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Unit 9 > Week 1: Immunology workshop > Flashcards

Week 1: Immunology workshop Flashcards

1
Q

What are the histological features of fibroblasts?

A

Active - spindle shaped cell, often only nucleus is visible darker stained and ovoid in appearance

Inactive (fibrocyte) - elongated shaped cell, nucleus is smaller, flattened, elongated and more darkyl stained

Cytoplasm is highly eosinophilic typically indistinguishable from surrounding collagen.

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2
Q

What is the function of a fibroblast?

A

Permanent residents of connective tissue, that produce and secrete the ECM, mainly collagen and elastin.
Some differentiate into myofibroblasts which have a role in wound contraction hence and wound healing.

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3
Q

What tissue resident cells should be identifiable in connective tissue?

A

Fibroblasts
Macrophages

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4
Q

What does collagen look like under histological imaging?

A

Typically pink bundles
Often associated with fibroblast nuclei

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5
Q

What are the histological features of a monocyte?

A

Largest of white blood cells
Large eccentrically placed kidney bean shaped nucleus.
Abundant cytoplasm with some fine granules

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6
Q

Draw diagrams to represent the histological appearance of neutrophils, lymphocytes, monocytes/macrophages, eosinophils, basophils and plasma cells.

A

Plasma cells - large eccentric round nuclei, with clock face chromatin

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7
Q

What are the histological features of cardiac muscle?

A

Straited
Intercalated disks
Single centrally located round nucleus
Branched appearance appearance

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8
Q

What are the histological features of skeletal muscle?

A

Eosionophilic cytoplasm
Many peripheral nuclei
Striated
Unbranched structure
Fibrocollagenous septa containing blood vessels

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9
Q

What are the histological features of smooth muscle?

A

Single Centrally located nucleus
Not striated
Spindle shaped cells
Gap junctions

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10
Q

How does the regenerative capacity of the different types of muscle vary?

A

Cardiac muscle - permanent, no regeneration
Smooth muscle - stable regenerates by mitosis
Skeletal muscle - stable, satellite cells (small population of stem cells)

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11
Q

Describe the histology of neural tissue?

A

Nerve axons (eosinophilic), typically surrounded by a myelin sheath (thicker indicates more insulation), may identify nuclei on the edge of this sheath belonging to the shwann cells.

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12
Q

What is the basic histological structure of the gall bladder?

A

Consists of:
Mucosa: Epithelium - simple columnar with prominent folds till the bottom of the lamina propria.
Lamina propria - may contain crypts of epithelium
Muscularis mucosa - quite thick
Submucosa:
Muscularis externa:
Serosa:

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13
Q

What are the science names for gall stones?

A

Cholithiasis in the gall bladder
Choledocholithiasis - in the bile duct

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14
Q

Describe the histological features of the lung parenchyma/alevoli?

A

Thin walled - type 1 and type 2 pneumocytes
Type 1: thin walled simple squamous epithelium with a flattened nucleus
Type 2: septal cells, source of surfactant, round and bulge into alveolar spaces
Walls around a large air spaces, surrounded by smaller capillaries marked by smaller lumens and singular flattened nuclei.

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15
Q

What are the key microscopic features of acute inflammation?

A

Neutrophil migration
Oedema - tissue exudate
Macrophage proliferation
Vascular congestion - indicate slowing of blood flow and coagulation.
Made see indication of vasodilation in widened spaces between endothelial cells.

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16
Q

What are the possible outcomes of acute inflammation?

A
  1. Progression to chronic inflammation is damaging stimuli is not removed
  2. Damaging stimuli removed and regeneration (return to normal function)
  3. Damaging stimuli removed and healing by fibrosis (scar) (no functional)
  4. A combination of repair and regeneration can lead to partially functional tissue
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17
Q

What are the key features of chronic inflammation?

A

Inflammatory damage and attempts at repair occur simultaneously
Identify macrophages and lymphocytes in infiltrate
Collagen, fibroblasts indicate fibrous tissue (scar) formation, this changes the ECM where there was previously parenchymal or stromal tissue.
Granulation tissue

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18
Q

What is the key outcome of chronic inflammation?

A

Typically: healing by fibrosis resulting in loss of tissue function

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19
Q

What are the key histological features of granulomatous inflammation?

A

Macrophages - epithelioid cells, foam cells, Multinucleate giant cells and activated macrophages
These ring around a core containing the pathogen, is often also necrotic
May be surrounded by an outer ring of lymphocytes
May be an additional outer ring of fibrosis

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20
Q

What are the factors that affect wound healing?

