Category: Quiz

Forms of Amyloid

Forms of Amyloid

Q. 1

The accepted nomenclature of amyloidosis is AX. What stands for A and X:

 A

A-Amyloid X protein in the fibril

 B

A- Amyloid X- beta pleated structure

 C

A-Amyloid X- helical structure

 D

A- Amyloid X -birefringent

Q. 1

The accepted nomenclature of amyloidosis is AX. What stands for A and X:

 A

A-Amyloid X protein in the fibril

 B

A- Amyloid X- beta pleated structure

 C

A-Amyloid X- helical structure

 D

A- Amyloid X -birefringent

Ans. A

Explanation:

Amyloid diseases are classified according to whether they are systemic or localized, acquired or inherited.

The accepted nomenclature is AX
A indicates amyloidosis  
X represents the protein in the fibril. 
Ref: Harrison, Edition-18, Page-942.

Q. 2

In hemodialysis associated amyloidosis, which of the following is seen

 A

Transthyretin

 B

Beta-2 microglobulin

 C

SAA

 D

Alpha microglobulin

Q. 2

In hemodialysis associated amyloidosis, which of the following is seen

 A

Transthyretin

 B

Beta-2 microglobulin

 C

SAA

 D

Alpha microglobulin

Ans. B

Explanation:

Ans. is ‘b’ i.e., B2 microglobulin


Q. 3

Amyloid (AA) originates from –

 A

RBC

 B

Plasma cell

 C

Reticulo-endothelial cell

 D

Lymphocytes

Q. 3

Amyloid (AA) originates from –

 A

RBC

 B

Plasma cell

 C

Reticulo-endothelial cell

 D

Lymphocytes

Ans. C

Explanation:

Ans. is ‘c’ i.e., Reticulo-endothelial cell

o SAA is produced in liver as an acute phase reactant in inflammatory process.

o The SAA is released into the circulation is an amyloid precursor and is transformed to AA-amyloid in lysosomes of macrophages and other cells of reticuloendothelial system.

Quiz In Between


Q. 4

AL type of amyloid is seen in –

 A

Medullary caracinoma thyroid

 B

Primary amyloidosis

 C

Multiple myeloma

 D

b and c

Q. 4

AL type of amyloid is seen in –

 A

Medullary caracinoma thyroid

 B

Primary amyloidosis

 C

Multiple myeloma

 D

b and c

Ans. D

Explanation:

Ans. is ‘b’ i.e., Primary amyloidosis & ‘c’ i.e., Multiple myeloma


Q. 5

Deposition of protein ‘A beta 2m’ is seen in which clinicopathologic category of amyloidosis –

 A

Familial Mediterranean fever

 B

Hemodialysis associated

 C

Senile cerebral

 D

Systemic senile

Q. 5

Deposition of protein ‘A beta 2m’ is seen in which clinicopathologic category of amyloidosis –

 A

Familial Mediterranean fever

 B

Hemodialysis associated

 C

Senile cerebral

 D

Systemic senile

Ans. B

Explanation:

Ans. is ‘b’ i.e., Hemodialysis associated

Quiz In Between



Amyloidosis- introduction

Amyloidosis- introduction

Q. 1

All are TRUE about amyloidosis, EXCEPT:

 A

It is an extracellular deposit

 B

Insoluble polymeric protein fibrils

 C

Amyloid fibrils share a common pleated structure

 D

The term amyloid was coined by Lister

Q. 1

All are TRUE about amyloidosis, EXCEPT:

 A

It is an extracellular deposit

 B

Insoluble polymeric protein fibrils

 C

Amyloid fibrils share a common pleated structure

 D

The term amyloid was coined by Lister

Ans. D

Explanation:

Amyloidosis is the extracellular deposition of insoluble polymeric protein fibrils. This disorder is due to misfolding of proteins. 

Eg:
  • Alzheimer’s disease and other neurodegenerative diseases, 
  • Transmissible prion diseases,
  • Certain of the cystic fibrosis mutations. 
Amyloid fibrils share a common beta-pleated sheet structural conformation. It has unique staining properties. 
 
