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Pathological processes > Cel injury and inflammation > Flashcards

Cel injury and inflammation Flashcards

1
Q

Give come causes of cell injury

A

hypoxia, toxins, trauma, tempreature, pressure, electic currents, radiation, microorganisms, dietary excess and deficiencies

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2
Q

What is hypoxia?

What are the 4 types of hypoxia?

A

Oxygen deprivation -

Hypoxaemic hypoxia, anaemic hypoxia, ischaemic hypoxia (interruption of blood supply), histotoxic hypoxia

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3
Q

What is hypoxaemic hypoxia and when does it occur?

A

oxygen content of arterial blood is low- eg at altitude or from lung disease

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4
Q

What is anaemic hypoxia?

A

decreased ability of Hb to carry blood- CO poisoning or anaemia

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5
Q

What is histotoxic hypoxia and when does it occur?

A

inability for the tissues to utilise O2 due due to inactivated oxidative phosphylation proteins - e.g.:
In cyanide poisoning

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6
Q

What is the difference between reversible and irreversible cell injury to hypoxia?

A

There is a massive influx of calcium which means that the injury becomes irreversible

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7
Q

When cell injury due to hypoxia is reversible, there is decreased ATP due to decreased oxidative phosphorylation, what effects to the cell does this have? (3)

A

1) Na/ K pump stops- influx of Na and H20 + Na/K pump reverses so Ca comes in, K+ leaves. (Na+, Ca2+ + H20 influx, K+ efflux)
2) Glycolysis increases, less glycogen and more lactate
3) detachment of ribosomes so decreased protein synthesis and more lipid deposition (leads to fatty liver)

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8
Q

What effects does the reversal of Na/ K pump leading to H20, Na and Ca influx and K+ efflux have?

A 
cell swelling
loss of microvilli
blebbing
ER swelling
myelin figures
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9
Q

What effects does massive Ca2+ influx with irreversible damage have?

A
  • Decreased ATPase activity (decreased ATP)
  • Phospholipase activated (destroys membrane integrity)
  • Protease activated (membrane and cytoskeletal as well as enzymes denatured)
  • Endonuclease activated (chromatin damaged)
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10
Q

What are signs of ischaemia?

A

4 Ps

  • pain
  • pulelessness
  • paleness (pallor)
  • pins and needles (paraesthesia)
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11
Q

What is a free radical?

A

A molecule with a single unpaired electron in their outer orbit.

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12
Q

Give 3 examples of free radicals

A

H202, O- (superoxide), OH˚ (hydroxyl - most dangerous)

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13
Q

How are free radicals produced?

A

Metabolic reactions (oxidative phosphylation)
Inflammation (respiratory bursts by neutrophils)
Radiation (H20 into OH* + H)
Contact with unbound iron and copper (eg in haemochromatosis)
Drugs and chemicals (metabolism of paracetamol)

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14
Q

Give 3 methods of protection against free radicals

A

1) anti oxidants (vitamins A, C and E will donate them electrons
2) Metal carriers and storage compounds such as transferrin and ceruloplasmin sequester iron and copper which will give/ take electrons
3) enzymes that neutralise free radicals

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15
Q

What 3 enzymes neutralise free radicals?

A

Superoxide dismutase (SOD) - O2* to H2O2
Catalase - H2O2 to O2 + H20
Glutathione peroxidase

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16
Q

how do free radicals cause cell injury?

A
  • overwhelm antioxidant system
  • cause lipid peroxidation (electrons taken from lipids in membranes, causes a chain of redox reactions which produces more free radicals and disrupts membrane integrity)
  • oxidise proteins, carbs and DNA causing structural changes - i.e.: fragmentation or strand breaks
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17
Q

What system is in place to repair misfolded/ damaged proteins after cellular injury

A

Heat shock proteins/ unfoldases/ chaperonins will mend misfolded proteins

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18
Q

Give an example of a heat shock protein

A

ubiquitin, hsp70/hsp90

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19
Q

How can cell death be diagnosed under a microscope?

