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ESA2 Callum's Cards - Complete > MoD S1+2 - Cell Injury > Flashcards

MoD S1+2 - Cell Injury Flashcards

1
Q

What is the difference in cell response to mild versus severe changes in environment?

What if the cell cannot respond appropriately?

A

Cells can maintain homeostasis when subject to mild changes

Cells must undergo physiological and morphological changes to attempt to stay viable in the face of severe change

If the cell cannot respond appropriately (have reached the limits of their adaptive response) they show evidence or reversible injury or irreversible injury and death

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2
Q

What are the major causes of cell injury?

A 
Hypoxia
Physical agents
Chemical agents and drugs
Microorganisms
Immune mechanisms
Dietary insufficiency or excess
Genetic abnormalities
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3
Q

What is the result of hypoxia in general terms?

A

Results in decreased aerobic respiration (although glycolytic respiration can continue)

If this is persistent this can cause Atrophy, cell injury or cell death

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4
Q

What are the 4 major types of hypoxia?

Give a brief description and example of each

A

Hypoxaemic:
Arterial pO2 is low E.g. Reduced inspired PO2 at altitude

Anaemic:
Decreased ability for haemoglobin to carry O2 E.g. anaemia, CO poisoning

Ischaemic:
Interruption to blood supply E.g. Vessel blockage

Histiocytic: Inability to utilise O2 in cells due to disabled oxidative phosphorylation E.g. Cyanide poisoning

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5
Q

What is meant by Ischaemia and what causes it?

A

Loss of blood supply caused by:

Reduced arterial supply (obstruction of artery, hypotension)

Reduced venous drainage

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6
Q

Why does Ischaemia cause more severe damage than other forms of hypoxia?

A

Reduced supply of oxygen AND respiratory substrates E.g. Glucose leads to damage occuring more rapidly and more severe damage than hypoxia

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7
Q

How does the length of time cells can tolerate hypoxia vary? Give examples

A

Differs greatly between cell types

Eg. Some neurones can only tolerate minutes, while fibroblasts can tolerate a number of hours

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8
Q

What occurs during reversible hypoxic injury?

Hint: One direct result of hypoxia leads to 3 main effects of this, each with their own concequences

A

As the cell becomes deprived of oxygen, there is a decrease in ATP production by oxidative phosphorylation.

When ATP concentrations fall to 5-10% of normal concentrations, cellular process are interrupted:

  • Loss of Na+/K+ pump activity causing intracellular Na+ concentration to rise causing swelling. Ca2+ also enters the cell and damages cellular components
  • Cell switches to anaerobic glycolysis for energy resulting in reduced pH intracellularly, low pH affects many enzymes, chromatin clumping is also seen
  • Ribosomes detach from RER and protein synthesis is disrupted, this results in accumulations of fat and denatured proteins in the cell
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9
Q

When does cell injury progress from reversible to irreversible?

A

Not really known/not well understood

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10
Q

What is the result of irreversible hypoxic injury?

Hint: Don’t go into detail on the effects of Calcium

A

Usually appears as necrosis

Profound disturbances in membrane integrity

Massive cytosolic accumulation of Ca2+

Intracellular substances leak out into circulation (E.g. Enzymes such as transaminases from liver cells) and can indicate cellular damage is occuring

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11
Q

How is Ca2+ involved in irreversible cell damage?

What is the effect of Ca2+ accumulation on a cell experiencing irreversible damage?

A

Ca2+ enters cells across the damaged plasma membrane and is released from stores in the RER and mitochondria causing Cytosolic build-up

Activates a host of enzymes such as:

ATPases - reduce ATP concentration further

Phospholipases - Cause further membrane damage

Proteases - Breakdown of membrane and cytoskeletal proteins

Endonucleases - Breakdown DNA

Causes leakage of lysosymes (by causing enzymes to damage their membranes) and hence further cell damage

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12
Q

What is Ischaemia-reperfusion injury?