The term amyloid was coined by Rudolf Virchow.
Ref: Harrison, Edition-18, Page 942

Q. 2

Stains used in amyloidosis –

 A

Congo red

 B

Thioflavin

 C

Reticulin

 D

a and b

Q. 2

Stains used in amyloidosis –

 A

Congo red

 B

Thioflavin

 C

Reticulin

 D

a and b

Ans. D

Explanation:

Ans. is ‘a’ i.e. Congo red,’b’ i.e. thioflavin


Q. 3

In amyloidosis Beta pleated sheet will be seen in

 A

X-ray crystallography

 B

Electron microscope

 C

Spiral electron microscope

 D

Congo red stain

Q. 3

In amyloidosis Beta pleated sheet will be seen in

 A

X-ray crystallography

 B

Electron microscope

 C

Spiral electron microscope

 D

Congo red stain

Ans. A

Explanation:

Ans. is ‘a’ i.e. X-ray crystallography

Quiz In Between


Q. 4

The etiology of amyloidosis is –

 A

Automimmune

 B

T-cell mediated

 C

B cell mediated

 D

Unknown

Q. 4

The etiology of amyloidosis is –

 A

Automimmune

 B

T-cell mediated

 C

B cell mediated

 D

Unknown

Ans. D

Explanation:

Ans. is ‘d’ i.e., Unknown


Q. 5

Which of these is characteristic of amyloidosis

 A

Beta pleated, metachromosis, PAS + ye

 B

Congophilic, beta pleated, PAS +ve

 C

Beta pleated, fibrillary, congophilic

 D

Alpha pleated, small fibrils

Q. 5

Which of these is characteristic of amyloidosis

 A

Beta pleated, metachromosis, PAS + ye

 B

Congophilic, beta pleated, PAS +ve

 C

Beta pleated, fibrillary, congophilic

 D

Alpha pleated, small fibrils

Ans. C

Explanation:

Ans. is ‘c’ i.e., Beta pleated, fibrillary, congophilic


Q. 6

Stain used to diagnose amyloidosis:     

September 2008

 A

Methylene blue

 B

Acid fast stain

 C

Rose bengal

 D

Congo red

Q. 6

Stain used to diagnose amyloidosis:     

September 2008

 A

Methylene blue

 B

Acid fast stain

 C

Rose bengal

 D

Congo red

Ans. D

Explanation:

Ans. D: Congo red

Quiz In Between



Edema- basics

Edema- basics

Q. 1

Edema is visible when the amount of fluid accumu­lated is:         

March 2013 (d, f)

 A

2-3 litres

 B

3-4 litres

 C

4-5 litres

 D

5-6 litres

Q. 1

Edema is visible when the amount of fluid accumu­lated is:         

March 2013 (d, f)

 A

2-3 litres

 B

3-4 litres

 C

4-5 litres

 D

5-6 litres

Ans. D

Explanation:

Ans. D i.e. 5-6 litres


Q. 2

What is the pathology of edema in nephrotic syndrome

 A

Reduced plasma protein

 B

Sodium and water retention

 C

Increased venous pressure

 D

Hyperlipidemia

Q. 2

What is the pathology of edema in nephrotic syndrome

 A

Reduced plasma protein

 B

Sodium and water retention

 C

Increased venous pressure

 D

Hyperlipidemia

Ans. B

Explanation:

Ans. b. Sodium and water retention

Sodium and water retention is the pathology of edema in nephrotic syndrome.

The nephrotic syndrome is characterized by proteinuria, edema, and hypoalbuminemia. Renal sodium retention and changes in variables of the Starling equation are fundamental to the pathophysiology of nephrotic edema. There is evidence for both intravascular volume expansion (overfilling) and intravascular volume depletion (under filling) in patients with nephrosis. Microvascular fluid exchange is described using a formulation of the Starling driving forces (DP and Dp) and it is through this equation that nephrotic edema is conceptualized. Previous theories have focused on abnormalities in DP and Dp to explain nephrotic edema. Studies have shown that hypoalbuminemia (and thus Dp) is not a likely cause of edema formation in most nephrotic patients owing to a parallel decrease in interstitial fluid albumin and an increase in interstitial fluid pressure, both of which serve to maintain edema driving forces constant. There is limited evidence suggesting that abnormalities in vascular permeability (Kf and s) may contribute to edema formation. A major advance in our understanding of the pathophysiologic basis of edema formation in the nephrotic syndrome is the discovery that proteinuria can cause primary renal sodium retention through ENaC activation. This mechanism is likely active in all patients with nephrotic syndrome, regardless of their intravascular volume status. Other causes of primary renal sodium retention include increased renal efferent sympathetic nerve activity, ANPase, and in the expression and activity of the Ne—le in the collecting duct in animal models. Furthermore, excess serum vasopressin levels have been found to contribute to free water retention in some patients with the nephrotic syndrome.”- Eric Siddall and Jai Radhakrishnan. The pathophysiology of edema formation in the nephrotic syndrome

Nephrotic Syndrome

Manifestations of Nephrotic Syndrome

  • 1.      Massive proteinuria, with the daily loss of 3.5 gm or more of proteinQ
  • 2.      Hypoalbuminemia, with plasma albumin levelsQ
  • 3.      Generalized edemaQ
  • 4.      Hyperlipidemia and lipiduriaQ

Pathophysiology:

  • Renal sodium retention and changes in variables of the Starling equation are fundamental to the pathophysiology of nephrotic edema.
  • There is evidence for both intravascular volume expansion (overfilling) and intravascular volume depletion (under filling) in patients with nephrosis.