A

A dye exclusion test- living cells will not take up the special dye

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20
Q

Do injured (but not dead) cells look different under microscope to alive cells?

A

they look slightly swollen, small blebs may start to be seen, chromtin clumps, ER swells and ribosomes disperse, mitochondira swell

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21
Q

Define oncosis

A

The process of cell death by swelling and the associated spectrum of changes that occur due to injury prior to death

22
Q

Define necrosis

A

The morphological changes that occur after the cell has died in a living organism. These changes take 12- 24 hrs to occur.

23
Q

What process dominates in coagulative necrosis and in liquifactive necrosis ?

A

Coagulative- protein denaturation

Liquifactive- Enzyme release

24
Q

Where does coagulative necrosis occur and what does it look like?

A

Occurs in ischaemia of solid organs with connective tissue (kidneys, heart, adrenal glands). Cells have more pink staining and the GHOST OUTLINE OF THE CELL IS STILL PRESENT w/some neutrophil accumulation

25
Q

Where does liquifactive necrosis occur and what does it look like?

A

in loose tissue (brain) and/ or when there are many neutrophils present (infection). It just looks like a hole.

26
Q

When does caseous necorsis occur and what does it look like?

A

only found in infections, by far most common cause it TB. structurless debris is found without proper cell outlines.

27
Q

When does fat necrosis commonly occur?

A

Due to direct trauma to a fatty area- eg tennis ball hitting breast- creates hard lump which is often mistaken for cancer.
Also in pancreatitis due to lipase release

28
Q

What occurs in fat necrosis?

A

Lipases leak out and attack lipids. This causes lipids bonding with calcium and creates a hard soap which looks like candle wax.

29
Q

Why does reperfusion injury occur?

A
  • increased production of O2 free radicals with reoxygenation
  • increased number of neutrophils so more inflammation/tissue injury
  • delivery of complement proteins
30
Q

What will be abnormal in blood results in hepatits?

A

ALT and AST and LDH (from hepatocytes), bilirubin (no longer excreted), decreased albumin and raised PT and ammonia (liver not functioning properly)

31
Q

What will be abnormal in blood results for acute and chronic alcoholic liver disease?

A

acute- same as hepatitis

chronic- raised bilirubin, raised alkaline phosphate and raised gamma GT

32
Q

Where do alkaline phosphate and gamma GT come from? Other than chronic alcholic liver disease, when are they released?

A

they are plasma membrane enzymes. also raised with damage to bile canaliculus- eg gall bladder stones

33
Q

What is abnormal in blood results for acute pancreatitis?

A

serum amylase for first 24 hrs
serum lipase from 72-96 hrs
in 10% see glycosuria
hypocalaemia possible if precipitation of calcium salts in fat necrosis

34
Q

What effect does excessive alcohol intake have on the liver?

A
  • Fatty liver (steatosis) from fat deposition- acetaldehyde build up is toxic to hepatocytes, less lipoprotein synthesis so less lipid removal- liver is main center of lipogenesis
  • alcoholic hepatitis- alcohol and fat accumulation leads to hepatocytes injury and death, leading to inflammation
  • Cirrosis- fibrotic repair of the parenchyma leading to loss of function
35
Q

How does hepatitis B present?

A
  • infection so causes flu like symptoms but incubation period to 40-160 days
  • jaudice in 50-60% adults
  • anorexia
  • nausia
  • pain in upper right quadrant of abdomen
  • fever, malaise
  • hepatomegaly
36
Q

How can hepatitis B be diagnosed?

A

HBsAg, HBeAg (Heb B surface antigens)

37
Q

What is hereditary Haemochromatosis and its presentation?

A

where much more iron is absorbed from the diet so it is deposited in skin, liver, pancreas and endocrine organs.
present with tanned skin, tiredness, weakness, joint pain, amenorrhea, hypogonadism

38
Q

What are complications of hereditary Haemochromatosis and how is it treated?

