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Pathological Processes > Session 2 > Flashcards

Session 2 Flashcards

1
Q

What is acute inflammation?

A

The response of living tissue to injury; protective mechanism.

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2
Q

What are the main features of acute inflammation?

A
  • Innate
  • Always the same regardless of stimulus
  • Short duration
  • Immediate
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3
Q

What causes inflammation?

A
  • Microorganisms
  • Foreign bodies
  • Hypersensitivity
  • Necrosis
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4
Q

What are clinical signs of acute inflammation?

A
  • Tumor = swelling
  • Rubor = redness
  • Calor = heat
  • Dolor = pain
  • Loss of function
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5
Q

What are the changes in the vascular phase?

A
  • Transient vasoconstriction (seconds)
  • Vasodilatation (causes heat and redness - more blood flow)
  • Increased permeability that allows fluid and cells to escape
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6
Q

What is movement of fluid controlled by?

A

Starling’s law.

  • Hydrostatic pressure: pressure exerted on vessel wall by fluid (pushes fluid out)
  • Oncotic pressure: pressure exerted by proteins that draws fluid in

Both exist in the vessels and interstitium and when balance, there is no water flow.

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7
Q

How do pressures change in acute inflammation?

A
  • Vasodilatation causes increased HYDROSTATIC pressure
  • Increased vessel permeability allows plasma proteins to move into interstitium and increase INTERSTITIAL ONCOTIC PRESSURE
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8
Q

What do pressure changes cause?

A

Oedema/tumor

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9
Q

What is a result of fluid moving out of vessel?

A

Increased blood viscosity - blood is thicker and not as diluted by fluid and therefore causes STASIS (reduced flow through vessel)

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10
Q

What type of interstitial fluid is exudate?

A
  • Increased vascular permeability
  • Protein rich fluid to deliver proteins into area of trauma

= INFLAMMATION

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11
Q

What type of interstitial fluid is transudate?

A

Unchanged vascular permeability. Fluid moves due to either:

  • Reduced capillary oncotic pressure
  • Increased capillary hydrostatic pressure
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12
Q

When does transudate occur?

A
  • Heart failure (blood pooling causes increased capillary hydrostatic pressure)
  • Liver failure (less protein synthesis = reduced capillary oncotic pressure)
  • Renal failure
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13
Q

How does a vessel become permeable and how is it controlled?

A

Retraction of endothelial cells that creates gaps.

  1. Controlled by CHEMICAL MEDIATORS:
    - Leukotrienes, Histamine, Nitric oxide
  2. DIRECT INJURY
    - Burns, trauma, toxins - allows proteins and cells to escape
  3. LEUCOCYTE DEPENDENT INJURY
    - Reactive oxygen species released by activated neutrophils
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14
Q

How is the vascular phase effective?

A
  • Interstitial fluid dilutes toxin
  • Exudate delivers proteins that limit spread of toxin (fibrin)
  • Exudate delivers immunoglobulins as part of adaptive immune response to destroy the toxin
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15
Q

Where does interstitial fluid drain and why?

A
  • Drains into lymph nodes

- Delivers antigens to stimulate the adaptive immune response

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16
Q

What is the cellular phase of inflammation controlled by?

A

The neutrophil.

Enter tissues - trilobed nuclei stain purple

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17
Q

How do neutrophils escape vessels?

A
  • MARGINATION: Increased viscosity causes neutrophil to stick to the edge of the vessel
  • ROLLING: weak intermittent bond with the vessel
  • ADHESION: binding tighter to the edge of vessel
  • EMIGRATION/DIAPEDESIS: neutrophils changes conformation to squeeze through endothelial cells
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18
Q

What adhesion molecules help with neutrophil vessel escape?

A
  • Selectins: on endothelial cells activated by chemical mediators
    Responsible for rolling (weak binding)
  • Integrins: on neutrophil surface, change from low to high affinity state
    Responsible for adhesion (tight binding)
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19
Q

How do neutrophils move through interstitium?

A

Chemotaxis - along an increasing chemical gradient of chemoattractants (e.g. bacterial peptides and inflammation mediators)

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20
Q

What is the function of neutrophils?

A

Phagocytosis (cover in MEH, revisit) and release of inflammatory mediators. Also releases debris from phagocytosis to dissolve in blood via exocytosis.

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21
Q

How do neutrophils recognise what to phagocytose?

A
  • Opsonisation
  • Pathogen gets covered by FC and C3b opsonins
  • Receptors found on neutrophil surface = binds to introduce neutrophil to pathogen
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22
Q

What are neutrophil oxygen-dependent killing mechanisms?

A
  • Reactive oxygen intermediates (superoxide, hydroxyl radical, hydrogen peroxide)
  • Reactive nitrogen intermediates (nitric oxide and dioxide)
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23
Q

What are some oxygen-independent killing mechanisms?

A
  • Lysozyme
  • Hydrolytic enzymes
  • Defensins
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24
Q

How is the cellular phase effective?

A
  • Removal of pathogens and necrotic tissue

- Release of inflammatory mediators

25
Q

What are inflammatory mediators?

A

Chemical messengers that control and co-ordinate the inflammatory response. Have overlapping functions.

26
Q

What do inflammatory mediators originate from?

A
  • Activated inflammatory cells
  • Platelets
  • Endothelial cells
  • Toxins
27
Q

What mediates vasodilatation?

A
  • Histamine
  • Serotonin
  • Prostaglandins
  • Nitric oxide
28
Q

What mediates vascular permeability?

A
  • Histamine
  • Bradykinin
  • Leukotrienes
  • C3a & C5a
29
Q

What mediates chemotaxis?