Nephrotic Syndrome

Mechanisms of Sodium Retention in the Nephrotic Syndrome

  • Increased angiotensin 11-independent afferent and efferent arteriolar tone because of increased efferent sympathetic nerve activity.
  • Tubular resistance to atrial natriuretic peptide (ANP).
  • Increased number of open epithelial sodium channel (ENaC) channels in the cortical collecting duct due to proteolytic activation of ENaC by plasmin.
  • Increased number and activity of cortical collecting duct Na/K ATPase channels

Most important facts about Nephrotic syndrome

  • The lipid appears in the urine either as free fat or as oval fat bodies, representing lipoprotein resorbed by tubular epithelial cells and then shed along with the degenerated cells.
  • Most proteins are decreased in nephrotic syndrome except Fibrinogen and lipoproteins, due to increased synthesis.
Proteins decreased Consequence
Albumin Edema due to hypoalbuminemiaQ
Transferrin Iron resistant microcytic anemiaQ
Cholecalciferol binding proteins HypocalcemiaQ
Thyroxin binding globulin Decreased thyroxin (Hypothyroid state)Q
IgG Increased susceptibility of infectionsQ
  • Renal vein thrombosis is particularly common (up to 40%) in patients with nephrotic syndrome due to membranous glomerulopathy, memranoproliferative glomerulonephritis, and AmyloidosisQ.
  • As a consequence of hypercoagulability and changes in proteins, patients can develop spontaneous peripheral arterial or venous thrombosis, renal vein thrombosis, and pulmonary embolismQ

Quiz In Between



Hyperemia & Congestion

Hyperemia & Congestion

Q. 1

All of the following are true about chronic venous congestion of liver except –

 A

Gamma Gandy bodies are seen

 B

Nutmeg liver is seen

 C

Dilated blood channels are seen

 D

All

Q. 1

All of the following are true about chronic venous congestion of liver except –

 A

Gamma Gandy bodies are seen

 B

Nutmeg liver is seen

 C

Dilated blood channels are seen

 D

All

Ans. A

Explanation:

Ans. is ‘a’ i.e., Gamma Gandy bodies are seen

Gamma Gandy bodies are seen in the congestion of spleen (not liver).


Q. 2

Venous congestion of liver affects ‑

 A

Midzone

 B

Perihepatic zone

 C

Centrilobular zone

 D

All the above

Q. 2

Venous congestion of liver affects ‑

 A

Midzone

 B

Perihepatic zone

 C

Centrilobular zone

 D

All the above

Ans. C

Explanation:

Ans. is ‘c’ i.e., Centrilobular zone

Nutmeg liver or chronic passive congestion or Congestive hepatopathy :‑

  • Chronic passive congestion is liver dysfunction due to venous congestion, usually right sided cardiac dysfunction (right sided cardiac decompenstion).
  • When there is right sided cardiac decompensation, the blood begins to return back in the IVC and hepatic veins.
  • This results in increase venous pressure and passive congestion of centrilobular region and hemorrhagic necrosis of centrilobular region.
  • The liver takes on a variegated mottled appearance, reflecting hemorrhage and necrosis in the centrilobular region, known as ‘nutmeg liver’.

Quiz In Between



WOUND HEALING- Complications, Factors & Strength

WOUND HEALING- Complications, Factors & Strength

Q. 1

Wound healing is affected by:

 A

Age

 B

Nutrition

 C

Dryness or wetness of wound

 D

a and b

Q. 1

Wound healing is affected by:

 A

Age

 B

Nutrition

 C

Dryness or wetness of wound

 D

a and b

Ans. D

Explanation:

Ans. is ‘ a ‘ , ‘ b ‘

Factors that adversely affect wound healing

•   Local

•   Abnormal blood supply (ischemia due to arterial disease or impaired venous drainage, e.g.

arteriosclerosis, varicose veins)

•   Infection

•   Presence of foreign material, necrotic tissue or excessive blood (hematoma)

•   Movement in injured area

•   Tension in injured area

•   Irradiation (decreases the viability of cells)

•   Denervation

•   Systemic

•   Advanced age

•   Failure of collagen synthesis d/t

– vitamin C deficiency

– protein deficiency

– zinc deficiency

– Ehlers-Danlos syndrome (disorder characterized by defective collagen formation,

hyperextensible joints, fragile tissues and impaired wound healing)

•     Diabetes mellitus

•     Corticosteroid excess (administration of exogenous corticosteroids or Cushing’s syndrome)

•     Malnutrition

•     Anemia

•  Obesity

•   Drugs (steroids, cytotoxic medication, intensive antibiotic therapy)

•   Genetic disorders (osteogenesis imperfecta, Ehler-Danlos syndrome, Marfan syndrome)

•   Systemic infection

•   Malignant disease

•  Temperature

•  Trauma, hypovolemia and hypoxia

•   Uremia

•   Bleeding disorder


Q. 2

The Vitamin which has inhibitory effect on wound healing is –

 A

Vitamin -A

 B

Vitamin – E

 C

Vitamin -C

 D

Vitamin B-complex

Q. 2

The Vitamin which has inhibitory effect on wound healing is –

 A

Vitamin -A

 B

Vitamin – E

 C

Vitamin -C

 D

Vitamin B-complex

Ans. B

Explanation:

Ans. is ‘b’ i.e., Vitamin-E. 


