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foundations of medicine > TBL 13 Cell Injury > Flashcards

TBL 13 Cell Injury Flashcards

1
Q

When cells are placed under increased stress, there are two outcomes.

A
  1. Adapt

2. No longer able to adapt –> cell injury and death

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2
Q

Cell injury could be due to:

  1. Oxygen deprivation (aka _______)
  2. Chemical agents
  3. Infectious agents
  4. Autoimmunity
  5. Genetic defects
  6. Nutritional imbalances
  7. Physical agents
  8. Aging
A

Hypoxia (due to ischaemia, cardiorespi failure, anaemia)

=> insufficient delivery of oxygen to heart muscles

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3
Q

Intracellular systems that are vulnerable to cell injury: (4)

A
  1. Cell membrane integrity
  2. ATP generation
  3. Protein synthesis
  4. DNA damage
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4
Q

______ is the shrinkage in cell/organ size by loss of cell substance.

A

Atrophy

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5
Q

Pernicious anaemia is an ________ disease with fewer crypts and various cell types in the ________ (organ/tissue) due to inflammatory destruction. This leads to loss of body mucosa and thus atrophy.

A

Pernicious anaemia:

  • autoimmune disease
  • fewer cell types in gastric mucosa
  • inflammatory destruction
  • atrophy
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6
Q

_______ is an organ-wide atrophy due to the loss of brain structure.
Sulci are widened, while gyri are shrunken. The ventricles (which are chambers containing CSF) are noticeably (enlarged/smaller).

A

Dementia

  • Gyri shrunken
  • Ventricles enlarged
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7
Q

_________ is the increase in cell/organ size.

involves an increase in PROTEIN concentration rather than cytosol

A

Hypertrophy

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8
Q

Physiological hypertrophy is caused by:

A

an increase in functional demand or specific hormonal stimulation

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9
Q

Which two organs have increased susceptibility to physiological hypertrophy?

A

Heart and kidneys

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10
Q

__________ hypertrophy is characterised by tissue dysfunction and increased cellular mortality.

A

Pathological hypertrophy

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11
Q

_______ is an increase in the number of cells in an organ due to increased cell division.

A

Hyperplasia

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12
Q

________ hyperplasia allows for tissue and organ regeneration after damage has occurred.
This is common in the ____ and epithelial cells.

A

Compensatory hyperplasia;

common in the liver

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13
Q

________ hyperplasia occurs in organs which depend on oestrogen.

E.g. Endothelial proliferation during the menstrual cycle in response to oestrogen secretion.

A

Hormonal hyperplasia

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14
Q

_________ hyperplasia is an abnormal increase in cell division due to excessive stimulation by hormones or growth factors.
E.g. Carcinoma

A

Pathological hyperplasia

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15
Q

Endometrial proliferation (_________) vs. Endometrial hyperplasia (_________)

A

Endometrial proliferation - Physiological hyperplasia

Endometrial hyperplasia - Pathological hyperplasia (uterine lining becomes too thick due to excessive secretion of oestrogen without progesterone)

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16
Q 
\_\_\_\_\_\_\_\_ is when one differentiated adult cell type is replaced by another. 
It is (reversible/irreversible).
A

Metaplasia

reversible

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17
Q

__________ is a condition in which the acid reflux causes the non-keratinising _______ epithelium to convert to _______ epithelium lining the oesophagues.

If this persists, __________ may be induced in the epithelium.

A

Barrett’s oesophagus

Non-keratinising squamous epithelium to convert to columnar epithelium
(metaplasia)

Persist –> Dysplastic pre-cancerous changes induced in the columnar epithelium

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18
Q

________ is when the normal columnar epithelial cells of the cervix transforms into ________ epithelial cells.

Might be due to puberty which leads to a rise in the _______ levels.

