation?

Ongoing, long-term response to endogenous or exogenous inflammatory stimuli and is characterized

by continued accumulation of mononuclear leukocytes (macrophages and lymphocytes),
accompanied by tissue injury due to the prolonged inflammatory response.
What do lymphocytes and plasma cells indicate at the site of inflammation?

Indicate terminology principles of inflammation

Organ or tissue + itis ex) bronchitis, myocarditis , pulpitis, gastritis

Exception pneumonia (in lungs)

What is the composition of serous exudate? Present examples of serous inflammation.

Composed of a small amount of desquamated epithelium or mesothelium.

Causes → Viruses (blisters in herpetic infection), or physical agents ex) high temp or skavsår. Or
catarrhal inf. in mucous membrane in respiratory tract ex) sneezing

Outcome → Healing or progress to other types of inf. most commonly purulent.

What are the most common etiological factors (causes) of fibrinous inflammation?

Occurs when greater vascular permeability larger molecules such as fibrinogen pass the vascular
barrier and fibrinogen is converted to fibrin.

Causes → Bacteria ex) streptococcus pneumoniae, corynebacterium diphtheriae, mycobacteria,

shigella and toxic agents (in case of uraemia jani increase of renal failure)

Outcome →

- Resolution (healing): Fibrinous exudate removed by fibrinolysis and debris by macrophages

so normal tissue can get restored.
- Organisation: : Fibrinous exudate converted to CT leading to synechiae or adhesion
formation in serious cavities (develop obliteration)
- Fibrinous ulcerative Inflammation in respiratory tract can lead to asphyxia (suffocation)
- Fibrinous ulcerative Inflammation can lead to scarring of mucus lining
What are the forms of fibrinous inflammation?

- Fibrinous inflammation can be in serous body cavities lined by mesothelium, mucous

membranes, and parenchymal organs (lungs)
- Fibrinous ulcerative (diphtheric or pseudomembranous inflammation); it develops in
diphtheria, dysentery, uremia

What are the morphological features of the forms of fibrinous inflammation?

What components do form purulent exudate and what are the forms of purulent inflammation?

Composed of neutrophils, necrotic cells, bacteria and plasma proteins.

Causes → Pyogenic bacteria (*pus forming bacteria) ex) staphylo & streptococcus and Neisseria
meningitidis & gonorrhoeae.

Forms → Abscess, phlegmone and empyema, furuncles and carbuncles

What is abscess, phlegmone, and empyema? What is furuncle and carbuncle?

Abscess → Has pyogenic capsule, so the pus is surrounded by capsule

Phlegmone → No capsule so the purulent inf. can spread in the tissues

Empyema → Purulent inf. in preformed cavities, pus is only accumulating and not destroying.

Furuncles → Purulent inf. of hair follicles

Carbuncles → Clusters/multiple of furuncles = carbuncles

What are the outcomes of purulent inflammation?

- Abscessus can drain through the fistula, if it's in the brain the patient will die but if it's in the
subdermal area/ muscles it will lead to healing.
- If the abscessus is large it will lead to formation of CT or scar.
- If the purulent inf. spreads to bloodstream it can lead to sepsis
- When its chronic purulent inf. It can lead to amyloidosis.

What are the morphological features of purulent inflammation manifesting in bones?

What is catarrhal inflammation and where does it usually manifest?

Catarrhal inflammation (inflammatio catarrhalis) is a serous inflammation in mucous membranes.

Catarrhus of upper respiratory tract – rhinitis, nasopharyngitis

When is the hemorrhagic inflammation in process?

Hemorrhagic inflammation (inflammatio haemorrhagica) – exudates with a great amount of RBC.

Haemorrhagic features can have other types of inflammation (serous, fibrinous) when there are
other pathological states affecting small vessels; It can be due to vit. C deficiency, thrombocytopenia

Causes → viruses (influensa, sneezing w blood), bacterial toxins (antrax, pestis); medicines (if using
anticoagulant or antiaggregants) increases the possibility for the inflammation.

Outcomes → depends on the main disease