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Semester 2 > MoD Session 1 > Flashcards

MoD Session 1 Flashcards

0
Q

What does all disease start with?

A

Cell injury

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1
Q

What can disease be considered as?

A

Consequence of failed homeostasis w/consequent morphological and functional disturbance

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2
Q

What are the increasing levels of response mounted by a cell as a stimulus moves from being physiological to harmful?

A

Homeostasis
Cellular adaptation
Cellular injury
Cell death

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3
Q

At what point does cell injury become cell death?

A

When the injury becomes irreversible

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4
Q

What can cause cell injury?

A 
Hypoxia
Toxins
Physical agents
Radiation
Micro-organisms
Immune mechanisms
Dietary insufficiency
Genetic abnormalities
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5
Q

What is hypoxaemic hypoxia?

A

Decrease in arterial oxygen content due to altitude or lung disease

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6
Q

What is anaemic hypoxia?

A

Decreased oxygen carriage by haemoglobin caused by anaemia or carbon monoxide poisoning

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7
Q

What is ischaemic hypoxia?

A

Interrupted blood supply caused by BV blockage or heart failure

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8
Q

What is histiocytic hypoxia?

A

Inability of a cell to use oxygen due to disabled oxidative phosphorylation enzymes caused by cyanide poisoning

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9
Q

How does the tolerance of hypoxia vary between neurones and fibroblasts before irreversible injury is caused?

A

Neurones can tolerate a few minutes

Fibroblasts can tolerate a few hours

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10
Q

Give examples of toxins that could cause cellular injury.

A

Glucose/salt in hypertonic solutions
Oxygen at high concentration
Therapeutic drugs

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11
Q

Give examples of physical agents that may cause cellular injury.

A

Direct trauma
Extreme temperature
Changes in pressure
Electric currents

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12
Q

How is urticaria (hives) caused?

A

Hypersensitivity reaction causes host tissue to be injured secondary to an overly vigorous immune response

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13
Q

How does Grave’s disease cause cellular injury?

A

Autoimmune reaction which fails to distinguish b/w self and non-self

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14
Q

What shows cellular injury when caused by immune mechanisms?

A

Redness

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15
Q

Give an example of a genetic abnormality which can cause cellular injury.

A

Inborn errors of metabolism

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16
Q

By what mechanisms can cellular injury be caused?

A 
Target:
Cell membranes, especially lysosomes
Nucleus
Proteins (structural cytoskeleton and enzymes)
Mitachondria
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17
Q

How can hypoxia cause reversible cell injury?

A

Ischaemia decreases oxidative phosphorylation –> decreases ATP to 5-10% of normal concentration –> cell reacts

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18
Q

Why does lipid deposition occur in reversible cell injury caused by hypoxia?

A

Ribosomes detach from the ER –> protein synthesis is decreased –> lipid is deposited

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19
Q

Why does chromatin clump during reversible cell injury caused by hypoxia?

A

Increased glycolysis lowers pH which in turn causes chromatin to clump

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20
Q

How are blebs formed in reversible cell injury caused by hypoxia?

A

The sodium/potassium pump is disrupted so cell swells as osmotic ions move in w/water allowing blebs to form

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21
Q

Why does cytosolic calcium levels increase in irreversible cell injury caused by hypoxia?

A

Leaky CSM allows calcium entry

ER and mitochondria also increase calcium levels

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22
Q

Which enzymes are affected by the increase in cytosolic calcium in irreversible cell injury caused by hypoxia?

A

ATPase
Phospholipase
Protease
Endonuclease

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23
Q

What effects does the high cytosolic calcium levels acting on enzymes within the cell have in irreversible cell injury caused by hypoxia?

A

Decreases ATP levels
Decreases phospholipid levels
Disrupts membrane and cytoskeleton proteins
Causes nuclear chromatin damage

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24
Q

Is the pathogenesis of cell injury due to all insults the same?

A

No, it may vary and attack different key structures

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25
Q

Which three free radicals are of biological significance?

A

Hydroxyl
Superoxide
Hydrogen peroxide

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26
Q

How does the Fenton reaction form free hydroxyl radicals?

