Pathophys 2018 + 2018 retake

An educational illustration depicting the human immune system interacting with pathogens and inflammatory processes, vibrant colors, educational style.

Pathophysiology Quiz 2018

Test your knowledge on pathophysiology with our engaging quiz that covers essential concepts related to inflammation, immune response, and gastrointestinal health.

Features of the quiz:

  • Multiple-choice questions
  • Focus on key pathophysiological concepts
  • Great for students and professionals alike
43 Questions11 MinutesCreated by AnalyzingCells57
The gut:
Is an organ to digestion and immunization
allows for absorption of the basic organic compounds of food, fatty acids, etc.
is the largest immune organ
Allows for absorption of larger pieces of organic matter due to presence of the M-cells
Macrophages:
Can prevent development of the inflammation by effective removing of the invading microorganisms
Can prevent pus formation
Clean the inflammatory site from debris in the late phase of the acute inflammation
Have the Fcy receptors, thus can act in ADCC reaction
The following humoral factors have similar action on the capillary blood vessel in inflammation
Serotonin
Histaminase
Prostaglandin
Prostacyclin
Basophils:
Are the least frequently of all granulocytes
Along with macrophages clean the tissues in the late phase of acute inflammation
In some way are similar to mast cells
Very efficiently phagocyte soluble immune complex
Vasoactive reaction in inflammation include:
Activation by histamine, serotonin, integrin, C3a and other factors
Drop of hydrostatic pressure in the capillary due to escape of globulins with exudate
Relaxation of the intercellular junction in capillary endothelium
Concentration of the post-capillary smooth muscles
The colloid osmotic pressure of the serum inflammation:
Is a minor factor in generation of the exudate as compared to hydrostatic pressure of blood in the capillaries
Drops markedly in the venous end of the capillaries due to escape of globulins with exudate
Remains practically unchanged in the capillaries because the protein are lost along with water
Increase in the arterial end of the capillaries because water escapes with transudate fluid
Rolling in the capillary:
Initiates events of leukocytes extravasation
May end up with leukocyte falling off the capillary wall
Is usually followed by fixation of the leukocyte
Is mediated by integrins
The important action of histamine in inflammation include
Concentration of the smooth muscle in pre-capillary blood vessel
Relaxation of the capillary endothelial cell junctions
Relaxation of the post-capillary smooth muscles
Increase of permeability in the capillary vessels
The long-term consequence of inflammation include:
High fever
Excessive swelling
Abscess formation
Scar formation in the organ/tissue leading to its
Among humoral factors directly destroying tissues in inflammation we find:
Elastase
Metalloproteinases
Reactive oxygen species
Histamine
Which of the following reflect possible sequence of events in acute inflammation?
Local tissue irritation -> local and generalized inflammatory events -> downregulation of the defence mechanism -> damage repair
Tissue damage -> infiltration with the inflammatory cells -> activation of local tissue inflammatory elements damage repair
Inflammatory factor -> inflammatory mediators -> vasoactive reaction-> infiltration with the inflammatory cells
Inflammatory stimuli -> activation of generalized inflammatory mechanism -> activation of local inflammatory mechanisms -> downregulation of the defence mechanism
Following are the valid pairs of sources - product of vasoactive stimulation towards inflammation development in human:
Platelets - leukotrienes
Complement system - C5a
Mast cell - C3a
4. Tissue kinin system-bradykinin
Macrophages can effectively present antigen in context of MHC molecule of:
Class I to Th cells
Class II to Th cells
Class I to B cells
Class I to Tc cells
Chemotaxis:
Provides recruitment of leukocytes from blood to the inflammatory tissue
Allows the acute phase protein to reach the inflammation site
Depends on the presence of variety of cytokines in the tissues
For leukocytes provided by activation of the complement and mast cells
Th2 type of reaction
Prevents the development of th1 type reaction with interleukin - 10
Often leads to allergy based on type I hypersensitivity reaction
Stimulates B-lymphocytes to produce antibodies on various classes
Induces NK cells, macrophages and Tc-cells
Rheumatoid arthritis:
Is a result of type II hypersensitivity reaction
Is restricted synovial membrane
First symptoms are in the knee joints
Is a disease of unknown, possible viral etiology
The immunodeficiency patient may typically suffer from infection
Of recurrent type
Of severe type
Caused by opportunistic microorganisms
Of all type except for viral infections (
B-lymphocytes can
Secrete antibodies of the same specificity as their surface immunoglobulins
Present antigen of the same specificity as their surface antibodies
Present antigen of specificity different form their surface antibodies
Secrete antibodies of specificity different from their surface immunoglobulins
Features of organ non-specific autoimmune diseases are prevalent in:
Grave’s disease
Myasthenia gravis
Type 1 diabetes
Rheumatoid arthritis
Good example of translation of specific immune response to inflammation can be:
Complement activation in hypersensitivity type I
Mast cell activation in hypersensitivity type