A

Tissue injury can be worse if blood flow is restored and the tissue is not yet necrotic

This may be due to:

  • Increased production of ROS with reoxygenation
  • Increased number of neutrophils causing more inflammation and injury
  • Delivery of complement proteins and activation of complement pathway
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13
Q

Give examples of physical agents that may cause cell damage

A 
Direct Trauma
Extreme temperatures
Sudden change in atmospheric pressure
Electric currents
Radiation
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14
Q

Give examples of chemical agents and drugs that might cause cell damage

A 
Glucose or salt in hypertonic solutions
O2 at high concentrations
Poisons
Insecticides
Herbicides
Asbestos
Alcohol
Illicit drugs
Therapeutic drugs
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15
Q

How might immune mechanisms lead to cell damage?

A

Hypersensitivity reactions where the host tissue has an overly vigorous immune reaction and causes injury (E.g. Urticaria)

Autoimmune reactions where the self is mis-identified as the non-self (E.g. Grave’s disease)

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16
Q

What are the 4 components of cells that are the principal targets for cell injury?

A

Cell membranes
Nucleus
Proteins
Mitochondria

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17
Q

How does chemical damage to a cell occur?

Give an example

A

Some chemicals will act by combining with a cellular component

E.g. Cyanide binds to mitochondrial cytochrome and blocks oxidative phosphorylation

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18
Q

What types of injury produce high levels of free radicals?

A 
Chemical
Radiation
Ischaemia reperfusion
Cellular ageing
High O2 concentration
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19
Q

What are some of the effects of free radicals on cells?

A

Attack membrane lipids and cause lipid peroxidation

Damage proteins and nucleic acids

Mutagenic

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20
Q

What are the three free radicals of biological significance?

A

OH* - Most dangerous

O2- (superoxide)

H2O2

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21
Q

How are OH* free radicals formed?

A

Radiation can directly lyse water

Fenton and Haber-Weiss reactions produce OH* from H2O2 and O2- (Note: This is one reason to remove these ROS quickly, to prevent OH* being formed)

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22
Q

Briefly, how is the body protected against free radicals and why it important for this to exist?

A

The anti-oxidant system protects against free radicals

Imbalance in free radial production and scavenging leads to ROS build up and cell injury (This is oxidative stress)

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23
Q

What 3 elements is the anti-oxidant system comprised of?

Give a brief explanation of each

A

Enzymes:

  • Superoxide dismutase (SOD) catalyses the O2- —–> H2O2 reaction (H2O2 is less toxic)
  • Catalases and peroxidases complete the process of ROS removal (H2O2 —–> O2 + H2O

Free radical scavengers such as:
Vitamins A, C and E
Glutathione

In the extracellular matrix storage proteins (E.g. Transferrins and ceruloplasmin) sequester transitional metals (E.g. Copper and iron) which catalyse the formation of free radicals

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24
Q

What is the function of heat shock proteins?

A

When protein folding or denaturation they ensure they are refolded correctly

If not possible, the protein is destroyed

Heat shock response plays a role in maintaining viability of proteins and thus maximising cell survival

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25
Q

What are the three main changes seen in cells seen with cell injury?

A

Cytoplasmic changes:

  • Reduced pink staining due to accumulation of water (reversible)
  • Followed by increased pink staining due accumulation of denatured proteins and ribosomes that have detached from the RER (irreversible)

Nuclear changes:

  • Chromatin clumped slightly (reversible)
  • Pyknosis (shrinkage), Karryohexis (fragmentation) and karryolysis (dissolution) of the nucleus (irreversible)

Abnormal cellular accumulations

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26
Q

What reversible changes to injured cells can be seen with an electron microscope?

Give a brief reason for each

A

Swelling of both cell and organelles due to Na+/K+ pump failure

Blebs - (small area of detachment of the plasma membrane from cytoskeleton, appears as a small swelling)

Clumped Chromatin due to low pH

Ribosomes separation from RER due to failure of energy dependant process that keeps ribosomes attached.

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27
Q

What irreversible changes to injured cells can be seen with an electron microscope?

A

Further cell swelling

Nuclear changes (pyknosis, karryohexis, karryolysis)

Swelling or rupture of lysosymes

Membrane defects/damage

Appearance of myelin figures (which are damaged membranes)

Lysis of ER due to membrane defects

Amorphous densities

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28
Q

Define Oncosis

A

The spectrum of changes that occurs in injured cells prior to death

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29
Q

Define Necrosis

A

The morphological changes that follow cell death in living tissue, largely due to the progressive degradative action of enzymes on a lethally injured cell

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30
Q

Where is necrosis found?

