Inflammation and immune response Flashcards
Which of the following is the first reaction in acute inflammation?
A. Vasoconstriction
B. Vasodilation
C. Stasis of blood flow
D. Oedema
B
Explanation
Vasodilitation follows a transient constriction of arterioles that lasts a few seconds.
Note: the current textbook has changed the wording to “vasodilation is one of the earliest manifestations of acute inflammation; SOMETIMES it follows a transient constriction of arterioles lasting a few seconds”. In the older editions, it did not say sometimes, but that vasoconstriction did occur a few seconds before vasodilatation.
Latest update: the current textbook: does not describe the transient arteriole constriction. It now describes the three components of acute inflammation- dilatation of small vessels, increased permeability and emigration of leukocytes.
Latest latest update: edition 10: vasodilation is induced by the action of several mediators, notable histamine, on vascular smooth muscle. It is one of the earliest manifestations of acute inflammation, and may be preceded by transient vasoconstriction.
Latest:
Acute inflammation has three major components: (1) dilation of small vessels leading to an increase in blood flow, (2) increased permeability of the microvasculature enabling plasma proteins and leukocytes to leave the circulation, and (3) emigration of the leukocytes from the microcirculation, their accumulation in the focus of injury, and their activation to eliminate the offending agent
I think the older questions which mention transient vasoconstriction prior to vasodilation should be removed now – as the current text makes no reference to dilation.
egarding chronic inflammation, which of the following statements is correct?
A. Frequently resolves spontaneously
B. Characterised by increased vascular permeability and oedema
C. It always follows acute inflammation
D. Macrophages are the major cellular players
D
Explanation
Macrophages are the major cellular players and have a half life of several months to a year. Monocytes have a half life of one day. Acute inflammation is characterised by hyperaemia, oedema and leucocyte infiltration. Chronic inflammation is not always preceded by acute inflammation but may follow it. Chronic inflammation includes some of the most common and disabling human disease such as rheumatoid arthritis, tuberculosis and artherosclerosis
Which of the following options is correct in relation to chronic inflammation?
A. It is always preceded by acute inflammation
B. The most frequent outcome is full resolution
C. Monocytes use the same chemotactic pathway as neutrophils
D. It is characterised by hyperaemia, oedema and leucocyte infiltration
C
Explanation
Acute inflammation is characterised by hyperaemia, oedema and leucocyte infiltration. Chronic inflammation is not always preceded by acute inflammation but may follow it. Chronic inflammation includes some of the most common and disabling human disease such as rheumatoid arthritis, tuberculosis and artherosclerosis
Migration of monocytes is analogous to migration of neutrophils in acute inflammation
In relation to compliment factor C5a, which of the following statements is false?
A. Increases vascular permeability and causes vasodilation
B. Acts as an opsonin and favours phagocytosis by neutrophils
C. Stimulates arachidonic acid (AA) metabolism
D. Is chemotactic for neutrophils
B
Explanation
C5a, a powerful inflammatory mediator, is chemotactic for neutrophils, eosinpohiles and basophiles. C5a activates the lipoxygenase pathway of arachidonic acid (AA) metabolism in neutrophils and monocytes. C5a also plays a role in increased vascular permeability and chemotaxis. C3b and C3Bi, but not C5a, when fixed to bacterial cell walls act as opsonins and promote phagocytosis by neutrophils and macrophages.
The complement system has three main functions
Inflammation- C3a, C5a and to a lesser extent C4a. C5a is also a chemotactic agent for neutrophils, monocytes, eosinophils and basophiles. C5a also activates the lipoxygenase pathway of AA metabolism
Opsonization and phagocytosis- C3b, iC3b
Cell lysis- MAC complex
Regarding mast cells, which of the following statements is correct?
A. They are only found in mucosal membranes
B. ADP is a stimulator of mast cell degranulation
C. They can degranulate without IgE
D. They are derived from thymus
C
Explanation
Mast cells are derived from the bone marrow and are widely distributed in the tissues. They are found predominantly near blood vessels, nerves and subepithelial sites. Mast cells participate in both acute and chronic inflammatory reactions. Mast cells release multiple primary and secondary mediators but not lysosomes. Adenosine triphosphate provides the energy for mast cell degranulation.
Other stimulators of mast cell degranulation are C5a, C3a, IL8 (interleukine 8 cytokine),drugs such as codeine, morphine, adenosine and mellitin along with physical stimuli
Which of the following statements is correct in relation to bradykinin?
