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ESA 2 - Pathological Processes > 2. Acute inflammation - clinical conditions > Flashcards

2. Acute inflammation - clinical conditions Flashcards

1
Q

Name 3 inherited disorders of acute inflammation.

A
  1. hereditary angio-oedema
  2. alpha-1 antitrypsin deficiency
  3. chronic granulomatous disease
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2
Q

What causes hereditary angio-oedema?

A
  • autosomal dominant inherited condition (extremely rare)
  • deficiency of C1-esterase inhibitor (component of complement system)
  • reduced levels of C2 and C4
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3
Q

What are the symptoms of hereditary angio-oedema?

A
  1. attacks of non-itchy cutaneous angio-oedema (rapid oedema of the dermis, subcutaneous tissue, mucosa and submucosa)
  2. recurrent abdominal pain due to intestinal oedema
  3. family history of sudden death due to laryngeal invovlement
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4
Q

What is alpha-1 antitrypsin deficiency?

A
  • autosomal recessive disorder with varying levels of severity
  • low levels of alpha-1 antitrypsin
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5
Q

What is the function of alpha-1 antitrypsin?

A

protease inhibitor which deactivates enzymes released from neutrophils at site of inflammation

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6
Q

What are the symptoms of alpha-1 antitrypsin deficiency, and why do these occur?

A
  1. emphysema - proteases released by neutrophils within the lungs act unchecked and destroy normal parenchymal tissue
  2. liver disease - hepatocytes produce incorrectly folded version of protein which polymerises and cannot be exported from ER, causing hepatocyte damage and cirrhosis
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7
Q

What is chronic granulomatous disease?

A

X-linked or autosomal recessive genetic deficiency in one of components of NADPH oxidase responsible for generating superoxide… can’t generate respiratory burst to kill phagocytosed bacteria.

Results in:

  • many chronic infections in 1st yr of life
  • numerous granulomas and abscesses affecting skin, lymph nodes, and sometimes lungs, liver and bone (but ineffective at eliminating infectious agents)
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8
Q

What is meningitis?

A

Acute inflammation of the meninges (protective membranes covering the brain and spinal cord) caused by infection (viruses, bacteria or other MOs).

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9
Q

What are the symptoms of meningitis?

A
  1. fever
  2. headache
  3. stiff neck
  4. vomiting
  5. photophobia
  6. confusion or altered consciousness
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10
Q

Which bacteria commonly cause meningitis (according to age group)?

A

Neonates:

  • Strep. pneumoniae
  • Listeria monocytogenes
  • E. coli
  • Group B Step.

Children:

  • Strep. pneumoniae
  • Neisseria meningitidis
  • Haemophilus influenza type B
  • Group B strep.

Young adults:

  • N. meningitidis
  • Step. pneumoniae

Older adults:

  • Strep. pneumoniae
  • N. meningitidis
  • H. influenza type B
  • Group B Step.
  • L. monocytogenes
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11
Q

What are the immediate possible complications of meningitis?

A

Acute inflammation causes:

1- purulent exudate in brain sulci (cerebral oedema)… increased intracranial pressure… brain herniation through foramen magnum.

2- disseminated intravascular coagulation (excessive blood clotting)…

a) thrombosis… reduced cerebral perfusion… cerebral thrombophlebitis or cerebral infarction due to obliterative endarteritis of local arteries
b) gangrene of limbs

3- haemorrhaging of adrenal glands… Waterhouse-Friderichsen syndrome… adrenocortical insufficiency… often fatal

4- cerebral abscess

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12
Q

Which long term complications can bacterial meningitis cause?

A

Neurological damage as a result of:

  • compression of cranial nerves from increased intracranial pressure
  • obstructive hydrocephalus due to subarachnoid adhesions blocking flow of CSF
Problems inc.:
1- epilepsy
2- learning and behavioural difficulties
3- sensorineural hearing loss
4- blindness
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13
Q

How would the appearance of an acutely inflamed appendix differ from that of a normal one?

A

1) swollen due to accumulation of inflammatory exudate
2) prominent BVs (starling forces)
3) partly covered with fibrino-purulent exudate (fibrin = acute phase protein)
4) ruptured appendix wall due to ischaemia and coagulative necrosis

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14
Q

What complication is likely to follow appendix rupture?

A

Peritonitis as bacteria leak out of ruptured wall… sepsis… death.

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15
Q

Apart from peritonitis, what are the possible complications of acute appendicitis?

A
  1. periappendiceal abscess - intraperitoneal
  2. subphrenic abscess - between diaphragm, liver and spleen
  3. liver abscess
  4. portal vein pyaemia (widespread metastatic abscesses) and risk of portal vein thrombosis
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16
Q

What happens to the mucosa in appendix inflammation?

A

Ulcerates - complete loss of epithelium due to neutrophil enzymes

17
Q

What are the predisposing factors for appendicitis?

A
  1. impaction of appendix neck by faecalith (calcified faecal deposit)
  2. presence of seeds or pinworms in appendix
  3. lymphoid hyperplasia with appendix wall (occurs in childhood and some viral infections such as adenovirus and measles)
  4. appendix tumour
18
Q

What will happen to the WBC count during AI? How is this brought about?

A

It will increase - leucocytocis, esp. of neutrophils.