A

Cervical ectropion/eversion

Normal columnar epithelial cells of the cervix convert into stratified squamous epithelium

Rise in oestrogen levels

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19
Q 
\_\_\_\_\_\_\_\_ refers to abnormal changes in cellular shape, size and organisation which are strongly associated with carcinogenesis.
It is (reversible/irreversible).
A

Dysplasia

Reversible

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20
Q

What is the difference between dysplastic and cancerous cells?

A

Dysplastic cells are not yet invading underlying tissues.

They show the genetic and cytological features of malignancy

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21
Q

Reversible cell injury may result in 2 consequences:

  1. Fatty change (also known as ______)
  2. Cellular swelling
A
  1. Fatty change - Steatosis

2. Cellular swelling

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22
Q

______ refers to the abnormal retention of lipids within the cells. This is due to the impairment of _______ and ______, causing excess lipid to accumulate in vesicles which displace the cytoplasm.

A

Steatosis (fatty change)

impairment of lipogenesis and lipolysis

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23
Q

Persistent steatosis may lead to ballooning degeneration of cells. This is due to damage to _________ causing fluid to flow into the cells, and due to failure of _____ export resulting in accumulation inside the cytoplasm.

A

Ballooning degeneration of cells:

  1. Plasma membrane damage
  2. Failure of protein export
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24
Q

Irreversible cell injury results in ________ or ________.

A

necrosis or apoptosis

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25
Q

________ necrosis is characterised by the formation of gelatinous substance in dead tissues that maintains the tissue structure.

A

Coagulative necrosis

outline of cells can still be observed

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26
Q

In myocardial infarction, _______ necrosis occurs, such that the cellular structure of cardiomyocytes can still be observed though they are dead and anucleate.

A

coagulative necrosis

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27
Q

_________ necrosis is charcterised by the digestion of dead cells to form a viscous, liquid mass. (abscess formation)

A

Liquefactive necrosis

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28
Q

Liquefactive necrosis often occur in _______ and _____ infections as they stimulate inflammatory responses.

A

bacterial and fungal infections

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29
Q

Hypoxic infarcts in the brain tissue usually presents as ________ necrosis as the brain contains little connective tissue to hold the cells in place. Cells contain large amounts of digestive enzymes and lipids, thus it is easy for cells to be digested by own enzymes.

A

Liquefactive necrosis (for old cerebral infarct)

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30
Q

_______ necrosis is characterised by amorphous granular debris enclosed within a distinctive inflammatory border. It is a combination of coagulative and liquefactive necrosis.

A

Caseous necrosis

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31
Q

__________ will form a TB lesion that is made up of a central caseous necrosis and surrounded by epithelioid macrophages.

A

Pulmonary tuberculosis

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32
Q

____ necrosis (Balser’s necrosis) is the specialised necrosis of fat tissue due to action of _________ on fatty tissues such as pancreas.

A

Fat necrosis - action of activated lipases on fatty tissues

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33
Q

In _________, there is abnormal activation of digestive enzymes within the pancreas, which leak out into the peritoneal cavity and liquefy the membrane by splitting triglycerides into fatty acids. The lesions produced can bind ______ to produce deposits (gritty white spots).

A

Acute pancreatitis (fat necrosis)

Lesions bind calcium to form calcium deposits.

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34
Q

_______ is the abnormal increase in interstitial fluid volume which surrounds cells of various tissues. This is due to the imbalance of the two forces that pushes fluid out into the IF.

A

Oedema

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35
Q

Water volume is usually very closely regulated by two forces that are in balance to each other.

A
  1. Colloid osmotic pressure (plasma proteins in the blood)

2. Vascular hydrostatic pressure

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36
Q

__________ is when fluid first accumulates in the interstitial spaces, then spills over into the alveolar spaces.

A

Pulmonary oedema

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37
Q

Pulmonary oedema is often caused by:

A

Left ventricular failure
(heart is unable to pump blood to the rest of the body from the left ventricle –> blood backs up to the lungs and leads to increased hydrostatic pressure in pulmonary capillary)

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38
Q

Main symptoms of pulmonary oedema are:
1. Breathlessness (known as ______)

  1. Breathlessness worse when lying flat (_________)
A
  1. Dyspnoea

2. Orthopnoea

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39
Q

_______ is a complication of pulmonary oedema as the fluid allows for bacterial growth.

A

Pneumonia

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40
Q

________ oedema is seen in brain tissues surrounding the intracranial lesions.

A

Cerebral oedema

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41
Q

Cerebral oedema is often caused by a disruption to _______.