A
  • C5a
  • Tumour necrosis factor
  • IL-1
  • Bacterial peptides
30
Q

What mediators are pyrogens?

A
  • Prostaglandins
  • IL-1 and IL-6
  • TNF-a
31
Q

What inflammatory mediators induce pain?

A
  • Bradykinin

- Prostaglandins

32
Q

What are local complications of acute inflammation?

A

Swelling - dangerous if compresses tubes (eg. airways/intestines)

Compression of organs by exudate - eg. cardiac tamponade

Loss of fluid - severe dehydration (burns)

Pain - muscle atrophy and psychosocial consequences

33
Q

What are systemic complications of acute inflammation?

A

Fever - pyrogens act on hypothalamus to alter temperature

Leucocytosis - increased white cell production as inflammatory mediators act on bone marrow.

Acute phase response - feeling unwell, tachycardia - induces rest

Acute phase proteins - CRP (sensitive not specific)

34
Q

How is fever brought down?

A

NSAIDs - block cyclo-oxygenase enzymes and therefore production of prostaglandin so that fever is reduced

35
Q

What are the differences between viral and bacterial leucocytosis?

A

Viral: lymphocytes
Bacterial: neutrophils

36
Q

What is septic shock?

A

A systemic complication.

  • Huge release of chemical mediators that spread throughout body
  • Vasodilatation in whole body - lower TPR = tachycardia, hypotension and multi organ failure
  • IV AND ANTIBIOTICS IMMEDIATELY!
37
Q

What happens after acute inflammation in complete resolution?

A
  • Mediators degraded/inactivated due to short half-lives.
  • Neutrophils apoptose
  • Exudate drains via lymphatics to reduce oedema
  • If tissue architecture preserved - regeneration
38
Q

What happens after acute inflammation in fibrosis?

A
  • Fibrosis
    Repair with connective tissue when a lot of tissue destruction
  • Progression to chronic inflammation
    Long inflammation with repair; acute not adequate
39
Q

What causes appendicitis?

A
  • Blocked lumen from faecolith
  • Accumulation of bacteria and exudate
  • Increased pressure can lead to perforation
40
Q

What causes pneumonia?

A

(Streptococcus pneumoniae
Haemophilus influenzae)

Buildup of exudate in lungs - impairs gas exchange. Causes sputum, fever, shortness of breath. Neutrophils in alveoli.

41
Q

What are risk factors for pneumonia?

A
  • Lung conditions (asthma, COPD)

- Smoking

42
Q

What causes bacterial meningitis?

A

(Neisseria meingitides)
Inflammation + exudate in narrow meningeal space

Causes headache, photophobia and altered mental state

43
Q

What are abscesses?

A

Accumulation of dead neurophils - liquefactive necrosis)

Can compress surrounding structures and cause pain and duct blockages

44
Q

What serous cavities can get inflamed?

A
  • Pleural and pericardial space (effusions)
  • Peritoneal space - ascites

Exudate into serous cavities.

45
Q

What is hereditary angio-oedema?

A
  • Inherited deficiency of C1-esterase inhibitor so patients have attacks of itchy oedema and intestinal oedema.
46
Q

What is alpha-1 antitrypsin deficiency?

A

Condition that allows uninhibited inflammation (especially in lungs) which can cause tissue destruction and fibrosis as AAT usually deactivates enzymes released from neutrophils to protect own tissues.

  • Liver disease (protein incorrectly folded, can’t be exported = CIRRHOSIS)
47
Q

What is chronic granulomatous disease?

A
  • Phagocytes unable to generate superoxide
  • Cannot kill bacteria
  • Chronic infections when young
48
Q

What are medicolegal autopsies?

A
  • Performed on behalf of HM Coroner

- No consent needed

49
Q

What are forensic autopsies?

A
  • Also coroner’s post mortems

- Performed in suspicious deaths (eg. murders, suicides)

50
Q

What are hospital/consent autopsies?

A
  • Need consent from next of kin
51
Q

When are coroner’s autopsies performed?

A
  • When doctor can’t determine cause of death
  • When deceased is unknown
  • When death is obviously unnatural
  • When death is related to work accident
  • When death is related to medical treatment
  • Individuals detained by state (prisoners)
52
Q

What is involved in an autopsy?

A
  • History
  • External examination: natural disease? injury? imaging?
  • Internal examination: all systems examined unless no consent
53
Q

What additional tests have to be done?

A
  • Histology: make/confirm diagnosis
  • Toxicology: drugs, blood, urine, bile
  • Microbiology: bacteria, viruses, fungi
  • DNA fingerprinting: genetic diseases, suspects
  • Biochemistry: ketoacidoses, renal failure
54
Q

What are some causes of sudden death (head)?

A
  • Subdural haemorrhage (between dura and arachnoid maters)
  • Extradural haemorrhage (between dura mater and skull)
  • Subarachnoid haemorrhage (rupture of ‘berry’ aneurysm)
  • Haemorrhagic/ischaemic strokes
55
Q

What are some causes of sudden death (heart)?

A
  • Coronary thrombosis (rupture causes haemopericardium)
  • Valvular disease
  • Cardiomyopathies
  • Aortic aneurysms that rupture
  • DVT
56
Q

What are causes of sudden death (lungs + other)?

A
  • Bronchopneumonia
  • Pulmonary embolism (DVT)
  • Peritonitis
57
Q

What is neuropathology?

A

Branch of autopsy dealing with trauma, neurodegenerative disease & research

58
Q

What is paediatric pathology?

A

Child autopsies.

  • In-utero & perinatal deaths
  • Sudden infant death
  • Suspicious deaths
  • Medicolegal & safeguarding issues
  • Provide answers for families

Pathological Processes (10 decks)

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