What does it cause?

What kind of timescale does it occur on?
Give an example of this

A

Necrosis is found where there is damage to the cell membranes and lysosomal enzymes are released into the cytoplasm and digest the cell

As a result cell contents often leak out and inflammation is often seen, the ultrastructural changes are those seen in irreversible cell injury

Necrotic changes develop over a number of hours (E.g. after Myocardial infarction it takes 4-12 hours before microscopic changes are seen)

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31
Q

What happens to necrotic tissue?

A

Normally removed by enzymatic degradation and phagocytosis by white cells

Any remnants may calcify (dystrophic calcification)

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32
Q

What are the two main types of necrosis?

What are the two special types that may only occur in a limited set of circumstances?

A

Normal:

Liquefactive
Coagulative

Special:

Caseous
Fat necrosis

33
Q

Describe coagulative necrosis

Hint: What it is, progression

Where is it commonly seen?

A

Denaturation of proteins dominates over release of active proteases

Dead tissue has a solid consistency due to protein clumping

Cellular architecture is somewhat preserved, this forms a ‘ghost outline’ of cells

This ghost appearance is only seen for a few days, after that the appearance is modified by acute inflammatory reaction to the dead tissue with consequent infiltration of phagocytes

Commonly seen in solid organs that have experienced ischaemia

34
Q

Describe Liquefactive necrosis

Hint: What, Where, Concequences

A

Active enzyme degradation is substantially greater than denaturation and this leads to enzymatic digestion of the tissues (liquefaction)

Often seen in massive neutrophil infiltration (E.g. In abscesses) because neutrophils release protease

Also commonly found in bacterial infection and the brain (Fragile tissue without support from collagenous matrix)

Tissue becomes a viscous mass and if there is acute inflammation there is pus present

35
Q

Describe the appearance of Caseous necrosis

What is it commonly associated with?

A

Has a cheesy appearance macroscopically

Characterised by amorphous debris (no ghost outlines)

Particularly associated with infection, especially Tuberculosis.

Often associated with granulomatous inflammation

36
Q

Describe Fat necrosis

Hint: Appearance, 2 causes

A

Occurs where there is destruction of adipose tissue

Causes release of fatty acids which can react with calcium to form chalky deposits (calcium soaps) in fatty tissue, these can been seen in X-rays and with the naked eye in surgery or autopsy

Typically seen as a consequence of acute pancreatitis as there is release of lipases from the pancreatic acinar cells, causing fat necrosis in the abdominal cavity.

Also occurs after direct trauma to fatty tissue, especially breast tissue, can leave an irregular scar after healing which may mimic a cancerous breast nodule

37
Q

What is gangrene?

A

NOT a ‘type’ of necrosis

It’s the clinical term used to describe necrosis that is visible to the naked eye

Gangrene can be ‘dry’ (coagulative necrosis) or ‘wet’ (liquefactive)

Wet gangrene is normally due to infection and can result in septicaemia

Gangrene is seen most commonly clinically as a result of ischaemic limbs

Gangrenous tissue is dead and cannot be salvaged

38
Q

What is an Infarct?

What can cause an infarct?

A

An area of Ischaemic necrosis

Can result in gangrene

Mostly due to thrombosis or embolism

Can also be due to:

External compression of a vessel (by tumour or within a hernia)

Twisting of a vessel (E.g. Testicular torsion)

39
Q

How does necrosis due to infarction present?

Give examples of the presentations

How else can infarcts be classified?

A

Necrosis due to infarct can present as liquefactive (E.g. Cerebral infarction) or coagulative (E.g. Myocardial infarction)

Can be described by colour, white or red

40
Q

Describe how white infarct appear and how/where they commonly present

What type of necrosis is present?