Q. 3

Fibroblasts in healing wound are derived from –

 A

Local mesenchyme

 B

Epithelium

 C

Endothelium

 D

Vascular fibrosis

Q. 3

Fibroblasts in healing wound are derived from –

 A

Local mesenchyme

 B

Epithelium

 C

Endothelium

 D

Vascular fibrosis

Ans. A

Explanation:

Ans. is ‘a’ i.e. Local mesenchyme 

Fibroblasts are specialized cells that differentiate from resting mesenchyme cells in connective tissue. They do not arrive in the wound cleft by diapedesis from circulating cells.

Quiz In Between


Q. 4

A patient of total parenteral nutrition develops delayed wound healing, loss of taste, deficient immunity and diarrhea. Most probably it could be due to deficiency of:          September 2008

 A

Selenium

 B

Copper

 C

Zinc

 D

Iron

Q. 4

A patient of total parenteral nutrition develops delayed wound healing, loss of taste, deficient immunity and diarrhea. Most probably it could be due to deficiency of:          September 2008

 A

Selenium

 B

Copper

 C

Zinc

 D

Iron

Ans. C

Explanation:

Ans. C: Zinc

Symptoms of Zinc Deficiency

  • Poor Immune system
  • Weight loss
  • Intercurrent infections
  • Hypogonadism in males
  • Lack of sexual development in females
  • Growth retardation
  • Dwarfism
  • Delayed puberty in adolescents
  • Rough skin
  • Poor appetite
  • Mental lethargy
  • Delayed wound healing
  • Short stature
  • Diarrhea

Congenital abnormalities causing zinc deficiency may lead to a disease called acrodermatitis enteropathica.


Q. 5

Most important vitamin, which promotes wound healing ?

 A

Vitamin C

 B

Vitamin D

 C

Vitamin A

 D

Niacin

Q. 5

Most important vitamin, which promotes wound healing ?

 A

Vitamin C

 B

Vitamin D

 C

Vitamin A

 D

Niacin

Ans. A

Explanation:

 

  • Vitamin C is required for collagen synthesis.
  • Due to its important role in collagen synthesis, vitamin C is required for adequate wound healing.

Q. 6

False about wound healing ‑

 A

Inhibited by infection

 B

Inhibited by DM

 C

Inhibited by hematoma

 D

Inhibited by foreign body

Q. 6

False about wound healing ‑

 A

Inhibited by infection

 B

Inhibited by DM

 C

Inhibited by hematoma

 D

Inhibited by foreign body

Ans. C

Explanation:

Ans. is ‘c’ i.e., Inhibited by hematoma 

Factors causing impairment of wound healing

A. Systemic factors

  • Poor nutrition (protein deficiency, vitamin C deficiency).
  • Metabolic abnormalities (Diabetes mellitus).
  • Poor circulatory status (Inadequate blood supply).
  • Hormones, e.g. glucocorticoids.

B. Local factors

  • Infection is the single most important factor.
  • Mechanical factors, e.g. early mobilization.
  • Foreign bodies (unnecessary sutures, fragments of steel or glass).
  • Wound in poorly vacularized area, e.g. foot.

Quiz In Between



Healing of Skin wounds

Healing of Skin wounds

Q. 1

Maximum collagen in wound healing is seen at –

 A

End of first week

 B

End of second week

 C

End of third week

 D

End of 2 months

Q. 1

Maximum collagen in wound healing is seen at –

 A

End of first week

 B

End of second week

 C

End of third week

 D

End of 2 months

Ans. B

Explanation:

Ans. is ‘b’ i.e., End of second week

o During second week there is continued accumulation of collagen and proliferation of fibroblast. Maximum collagen is seen in second week.


