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Pathology-Alaa > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

What type of cell does paracetamol damage

A

Liver hepatocytes

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2
Q

Give some causes of cell injury and death (6)

A 
Infection
Hypoxia
Chemicals & drugs
Physical agents ( radiation , trauma)
Nutritional factors (dietry insufficiency)
Immunological factors
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3
Q

tuberculosis- What category of agent causes this cell injury?

A

Immunological

Infection

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4
Q

Give an example of a case in which a change in the blood deprives the neurones of a vital nutrient and leads to cell injury.

A

Hypoglycaemia in blood, and brain gets its nutrients directly from glucose ( if diabetic patient injects too much insulin)

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5
Q

cell can become injured as a result of damage to any of four vital structures:

A
  • Er
  • mitochondria
  • nucleus
  • membranes
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6
Q

What structures would be damaged by taking cyanide? What does it imterfere with

A

Mitochindra-oxidative phosphorolation

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7
Q

What about hypoxia? Which structure does it damage

A

Membranes

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8
Q

The point of no return for the cell( irreversible damage) is thought to be marked by influx of a certain ion

A

Ca+

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9
Q

type of cell death that results from this massive influx of calcium into the cytosol is given a special name.

A

Necrosis

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10
Q

Whenever there are necrotic cell we find an inflammatory reaction.

Indeed, we can often recognise necrosis because of the inflammation.

A

Just saying

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11
Q

when the cell membranes break down, an important mediator is formed from the phospholipid that makes up the membrane itself.

What’s this mediator called?

A

It’s called arachidonic acid.

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12
Q

What is function of arachadonic, how does is mediate inflammation

A

Arachidonic acid then breaks down into chemicals, ( prostaglandins and leukotrienes) which mediate various components of the acute inflammatory reaction

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13
Q

What term is applied to the changes that occur in the membrane when free radicals damage it

A

Lipid peroxidation

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14
Q

cell can be digested by its own enzymes? What effect does this have on the cell?

A

Autolysis, can cause the tissue to become soft.
So infarcts in the heart or brain often become soft.
This makes the tissue liable to break down and even burst.

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15
Q

This time it’s a young woman, who becomes very ill, with nausea and vomiting. She becomes jaundiced and is brought into hospital. She’s thought to have hepatitis. What can be measured

A

ALT
AST
GT

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16
Q

Explain what happens when cell injury becomes irreversible & how the changes trigger the inflammatory response

A

The membranes become damaged. The cell membrane damage leads to water influx due to breakdown of the sodium-potassium pump. Calcium also enters the cell.
Calcium also flows out of the mitochondria (mitochondrial permeability transition) and the enzymes there stop functioning. Calcium flows from endoplasmic reticulum and lysosomes into the cytosol, where the level rises very highly.

Phospholipase becomes activated and digests the cell membranes, releasing, among other things, arachidonic acid, which breaks down to form inflammatory mediators, such as prostaglandins and leukotrienes. These attract neutrophils and promote the other aspects of acute inflammation.

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17
Q

Causes of hypoxia can be classified as:

A

Hypoxemic
Anemic
Ischeamic
Histoxic

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18
Q

What is ischemic reperfusion injury

A

When blood flow is restored to an “ischemic cell” is restored.
The absence of oxygen and nutrients from blood during the ischemic period creates a condition in which the restoration of circulation results in inflammation and oxidative damage through the induction of
oxidative stress rather than restoration of normal function.

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19
Q

What are free radicals? How do they cause damage?

A

Free radicals are reactive oxy species, they have an unpaired electron, and this makes them to want to “steal” an electron from a neighbouring atom.
»attach lipids on membrane&raquo_space; lipid peroxidation
»damage proteins, carb, nucleic acids

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20
Q

Name 3 free radicals

A

OH hydroxyl(most damage)
02- superoxide
H202 hydrogen peroxide

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21
Q

What r the antioxidant system in our body? and how does each work (3)

A

Enzymes> neutralise free radicals (catalase, superoxide dismutase, glutathione peroxidse)
Vit A C E
Storage proteins and metal carriers (transferrin) > sequester iron and copper

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22
Q

What are heat shock proteins? how to they function? name some

A

HSPS, ex: ubiquitin, stress proteins, unfoldases, chaperonins

ta9fee6 il malabis ;P
***They MEND other proteins, so when other proteins r misfolded or damaged as a result of injury, they bind to them and guide them through proper folding

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23
Q

What r the 2 main types of necrosis? And how do they appear on a microscope? give an example of which organ can u see each one?

A

1) Liquafactive»enzyme release» cant really see shit…Brain
2) Cooagulative»protein denaturation in cell, and clumps> ghost like…kidney

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24
Q

What is gangrene, name 2 types

A

Necrosis visible to the naked eye

Dry~ exposed to air
Wet~ Liquafactive necrosis

Gas gangrene is wet gangrene w/ infectivd mixed bacterial culture (exudate)

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25
Q

What is an infarction? infarct?