A

White occurs in solid organs with good stromal support after the occlusion of an ‘end’ artery (i.e. an artery which is the sole arterial supply for a segment of the organ

The solid nature of the tissue limits the amount of haemorrhage that can occur into the infarct from adjacent capillaries

Appears white due to the lack of blood into the tissue

Commonly occur in the heart, spleen and kidneys

Most are wedge shaped with the occluded edge at the apex

Coagulative necrosis

41
Q

What is a red infarct?

A

An infarction that results in significant haemorrhage

42
Q

In what situations can red infarcts appear?

Hint: 5 appearances

Provide examples of where each may occur if possible/applicable

A

In organs with dual blood supply (E.g. Lungs) Occlusion of the main artery causes infarct, the secondary supply is insufficient but does allow blood to enter, hence red infarct

If numerous anastomoses (capillary beds of two separate arterial supplies merge) are present (E.g. Intestines) red infarct appears for same reason as above

In loose tissue (E.g. Lung) where there is poor stromal support for capillaries there is therefore more than normal haemorrhage into the dead tissue

Where there has been previous congestion (E.g. Congestive heart failure) there is more than normal amount of blood in the necrotic tissue

Where there is raised venous pressure, pressure is transmitted to capillary beds, as tissue pressure rises there is reduced arterial filling pressure in the tissue that causes ischaemia and necrosis, because tissue was previously engorged with blood a red infarct appears

43
Q

What does the severity of an infarct depend on?

A

Whether the tissue has an alternative blood supply (E.g. In the lung and forearm)

How quickly the ischaemia occurs (if slowly there is time for additional perfusion pathways to develop)

How vulnerable a tissue is to hypoxia

The oxygen content of the blood (an infarct occurring in an anaemic patient will be more serious)

44
Q

Define Apoptosis

A

Cell death induced by a regulated intracellular program where a cell activates enzymes that degrade its own nuclear DNA and proteins

45
Q

Where is apoptosis seen?

A

When cells are no longer needed to maintain a steady state

During hormone controlled involution

Cytotoxic T cell killing of virus infected cells or neoplastic cells

Embryogensis

46
Q

When does apoptosis occur?

A

When a cell is particularly damaged, particularly when damage is to the cell’s DNA or proteins

47
Q

How do apoptic cells appear under a light microscope?

A

Shrunken

Intensely eosinophilic

Chromatin shrinkage

Pyknosis, karryohexis

Affects single cells or small groups

48
Q

How do apoptic cells appear under an electron microscope?

How does this appearance change as apoptosis progresses?

A

Cytoplasmic blebbing is seen in addition to those features found in light microscopy

Blebbing progresses to fragmentation into membrane bound apoptic fragments which contain organelles and nuclear fragments

These fragments are eventually removed by macrophages

49
Q

Why does apoptosis not cause inflammation?

A

No leakage of cell contents

50
Q

What are the three key stages of apoptosis?

A

Initiation

Execution

Degradation/Phagocytosis

51
Q

Describe the initiation phase of apoptosis

A

Triggered by intrinsic and/or extrinsic processes which both result in the activation of capases

Extrinsic apoptosis is ligand driven (as a result of ligand binding) such as TRAIL or Fas that bind to death receptors leading to capase activation

Intrinsic apoptosis has mitochondria as a central player, all apoptic machinery is internal to the cell

Various triggers including DNA damage, withdrawal of growth factors, hormones or p53 protein

Triggers lead to increased mitochondrial permeability resulting in the release of cytochrome c from mitochondria, this interacts with APAF1 and capase 9 to form an apotosome the activates various downstream capases

52
Q

Describe the execution phase of apoptosis

A

Capases are released

They are proteases that mediate the cellular effects of apoptosis

They act by cleaving proteins breaking up the cytoskeleton and initiating the degradation of DNA

53
Q

Describe the Degradation/Phagocytosis phase of apoptosis

A

Cell breaks into membrane bound fragments called apoptic bodies

They express molecules on their surface that induce their phagocytosis by neighbouring cells or phagocytes

54
Q

What are the important apoptic molecules?