Q. 2

Which occurs first in wound healing –

 A

Thin continuous epithelial cover appears

 B

Fibroblasts lay down collagen fiber

 C

Granulation tissue fills the wound

 D

Neutrophils line the wound edge

Q. 2

Which occurs first in wound healing –

 A

Thin continuous epithelial cover appears

 B

Fibroblasts lay down collagen fiber

 C

Granulation tissue fills the wound

 D

Neutrophils line the wound edge

Ans. D

Explanation:

Ans. is ‘d’ i.e., Neutrophils line the wound edge


Q. 3

Wound healing is the summation of following processes except –

 A

Coagulation

 B

Matrix synthesis

 C

Angiogenesis

 D

Fibrolysis

Q. 3

Wound healing is the summation of following processes except –

 A

Coagulation

 B

Matrix synthesis

 C

Angiogenesis

 D

Fibrolysis

Ans. D

Explanation:

Ans. is ‘d’ i.e., Fibrolysis

Quiz In Between


Q. 4

Primary intentional healing which is true ‑

 A

Neovascularization is maximum by day 5

 B

Neovascularization is maximum by day 3

 C

Neutrophils appear at wound margins on day 3

 D

The epidermis recovers its maximum thickness by day 7

Q. 4

Primary intentional healing which is true ‑

 A

Neovascularization is maximum by day 5

 B

Neovascularization is maximum by day 3

 C

Neutrophils appear at wound margins on day 3

 D

The epidermis recovers its maximum thickness by day 7

Ans. A

Explanation:

Ans. is ‘a’ i.e., Neovascularization is maximum by day 5

Skin wound healing

  • Skin wounds are classically described to heal by primary or secondary intention.

A. Healing by primary intention

  • It occurs in wounds with opposed edges, e.g., surgical incision.
  • The healing process follows a series of sequantial steps : ‑

Immediate after incision

  • Incisional space filled with blood containing .fibrin and blood cells.
  • Dehydration of the surface clot forms scab that covers the wound.

Within 24 hours

  • Neutrophils appear at the margins of wound.

In 24-48 hours

  • Epithelial cells move from the wound edges along the cut margin of dermis, depositing basement membrane components as they move.
  • They fuse in the midline beneath the surface scab, producing a continuous but thin epithelium layer that closes the wound.

By day 3

  • Neutrophils are largely replaced by macrophages.
  • Granulation tissue progressively invades the incision space.
  • Collegen fibers now present in the margin but do not bridge the incision.

By day 5

  • Incisional space is largely filled with granulation tissue.
  • Neovascularization is maximum.
  • Collegen fibrils become more abundant and begin to bridge the incision.
  • The epidermis recovers its normal thickness.

During second week

  • Leukocytes and edema have disappeared.
  • There is continued accumulation of collegen and proliferation of fibroblast.
  • By the end offirst month
  • Scar is made up of a cellular connective tissue devoid of inflammatory infiltrate covered now by intact epidermis.

B. Healing by secondary intention

  • It occurs in wounds with seperated edges in which there is more extensive loss of cells and tissue.
  • Regeneration of parenchymal cells cannot completely restore the original architecture, and hence abundant granulation tissue grows.

Healingby secondary from primary intention in several respects :

  • Inflammatory reaction is more intense.
  • Much larger amounts of granulation tissue are formed.
  • Wound contraction occurs → Feature that most clearly differentiate secondary from primary healing.
  • Permanent wound contraction requires the action of myolifibroblasts – Fibroblasts that have the ultrastructural characteristic of smooth muscle cells.

 

 


Q. 5

Two types of Healing of wounds are shown in the image.The characteristics of ‘A’ type of wound healing as compared to ‘B’ type of wound healing are all except:

 

 A

Wound is clean

 B

Scanty granulation tissue

 C

Sutures are not used

 D

Outcome is neat linear scar

Q. 5

Two types of Healing of wounds are shown in the image.The characteristics of ‘A’ type of wound healing as compared to ‘B’ type of wound healing are all except:

 

 A

Wound is clean

 B

Scanty granulation tissue

 C

Sutures are not used

 D

Outcome is neat linear scar

Ans. C

Explanation:

Ans:C.)Sutures are not used

Image shows:’A’:Healing by primary intention,’B’:Healing by secondary intention.

Quiz In Between



Wound healing & repair

Wound healing & repair

Q. 1

Which are not labile cells‑

 A

Bone marrow

 B

Epithelium of skin

 C

Intestitial mucosa

 D

Hepatocytes

Q. 1

Which are not labile cells‑

 A

Bone marrow

 B

Epithelium of skin

 C

Intestitial mucosa

 D

Hepatocytes

Ans. D

Explanation:

Ans. is ‘d’ i.e., Hepatocytes

When a cell proliferates, it pass through a cell cycle


Q. 2

Early granulation tissue  

 A

Type I collagen

 B

Type IV collagen

 C

Type I & IV collagen

 D

None 

Q. 2

Early granulation tissue  

 A

Type I collagen

 B

Type IV collagen

 C

Type I & IV collagen

 D

None 

Ans. C

Explanation:

  • Early granulation tissue- Type I & III collagen

Quiz In Between



Granulomatous inflammation

Granulomatous inflammation

Q. 1

A sarcoidosis patient developed non caseating granulomas. Which type of hypersensitivity is responsible for developing granulomatous inflammation in this patient?