A Causes relaxation of smooth muscles
B Is not painful when injected into the skin
C Causes vasodilation
D Is formed from pre kallikrein
C
Explanation
Kininogens form vasoactive peptides and the enzymes involved are kallikriens. Bradykinin causes increased vascular permeability, contraction of smooth muscle, dilatation of blood vessels and pain when injected into the skin
Which of the following is released by macrophages?
A Serotonin
B Histamine
C IL-17
D Toxic oxygen metabolites
D
Explanation
Factors released by macrophages include toxic oxygen metabolites, proteases, neutrophil chemotactic factors, coagulation factors, arachidonic acid (AA) metabolites (I would include PGs and Leukotrienes), nitric oxide, growth factors, angiogenesis and remodelling collagenases.
Others include: PAF, TNF, IL-1, IL-6, Chemokines, IL-12
Which of the following is not chemotactic?
A Leukotriene B4
B Bacterial polypeptides
C Bradykinin
D Histamine
C
Explanation
Other chemotactic factors include kallikrein, platlet activating factor (PAF), lysosomal proteins, chemokines and fibrinopeptides. Histamine is chemotactic for eosinophils.
Bradykinin direct effects are: smooth muscle contraction, arteriolar dilatation, increased permeability of venules, pain. Bradykinin is inactivated by kininases.
Regarding phagocytosis, which of the following statements is correct?
A IgM is a potent opsonin
B Bacterial killing occurs by mainly O2 dependant mechanisms
C C5a is an opsonin
D Occurs in 2 steps: engulfment and killing
B
Explanation
Phagocytosis occurs in three steps;
- recognition and attachment
- engulfment
- degradation
C5a is not an opsonin. IgG is a potent opsonin as is the C3b breakdown product and certain plasma lecitins. Phagocytosis is greatly enhanced by opsonisation
By itself, IgM is an ineffective opsonin; however it contributes greatly to opsonization by activating complement and causing C3b to bind to the antigen
Regarding fatty change, which of the following statements is false?
A May result from diabetes mellitus
B May represent unmasking of normal cell fat content
C Fatty acids are oxidised in the mitochondria
D May result from protein malnutrition
B
Explanation
Fatty change and steatosis describe abnormal accumulations of triglycerides within parenchymal cells. It occurs most often in the liver but also in the kidney, heart and muscles. Causes include alcohol (most common), diabetes mellitus (DM), protein malnutrition, toxins, obesity and anoxia. Fatty change per se, is reversible. Mild accumulation in an organ will not impair cellular function. Severe accumulation may impair function and even cause cell death.
The first vascular response to injury is which of the following?
A Recruitment of vascular beds
B Capillary engorgement
C Slowing of the circulation
D Arteriolar vasoconstriction
D
Explanation
Vasodilation follows a transient constriction of arterioles lasting a few seconds.
Note; The actual main change of the vessel in acute inflammation is vasodilation. However as you read the fine print, it SOMETIMES follows a transient constriction of the arterioles, lasting a few seconds. This initial vasoconstriction is likely due to an traumatic injury resulting in inflammation. Probably doesn’t happen in non-trauma cases
Mechanism:
Initial Vasoconstriction:
Immediately following an injury or inflammatory stimulus, there may be a brief period of vasoconstriction. This initial response is mediated by the release of substances such as endothelin and the action of reflex sympathetic nervous system activation. It serves to minimize blood loss in the case of tissue injury.
Vasodilation:
Following this transient vasoconstriction, there is a significant and sustained vasodilation. This vasodilation is primarily mediated by mediators such as histamine, prostaglandins, and nitric oxide released from various cells in the injured or inflamed area.
The vasodilation increases blood flow to the affected area, leading to the classic signs of inflammation: redness (erythema) and heat.
Outcome:
The increased blood flow during the vasodilation phase facilitates the delivery of immune cells, nutrients, and oxygen to the site of injury, which is critical for effective inflammation and subsequent healing.
Therefore, the sequence of transient vasoconstriction followed by vasodilation is a normal part of the physiological response during acute inflammation.
Rather a tricky MCQ-but none of the stems say vasodilation-making it easier to answer
Which statement is CORRECT regarding the movement of leucocytes towards the sire of injury?