A

Necrosis caused by reduction in blood supply

an AREA of necrotic tissue which is the result of loss of arterial blood supply.

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26
Q

What is gas gangrene ? Feautures?

A

Motercycle pic in lecture
caused by ANEROBIC bacteria in soil that enter the wound causes gas gangrene

Feature> palpable bubbles of gas w/ in the tissue

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27
Q

What is caseous necrosis? What does it look like?

A

Caseous necrotic debris (looks like cottage cheese). MOSTLY IN TB

(Fits in btw coagulative and necrotic)

U get a mess

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28
Q

What r 2 common causes of infarction

A

Thrombosis

Embolism

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29
Q

Red and white infarction, in which type of organ does each occur in?

A

White infarction (anaemic)»SOLID organs > in end arteries mostly, no blood supply, often wedge shaped, coagulative necrosis

Red» Infarct complicated by HEMMORHAGE > blood leaks and u becomes read (happens mostly to Loose tissues)

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30
Q

When membranes become leaky, can molecules leak out as well?

A

Yes

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31
Q

What r the 3 important things that leak out of the cell

A

Pottasium» leads to cardiac
Enzymes» troponin/AST/Ck
Myoglobin

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32
Q

It takes ________to be able detect the morohological changes in a necrtotic tissue under a light microscope. (Ex MI)

A

12-24 hrs

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33
Q

What is pathalogical calcification

A

Abnormal deposition of ca salts in within tissues

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34
Q

In what case do u see lipids accumalating into the cells? Why?

A

In steatosis (fatty liver) bc that where most fat metabolism occurs

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35
Q

What causes a fatty liver?

A
  • diabetes
  • obesity
  • alchohol
  • toxins
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36
Q

In what clinical conditions to proetins accumalate in cells?

A
  • Emphysema ( lack of a1- antitrypsin ) u get accumaltes of proteases in lung
  • alcholoic liver disease (mallorys hyaline) damaged keratin filaments
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37
Q

What is accumalating in jaundince

A

Bilirubin, (breakdown if heme)

38
Q

Dystrophic vs metastatic calcification

A

-Dystrophic is localized ; more common
There is no abnormality in calcium salts, but the disturbance of the tissue favoured deposittion of hydroxyapatite crystals.

-Metastatic (usually asymptomitic but LETHAL)
Hydroxyapetite is laid down due to disturbed calcium metabolism that caused hypercalcemia!

***METAstatic=METAbolism

39
Q

Blebbing happens in ________

Buddimg happens in________

A

Necrosis

Apoptosis

40
Q

What r the 3 steps of apoptosis?

A

1) initiation
2) execution
3) degredation and phagocytosis

41
Q

In apoptosis, does the cell shrink or swell?

how do phagocytes recognise them?

A

Shrink, and form apoptotic bodies, that express proteins on their surfaces, these r recognised by phagocytes.

42
Q

The plasma membrane in apoptosis is intact/lysed?

A

Intact

43
Q

When does fluid accumalate in the cells? In which organ is this a serious problem amd why?

A

When they get hypoxic, low 02, more na & water flood inside the cell.
In the brain, bc the brain sitsin a restricted area.

44
Q

What is heridetary haemochromatosis, which organs r mostly effected? how do patients look like? how do u treat it?

A

Genetically inherited disorder, Increased absorbtion of IRON.
excess iron is deposited as hemosdierin in various organs, skin, (mostly with liver cihrossis and pancreas scarring) .

bc iron is deposited in skin, they look tanned!

-just bleed the patient!!

45
Q

What r mallory bodies? What causes them

A

Deposits of clumped abmormal cytoskeletal filaments in hepatocytes
Alchohol

46
Q

What is karyolysis? pyknosis?

A

Nucleus just gradually disappeared. This is due to digestion of the DNA in the nucleus by certain enzymes that are released by the injured cell.

is the irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis.

47
Q

what enzymes have digested the nuclei to give it this karyolytic appearance?

A

Enzymes called endonucleases break down the DNA in karyolysis.

48
Q

___________&___________are the most common types of change we see in the NUCLEUS when the cell dies. If we see these changes, we can say for certain that the cell is dead, deceased, no more: no ifs and buts about it.

A

Karyolysis & pyknosis

49
Q

Eosinophilia is an early sign of necrosis. Why does this pink staining occur?

A

It happens because cytoplasmic proteins become denatured, leading to increased exposure of basic amino acid groups, which react with acidic dyes, such as eosin.

50
Q

Example of coagulative necrosis would be in

A

MI

51
Q

What’s the aetiological mechanism underlying this type of necrosis (colliquative necrosis)?