A

Iron(II) is oxidised to iron(III) whilst hydrogen peroxide becomes an hydroxide ion and hydroxyl free radical

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27
Q

How does the Haber-Weiss reaction form hydroxyl free radicals?

A

An oxide ion, hydrogen ion and hydrogen peroxide react to form oxygen, water and a hydroxyl free radical

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28
Q

Which free radical is the most dangerous biologically?

A

Hydroxyl

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29
Q

Why must hydrogen peroxide and oxide ions be rapidly removed by the body?

A

To prevent formation of more dangerous hydroxyl free radicals

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30
Q

Why is the Fenton reaction important in bleeding?

A

Iron is available so there is an increased risk of hydroxyl free radical formation

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31
Q

What insults particularly cause free radical production?

A 
Chemical (paracetamol)
Radiation
Ischaemia-reperfusion
Cellular aging
High oxygen concentration
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32
Q

What damage do free radicals cause to cellular structures?

A

Lipid peroxidation

Bent/broken/cross-linked proteins, carbohydrates and nucleic acids

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33
Q

Why are free radicals required by leucocytes?

A

Killing bacteria

Cellular signalling

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34
Q

How are free radicals removed?

A

Antioxidant system

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35
Q

Which enzymes are involved in the antioxidant system?

A

Superoxide dismutase
Catalases
Peroxidases

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36
Q

What are free radical scavengers?

A

Vitamins A, C, E which can sequester metal ions and prevent Fenton reaction

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37
Q

What type of proteins are used in the antioxidant system?

A

Storage

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38
Q

What is ischaemia reperfusion injury?

A

When bloodflow is returned to damaged but not yet necrotic tissue causing damage worse than if the bloodflow was not restored

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39
Q

What mechanisms can cause reperfusion injury?

A

Increased ROS w/reoxygenation
Increased neutrophils causing more inflammation and tissue injury
Delivery of complement proteins activating the complement pathway

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40
Q

What cells are heat shock proteins present in?

A

All at low concentrations

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41
Q

What is the function of heat shock proteins?

A

Mend mis-folded proteins

Maintain cell vitality

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42
Q

What type of proteins are heat shock proteins?

A

Unfoldases/chaperonins e.g. Ubiquitin

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43
Q

How does the cell use heat-shock proteins to maintain cell vitality?

A

Turns off production of other proteins and increases heat-shock protein synthesis

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44
Q

What happens to a mis-folded protein if it cannot be re-folded?

A

It is destroyed

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45
Q

What are the stages of cell injury as seen by light microscopy?

A

Alive –> injured –> dead-pyknosis –> karyorrhexis –> karyolysis

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46
Q

What is pyknosis?

A

Irreversible cell shrinkage

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47
Q

Why does an injured cell become more darker staining as its injury becomes less reversible?

A

Denatured proteins accumulate

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48
Q

When does chromatin clumping remain reversible until?

A

Pyknosis

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49
Q

In reversible cell injury, what cellular changes are seen by electron microscopy?

A 
Cell swelling and blebs
Autophagy by lysosomes
Chromatin clumping
Mitochondrial and ER swelling
Dispersion of ribosomes
Aggregation of intramembranous particles
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50
Q

In irreversible cell injury, what cellular changes are seen by electron microscopy?

A 
Rupture of lysosomes and autolysis
Pyknosis of nucleus
Mitochondrial swelling w/large densities formed inside
Lysis of ER
Myelin figures
Defects in CSM
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51
Q

What is oncosis?

A

Cell death w/swelling

Spectrum of changes that occur in injured cells prior to death

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52
Q

What is the relationship between ATP and oncosis?

A

There is none - it is an ATP independent process

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53
Q

What cellular changes are seen in oncosis?

A

Cell and mitochondrial swelling

Plasma membrane rupture

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54
Q

What is necrosis?

A

Morphological changes that occur in a living organism after a cell has been dead for some time

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55
Q

Typically what period of time after cell death is necrosis seen?

A

4-24 hours

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56
Q

What is apoptosis?