A

Liver fibrosis and cirrhosis and hepatocellular carcinoma from iron overload, pancreatitis, heart failure/ arrhythmias, hypogonadism, diabetes

treat with regularly draining blood (phlebotomy)

39
Q

What is alpha1 antitrypsin deficiency and what is its effect?

A

Alpha1 antitrypsin is normally a protease inhibitor which deactivates the elastase produced by neutrophils at the sites of inflammation- due to infection or damage from smoking ect.
In lungs this leads to loss of elastin from alveoli walls and fibrosis which leads to mimicking of emphysema.
A1AT is produced in hepatocytes. Since is it defective it is not transported out the hepatocytes which leads to their death resulting in hepatitis, fibirosis and then cirrhosis in some people.

40
Q

What is the presentation and complications of alpha1 antitrypsin deficieny?

A

presentation:
- Symptoms similar to COPD- wheezing cough, emphysema, dynsopnea emerging in 30s/ 40s
- Most ppl get liver disease: jaundice, fibrosis
Complications
- liver failure, fibrosis, ciriohsis

41
Q

What are the 4 mechanisms of intra cellular accumulations due to cell injury?

A
  • abnormal metabolism
  • alterations in protein folding and transport
  • deficiency in critical enzymes
  • inability to degrade and phagocytose particles
42
Q

How does jaundice occur?

A

accumulations of bilirubin from haem breakdown
- bile flow obstructions
- liver failure
both mean it is deposited in macrophages or extracellualr space (first sclera, then skin, kidney, brain ect)

43
Q

What is calcification?

When does localised calcification occur ?

A

Abnormal deposition of calcium salts within tissues

when tissues are dying- eg in atheromatous plaques, aging, damaged valves, TB ect)

44
Q

Why does general calcification occur?

A

abnormal calcium metabolism (possibly due to increase in parathyroid hormone) causing hypercalcaemia - so due to hypercalcaemia in otherwise healthy tissue.

45
Q

What would be seen microscopically in a liver of an alcoholic?

A

Mallory’s hyaline cells- cells with clumps of cytokeratin in
Fat deposits
Fibrosis

46
Q

What are the main differences in structural changes between apoptosis and oncosis?

A
  • cellular contents intact vs enzymatic degradation
  • single cell vs contiguous groups of cells
  • membrane integrity maintained vs disrupted
  • Cell shrinks vs Cell swells
  • often physiological vs often pathological
47
Q

How is apoptosis triggered?

A

INTRINSIC MECHANISM: DNA damage usually, P53 activated, outer mitochondrial membrane becomes leaky, cytochrome C released, activates caspases
EXTRINSIC MECHANISM: signals like TNFa from T cell in response to foreign cells bind to death receptors, caspase 8 activates, which activates caspase 3

48
Q

Describe what happens in apoptosis

A
  • DNA and proteins in cytoplasm degraded in controlled manner
  • cells shrinks and condenses (looks smaller and darker red under microscope)
  • parts of cell wall budd off
  • fragments phagocytosed without inflammation
49
Q

What leads to intracellular accumulations? (4)

A
  • abnormal metabolism
  • alterations in protein folding and transport
  • deficiency of crucial enzymes
  • inability to degrade phagocytosed particles
50
Q

What are the 4 pathological stages of lobar pneumonia?

A
  1. congestion- exudate forms due to vascualr congestion
  2. red hepatisation- lots of neutrophils and rbc and fibrin means exudate becomes fibrous
  3. grey hepatisation- lung tissue goes from red to grey as it dries and rbcs are lysed
  4. resolution- exudate us enzymatically digested
51
Q

What are complications of lobar pneumonia?

A
  • pleural effusion
  • lung fibrosis
  • meningitis, endocarditis ect if spread into blood
  • abcesses
  • emphysema

Pathological processes (8 decks)

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