Gen Path - Cell damage + Acute/Chronic infl.

Question 1

Name 3 cellular adaptations.

Answer 1

Increased cellular activity - hypertrophy (SIZE), hyperplasia (NO.), both
Decreased cellular activity - hypotrophy, hypoplasia, both
Metaplasia

Impt to discern if its pathological or physiological!!

Question 2

Early vs Late changes following cell injury and significance?

Answer 2

Essentially: swelling + clumping = early thus reversible; everything else is late changes

Question 3

3 ways of cell death?

Answer 3

1. Autolysis (suicide - enzymatic digestion of cells released from lysosomes)
2. Apoptosis (programmed cell death; can be pathological/ physiological)
3. Necrosis (Unplanned; large area; alw pathological)

Question 4

Name the types of necrosis + what cdns they can be found in.

Answer 4

(Chocolate Casing Got Liquefied How Sad Fat Fibrinoids)

• Coagulative - ischaemia
  -Caseous - TB
  -Liquefactive - stroke (‘brain’)/ abscess
  -Haemorrhagic - in organs with dual blood supply (2 Ls - lung, liver)
  -Suppurative - purulent (bacterial) infection
  -Fat - acute pancreatitis
  -Gangrenous - diabetes
  -Fibrinoid – vasculitis

Question 5

Note:
- coagulative necrosis can’t occur in brain
- caseous necrosis is cheesy & crumbly
- liquefactive necrosis is in BRAIN or aft lung abscess bursts

Question 6

Why does cellular aging occur?

Answer 6

(mainly) lack of telomerase in somatic cells → telomeric shortening of ends of DNA after every cycle of DNA rep w/o replacement

Question 7

Explain these 2 instances of metaplasia:
1. Intestinal metaplasia in esophagus (‘Barrett’s esophagus’)
2. Cervical metaplasia

Question 8

Causes of Acute inflammation (and/ chronic infl.)?

Answer 8

FINI

Foreign bodies
Infections by microbes
Necrosis - hypoxic cells calling wbcs for help (like a desperation call kinda)
Immune rxns (hypersensitivity rxns, autoimmunity)

Question 9

5 cardinal signs of acute infl.? (LOCAL signs)

Answer 9

(see nice pic)
Warmth
Redness
Swelling
Pain
Loss of fxn

aka. Pain RWS Loss

Question 10

SYSTEMIC signs of acute infl.?

Answer 10

Pyrexia
Constitutional symptoms (malaise, anorexia, nausea)
Loss of weight
Loss of appetite

Question 11

Primary cells seen in acute vs chronic infl.?

Answer 11

Acute:
Infection: neutrophils
Allergy: Eosinophils, mast cells

Chronic:
- macrophages (ig cuz they produce cytokines to activate more lymphocytes)
- lymphocytes

Question 12

Describe the whole process of acute inflammation.

Answer 12

Hint:
1. FINI –> DAMPS + residential tissues
2. Vasodil
–> 3.1 Exudate (PPC)
–> 3.2 Neutrophilic mvmt (MMA-T)
3. Neutrophil MOA
4. Systemic how? + enhancement of acute infl. rxns?

To think: after neutrophil actions, how are other WBCs recruited?

Question 13

Note: Chemokines are a special kind of cytokines that causes chemotaxis - migration of cells from one place to another.

Question 14

Now allude each step of Acute infl. to when and how the 5 cardinal signs of acute infl. occur.

Hint:

Answer 14

Warmth: vasodilation
Redness: vasodilation
Swelling: exudation (and accumulation of the exudate in interstitial tissues)
Pain: stimulation of nerve endings by bradykinin and PGE2
Loss of function: (due to pain)

Question 15

What 2 things cause Fever (a systemic sign of infl.)?

Answer 15

IL-1 + TNFalpha

Question 16

4 Outcomes of acute inflammation?

(RFAC)

Answer 16

Resolution - healingnrepair

Fibrosis - healingnrepair

Abscess formation - ‘sequelae’ of acute infl. –> due to accumulation of neutrophils

Chronic inflammation (usually if injurious stimuli doesn’t clear)

Question 17

Exudate vs Transudate - compare:
(i) cause
(ii) what they contain

Answer 17

Exudate:
i. vasodil (so increased blood flow) + increased vascular perm
ii. high protein, plasma, more cells (eg. neutrophils to go to inflamed tissue)

Transudate:
i. increased hydrostatic p.a. in BV/cap +- decreased oncotic p.a (think: Starling’s forces)
ii. low protein, plasma, less cells

Question 18

Is inflammation = infection?

Answer 18

No. Infection is 1 cause of infl.

Question 19

Name the 4 special patterns of acute inflammation. (FUSS)

Answer 19

FUSS:
F - Fibrinous
- fibrinous is NOT fibrous
- fibrinous = more fibrin threads from increased fibrinogen there
- fibrous = more collagen fibres (eg. scar tissue)

U - Ulcerative
- when there’s defect in epithelial surface

S - Serous
- cell-poor, protein-poor EXUDATE (usually early in infection when neutrophils haven’t come alot)

S - Suppurative
- when there’s pus

Question 20

What does pus consist of?

Answer 20

Neutrophils (dead/ alive)
Necrotic cell debris (“large area of unplanned cell death” = necrosis!)
Bacteria

Question 21

Localised pus = ?

Answer 21

Abscess

Question 22

Pus contained in body cavity = ?

Answer 22

Empyema

Question 23

Systemic inflammation = ?

Answer 23

Sepsis

Sepsis can be due to:
- septicaemia (systemic bloodstream inf by bact/ mirobials)
- bacteraemia (=^ by bact only)
- viraemia (=^ by viruses only)

Question 24

Why does body even have infl.? (good)

Answer 24

To clear out injurious stimuli

Question 25

Define chronic inflammation with 4 keywords

Answer 25

1. prolonged duration of infl.
2. varying combis of:
   - Inflammation
   - Tissue injury
   - Attempts at healing n repair

Question 26

Name the 2 more common causes of chronic infl. out of FINI.

Answer 26

I+I
Infection, toxins
Immune rxns- eg. autoimmune, hypersensitivity - allergies

Question 27

Name a special type of chronic inflammation. + common causes? + histology?

Answer 27

• Granulomatous infl.

Causes:
- caused by (hard to digest things):
1. Infections - M. Tb; Parasites; Syphilis
2. hard-to-digest materials: Keratin, silica, etc
3. Specific chemicals: Beryllium
4. Drugs: Allupurinol; Sulphonamides
5. Unknown: Sarcoidosis; Crohn disease; Wegener Granulomastosis

Histo:
- aggregates of epithelioid histiocytes
- surrounded by cuff of T lymphocytes
- Langhan’s giant cells (aka. multinucleated giant cells)
- necrotic center (for some cases - eg. Tb)

Question 28

Bacterial infection or viral infection usually causes abscess + why?

Answer 28

Bacterial.
Viruses usually intracellular while neutrophils feast on (mostly extracellular bact) to form pus.

Question 29

Describe WBCs under microscopy:
Neutrophils -
Plasma cells -
Langhans giant cells -

Answer 29

Neutrophils: multi-lobated
Plasma cells - clock-face
Langhans giant cells - Nuclei in horseshoe pattern on one or both poles of the cell