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Path Pro Flashcards

1
Q

What are the stages of acute inflammation

A
  1. Stimulus
    2.Vascular stage - slowing the circulation and forming exudate at the site of inflammation
  2. Cellular stage - the migration of neutrophils to the site
  3. Resolution or persistance (develops into chronic inflammation)
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2
Q

Describe vascular phase of acute inflammation

A

vasoconstriction for a few seconds
then vasodilation=>
-↑ blood flow to affected area
-↑ permeability=allows fluid, cells and proteins to exit
-↑ viscosity of blood due to less fluid

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3
Q

how is vascular phase regulated?

A

For the first 30 mins, main mediator is histamine (released by mast cells, basophils, platelets). As the inflammatory response continues, it is mediated by leukotrienes, bradykinins

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4
Q

What is the purpose of exudate?

A

-deliver proteins (fibrin, immunoglobulins, and inflammatory mediators)
-dilutes toxins to reduce damage
-increases lymphatic drainage

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5
Q

How is exudate formed?

A

-↑ hydrostatic pressure in the vessel (the pressure exerted by a fluid which forces fluid out)
-↑ oncotic pressure in the interstitium (osmotic pressure exerted by proteins which draws fluid in).
-endothelial contraction

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6
Q

What causes vascular leakage?

A

-Retraction of endothelial cells (mediated by histamine, nitric oxide, leukotrienes)
-direct injury (burns, toxins, etc.)
-leucocyte dependent injury (ROS, enzymes from leukocytes)

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7
Q

Types of exudate

A

-Pus- neutrophil rich, infections of pyogenic bacteria
-Haemorrhage- presence of RBC’s, significant vascular damage
-Serous- clear fluid with leukocytes, blisters and burns
-Fibrinous- deposition of fibrin, friction betwen serosal surfaces, seen in pericarditis

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8
Q

What does the presence of neutrophils indicate? Identifying feature?

A

Indicates pathogenic organism or injury
trilobed nucleus

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9
Q

What happens in the cellular phase of acute inflammation

A

Neutrophils are attracted to affected area
Removal of pathogens and necrotic tissue
Release of inflammatory mediators

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10
Q

How do circulating neutrophils infiltrate site of injury?

A

-Margination- due to increased viscosity, blood contents including neutrophils move to the walls of the vessel
-Rolling- roll along the endothelial wall forming weak bonds
-Adhesion- neutrophils form strong bonds with the endothelial cells; mediated by adhesion molecules
-Diapedesis/Emigration- neutrophils exit directly through the endothelial cells or between them

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11
Q

Adhesion Molecules (neutrophils, AI)

A

-Selectins- expressed on endothelial cell, form weak bonds (Rolling)
-Integrins- expressed on neutrophil surface, can change from low affinity to high affinity, tight bonds (Adhesion)

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12
Q

How do neutrophils reach site of injury (AI)

A

Chemotaxis- Neutrophils are attracted to chemoattractants (bacterial peptides, inflammatory mediators) that are released at site of injury

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13
Q

How do neutrophils destroy pathogens?

A

Phagocytosis
Engulf→ phagosome→ phagolysosome→ digestion→ release of debris

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14
Q

How do neutrophils recognize what to phagocytose?

A

Pathogens are recognised by opsonisation
Opsonins=cell tags that flag it for phagocytosis, ex- Fc, C3b

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15
Q

Where are inflammatory mediators released from?

A

Activated inflammatory cells
platelets
endothelial cells
toxins

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16
Q

Inflammatory mediators that cause vasodilation

A

Histamine
Serotonin
Prostaglandins
Nitric Oxide

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17
Q

Inflammatory mediators that cause vascular permeability

A

Histamine
Bradykinin
Leukotrienes
C3a, C5a

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18
Q

Inflammatory mediators that cause chemotaxis

A

C5a
TNF-a
IL-1
bacterial peptides

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19
Q

Inflammatory mediators that cause pyrexia

A

Prostaglandins
IL-1, IL-6
TNF-a

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20
Q

Inflammatory mediators that cause pain

A

Bradykinin
Substance P
Prostaglandins

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21
Q

Local complications of AI

A

-Swelling- compression of tubes (airways, bile ducts, etc.)
-Exudate- compression of organs (cardiac tamponade)
-Loss of fluids- dehydration (burns)
-Pain- Muscular atrophy, psycho-social complications

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22
Q

Systemic complications of AI

A

-Fever
-Leucocytosis (inc. prodn. of WBC’s)
-Acute Phase Response (malaise, red. appetite, altered sleep)

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23
Q

What causes Acute Phase Response

A

Acute Phase Proteins, ex- C-reactive Protein, Fibrinogen, α1 antitrypsin

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24
Q

How do NSAIDS work

A

Non-Steroidal Anti-Inflammatory Drugs (ex-aspirin, ibuprofen) block cyclo-oxygenase enzymes which are involved in production of prostaglandins