Colony stimulating factor is produced by macrophages and endothelial cells at site of acute inflammation - stimulates neutrophil production by bone marrow.

19
Q

Name 3 possible causes for pyogenic liver abscesses.

A
  1. biliary disease (conditions affecting liver, pancreas and gallbladder), e.g. cholecystitis - most common
  2. bacterial infection from a ruptured appendix
  3. septicaemia
  4. pancreatic/colon cancer
  5. liver trauma
20
Q

Why are raised serum [bilirubin, alanine transaminase and alkaline phosphatase] seen in a liver abscess?

A

hepatocellular damage causes intracellular proteins to leak into extracellular space and then into bloodstream

21
Q

How can gallstones cause a hepatic abscess?

A

Gallstones can obstruct the bile duct causing bacterial infection and inflammation - ascending cholangitis. Infection then spreads to liver where an abscess can form.

22
Q

What are gallstones?

A

Small stones, usually made of cholesterol, that form in the gallbladder as a result of too much cholesterol and not enough bile salts in bile.

23
Q

Which bacteria are most often implicated in ascending cholangitis?

A

GNB:

  • E. coli (25-50% of cases)
  • Klebsiella (15-20% of cases)
  • Enterobacter (5-10% of cases)
24
Q

What is the difference between cholangitis and cholecystitis?

A 
Cholangitis = inflammation of the bile duct/biliary tree
Cholecystitis = inflammation of the gallbladder
25
Q

Name 4 complications of gallstones and explain why they occur.

A
  1. biliary colic and jaundice - due to impaction of a stone in the common bile duct leading to biliary obstructution
  2. ascending cholangitis - due to impaction of a stone in the common bile duct leading to biliary obstructution, followed by bacteria infection
  3. pancreatitis - inflammation of pancreas due to impaction of a gallstone distal to opening of pancreatic duct
  4. cholecystitis - inflammation of gallbladder caused by impaction of a stone in the neck of gallbladder or cystic duct
  5. gallstone ileus - intestinal obstruction by gallstone that has entered gut through a fistulous connection with gallbladder
  6. predisposition to gallbladder carcinoma - pathogenesis unclear, could be due to repeated trauma to epithelium, resulting in increased epithelial turnover and increased risk of mutation during DNA replication
26
Q

Give 3 differences between lobar pneumonia and bronchopneumonia.

A

Lobar pneumonia:

  • involves a large portion, or an entire lobe of lung
  • S. pneumoniae in 95% of cases
  • typically affects young healthy adults (primary pneumonia)

Bronchopneumonia:

  • patchy foci of consolidation centred on bronchi and surrounding alveoli (lobular), scattered in 1 or more lobes of 1 or more lungs
  • caused by a wider variety of organisms (most commonly Staphylococci, also Streptococci, H. influenzae and P. aeruginosa)
  • tends to occur at extremes of life or as a secondary condition
27
Q

Describe the 4 pathological stages of lobar pneumonia.

A
  1. Congestion (day 1-2):
    - Lobe is heavy, red and boggy. There is vascular congestion.
    - Microscopy: alveoli lumen contain serous exudate with many bacteria and rare neutrophils
  2. Red hepatisation (day 3-4):
    - Lobe is red with a liver-like consistency.
    - Microscopy: alveoli lumen packed with neutrophils, RBCs and fibrin. Fibrinous exudate on adjacent pleura.
  3. Grey hepatisation (day 5-7):
    - Lobe is grey with a liver-like consistency.
    - Microscopy: RBCs are lysed, fibrous exudate persists.
  4. Resolution (day 8 – 3 wks):
    - Exudate with alveolar spaces is enzymatically digested and drained through lymphatics and airways (“productive” cough). Basic architecture of lung is left intact.
28
Q

What complications can arise following lobar pneumonia?

A
  1. bacteraemia - can result in meningitis, arthritis or endocarditis
  2. Lung abscesses
  3. pleural effusion (build up of fluid between pleura), e.g. Empyema
  4. lung fibrosis
29
Q

What are the symptoms of lobar pneumonia?

A
  • worsening fever
  • dry cough and breathlessness
  • hypoxaemia over a few days
  • prostration
30
Q

What are the causes, predominant features and consequences of a skin blister?

A

Causes:

  • heat
  • sunlight
  • chemicals

Predominant features:

  • pain (main pain Rs)
  • profuse exudate - clear as relatively few inflammatory cells (unless bacterial infection develops) - risk of dehydration if large area
  • collection of fluid strips off overlying epithelium

Consequences: resolution or scarring

31
Q

What is an abscess? How does this injure the body?

A
  • In solid tissues, inflammatory exudate forces tissue apart.
  • Liquefactive necrosis in centre.
  • May cause:
    • high pressure and therefore pain
    • tissue damage/compression of adjacent structures
32
Q

What are the consequences of acute inflammation in serous cavities?

A

Exudate pours into cavity, causing:

  • ascites (oedema in peritoneal cavity)
  • pleural effusion
  • pericardial effusion

May result in:

  • respiratory/cardiac impairment (i.e. cardiac tamponade)
  • localised fibrin deposition
33
Q

What is “bread and butter” pericarditis?

A

shaggy fibrinous inflammatory exudate - can cause friction rub on physical examination as fibrin strands on pericardium and epicardium rub against each other

ESA 2 - Pathological Processes (21 decks)

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