Session 3 Flashcards

(61 cards)

1
Q

What is chronic inflammation?

A

Chronic response to injury with associated fibrosis

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2
Q

In what three ways can chronic inflammation develop?

A

May ‘take over’ from acute inflammation if damage too severe to be resolved within a few days, may arise ‘de novo’, or may develop alongside acute inflammation in severe persistent/repeated irritation

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3
Q

What are the most important characteristic in chronic inflammation?

A

The type of cells present (chronic inflammation is much more heterogeneous than acute inflammation)

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4
Q

What cells are found in chronic inflammation?

A

Macrophages (derived from blood monocytes), lymphocytes, eosinophils, fibroblasts/myofibroblasts

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5
Q

What are macrophages derived from?

A

Blood monocytes

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6
Q

Describe the histological appearance of macrophages (blood monocytes)

A

Large, folded nucleus; grey/blue granular cytoplasm

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7
Q

Describe the difference in phagocytosis between macrophages and neutrophils

A

Macrophages are better with dead tissue, polymorphs are better with bacteria

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8
Q

What are the functions of macrophages?

A

Phagocytosis, antigen presentation, synthesis of cytokines, complement components, blood clotting factors and proteases (signalling), and the control of other cells by this cytokine release

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9
Q

What are the functions of lymphocytes?

A

Complex, mainly immunological; B cells produce antibodies (plasma cells), T cells are involved in the control of the immune action, and some cytotoxic actions. The presence of lymphocytes is not necessarily indicative of inflammation

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10
Q

How long does plasma cell appearance usually take in an immune reaction?

A

Around a week

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11
Q

What is the appearance of plasma cells likened to?

A

A clock-face

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12
Q

What situations are eosinophils commonly found in?

A

Allergic reactions, parasite infections, some tumours

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13
Q

What are the predominant cells in rheumatoid arthritis?

A

Plasma cells

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14
Q

What are the predominant cells in chronic gastritis?

A

Lymphocytes

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15
Q

What are the predominant cells in leishmaniasis (a protozoal infection)?

A

Macrophages

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16
Q

What are giant cells? What is the commonest theory for their formation?

A

Multinucleate cell made by the fusion of macrophages; frustrated phagocytosis

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17
Q

What are the three types of giant cells commonly seen?

A

Langhans, foreign body type, Touton

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18
Q

What are Langhans giant cells commonly seen in? Describe their structure

A

Tuberculosis (can be seen in other diseases); usually a horseshoe shaped nuclei arrangement, around granular cytoplasm

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19
Q

What is the function of foreign body type giant cells?

A

Prevent spread by localisation of foreign body

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20
Q

What situation are Touton giant cells commonly seen in?

A

Fat necrosis; the gat like foam is due to the emptiness of the cells

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21
Q

What are the four principle effects of chronic inflammation?

A

Fibrosis, impaired function (rarely increased), atrophy, stimulation of immune response

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22
Q

What is chronic cholecystitis?

A

Inflammation of gall bladder most commonly due to gallstone in cystic duct; the acute inflammatory response causes the gallstone to pop out, the gallstone blocks the duct again and the process continues

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23
Q

Why does chronic inflammation occur in cholecystitis?

A

The repeated acute inflammatory response results in chronic inflammation

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24
Q

Why does the wall of the gallbladder appear white in colour in cholecytitis? What is the normal colour?

A

Translucent; chronic inflammation results in formation of fibrous tissue

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25
What does the cystic duct connect the gallbladder with?
The common bile duct
26
What are some causes of acute gastritis and chronic gastritis respectively?
Acute: alcohol, drugs e.g. aspirin Chronic: helicobactor pylori
27
Why gastric ulceration occur?
Imbalance of acid production and mucosal defence, acid causes damage to the mucosa stimulating an acute inflammatory response forming an ulcer
28
What is an ulcer?
An area of necrosis through the mucosa
29
What is the potential result of an untreated gastric ulcer?
It can burn through the wall of the GI tract (perforation) allowing digestive juices and food to leech into the abdominal cavity
30
What causes inflammatory bowel disease?
It is idiopathic
31
With what two symptoms will a patient with inflammatory bowel disease commonly present?
Diarrhoea and rectal bleeding
32
What is the typical site of ulcerative colitis?
Large intestine, however small intestine may show inflammation in some people
33
How much of the bowel wall is affected by ulcerative colitis?
It is superficial and inflammation tends to be continuous throughout inflamed areas
34
How does ulcerative colitis appear histologically?
No granulomas, mucosa ulcerated, crypt architecture distorted; presence of inflammatory cells
35
What is the typical site of Crohn’s disease?
Inflammation can occur anywhere along the digestive tract, and tends to do so in patches
36
Why is Crohn’s disease described as ‘transmural’?
It affects the full thickness of the bowel wall
37
What does Crohn’s disease cause in the bowel?
Strictures, fistulae and cobblestoning
38
What are ‘strictures’?
Narrowing of the bowel
39
What are ‘fistulae’?
Connection between 2 mucosal surfaces that shouldn’t otherwise be linked
40
What is cobblestoning?
Deep ulceration around surviving areas of mucosa, and the thickening of the mucosal wall; there is a distinct appearance
41
What is a key indicator of Crohn’s in a biopsy?
Presence of granulomas
42
What are possible treatments of inflammatory bowel disease?
Corticosteroids, anti-inflammatories, surgery
43
What is cirrhosis a consequence of?
Chronic liver disease
44
What are common causes of cirrhosis?
Alcohol, infection (hep B/C), immunological, fatty liver disease, drugs and toxins
45
What is a typically seen in cirrhotic liver histology?
Nodules of fibrosed tissue, caused by damage to the architecture with attempted regeneration; there is disruption to blood flow as a result
46
What is the pathophysiology of Grave’s disease?
Antibodies produce that stimulate TSH receptors, mimicking TSH; there is chronic inflammation
47
Why can atrophy cause hypochloridia in the stomach?
Chronic inflammatory cells replace glands
48
What is a granuloma?
Mixture of chronic inflammatory cells; macrophages (epitheloid histiocytes) group together and lymphocytes (T cells predominate) are usually associated
49
What are the main causes of granulomatous inflammation
Mildly irritant ‘foreign’ material, infections, unknown causes
50
Why do granulomas arise?
Persistent, low grade antigenic stimulation
51
Name three diseases in which the cause of granulomatous inflammation is unknown?
Sarcoidosis, Wegener’s granulomatosis, and Crohn’s (around 50% of cases have granulomas)
52
Which common vaccination results in the formation of a granuloma?
BCG (for tuberculosis)
53
What causes sarcoidosis?
It is idiopathic
54
What structures does sarcoidosis affect?
Lungs, lymph nodes
55
What are the granulomas like in sarcoidosis?
Beautiful! Neat, tight groups of macrophages (non-caseating)
56
Why do giant cells form with tuberculosis?
The organism is very resistant to phagocytosis by macrophages
57
How does tuberculosis cause disease?
Persistence and induction of cell-mediated immunity; granulomas are a localisation of this and last for a very long time
58
What do tuberculosis granulomas contain?
Central caseous necrosis, macrophages (epitheloid histiocytes), lymphocytes and Langhans type giant cells
59
What is tuberculosis empymena?
Infection of pleural space caused by tuberculosis
60
Why can tuberculosis be seen on an X-ray?
It causes fibrosis and scarring in the lungs?
61
What is tuberculosis called when it affects many organs?
Miliary tuberculosis