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25
How does chronic inflammation arise?
-Takes over from acute inflammation (if resolution is not possible from AI alone) -Develops alongside AI (severe/persistent insult) -De novo chronic inflammation (ex- autoimmune diseases)
26
Macrophages- identifying histology features
large foamy cytoplasm (full of lysosomes) sometimes indented nucleus
27
Role of macrophages?
-phagocytosis -antigen presentation to immune system -synthesis and release of inflammatory mediators
28
lymphocyte histology appearance
small cells, large round nucleus, small cytoplasm
29
Role of Lymphocytes
-Helper T cell: assist other inflammatory cells -Cytotoxic T cells: directly destroy pathogens -B cells: mature into plasma cells which produce antibodies
30
Plasma cell histology appearance
large cells acentric nucleus with clockface pattern peri-nuclear clearing (dues to prominent golgi bodies)
31
Eosinophil histology appearance
similar size to lymphocyte, bilobed nucleus, granular red staining cytoplasm 'tomato wearing sunglasses)
32
Eosinophil function
release of a variety of mediators especially during hypersensitivity reactions and parasitic infections
33
how are giant cells formed?
formed by fusion of multiple macrophages (frustrated phagocytosis)
34
Types of giant cells
-Foreign body GC (in response to a foreign body, scattered nuclei) -Langhans GC (Nuclei arranged as a ring or horseshoe shape at the cell border; seen in TB) -Touton GC (ring of nuclei in the middle; seen in fat necrosis)
35
Which is the main cell type in CI?
generally non-specific but sometimes can indicate a diagnosis Rheumatoid arthritis- plasma cells Chronic gastritis- lymphocytes Whipples disease (bacterial)- macrophages Parasitic- eosinophils
36
Effects of Chronic inflammation
-Fibrosis (deposition of collagen) -Impaired function -Atrophy -Stimulation of immune response (antigen presentation) -rarely, increased function (ex-graves disease)
37
Crohns disease
-affects entire GI tract -discontinuous patches of inflammation -affects full thickness of bowel wall (transmural) -can sometimes cause granulomata -rectal bleeding rare
38
Ulcerative Colitis
-affects large bowel only -continuous inflammation -affects only superficial layers (mucosa and submucosa) -no granulomata -prone to rectal bleeding
39
Causes of cirrhosis
-alcohol -drugs/toxins -fatty liver disease -hepatitis
40
Granulomatous inflammation
chronic inflammation + granuloma
41
What is a granuloma
a collection of epithelioid histiocytes (macrophages) with surrounding lymphocytes
42
Difference btwn giant cell and granuloma
both are made of macrophages but in giant cells the macrophages are fused into one multi-nucleated cell, in granuloma the individual cells are still distinct
43
Types of granuloma
-Foreign body granuloma =few surrounding lymphocytes) -Immune mediated granuloma =destruction/ removal of pathogens (bacteria/fungi) =can undergo central (caseous) necrosis =many surrounding lymphocytes
44
Examples of infections characterized by granulomatous inflammation
Myobacterium infections -myobacterium tuberculosis (TB) -myobacterium leprae (leprosy)
45
Examples of idiopathic granulomatous inflammation
-Sarcoidosis (in lymph nodes, skin, lungs, etc.) -Crohns disease (in GI tract) (non-necrotising)
46
Define atherosclerosis
Disease Process Accumulation of intra and extracellular lipid in the intima and media of large and medium sized arteries
47
Define atheroma
Necrotic core of the atherosclerotic plaque causing thickening and hardening of arterial walls
48
what is the blood supply of blood vessels called
Vaso vasorum
49
Risk factors for chronic endothelial damage
Raised levels of LDL Hypertension Smoking-toxins Haemodynamic stessors
50
How are foam cells formed?
Chronic endothelial damage→ endothelial dysfunction smooth muscle cell proliferation and migration Lipids (LDL and Ch) cross into intima Macrophages engulf lipids in the intima Macrophages+sm cells=foam cells
51
What do foam cells do
secrete cytokines which leads to -further smooth muscle cell stimulation -recruitment of other inflammatory mediators
52
How are the necrotic center and fibrous cap of atherosclerotic plaque formed?
-Lipid debris secreted by macrophages in the center forms the necrotic contents -Covered by a fibrous cap (sm cells produce collagen, elastin and other proteins)
53
Components of atherosclerotic plaque
Cells: endothelial cells, platelets, neutrophils, macrophages, leucocytes, sm cells Lipid: intracellular(foam cells) and extracellular (pools) Extracellular Matrix: collagen, elastin, proteoglycans
54
Complications of unstable atherosclerotic plaque
unstable plaque→ can rupture → can allow platelet aggregation (thrombus formation)→ pressure atrophy of underlying media, weakening of elastic lamina
55
Complications of Atherosclerotic plaque
-Ulceration -Thrombosis (further stenosis or occlusion) -Vasospasm (local vasoconstrictor release) -Embolisation -Calcification (cholesterol cleft deposition) -Haemorrhage -Aneurysm formation -Rupture
56
Atherosclerosis in brain
-Transient Ischaemic Attacks (resolve within 24hrs) -Cerebral Infarction -vascular dementia -cerebral haemorrhage (stroke)
57
Atherosclerosis in heart
-sudden death -MI -angina pectoris -Arrythmias -Cardiac failure
58
Atherosclerosis in GI tract
acute- intestinal infarction chronic- ischaemic colitis, malabsorption
59
Atherosclerosis in peripheral arteries
-acute limb ischaemia -Ischaemic pain -Intermittent claudication -Gangrene
60
Risk factors for atherosclerosis
-Age -Gender (post-menopausal) -Hyperlipidaemia (including defects in lipid metabolism) -Smoking -Hypertension -Diabetes mellitus, obesity -Infection (chlamydia pneumoniae, helicobacter pylori, CMV) -Lack of exercise -Stress
61
Prevent/reduce atherosclerosis
-decrease Cholestrol and LDL in diet -Lipid lowering drugs (statins) -Low fat, high fibre diet -Aspirin (*small amounts of alcohol may be protective)

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