This causes a breakdown of the tight endothelial junctions which make up the ________ and allows the plasma proteins and fluid to penetrate the extracellular space.

A

Disruption to cerebral capillaries

Breakdown of tight endothelial junction which make up the blood brain barrier

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42
Q

Cerebral oedema can cause a rise in the ________, which may lead to brain herniation and death.

A

Rise in the intracranial pressure (ICP)

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43
Q

Generalised oedema refers to the widespread accumulation of interstitial fluids in ________ and ________ around the entire body.

A

subcutaneous tissues and serous cavities

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44
Q

Generalised oedema often presents as _______.

A

pitting oedema at the ankles and feet

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45
Q

The key pathophysiological factor behind the formation of generalised oedema is

A

the activation of the renin-angiotensin-aldosterone pathway

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46
Q

_________ is an adrenal hormone which is essential for sodium retention in the body.

In oedema, there is impaired (hormone) escape resulting in reduced sodium retention.

A

Aldosterone

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47
Q

Common causes of generalised oedema include:

  1. Right ventricular failure
  2. Nephrotic syndrome
  3. Hepatic failure

Explain how each of them causes generalised oedema.

A
  1. RV failure - causes backing of blood into the lower parts of the body due to gravitational forces => higher hydrostatic pressure
  2. Nephrotic syndrome - loss of plasma proteins from the blood into the urine, resulting in lowered colloid osmotic pressure.
  3. Hepatic failure - Liver failure leads to inability to make sufficient plasma proteins, resulting in lowered colloid osmotic pressure of the blood.
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48
Q

________ is the abnormal blood clot formation within blood vessels of the circulatory system.

A

Thrombosis

49
Q

Virchow’s triad states the 3 factors which contribute to the generation of thrombosis:

A
  1. Stasis
  2. Hypercoagulability
  3. Vessel wall injury
50
Q

Key factors of venous thrombosis are:

A
  1. Stasis

2. Hypercoagulability

51
Q

Key factor of arterial thrombosis is:

A

Vessel wall injury

52
Q

Key factor of cardiac thrombosis is:

A

Stasis

53
Q

The most common type of venous thrombosis is the ________.

A

deep vein thrombosis (DVT)

54
Q

Potential complication of venous thrombosis is:

A 
Pulmonary embolism 
(where the blood clot in the vein breaks off and enters the lung)
55
Q

Arterial thrombosis is almost always related to vessel wall injury due to ________ plaques.

A

atherosclerotic plaques

which make the arterial walls much more fragile; rupture of the plaques

56
Q

Arterial thrombosis may cause:

  1. Stenosis => _______
  2. Occlusion => ________
A
  1. Stenosis (narrowing of the artery lumen) => Ischaemia

2. Occlusion (complete blockage of the artery) => Infarction

57
Q

Cardiac thrombosis refers to blood clot within the chambers of the heart that is due to _____ and is almost always seen in the (right/left) side of the heart.

A

Due to stasis

Always seen in the left side of the heart

58
Q

Cardiac thrombosis in the left atrium might be due to

A 
atrial fibrillation (contracts irregularly) which may result in reduced blood flow into the left ventricle 
=> blood clot forms in the left atrium where there is low blood flow/blood pressure
59
Q

Cardiac thrombosis in the left ventricle might be due to a

A

previous myocardial infarction which result in the scarring of the left ventricle => predispose blood to undergo thrombosis due to stasis of blood

60
Q

Formation of thrombus in the left side of the heart may potentially result in the thrombus becoming dislodged, and turn into an _______ in the __________.