A

Cell death w/shrinkage induced by a regulated intracellular programme where the cell activates enzymes that degrade its own nuclear DNA and proteins

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57
Q

Is apoptosis and active process?

A

Yes, it’s ATP dependent

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58
Q

What cellular changes are seen in apoptosis?

A 
Cell shrinkage
Chromatin condenses
Nuclear fragments
Membrane integrity preserved
Apoptotic bodies
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59
Q

What does this describe?

Seen w/damage to cell membranes –> cell contents leak out –> inflammation

A

Necrosis

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60
Q

What is fat necrosis?

A

Destruction of adipose

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61
Q

How are chalky deposits formed in fat necrosis?

A

Lipases free fatty acids which combine with calcium

62
Q

What can cause fat necrosis?

A

Pancreatitis

Trauma to adipose

63
Q

What can fat necrosis mimic?

A

Breast cancer nodule

64
Q

What is caseous necrosis?

A

Amorphous structureless debris associated with TB

65
Q

What is liquefactive necrosis?

A

Enzymatic digestion of tissues seen in tissues lacking stroma

66
Q

How is pus formed in colliquitive necrosis?

A

Increased inflammation and neutrophils

67
Q

What is coagulative necrosis?

A

Denaturation of proteins causing them to coagulate seen in solid organs

68
Q

Why is a ‘ghost outline’ seen in coagulative necrosis?

A

Cellular architecture is somewhat preserved

69
Q

How does coagulative necrosis appear histiologically?

A

Intense pink staining

Small nuclei

70
Q

How can liquefactive and coagulative processes be rescued when occurring in cells which are still alive?

A

Rescued by heat shock proteins

71
Q

What is gangrene?

A

Necrosis that is visible to the naked eye

72
Q

What is the difference between dry and wet gangrene?

A

Dry: tissue dries before infection can take hold
Wet: bacteria or fungi invade before drying completes

73
Q

How can wet gangrene cause septicaemia?

A

Microorganisms can easily leak into surrounding capillaries

74
Q

How does gas gangrene lead to the development of palpable pockets of gas in a tissue?

A

Wet gangrene w/anaerobic bacteria

75
Q

Which type of necrosis is associated with ischaemia?

A

Coagulative

76
Q

What is an infarct?

A

Area of ischaemic necrosis

77
Q

What two types of infarct are possible?

A

White

Red

78
Q

Which two types of necrosis can cause an infarct to form?

A

Coagulative e.g. MI

Liquefactive e.g. Cerebral infarct

79
Q

What can cause an infarction?

A

Thrombosis and embolism

Compression/twisting of BV - twisted spermatic cord, hernia, twisted bowel

80
Q

How is a wedge shaped white infarct formed?

A

Arteral insufficiency so not reperfused due to single blood supply –> occluded artery at apex of wedge of infarct

81
Q

How are red infarcts formed?

A

Venous insufficiency/reperfused/dual blood supply sufficient to cause haemorrhage but not rescue tissue

82
Q

What features are present in tissue which can form a red infarct?

A

Numerous anastomoses

Loose tissue w/poor stromal support

83
Q

What reduces arterial filling hence causing ischaemia in red infarction?

A

Capillaries leak causing venous pressure to increase

84
Q

What do the consequences of infarction depend on?

A

Alternative blood supply
Speed of ischaemia
Tissue involved
Oxygen content of blood

85
Q

What causes release of molecules by injured and dying cells?

A

Calcium entering damaged membranes

86
Q

What molecules are leaked by injured and dying cells?

A

Potassium
Enzymes
Myoglobin

87
Q

What are the affects of molecules released by injured and dying cells?

A

Local inflammation

General toxic effects on body

88
Q

Why can molecules released by injured and dying cells be used for diagnosis?

A

They may appear in blood

89
Q

What can cause potassium to explode out of dead cells?

A

Large MI
Severe burns
Tourniquet removal
Tumour necrosis syndrome

90
Q

What is tumour necrosis syndrome?

A

Where cancer cells are effectively killed so release lots of potassium

91
Q

Why is potassium used in cardiac surgery?

A

High levels stop the heart

92
Q

In what order are enzymes released by injured and dying cells?