A

p53 - ‘Guardian of the genome’ that mediates apoptosis in response to DNA damage

Cytochrome c, APAF1, capase 9 - together they are the apoptosome

Bcl-2 - Prevents cytochrome c release from mitochondria therefore inhibits apoptosis

Death ligands - E.g. TRAIL

Death receptors - E.g. TRAIL-R

Capases - Effector molecules of apoptosis

55
Q

What are abnormal cellular accumulations?

What might they consist of?

A

Occurs with sublethal or chronic injury when metabolic processes become deranged.

May be reversible or toxic

Can consist of:

Normal cellular constituents - E.g. Water, Lipids, Proteins, Carbohydrates

Abnormal substances - exogenous such as minerals or endogenous such as the products of abnormal metabolism

Pigments - Endogenous or exogenous

56
Q

What are two common types of abnormal lipid accumulation?

A

Steatosis

Cholesterol accumulation

57
Q

What is steatosis?

What are the causes of steatosis and where it is commonly found?

Does it affect cell function?

A

Accumulation of triglycerides

It is often seen in the liver (major site of lipid metabolism)

Common causes of liver steatosis include:

Alcohol abuse
Diabetes
Obesity
toxins (E.g. Carbon tetrachloride)

Mild steatosis doesn’t appear to affect function, more severe will have an effect

58
Q

Where is cholesterol likely to be found abnormally accumulating?

What effect does it have on cells?

A

Accumulates in smooth muscle cells and macrophages within athersclerotic plaques

Microscopically these cells appear to have foamy cytoplasm, so are known as ‘foam cells’

Also seen in macrophages in the skin of people with familial and acquired hyperlipidaemias.

The macrophages form small masses known as xanthomas

59
Q

How do abnormal protein accumulations appear in cells?

A

As eosinophilic droplets or aggregates in the cytoplasm

60
Q

Describe two examples of abnormal protein aggregation

A

Mallory’s hyaline is a damged protein seen in hepatocytes of those with alcoholic liver disease due to accumulation of altered keratin fliaments

alpha1-antitrypsin deficiency is a genetic disorder where the liver produces incorrectly folded alpha1-antitrypsin that accumulates in the ER and is not secreted

This leads to proteases in the lung acting unchecked and breaking down lung tissue, leading to emphysema

61
Q

Give examples of exogenous pigment accumulation

A

In tattoos, pigment is phagocytosed by macrophages and remains there indefinitely

Carbon coal dust inhalation, Dust particles phagocytosed by macrophages in the lung, this gives rise to blackened lung tissue (anthracosis)

If high exposure occurs lungs can become fibrotic or emphysema can develop, this is known as ‘coal workers pneumoconiosis’

62
Q

Give examples of endogenous pigment accumulation

A

Lipofusin:
Brown pigment in aging cells a sign of ROS injury and lipid peroxidation

Haemosiderin:
Derived from Hb, Yellow brown and contains iron, forms in local or systemic excess of iron. A common example of this is in a bruise

Systemic iron overload leads to deposition of this pigment in all organs (haemosiderosis), if severe can lead to heart, pancreas and liver damage

Haemosiderosis can be seen in haemochromatosis (increased intestinal iron absorption), blood transfusions and haemolytic anaemias

Bilirubin:
Bile pigment, can cause jaundice if in excess (as in abnormal liver function or haemolytic anaemias)

63
Q

What is pathological calcification?

A

Abnormal deposition of calcium salts in tissues

Can be dystrophic or metastatic

64
Q

What is dystrophic calcification?

A

Occurs in areas of dying tissue, athersclerotic plaques or damaged heart valves

There is no abnormality in serum Ca2+ concentration or calcium metabolism

Can cause organ dysfunction (E.g. Athersclerosis or calcified heart valves)

65
Q

What is metastatic calcification?

Hint: Four main causes

A

Calcium deposited in tissue secondary to hypercalcaemia and disturbances in calcium metabolism

Usually asymptomatic

Four main causes:

Increased PTH, for example due to parathyroid tumour or ectopic parathyroid tissue in tumours

Destruction of bone secondary to primary tumours of bone, for example in leukaemia, metastases in bone or immobilisation

Vit D disorders

Renal failure

66
Q

What happens to cells as they age?