A Largely in the arterioles
B The process of transmigration is mediated by ICAM and PECAM adhesion molecules
C In response to C3b
D Predominantly as monocytes on the first day post injury
B
Explanation
Leukocyte migration through endothelium (transmigration or diapedesis) - occurs mainly in post-capillary venules. - Chemokines act on the adherent leukocytes and stimulate the cells to migrate through interendothelial spaces toward the chemical concentration gradient, that is, toward the site of injury or infection where the chemokines are being produced. - Several adhesion molecules present in the intercellular junctions between endothelial cells are involved in the migration of leukocytes. These molecules include a member of the immunoglobulin superfamily called PECAM-1 (platelet endothelial cell adhesion molecule), ICAM (intercellular adhesion molecule 1) or CD31and several junctional adhesion molecules. After traversing the endothelium, leukocytes pierce the basement membrane, probably by secreting collagenases, and enter the extravascular tissue. The cells then migrate toward the chemotactic gradient created by chemokines and accumulate in the extravascular site.
Chemotaxis-leucocytes emigrate in tissues towards the site of injury along a chemical gradient. The leukocyte moves by extending a pseudopod and pulls the remainder of the cell in the direction of extension. The interior of the pseudopod consists of a branching network of filaments composed of actin and the contractile protein myosin
Regarding chemical mediators of inflammation, which of the following options is correct?
A The kinin system is activated in platelets
B Serotonin is preformed in platelets
C C3b is within macrophages
D Histamine is derived from plasma
B
Explanation
Histamine is derived from mast cells, basophils and platelets.
C3b is derived from liver and formed in plasma.
The kinin system is activated in plasma.
Nitric oxide is produced in macrophages
Chronic inflammation is characterised by which of the following options?
A Most frequently results in resolution
B The factors underlying monocyte infiltration are the same as for acute inflammation
C Characterised by hyperemia, oedema and leukocyte infiltration
D Always preceded by acute inflammation
B
Explanation
Macrophages are the major cellular players and have a half life of several months to a year. Monocytes have a half life of one day. Acute inflammation is characterised by hyperaemia, oedema and leucocyte infiltration. Chronic inflammation is not always preceded by acute inflammation but may follow it. Chronic inflammation includes some of the most common and disabling human disease such as rheumatoid arthritis, tuberculosis and artherosclerosis.
In the triple response, reactive hyperaemia is due to?
A Arteriolar dilatation
B Inflammatory mediators
C Exercise
D Blushing
A
Explanation
The triple response consists of;
- Red line
- Flare
- Wheal
Hyperaemia and reactive hyperaemia is an active process due to arteriolar dilitation
All of the following infections cause granulomatous infections EXCEPT?
A Syphilis
B Leprosy
C Lymphogranuloma venereum
D Schistosomiasis
C
Explanation
Causes of granulomatous disease infectious:
Bacterial: tuberculosis, leprosy, syphilis, cat-scratch disease
Parasitic: schistosomiasis
Fungal: Histoplasmosis; Blastomycosis
Inflammatory: temporal arteritis, chron’s disease, sarcoid, Inorganic particulates: silicosis, berylliosis Foreign body granuloma (suture or talc)
LGV is primarily an infection of lymphatics and lymphnodes. Chlamydia trachomatis is the bacterium responsible for LGV
Not a great question, don’t know if the answer is correct. Form the current text book “The lesions of lymphogranuloma venereum contain a mixed granulomatous and neutrophilic inflammatory response.” Left in the bank because it has appeared before.
What is the first step in the process of inflammation?
A Increased vascular permeability
B Vascular calibre and flow changesCorrect Answer
C Chemotaxis of inflammatory mediatorsYour Answer
D Adherence of inflammatory mediators
B
Explanation
Phase of acute inflammation include: 1) Vasodilation. Sometimes follows transient arteriolar vasoconstriction 2) Increased vascular permeability 3) Stasis/vascular congestion due to increased blood viscosity and concentration of RBCs 4) Emigration of leukocytes: leukocytes (mainly neutrophils) marginate along endothelium and migrate through vessel wall.
Rapid onset, duration of hours to days
Which of the following causes fever?
A Thromboxane A2
B Neutrophils
C Interleukin-1
D Arachidonic acid
C
Explanation
Fever: IL-1, TNF, Prostaglandins.
Which condition is not characterised by granulomatous inflammation?
A Sarcoidosis
B Cat Scratch disease
C Chancroid
D Leprosy
C
Explanation
Examples of diseases with granulomatous inflammation:
Tuberculosis (Mycobacterium tuberculosis)-caseating granuloma
Leprosy (Mycobacterium leprae)-non caseating granuloma
Syphilis (Treponema pallidum)-gumma (not chancroid)
Cat-scratch disease (Gram-negative bacillus)-rounded or stellate granuloma
Sarcoidosis- non caseating granuloma
Crohn disease-occasional non caseating granuloma