A

Smallest molecular weight first w/increasing weight w/increasing pore size

93
Q

Give three examples of enzymes released by injured or dying cells.

A

Creatine kinase
AST
Troponin

94
Q

How does myoglobin released by injured or dying cells cause brown coloured urine?

A

Dead myocardium or striated muscle releases myoglobin which plugs renal tubes –> greatly increases myoglobin levels in the urine

95
Q

What is apoptosis characterised by?

A 
Shrinkage
Consistent cleavage of DNA breakdown
Use of ATP
Maintained membrane integrity
Lack of lysosomal emzyme involvement
Rapid completion time
96
Q

What is apoptosis used physiologically for?

A

Sculpting during embryogenesis

Involution of hormones and cytotoxic killer T cells

97
Q

How can apoptosis be identified pathologically?

A

Individual cell destruction w/shrunken, intensely pink appearance

98
Q

What is the process seen by a cell undergoing apoptosis?

A

Normal cell –> condensation –> cell buds –> apoptotic bodies

99
Q

Why is there no inflammation in apoptosis?

A

Apoptotic bodies are removed by phagocytes therefore there is no release of cellular contents

100
Q

How does extrinsic intimation cause apoptosis?

A

Stressed cell expresses death receptors –> death ligand TRAIL binds –> activates caspase-8

101
Q

How does intrinsic initiation cause apoptosis?

A

Stimulated by DNA damage or hormone withdrawal –> p53 stimulates mitochondria which stimulates apoptosome –> activated caspase-9

102
Q

What is the process of degradation and phagocytosis seen in apoptosis?

A

Loss of microvilli and junctions +/- nuclear changes –> fragmentation creating apoptotic bodies –> apoptotic body expresses surface proteins for recognition by phagocytosis

103
Q

Name 7 important apoptotic molecules.

A 
Death receptors
Death ligands
Caspases
p53
Cytochrome C
APAFI
Bcl-2
104
Q

What are caspases?

A

Effector molecules of apoptosis

105
Q

What is p53?

A

‘Guardian of the genome’ which mediates apoptosis in response to DNA damage

106
Q

What does Bcl-2 do?

A

Prevents cytochrome C release from mitochondria therefore inhibiting apoptosis

107
Q

What causes abnormal accumulations in a cell?

A

If the cell cannot metabolise something

108
Q

What can abnormal accumulations in a cell derive from?

A

Cell’s own metabolism
Extracellular space - iron in bleeding
Outer environment - dust

109
Q

Can abnormal accumulations in a cell be reversed?

A

Yes, if cell metabolism recovers

110
Q

What four mechanisms can cause abnormal accumulations in a cell?

A

Abnormal metabolism
Alterations in protein folding and transport
Enzyme deficiency
Inability to degrade phagocytosed particles

111
Q

How does abnormal accumulation of water and electrolytes cause tissues to become heavy?

A

Vacuoles/hydropic swelling increase water content

112
Q

What very difficult to treat condition caused by water and electrolyte retention stops breathing?

A

Cerebral oedema

113
Q

What causes steatosis?

A

Alcohol
Diabetes mellitus
Obesity
Toxins

114
Q

How are xanthomas formed?

A

Cholesterol vesicle filled cells form foam cells as cholesterol is not broken down by the body so is stored in membrane bound droplets

115
Q

What forms myelin figures?

A

Phospholipids

116
Q

What is the first stage of liver disease?

A

Steatosis

117
Q

How does mild steatosis compare to advanced steatosis?

A 
Mild = asymptomatic
Advanced = increased weight and size of liver
118
Q

What causes abnormal accumulations of carbohydrates?

A

Secondary to inborn errors of metabolism

119
Q

How are abnormal accumulations of protein seen in cells?

A

Eosinophilia droplets in cytoplasm

120
Q

What is Mallory’s hyaline?

A

Damaged hepatocyte protein due to accumulation of keratin in alcoholic liver disease

121
Q

How does incorrectly folded alpha 1-antitrypsin lead to emphysema and hepatitis?

A

Causes alpha 1-antitrypsin deficiency –> accumulates in ER

122
Q

How do exogenous pigments remain in the skin?