 A

Type I

 B

Type II

 C

Type III

 D

Type IV

Q. 1

A sarcoidosis patient developed non caseating granulomas. Which type of hypersensitivity is responsible for developing granulomatous inflammation in this patient?

 A

Type I

 B

Type II

 C

Type III

 D

Type IV

Ans. D

Explanation:

Delayed-type hypersensitivity or or type IV hypersensitivity is a T-cell mediated or inflammatory response in which the stimulation of antigen-specific effector T cells leads to macrophage activation and localized inflammation and edema within tissues.

Three variants of type IV hypersensitivity reaction are recognized, contact, tuberculin type and granulomatous.

Contact hypersensitivity and tuberculin-type hypersensitivity both occur within 72 hours of antigen challenge.

Granulomatous hypersensitivity reactions develop over a period of 21-28 days – the granulomas are formed by the aggregation of macrophages and lymphocytes and may persist for weeks.

This is the most important type of hypersensitivity response for producing clinical consequences.

Examples of chronic diseases which manifest type IV granulomatous hypersensitivity are leprosy, tuberculosis, schistosomiasis, sarcoidosis, Crohn’s disease.

Ref: Immunology By David K. Male, 2006, Page 477, 486 ; Immunology by David K. Male, Jonathan Brostoff, Ivan Maurice Roitt, David B. Roth, Page 477-478


Q. 2

A 49 year old female with shortness of breath is found to have hilar lymphadenopathy on chest x-ray. Biopsy of one of the lymph nodes reveals granulomas, and is highly suggestive of sarcoidosis. Which of the following histological findings must have been present in the biopsy material to support the diagnosis of granulomatous inflammation?

 A

Asteroid bodies

 B

Caseous necrosis

 C

Epithelioid histiocytes

 D

Fibroblast proliferation

Q. 2

A 49 year old female with shortness of breath is found to have hilar lymphadenopathy on chest x-ray. Biopsy of one of the lymph nodes reveals granulomas, and is highly suggestive of sarcoidosis. Which of the following histological findings must have been present in the biopsy material to support the diagnosis of granulomatous inflammation?

 A

Asteroid bodies

 B

Caseous necrosis

 C

Epithelioid histiocytes

 D

Fibroblast proliferation

Ans. C

Explanation:

A granuloma is defined as a focus of chronic inflammatory reaction in which the predominant cell type is the epithelioid macrophage or histiocyte. Epithelioid histiocytes are recognized on standard H&E preparation by their pale pink cytoplasm and indistinct cell boundaries. Granulomas are generally surrounded by a ring of lymphocytes and infrequent plasma cells.
 
The granulomas of sarcoidosis usually contain many multinucleated giant cells, and frequently these giant cells contain stellate inclusions called asteroid bodies
 
Caseous necrosis describes the gross appearance of cheesy, necrotic debris filling a nodule of active tuberculosis, but also has come to describe its characteristic amorphous and eosinophilic appearance on H&E sections. Caseous necrosis is suggestive of tuberculosis, not sarcoidosis.
 
Over time, fibroblasts proliferate within the core of old, inactive granulomas, eradicating the histiocytes and stereotypical appearance and producing a dense collagenous scar. 
 

Q. 3

The epitheloid cell and multinucleated gaint cells of Granulomatous inflammation are derived from

 A

Basophils

 B

Eosinophils

 C

CD 4 – T lymphocytes

 D

Monocytes – Macrophages

Q. 3

The epitheloid cell and multinucleated gaint cells of Granulomatous inflammation are derived from

 A

Basophils

 B

Eosinophils

 C

CD 4 – T lymphocytes

 D

Monocytes – Macrophages

Ans. D

Explanation:

Ans. is ‘d’ i.e., Monocyte macrophages

In granulomatous inflammation

o Main cells involved  —->  Macrophages, CD-4 helper T cells.

  • Epitheloid cells – Macrophages that develop epithelial like appearance.
  • Multinucleated giant cells -4 Due to fusion of epitheloid cells.

Q. 4

Which of the following is not a cyclin dependent kinase (CDK) inhibitor?

 A

p21

 B

p27

 C

p53

 D

P57

Q. 4

Which of the following is not a cyclin dependent kinase (CDK) inhibitor?

 A

p21

 B

p27

 C

p53

 D

P57

Ans. C

Explanation:

 

p53 is a tumor supressor gene, that control some CDK inhibitors like p21, but p53 itself is not a CDK inhibitor.

Cell cycle Inhibitors

o The activity of cyclin – CDK complexes is tightly regulated by inhibitors, called CDK inhibitors.

o By inhibiting CDK they inhibit cell cycle and replication –> Act as tumor suppressors.

o There are two main classes of CDK inhibitors ‑

  1. The Cip/kip family
  2. The INK4/ARF family

o The Cip / kip family

      It has 3 components, p21, p27 and p57.