A

Hypoxia

52
Q

In apoptosis, in contrast to necrosis, there’s no inflammatory reaction.

Why is this so?

A

apoptosis, the bits of dead cell wrapped in plasma membrane So the fragments are never exposed to the extracellular environment and thus aren’t exposed to the immune system.

53
Q

How do free radicals damage cells

A
  • cause lipid peroxidation

- oxidise proteins (cross-link them), carbs & DNA

54
Q

What causes hypercalcemia?

A
  • increased secretion of PTH>resulting in bone resorption

- destruction of bone tissue

55
Q

Oncosis, necrosis, apoptosis

A

Oncosis» cell death with swelling
Apoptosis» cell death with shrinking
Necrosis» morphological chnages that occur AFTER death

56
Q

Give a common comdition of fat necrosis in the body

A

PANCREATITIS

Digestive Enzymes Leak out from pancreas into the abdominal cavity and attack the lipids in the abdomial cavity and break down the triglycerides, and the fatty acids produced will react with calcium forming CA soaps

Or they get into bv and u can detect them

57
Q

Anastomoses is different than dual blood supply

A

Dual blood supply, organ is getting blood supply from 2 seperate places (lungs)
Anastomoses, u know it alaa

58
Q

Graft vs host disease

A

…

59
Q

What do injured and dying cells look like jnder a microscope?

A
  • cytoplasmic changes
  • Nuclear changes
  • cellular accumalations
60
Q

Why is it bad to suddenly reperfuse an ischemic tissue?

A

It can lead to ischemic-reperfusion injury,

When u reperfuse highly oxygenated blood to an acidic hypoxic tissue, Its an environment that can produce FREE RADICALS!

61
Q

Function of igG antibody in infkammation

A

Most importamt opsonin, not oreseny when bacterium is encountered for the 1st time

62
Q

Apoptosis

A

Extrinsic» caspase 8

intrinsic&raquo_space; mitochondra release cytc C,APAF,cas 9

63
Q

Whats the organelle in the cell is related to intrinsic apoptosis

A

Mitochondria center
Cytocrome C leaves
And binds to APAF 1 & caspase 9

Which will work on CASPASE 3

64
Q

In apoptosis what is the convergence point in the cell

A

Caspase 3

65
Q

Role lf p53 in apoptosis? BCL-2

A

BCL-2 is prevents release of cyt C from the mitochondria
Less apoptosis occurs

**If it is over-expressed it causes CANCER

66
Q

explain in steps what happens during hypoxia

A
  1. Cell deprived of oxygen.
  2. Mitochondrial ATP production stops.
  3. The ATP-driven membrane ionic pumps run down.
  4. Na and water seep into the cell.
  5. The cell swells, and the plasma membrane is stretched.
  6. Glycolysis enables the cell to limp on for a while.
  7. The cell initiates a heat-shock (stress) response (see below), which
    will probably not be able to cope if the hypoxia persists.
  8. The pH drops as cells produce energy by glycolysis and lactic acid
    accumulates.
  9. Calcium enters the cell.
  10. Calcium activates:
    • phospholipases, causing cell membranes to lose phospholipid, • proteases, damaging cytoskeletal structures and attacking
    membrane proteins,
    • ATPase, causing more loss of ATP,
    • endonucleases, causing the nuclear chromatin to clump.
  11. The ER and other organelles swell.
  12. Enzymes leak out of lysosomes and these enzymes attack
    cytoplasmic components.
  13. All cell membranes are damaged and start to show blebbing.
  14. At some point the cell dies, possibly killed by the burst of a bleb.
67
Q

what happens if hypoxia is prolonged? what will the increased intracellular Ca+ activate? (4)

A

damage becomes irreversible.
massive influx of ca+ in cell

Activates enzymes!

  • ATPase> less ATP
  • Phospholipase>less phospholipids
  • Protease>cytoskeletal proteins destroyed
  • endonuclease>nuclear chromatin damage
68
Q

what is an end artery?

A

any artery that is the sole source of arterial blood to a segment of an organ

69
Q

what is emphysema?

A

a type of (COPD) involving damage to the air sacs (alveoli) in the lung.

Smoking»oxidizes a very important methionine chain in A1-ANTITRYPSIN (enzyme responsible to inhibit proteases in the lungs)

70
Q

what r the 3 enzymes that act as antioxidants? what do these enzymes do?

A

Enzymes> neutralise free radicals

  • catalase
  • superoxide dismutase
  • glutathione peroxidse)
71
Q

______necrosis occurs in solid tissues, like the kidneys..

A

coagulative

72
Q

intrinsic pathway vs extrinsic pathway in apoptosis?