A

Extreme age
Immunocompromised - HIV
Diseases - diabetes
Low perfusion - diabetes or obesity
Persistent damaging stimuli - infection
Mechanical forces - pulling open wound or picking scab
Nutritional status
Poor wound hygiene
Fibrin coating (supports healing)
necrosis (can harbour pathogens).

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21
Q

What blood tests can confirm suspected infection?

A

1.Full blood count - elevated wbcs, particularly lymphocytes, may be combined with a blood smear
2.Basic metabolic panel - Na+, K+ etc, determine severity of illness
3. Look for metabolic markers of inflammation such as C-reactive protein (and other acute phase proteins)
4.ESR - measures degree of inflammation, increase in infection
5. Blood culture - detect septicemia

22
Q

What blood tests may help confirm a diagnosis of pneumonia specifically?

A

Arterial blood gases - measure pH, O2 and CO2 to determine lung function
Mycoplasma testing - potential specific cause of pneumonia
Legionella testing - looking for legionella antigen, notifiable disease that can present as pneumonia
Usually produces a clear blood culture

23
Q

What is the blood marker for systemic inflammation?

A

Procalcitonin

24
Q

What are the changes in vital signs that you expect to see in pneumonia?

A

Elevated temperature
Elevated HR
Normal or slightly high BP
Elevated RR

25
Q

What is the mechanism underlying increased temperature during infection?

A

Endogenous/exogenous pyrogenes act on the hypothalamus to increase the homeostatis set point for temperature regulation.

This aims to denature pathogen enzymes and inhibit replication.

26
Q

What is the mechanism behind increased pulse in pneumonia?

A

Low oxygen levels = RAAS activation (long term)
In septic patient low BP =baroreceptor reflex
Mostly: central and peripheral chemoreceptors
Triggers an increase in the frequency of impulses intiated by the SAN increasing HR.
Accompanied by increased TPR and Pa often.

27
Q

What is the mechanism behind elevated blood pressure in pneumonia?

A

Low BP.
Detected by baroreceptors in the carotid bodies and aortic arch, send signals to the nucleus tractus solitarus by the vagus nerve and the glassopharangeal nerve respectivly.
Activates the vasomotor centre to cause vasoconstriction.

28
Q

What is the mechanism behind increased respiratory rate in pneumonia?

A

Low gas exchange as alveoli, leads to low arterial oxygen (detected by peripheral chemoreceptors) and high arterial carbon dioxide (detected by central chemoreceptors).
Signal is carried to the respiratory centres in the medulla oblangata.

Increased sympathetic tone.
Activates the phrenic nerves and intercostal nerves to increase the respiratory rate and depth of ventilation.

29
Q

What histological changes would you expect to be present in the lungs during pneumonia?

A

ACUTE: Excessive neutrophil infiltration into the alveolar air space and surrounding connective tissue.
Capillary congestion
Obstruction of bronchiolar lumen and alveoli by mucus
CHRONIC: Alveolar wall - thickened from fibrosis, occluding airways
BOTH: Fluid exudate - areas of white

30
Q

What are the potential outcomes of acute pneumonia?

A
  1. Progress to chronic granulatomous inflammation
  2. Resolution of acute - complete with regeneration and removal of insult
  3. Fibrosis and scar formation in sustained damage
31
Q

What is acute cholecystitis?

A

Acute - short term and rapid onset
Cholecy - of the gall bladder
itis - inflammation

32
Q

What are the gross changes to the gall bladder during acute cholecystitis?

A

Enlargement - oedema
Change in colour - becomes more red rather than green due to congested vessels. haemorrhage, fibrin deposition.
Thickened wall
Loss of smooth surface
Inside - loss of hollow centre

33
Q

What are the histological changes in acute cholecystitis?

A

Early: Loss of epithelial folds and ulceration of epithelium
Increased infiltrate of neutrophils and wbcs, purple nuclei cells
Fibrin deposition and odema.

Later: Mucosal necrosis, fresh thrombi within small veins.

34
Q

What is a good stock answer for histological changes during acute inflammation?