      This binds and inactivate cyclin – CDK complexes.

      Transcriptional activation of p21 is under the control of p53, a tumor suppressor gene that is mutated in a large proportion of human cancers.

o INK 4a/ARF family

      It consists p16INK4a and p14 ARF

     p16 INK4a competes with cyclin D for binding with CDK4, so it inhibits cyclin D-CDK4 complex.

     p14 ARF acts through p53 by preventing its degradation. p53 then activate p21 that inturn inhibit cyclin D-CDK4 complex.

Quiz In Between



Chronic inflammation

Chronic inflammation

Q. 1

All occurs in chronic inflammation except –

 A

Infiltration of macrophages

 B

Fibrosis

 C

Infiltration of neutrophils

 D

Angiogenesis

Q. 1

All occurs in chronic inflammation except –

 A

Infiltration of macrophages

 B

Fibrosis

 C

Infiltration of neutrophils

 D

Angiogenesis

Ans. C

Explanation:

Ans. is ‘c’ i.e., Infiltration of neutrophils

Chronic inflammation

  • Chronic inflammation is of prolonged duration in which active inflammation, tissue destruction and attempts of repair are proceeding simultaneously.
  • It may : ‑
  1. Begins insdiously without acute inflammation (more common). or
  2. Follows acute inflammation, when the injurious stimulus is persistent.
  • Chronic inflammation is characterized by

A. Mononuclear cell infiltration

  • The macrophages are the major cells involved in chronic inflammation.
  • Macrophages are derived from monocytes i.e., when these cell circulate in the blood, they are known as monocytes and when they come out from the circulation and become part of the tissue, they are called macrophages.
  • Macrophage accumulation persists in chronic inflammation by following mechanisms.
  1. Recruitment of monocyte from the circulation (most common).
  2. Local proliferation of the macrophages.
  3. Immobilization of macrophages at the site of inflammation.
  • Other cells involved in chronic inflammation are plasma cells, lymphocytes, eosinophils, mast cells.

B. Tissue destruction

  • The products of activated macrophages serve to eliminate injurious agents such as microbes and to initiate the process of repair.
  • These mediators also cause tissue injury because some of these are toxic to host cells, (reactive oxygen species) or extracellular matrix (proteases) and a variety of other substances may contribute to tissue damage in chronic inflammation.
  • So, tissue destruction is one of the hallmark of chronic inflammation.

C. Healing and Fibrosis

  • Attempt at healing by connective tissue replacement of damaged tissue is accomponied by proliferation of new small vessels (angiogenesis) and fibrosis.

Q. 2

Sign of chronic inflammation ‑

 A

Angiogenesis

 B

Purulent exudate

 C

Induration

 D

Edema

Q. 2

Sign of chronic inflammation ‑

 A

Angiogenesis

 B

Purulent exudate

 C

Induration

 D

Edema

Ans. A

Explanation:

Ans. is ‘a’ i.e. Angiogenesis

Chronic inflammation is characterized by :‑

  • Infiltration with mononuclear cells, which include → macrophages, lymphocytes, and plasma cells
  • Tissue destruction, induced → the persistent offending agent or by the inflammatory cells
  • Attempts at healing → connective tissue replacement of damaged tissue, accomplished by angiogenesis (proliferation of small blood vessels) and, in particular, fibrosis.

Quiz In Between



Plasma derived inflammatory mediator

Plasma derived inflammatory mediator

Q. 1

Which complement component is involved in both classical and alternative pathways –

 A

Cl

 B

C2

 C

C3

 D

C4

Q. 1

Which complement component is involved in both classical and alternative pathways –

 A

Cl

 B

C2

 C

C3

 D

C4

Ans. C

Explanation:

Ans. is ‘c’ i.e., C3

.       The central process in the complement cascade ( for both classical and alterante pathway) is the avtivation of C3, which is the major component of complement.


Q. 2

Complement binding immunoglobulin via the classical pathway is –

 A

IgG & IgM

 B

IgG & IgA

 C

IgG & IgD

 D

IgD & IgE

Q. 2

Complement binding immunoglobulin via the classical pathway is –

 A

IgG & IgM

 B

IgG & IgA

 C

IgG & IgD

 D

IgD & IgE

Ans. A

Explanation:

. Ans. is ‘a’ i.e., IgG and IgM


Q. 3

Actions of bradykinin include all of the following, except-

 A

Vasodilatation

 B

Bronchodilatation

 C

Increased vascular permeability

 D

Pain

Q. 3

Actions of bradykinin include all of the following, except-

 A

Vasodilatation

 B

Bronchodilatation

 C

Increased vascular permeability

 D

Pain

Ans. B

Explanation:

Ans. is ‘b’ i.e., Bronchodilatation

Effects of bradykin in

  • Increased vascular permeability.
  • Mediation of pain (Direct stimulation of free nerve ending and T PG production)
  • Vasodilatation (Largely mediated by endothelial cell NO & PGI2).
  • Visceral smooth muscle contraction : – Bronchoconstriction, Intestinal & uterine smooth muscle contraction.