A

Intrinsic pathway: signal come inside cell
P53 is activated
causes mitochondrial membrane to become leaky
Cytocrome c is released & activates caspases

Extrinsic pathway: signal comes from bara
triggered by tumor cells, virus cells
immune cells (t-killer) secrete TNFa
bind to 'DEATH recepters"
Capases activated!

ur notes alaa.

73
Q

when do pigments accumalate in cells?

how do these pigments reach peribronchial lymph nodes?

A
  • carbon/coal dust in air
  • inhaled and phagocytosed by alveolar macrophages

**alveolar macrophages will migrate from alveoli to the peribronchial lymph nodes and get trapped there

74
Q

what in anthracosis?

A

A chronic lung disease resulting from repeated inhalation of coal dust

75
Q

how does tattoos cause pigmentation? how does this reach the lymph nodes?

A

pigments is picked up by MACROPHAGES in the dermis and stay there> tattoo stain.

some macrophages will drain in the lymph nodes.

76
Q

what was once called bronze diabetes? why?

A

heridetery hemochromatosis,

bronze colour due to deposits of hemosiderin in skin & they used to get diabetes cuz their pancreas was being destroyed.

77
Q

It what cases can u get increased secretion of PTH? (3)

A

1) tumour of parathyroid
2) renal failure>retention of phosphate
3) ectopic> secretion of PTH by malignant tumors.

78
Q

It what cases can u destruction of bone tissue? (4)

A

1) primary tumor of bone marrow ex: leukaemia, multiple myeloma
2) immobilsation
3) pagets disease> accelerated bone turnover
4) diffuse skeletal metastases

79
Q

ends of chromosomes r called _____, white every replication the ______is ______.

A

telomeres= shortened.

when the telomeres reach a certain length, the cell can no longer divide.

80
Q

wha tis the function of telomerase? which cells have em?

A

it maintains the original length of telomeres, to make them live longer (ends of chromosomes that shorten within each replication).

GERM CELLS + STEM CELLS
cancer cells too!

81
Q

which enzymes/proteins will be elevated in the blood and why.

Hepatitis (4)

A
  • Raised serum ALT, AST and LDH. These are cytosolic hepatocellular enzymes and their presence in the blood indicates poor hepatocyte integrity.
  • Raised bilirubin (often conjugated) – indicates poor biliary excretory function.
  • Decreased albumin, raised PT (reliant on factors 2,7,9,10 produced by the liver),

raised ammonia – these findings indicate poor hepatocyte function.

82
Q

which enzymes/proteins will be elevated in the blood and why.

· Acute pancreatitis (4)

A

Raised serum amylase in first 24 hours.

Raised serum lipase from 72-96 hours.

In 10% see glycosuria.

Hypocalcaemia possible – due to precipitation of calcium salts in fat necrosis

83
Q

what r troponins? when do the peak?

A

Troponins are proteins that regulate contraction of muscle. They are increased in the blood at 2-4 hours post-MI and peak at 48 hours. They remain elevated for 7-10 days.

84
Q

you get____ necrosis when theres lots of neutrophils (mostly during inflammation)

A

liquafactive necrosis

85
Q

infarct in the brain is healed by____

A

gliosis

is a nonspecific reactive change of glial cells in response to damage to the central nervous system (CNS)

86
Q

do u see apoptosis in liver in hepatitis?

A

yas.

87
Q

The following would undergo irreversible cell injury within 60 minutes of complete cessation of blood supply? choose

a) myocardium
b) motor neurons
c) skeletal muscle
d) renal tubules
e) chondrocytes

A

a) myocardium
b) motor neurons
d) renal tubules

88
Q

Alcoholic liver disease

A

Acute alcoholic liver disease – a hepatic picture is seen. Chronic alcoholic liver disease – fulminant liver failure is seen.

Raised bilirubin, raised alkaline phosphatase, raised gamma GT (glutamyl transpeptidase). (NB: See raised alkaline phosphatase and gamma GT with damage to bile canaliculus (these are plasma membrane enzymes)).

89
Q

which enzymes/proteins will be elevated in the blood and why.

-Myocardial infarction

A

We measure blood levels of intracellular macromolecules that leak out of fatally injured myocardial cells through damaged cell membranes.

Now we measure primarily CARDIAC TROPONIN (TnT), troponin I (TnI), creatine kinase (CK, CK-MB), lactate dehydrogenase (LDH) and myoglobin.

Troponins are proteins that regulate contraction of muscle.

90
Q

when do Troponins increase in the blood? peak in the blood? how long do they remain for?

A

They are increased in the blood at 2-4 hours post-MI

PEAK at 48 hrs (2 ays)

They remain elevated for 7-10 days.

91
Q

When does apoptosis occur normally?

A

Embyrogeneis
Scultpting
Matamorphosis (butterfly)

92
Q

When does apoptosis occur normally?

A

Embyrogeneis
Scultpting
Matamorphosis (butterfly)

Pathology-Alaa (16 decks)

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