A

Neutrophil infiltrate
Fibrin deposition
Odema
Congested capillaries

35
Q

Summarise the pathogenesis of acute cholecystitis

A

1.Normally develops secondary to choleithiasis (gall stones) which form from excess cholesterol in bile.
2.Stone aggregate the gall bladder wall or block the bile duct cause bile build up, this damages the tissue causing inflammation.
3.Inflammation results in neutrophil migration, vasodilation, edema and ulceration of epithelium. Results in an enlarged and distended gall bladder
4. If injury persists can progress to chronic inflammmation.

36
Q

What are the gross changes to the gall bladder in chronic cholecystitis?

A

Appearance of yellow (due to high cholesterol) gall stones
Redness of the gall bladder wall - inflammation, haemorrhage and congested blood vessels
Thickening of the walls - fibrosis
Serosal adhesions

37
Q

What are the histological changes of chronic cholecystitis?
What causes these changes?

A

Ulceration of mucosal layer, penetrate down to the muscularis mucosae - due to irritation of stones removing necrotic epithelial cells.
Inflammatory cells are present shown by purple or blue layer
Thickening of smooth muscle layer/connective tissue layer (muscularis mucosae) - fibrosis, increased deposition of collagen by fibroblasts as part of repair process, smooth muscle thicken as continues to contract to try and force bile past blockage.

38
Q

What type of leukocytes are present in chronic cholecystitis?

A

Leukocytes

39
Q

Why does fibrosis occur in chronic inflammatory process?

A

Severe damage to cells and ECM means the regenerative capacity is lost and reduced number of parenchymal cells are present, hence when damaging stimuli is removed will heal by fibrosis
Macrophages and endothelial cells secrete growth factors, including fibroblast growth factor, this will cause tissue resident fibroblasts to proliferate and secrete collagen alongside other ECM components.
Results in thickening of the tissue

40
Q

What are the potential functional effect of fibrosis in the bowel?

A

Fibrosis results in unusual attachment of regions in the bowel to one another and other organs.
Reduced movement of the bowel, can inhibit peristalsis

41
Q

What are the functional effects of fibrosis in the peritoneum?

A

Fibrosis results in unusual attachment of the peritoneum to organs within it.
THis can restrict movement of the bowel and prevent urinary flow due to effect on ureters (retroperitoneal)

42
Q

What are the functional effects of fibrosis in the bile duct?

A

Fibrosis typically caused by gall stones
Results in thickening of gall bladder wall, biliary obstruction, jaundice and infections

43
Q

What is the functional effect and impact of fibrosis in the skin?

A

Deformation and contraction of the skin
results in restricted movement

44
Q

What is lymphadenopathy?

A

Swelling of the lymph nodes, can be secondary to infection, autoimmune disease and malignancy.

45
Q

What type of inflammation do you expect to see in tuberculosis resulting in lymphadenopathy?

A

Chronic granulomatous inflammation
In particular a caseating immune granuloma

46
Q

Label the components of the granuloma

A

A necrotic centre
B Multinucleate giant cell
C macrophage or epithelioid macrophage
D lymphocyte

47
Q

What abnormalities can be seen in TB infection in the lymph node?

A

Granulomatous inflammation
Necrotic centre
Multinucleate Giant Cell
Epithelioid cell

48
Q

What special stains should be performed after seeing a caseating/necrotic granuloma in H&E?
Why?

A

M. tuberculosis and atypical mycobacteria are not visible on routine H&E stains.
Further staining is used to confirm suspiscion of mycobacterial infection
This stain in Ziehl-Neelson stain for TB
Modified Ziehl-Neelson stain for atypical mycobacteria.

49
Q

List and briefly describe some causes of the various types of granulomatous inflammation

A
  1. Immune granuloma - around an infectious agent, surrounded by a lymphocyte ring, more likely to have specialised macrophages.
    These can then be subdivided into (non)necrotic (with a caseating centre) or fibrotic (surrounded by a fibrous ring
  2. Foreign body granuloma - centres around a non-infectious agent
50
Q

What outcomes do you expect to see in necrotising granulomatous inflammation?

A

Early stage: tissue damage from macrophage products and enzymes
Chronic as persistent infection
Severe damage to parenchymal tissue and ECM leads to loss of function.
Calcified granulomas can be left as scars, replacing functional tissue

51
Q

What is needed for the formation of granulation tissue?

A

Dependent on the nature of tissue that is wounded and the extent of wounding
Most common after chronic inflammatinon
Or from severe wound during acute inflammation

52
Q

What is an example of a non-caseating immune granuloma?

A

Crohns disease

Unit 9 (15 decks)

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