Stimulation of epithelial ion transport and fluid secretion in airways and GIT.

Quiz In Between


Q. 4

Bradykinin Causes –

 A

Vasoconstriction

 B

Pain at the site of inflammation

 C

Bronchodilatation

 D

Decreased Vascular bermeability

Q. 4

Bradykinin Causes –

 A

Vasoconstriction

 B

Pain at the site of inflammation

 C

Bronchodilatation

 D

Decreased Vascular bermeability

Ans. B

Explanation:

Ans. is ‘b’ i.e., Pain at the site of inflammation


Q. 5

Bradykinin is a clevage product of –

 A

Kininogen

 B

Prekallikrein

 C

Kallikrien

 D

Histamine

Q. 5

Bradykinin is a clevage product of –

 A

Kininogen

 B

Prekallikrein

 C

Kallikrien

 D

Histamine

Ans. A

Explanation:

Ans. is ‘a’ i.e., Kininogen


Q. 6

Which one of the following is a major component in activation of the complement via alternative pathway:

September 2007

 A

C1

 B

C2

 C

C3

 D

C4

Q. 6

Which one of the following is a major component in activation of the complement via alternative pathway:

September 2007

 A

C1

 B

C2

 C

C3

 D

C4

Ans. C

Explanation:

Ans. C: C3

Quiz In Between


Q. 7

Complement having cell lytic property ‑

 A

MAC

 B

C3b

 C

C3a

 D

C5a

Q. 7

Complement having cell lytic property ‑

 A

MAC

 B

C3b

 C

C3a

 D

C5a

Ans. A

Explanation:

Ans. is ‘a’ i.e., MAC


Q. 8

Anaphylotoxin in complement system ‑

 A

C3b

 B

C5_9

 C

C5a

 D

C1_3

Q. 8

Anaphylotoxin in complement system ‑

 A

C3b

 B

C5_9

 C

C5a

 D

C1_3

Ans. C

Explanation:

Ans. is ‘c’ i.e., Csa


Q. 9

Byproducts of complement system Anaphylactotoxins ‑

 A

C3b

 B

C4a

 C

C5a

 D

c and b both

Q. 9

Byproducts of complement system Anaphylactotoxins ‑

 A

C3b

 B

C4a

 C

C5a

 D

c and b both

Ans. D

Explanation:

Ans. is ‘c’ i.e., C5a > ‘b’ i.e., C4a

C5a.,C3a.,to a lesser extent C4a—> are called anaphylotoxin because they have effects similar to those of mast cell mediators that are involved in the reaction called anaphylaxis. These effects are due to stimulation of histamine release by these anaphylotoxin. The effects are increased vascular permeability and vasodilatation.


Q. 10

The role of bradykinin in process of inflammation is

 A

Vasoconstriction

 B

Bronchodilation

 C

Pain

 D

Increased vascular permeability

Q. 10

The role of bradykinin in process of inflammation is

 A

Vasoconstriction

 B

Bronchodilation

 C

Pain

 D

Increased vascular permeability

Ans. D

Explanation:

Ans. d. Increased vascular permeability

  • The role of bradykinin in process of inflammation is to increase vascular permeability.
  • “Bradykinin increases vascular permeability and causes contraction of smooth muscle, dilation of blood vessels, and pain when injected into the skin.”- Robbins 8/e p65

Kinins

  • Kinins are vasoactive peptides derived from plasma proteins, called kininogens, by the action of specific proteases called kallikreins.
  • The kinin and coagulation systems are also intimately connected.
  • The active form of factor XII, factor XIIa, converts plasma prekallikrein into an active proteolytic form, the enzyme kallikrein, which cleaves a plasma glycoprotein precursor, high-molecular-weight kininogen, to produce bradykinin
  • Bradykinin increases vascular permeability and causes contraction of smooth muscle, dilation of blood vessels, and pain when injected into the skinQ.
  • These effects are similar to those of histamine.
  • The action of bradykinin is short-lived, because it is quickly inactivated by an enzyme called kininase.
  • Any remaining kinin is inactivated during passage of plasma through the lung by angiotensin-converting enzyme.
  • Kallikrein itself is a potent activator of Hageman factor, allowing for autocatalytic amplification of the initial stimulus.
  • Kallikrein has chemotactic activity, and it also directly converts CS to the chemoattractant product C5aQ.

Quiz In Between



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