A

embolus in the systemic circulation

=> leading to infarction of distant organs

61
Q

______ are detached masses within the circulatory system that has been carried by the blood to a distant site from point of origin.

A

emboli

62
Q

As arteries supply blood from the heart to the systemic circulation, an arterial thromboemboli has the potential to affect anywhere in the body.

In the _____: ischaemic stroke

In the mesenteric arteries: __________

In the lower limb arteries:

A

In the brain: ischaemic stroke

In the mesenteric arteries: small bowel infarction

In the lower limb arteries: acute lower limb ischaemia

63
Q

________ refers to the extravasation of blood due to blood vessel rupture.

A

Haemorrhage

64
Q

_____________ is when the aneurysm ruptures, causing a large volume of blood to be lost due to haemorrhaging. It is a major vessel rupture.

A

Abdominal aortic aneurysm rupture

65
Q

________ haemorrhage is a small vessel rupture thtat occurs at a vital site. It occurs when diseased blood vessel within the brainstem bursts.

A

Brainstem haemorrhage

66
Q

____________ refers to slow and insidious chronic blood loss which may result in _______.

A

Chronic low grade haemorrhage

may result in iron deficiency anaemia

67
Q

_____ is a generalised failure of tissue perfusion.

A

Shock (tissues do not get enough blood due to circulatory collapse)

68
Q

Main causes of shock include:

  1. Pump failure caused by _________
  2. Peripheral circulation failure caused by _______ (leading to low blood volume); sepsis or anaphylaxis leading to ________.
A
  1. Pump failure due to acute MI
  2. Peripheral circulation due to
    - hypovolaemia (low blood volume)
  • sepsis and anaphylaxis (low blood pressure)
69
Q

________ is tissue necrosis due to ischaemia.

A

Infarction

70
Q

Myocardial infarction occurs due to blockage of the _________ in the heart, blocking off blood supply to the _________.

A

Blockage of the coronary artery which supplies blood to the heart; blocking off blood supply to the left ventricle of the heart.

71
Q

Small bowel infarction is the infarction of the small intestine, caused by a thromboembolus originating from the left side of the heart and travelled down the aorta, impacting the ____________ artery that supplies the bulk of the small intestine.

A

superior mesenteric artery

72
Q

__________ is an inflammatory disease characterised by the formation of lipid-rich plaques.

A

Atherosclerosis

73
Q

_________ is the key factor in the formation of atherosclerosis.

A

Endothelial injury (formation of plaque in response to the injury)

74
Q

_________ is when a patient feels normal at rest, but when exercising, he or she may experience symptoms or cardiac ischaemia like central chest pain.

A

Stable angina

75
Q

There are 4 components of inflammatory response:

A
  1. Cells
  2. ECM
  3. Soluble factors
  4. Vessels
76
Q

The cells involved in inflammation are:

A

Neutrophils, macrophages, eosinophils, mast cells, basophils

77
Q

ECM involved in inflammatory response include:

A

collagen, proteoglycans and fibroblasts

78
Q

Inflammation is a response primarily by the _______.

A

vascular tissues (including the blood vessels)

79
Q

Acute inflammation involves mainly ______ (cells); whereas chronic inflammation involves mainly ________(cells).

A

Acute inflammation - neutrophils; chronic inflammation - macrophages, lymphocytes and plasma cells

80
Q

Resolution/repair of tissue damage involves ________ and ________ (cells).

A

macrophages (alternatively-activated) and fibroblasts

81
Q

________ refers to the tissue architecture returning back to normal.
There are two conditions for this to occur:

A

Regeneration

  1. Cells are able to regenerate.
  2. Little structural damage has been done (framework).
82
Q

_____ of tissue occurs when the tissue loss is too great, and cells cannot regenerate, resulting in the replacement of normal tissue with ________.