A

Macrophages pick up pigment and stay indefinitely, replaced when they die and remain stained

123
Q

Why is some exogenous pigment found in lymph nodes?

A

Some is taken up by lymph fluid and taken to nodes

124
Q

Give three examples of endogenous pigments found in the body.

A

Bilirubin
Heamosiderin
Lipfuscin

125
Q

How is heam converted to a toxic endogenous pigment?

A

Haem –> biliverdin (non-toxic) –> bilirubin (toxic)

126
Q

What is the irreversible step in bilirubin production from biliverdin?

A

Breaking of porphyrin ring

127
Q

Why is bilirubin associated with liver disease when it can be formed by all tissues of the body?

A

It is transported w/albumin to the liver

128
Q

What is heamosiderin?

A

Iron storage molecule seen in systemic/local excess of iron

129
Q

What causes haemosiderin deposition in tissues?

A

Bruising

130
Q

What is hereditary haemochromatosis?

A

Absorption of too much iron which affects the liver and pancreas

131
Q

What is another name for hereditary haemochromatosis?

A

Bronze diabetes

132
Q

When is lipofuscin seen?

A

In age/wear and tear in tissues which have been damaged by free radicals

133
Q

What type of cells is lipofuscin not seen in?

A

Rapid turnover cells

134
Q

What are the three stages of excessive alcohol intake?

A

Steatosis - reversible
Acute alcohol hepatitis - reversible
Cirrhosis - irreversible

135
Q

What are the S/S of acute alcoholic hepatitis?

A

Fever

Liver tenderness

136
Q

How does the liver appear in cirrhosis?

A

Hard and nodular w/scar tissue and macrophages

137
Q

What is dystrophic calcification?

A

Pathological local deposition of calcium seen in tuberculous lymph nodes and atheroma

138
Q

Is there abnormal serum calcium or calcium metabolism in dystrophic calcification?

A

Nope

139
Q

What is favoured in dystrophic calcification?

A

Hydroxyapatite crystal formation

140
Q

Which is the commonest type of pathological calcification?

A

Dystrophic

141
Q

What is metastatic calcification?

A

Hypercalcaemia leading to deposition of hydroxyapatite crystals in all tissues

142
Q

What can cause metastatic calcification?

A

High PTH
Destruction of bone due to tumour
Paget’s disease
Immobilisation causing lack of bone formation stimulus

143
Q

What causes cellular aging?

A

Shortening of telomeres

144
Q

What occurs at a critical telomere length?

A

Replicating senescence

145
Q

Why can germ cells and stem cells replicate indefinitely?

A

They contain telomerase which replicates their telomeres

146
Q

How does the pattern of oncosis/necrosis compare to apoptosis?

A

Oncosis/necrosis: contiguous group of cells

Apoptosis: single cells

147
Q

How does the cell size in oncosis/necrosis compare to that in apoptosis?

A

Oncosis/necrosis: enlarged (swelling)

Apoptosis: reduced (shrinkage)

148
Q

How does the nucleus of a cell undergoing oncosis/necrosis compare to that of one undergoing apoptosis?

A

Oncosis/necrosis: pyknosis-karyorrhexis-karyolysis

Apoptosis: fragmentation into nucleosome size fragments

149
Q

How does the plasma membrane compare in oncosis/necrosis to apoptosis?

A

Oncosis/necrosis: disrupted, early lysis

Apoptosis: intact but w/altered structure, especially orientation of lipids

150
Q

How do the cellular contents compare in oncosis/necrosis and apoptosis?

A

Oncosis/necrosis: enzymatic digestion which may leak out of cell
Apoptosis: remain intact but may be released by apoptotic bodies

151
Q

Compare adjacent inflammation in oncosis/necrosis to apoptosis.

A

Oncosis/necrosis: frequent

Apoptosis: does not take place

152
Q

Does oncosis/necrosis have a physiological or pathological role?

A

Invariably pathological

153
Q

When is apoptosis physiological and when is it pathological?

A

Physiological to eliminate unwanted cells

Pathological after some forms of cell damage, especially DNA damage

Semester 2 (45 decks)

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