A

Accumulate damage to cellular components and DNA

May accumulate lipofuscin and abnormally folded proteins

Decline in replicative ability (Replicative senescence)

67
Q

How does replicative senescence come about and how is it avoided?

A

Ends of chromosomes (telomeres) shorten with every division, when they reach critical length that cell can no longer divide

Germ cells, stem cells and some malignant cells produce telomerase to maintain telomeres and avoid senescence (indefinitely for germ cells)

68
Q

How does metabolic tolerance to alcohol come about?

A

Induction of CYP2E1, increasing rate of ethanol metabolism and other drugs that are metabolised by this enzyme

69
Q

What are the three major effects of Chronic excessive alcohol intake on the liver?

A

Fatty change:
Toxicity of alcohol results in steatosis, which can cause hepatomegaly

This is acute change and is reversible and generally asymptomatic

Acute alcoholic hepatitis:
Alcohol and metabolites can cause hepatitis as they are toxic

A binge can result in AAH and focal hepatocyte necrosis the formation of mallory bodies and and neutrophilic infiltrate

Gives symptoms of fever, liver tenderness and jaundice, is usually reversible

Cirrhosis:
Occurs in 10-15% of alcoholics, can result in a hard, shrunken liver and histologically appears as micronodules of regenerating hepatocytes surrounded by bands of collagen

It is irreversible, serious and sometimes fatal

70
Q

How is paracetamol normally metabolised by the liver? (Metabolism Semester 1)

A

Detoxified in the liver by phase 2 sulphonation or glucuronidation

Small amounts are metabolised by CYP2E1 to NAPQI (phase 1) which is detoxified by glutathione (phase 2)

71
Q

If a large dose of paracetamol is taken, what happens?

A

NAPQI accumulates
Glutathione is depleted by NAPQI
NAPQI binds to sulphydryl groups on liver cell membranes causing hepatocyte necrosis and liver failure
Massive liver necrosis can occur 3-5 days after the overdose with a large dose, this can be fatal

72
Q

What makes someone particularly at risk of damage following a paracetamol overdose?

A 
Those who took alcohol with the overdose
Alcohol dependents
Malnourished people
People on enzyme inducing drugs (E.g. Carbamazepine)
People with HIV or AIDS
73
Q

What can be done for people following a paracetamol overdose?

How can severity of damage following overdose be gauged?

A

Can be given an antidote (N-acetyl cysteine / NAC) to increase availability of hepatic glutathione

To decide wether this is required 4 hours after overdose the serum concentration of paracetamol is measured

Prothrombin time after 24 hours indicates severity of liver damage

74
Q

What are the effects of aspirin normally?

A

Acetylates platelet cyclooxygenase and blocks thromboxane A2 production (a substance which activates platelet aggregation)

75
Q

What are the major consequences of aspirin overdose?

What indicates serious poisoning?

A

Aspirin stimulates the respiratory centre leading to respiratory alkalosis
Compensatory mechanisms result in metabolic acidosis

INterferes with carbohydrate, fat and protein metabolism and oxidative phosphorylation, resulting in an increase in lactate, pyruvate and ketones bodies, contributing to acidosis

Fall in serum pH indicates serious poisoning

Platelet cyclooxygenase inhibition causes decreased platelet aggregation and petechaie (small red/purple spot on skin indicating minor haemorrhage) may be present

Can also cause acute erosive gastritis leading to GI bleeding

76
Q

What is a common indication of liver damage due to hepatitis or alcoholic liver disease?

If you see this indication, what might be the next step towards diagnosing hepatitis?

A

Raised bilirubin and aspartate aminotransferase (ASP) and alanine aminotransferase (ALT) in the blood indicated liver damged

A liver biopsy

77
Q

What lab tests might be done if acute pancreatitis is suspected?

Raised values for these tests indicates what?

A

A serum amylase and lipase test

Raised result indicates cell injury/necrosis of the pancreatic cells

78
Q

What abnormal blood test results might indicate someone is having a myocardial infarction?

Why are these good tests?

A

Raised troponin - Only released from cardiac cells

Raised Creatine kinase MB (CKMB) - Found mainly in the heart

Good tests as they are fairly specific to MI

ESA2 Callum's Cards - Complete (36 decks)

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