Patophys
Acute Inflammation Quiz
Test your knowledge on the mechanisms and implications of acute inflammation! This comprehensive quiz covers a wide range of topics, including cellular responses, immune system interactions, and the roles of various mediators in inflammation.
Whether you're a student, educator, or simply interested in the subject, this quiz will enhance your understanding of critical physiological processes.
- 25 engaging questions
- Multiple choice answers
- Score as you go along!
The action of endothelial cells in acute inflammation
Migration to the inflammation site
Relaxation of the intracellular bonds in response to histamine
Adhesion to the mast cell
Expression of certain adhesion molecules
Following elements can be of higher importance in initiation of acute inflammation:
Endothelial cells
Post capillary SMC
Mast cells
Pre - capillary SMC
Macrophages
Can present antigen in MHC class I molecules
Clean the inflammatory site of debris in late phase of acute inflammation
May possess the Fc receptors on their surface helping better recognize and phagocyte opsonized bacteria
Are the main cells of chronic inflammation
Vasoactive reaction in acute inflammation
Is based on pre-capillary smooth muscle contraction
Depends on capillary smooth muscles relaxation
Relies on adrenergic receptors in post-capillary SMC
Is crucial event for exudate production and leukocyte extravasation
Following factors have similar direct action on the capillary blood vessel in inflammation
Serotonin
Adrenalin
Histamine
C5b
Inflammatory processes
Typically have destructive character
Chronic are frequently related to autoimmune processes
May help the immune system recognize the antigen
Were first described in XIX century
Complement activation products have very important functions in inflammation development. One or more of the following combinations reflect the actual possibility
C5b67 - chemotaxis
C5b - activation of mast cell
C3a - chemotaxis
C3b - opsonization of target cell
The most serious long-term consequences of the inflammation are
High fever
Widespread damage in the tissue
Abscess formation
Fibrotic changes
Which of the following sequences acceptably reflect(s) the sequence of events in acute inflammation
Tissue damage > activation of tissue inflammation elements > infiltration with the inflammatory cells > damage repair
Local tissue irritation > neutrophils infiltration > damage repair > down regulation of the defence
Irritating factor > inflammatory mediators > vasoactive reaction > infiltration with the inflammatory cells
Inflammatory stimulus > activation of generalized inflammatory mechanisms > activation of local inflammatory mechanisms > down regulation of the defence mechanisms
In inflammation
Complement C2a components are the common direct activators of the mast cells
Selectins and integrins help the monocyte migrate from blood to the tissue
Neutrophils attract the mast cells with chemokines
Bradykinin can act very similar to histamine in activating the capillary reaction
Complement in inflammation can be activated
On the alternative pathway through direct contact with bacterial glycoproteins
On the classical pathway through contact with fixed immune complexes
Outside of the blood vessels
Inside the blood
APCs can present certain antigens in the context of the following MHC molecules
Class II to Tc cells - intracellular antigens
Class I to Th cells - antigens derived from their content regarded as “self”
Class I to Tc cells - antigens present in their own cytoplasm
Class II to Th cells antigens obtained from phagocytosed matter
Chemotaxis
Depends on the ligand - receptor action
Is crucial for guided movement of leukocytes in the tissue
Relies on diffusion of chemotactic factors in tissue fluids and blood serum
Can be provided by both fixed and soluble chemotactic molecules
Adhesion molecules responsible for certain actions in the capillary are
Selectins for leukocytes rolling
Integrins for leukocytes firm stopping
Selectins for blood cells selection
ICAM-1 for cells diapedesis
Secondary immune deficiencies can result from
Tuberculosis
HIV infection
Chronic hepatitis
Latrogenic cause
IgA deficiency
Is typically a secondary immunodeficiency
Is always asymptomatic
Can be easily cured
Can be a secretory as well as serum immunoglobulin deficiency
Hypersensitivity of
Type I is very seldom
Type II is based on aggreagetd immune complexes deposition
Type III is a consequence of organ - specific action mediated by the antibodies
Type IV is developing very slowly and usually leading
Severe combined immunodeficiency disorder (SCID)
Is typically developing in myeloid lineage
Is a common disease (1:1000 births in Europe)
. Is developing at the early stages of hematopoiesis
Has a course characterized by severe and repeated infections with whole variety of pathogens (bacteria, viruses, fungi)
Abnormal appearance of certain types of infection can suggest existence of the following immunodeficiencies
Of the phagocytic cells - mainly viral
Of the T cells - mainly fungal
Of the complement - mainly bacterial
Of the B cells - bacterial, viral and fungal
Fc(epsilon)RI on the mast
Is a high affinity receptor as compared to Fc(epsilon)RII
Induces histamine release when dimerized 3. Induces histamine release when dimerized
Can be bridged with another Fc(epsilin)RI receptor through the IgE antibodies binding to allergen
Can be found in the tissue fluid in soluble form which blocks the Fc fragments of the IgE antibodies
SLE
Develop as a result of anti-IgG autonomies production
Results from inflammatory processes induced with complement activation by soluble immune complexes
Produces no typical symptoms
Is non-organ specific autoimmune disease
Autoimmune diseases
Are mostly of unknown etiology
Usually lead to destruction of tissue with chronic inflammation
Majority of symptoms in organ non-specific diseases are related to the III type of hypersensitivity
In most cases are related to incomplete positive selection in the thymus and resulting from it cytotoxic reaction with Tc cells
The intestine is the highly important immune organ because:
It can serve as auxiliary production site for leukocytes
All the immune reaction there are very effective defense type
Majority of immunization processes for the benefit of entire organism take place there
Of its well-built lymphatic structures and constant access to rich antigenic load
What Fasano discovered was that:
Infection with Vibrio cholera predisposes to celiac disease
Zonulin receptor can be blocked by zonula occludent toxin
Zonula occludens toxin analogue is produced by gut’s mucosa
Production of zonulin can be triggered by gluten
.Exceptional knowledge coming from discoveries in the field of Celiac disease pathogenesis helped us to learn that:
There is a strong link between the incompetent intestinal epithelium and development of autoimmunities
Gluten is a factor increasing permeability of the gut also in individuals who do not develop Celiac disease
The development of autoimmune reactions need to be propelled by the supply of external stimuli
Zonulin is a necessary link between ingestion of gluten and increased permeability of the gut
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