Platelets aggregation in blood vessel damage
Complement activation in hypersensitivity type II
The systematic, steady immunization taking place in Payer’s patches:
Can lead to development of active, defensive immune system
Can be disrupted by increased permeability of the intestinal barrier
Can lead to development of tolerance towards particular antigens
Strongly dependent on the appropriate function of the M-cells
Zonulin is:
A physiological protein keeping the intestinal barrier tight
Pathological protein which increases permeability of the internal barrier
Protein identical to ZOT (zonula occludens toxin) which is produced by Plasmodium malaria
A factor causing diarrhoea among other
Increase permeability of the gut may be directly or indirectly responsible for:
Inappropriate immunization towards development of autoimmune disease
Intoxication of the liver
Malabsorption
Inflammation within the gut’s wall
Among the causes of celiac disease, we find
Genetic predisposition (HLA DQ 4 and DQ 8)
Gluten intake
Enteropathy
Increased permeability of the intestinal barrier
24. Celiac disease is:
A primary malabsorption syndrome
An autoimmune disease
Gluten intoxication
Gluten dependent malabsorption syndrome with some genetic background
Hypersensitivity of:
Type I involves specific IgE overproduction
Type II is targeting the specific organs due to production of antibodies against certain self antigens
Type III leads to chronic inflammation due to immunocomplexes tuming from soluble to non-soluble
Type IV leads to chronic inflammation
Severe combined immunodeficiency disorder (SCID):
Is based on mutation of gene encoding γ subunit of several cytokine receptor
Is related to the early stages of lymphoid lineage
Has a characteristic course with severe and frequently infection with various pathogens (bacteria, viruses, fungi)
Is a very common disease (1:1,000 births in Europe
Increase of frequency of the following types of infections can be manifestation of the immunodeficiencies:
Of the complement - mainly fungal (
Of the phagocytic cells - all except for viral
Of the T cell - mainly parasitic
Of the B-cell - bacterial, viral, fungal
The symptoms associated with increased intestinal permeability that are frequently found in various organs and tissues, can be attributed to following pathomechanism:
Autoimmunity
Allergic reaction
Direct toxicity
Dysbiosis
The importance of endothelial cells in acute inflammation in related to:
Inhibition of the inflammation as a result of endothelium damage
Preventing the exudate fluid from leaking out of the blood vessel
Extravasation of selected leukocytes
Making the capillary vessel’s walls impermeable to
In the earliest phase of acute inflammation following elements usually do not play primary role:
Fibroblast
Lymphocytes
Macrophages
Endothelial cells
Complement activation can be triggered by:
Stimulatory action of c5b67
Opsonization of bacteria with immunoglobulins
Membrane attack complex
Fixed immune complex
Hypersensitivity of:
Type I involves IgE overproduction of certain specificity
Type II leads most often to organ specific autoimmune diseases
type III leads to chronic inflammation in the vicinity of the small blood vessels
Type IV is the most common in allergies
Inflammatory processes:
Help the immune system recognized the antigen
May have destructive character
chronic are often related to autoimmune processes
Were first described in XIX century
SLE:
Develops as a result of anti-nuclear auto-antibodies production
Is a non-organic specific autoimmune disease
Is a result of type III hypersensitivity reaction
Produces a typical rush on face
Complement is very important in inflammation development. One or more of the following combinations of the action in inflammation and complement element responsible for it reflect the real possibility:
C5b67 activation of the mast cell
C5a opsonization of the cell
C3b chemotaxis
C3a chemotaxis
Which of the following describes possible sequence of inflammatory elements activation
Mast cells ⇒ neutrophiles ⇒ macrophages
Endothelial cells ⇒ platelets ⇒ neutrophiles ⇒ macrophages
Complement ⇒ mast cells ⇒ endothelial cells
Macrophages ⇒ lymphocytes ⇒ neutrophiles
B lymphocytes
Can present extracellular antigen in the context of MHC class II molecule
Belong to the group of phagocytic cells
Of one clone can produce antibodies of one specificity only, regardless of the antibody class products
Do not have receptors specifically recognized antigen (similar to TCR found on T lymphocytes)
Appropriate antigen presentation
Can induce cellular immune response
In the thymus can mediated induction of the thymocytes death
Can influence humoral immune response
Can be provided by B-lymphocytes, dendritic cells and mast cells
Most often the following connections of adhesion molecules and their ligands can be found
Integrins > selectins
Integrins > immunoglobulin- like protein
Immunoglobulin-like protein> mucine-like glikoprotein
Selectins > mucine-like glikoprotein
Cells that specifically react with inflammatory factor thanks to their ability to create immune diversity and specificity are
Mast cells
NK cells
Macrophages
Lymphocytes
Macrophages effectively present antigen in context of MHC molecules of
class I to TH cells
Class II to TC cells
Class I to B cells
Class I to TC cells
Following leukocytes and endothelial cell interactions involve certain adhesion molecules
Rolling-integrins
Rolling-selectins
Stopping-selectins
Extravasation-PECAM-1
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