A

Repair

Replace normal tissue with fibrous scar tissue

83
Q

Repair of tissue after inflammation:

Involves mainly _______ (cells) which produce ______ that undergoes remodelling to give maximal tensile strength in the wound.

A

Fibroblasts which produce collagen that undergoes remodelling

84
Q

Repair of tissue damage:

Angiogenesis (newly formed capillaries) –> Migration and activation of fibroblasts (granulation tissue) –> Laying of ECM and collagen –> Remodelling

A

-

85
Q

Acute inflammation (on the body surface) is characterised by 5 cardinal signs:

A
  1. Loss of function
  2. Rubor (redness)
  3. Tumor (swelling)
  4. Calor (heat)
  5. Dolor (pain)
86
Q

Explain redness/erythema (rubor) and heat (calor) from acute inflammation.

A

Due to increased vascular supply to the area (increased blood flow)

87
Q

Explain swelling (tumor) from acute inflammation.

A

Due to oedema (due to increased vascular permeability)

88
Q

3 vascular changes to acute inflammation:

  1. _______ of blood vessels and increased blood flow to the injured site
  2. _________ are expressed on the local endothelium of blood vessels to allow inflammatory cells to stick to the vessel wall for ________.
  3. Increased __________ resulting in leaky capillaries for cells and mediators to enter the tissues.
A
  1. Dilation of blood vessels and increased blood flow to the injured site
  2. Adhesion molecules expressed on the local endothelium of blood vessels to allow inflammatory cells to stick to the vessel wall for extravasation.
  3. Increased vascular permeability => oedema and exudate
89
Q

______ is a protein-rich fluid made of the infiltrate from leaky capillaries within the extravascular space.

A

Exudate

90
Q

Exudate helps to _____ the pathogen and allow soluble mediators to spread more effectively.

A

dilute the pathogen

91
Q

_____ (protein) in exudate walls off the pathogen to stop it from spreading, giving inflammatory cells a substrate to hold on to.

A

Fibrin

92
Q

Exudate contains many soluble factors, classified into 2 categories -

  1. Factors produced locally by cells
  2. Circulating plasma proteins produced by the ______.
A
  1. Factors produced by cells
    A. Pre-formed: Histamine, lysosomal enzymes

B. Newly synthesised: Prostaglandins, leukotrienes, nitric oxide, cytokines

  1. Circulating plasma proteins produced by the liver
93
Q

The kinin system, which contain circulating plasma proteins produced by the liver, includes

A
  1. Fibrinogen

2. Plasmin

94
Q

The __________ in the exudate is a marker for inflammation

A

C-reactive protein (CRP)

95
Q

______ exudate is a watery fluid which is protein-poor. E.g. in blisters.

A

Serous exudate

96
Q

________ exudate occurs due to more severe injury and is rich in fibrin and proteins, where the fibrin forms thread-like material in the space.

It is typically seen in body cavity spaces e.g. in viral pericarditis

A

Fibrinous exudate

97
Q

_______ exudate is filled with pus, consisting of fibrin, acute inflammatory cells, debris and fluid.
E.g. in peritonitis following bowel rupture

A

Purulent

98
Q

__________ protein is a cationic protein found in eosinophils that targets parasites.

A

Major basic protein (MBP)

99
Q

_______ (protein produced by phagocytes) inhibits the growth of bacteria.

A

Lactoferrin

100
Q

How is acute inflammation terminated?

  1. _______ removed
  2. Inflammatory mediators and _______ die
  3. ________ are activated to release anti-inflammatory products
  4. ______ release anti-inflammatory products known as lipoxins.
A
  1. Stimulus removed
  2. Inflammatory mediators and neutrophils die
  3. M2 macrophages are activated to release anti-inflammatory products
  4. Mast cells release anti-inflammatory products known as lipoxins.
101
Q

There are 4 consequences to acute inflammation:

A
  1. Complete healing
  2. Healing by fibrosis
  3. Chronic inflammation
  4. Abscess formation
102
Q

How is acute inflammation terminated?

  1. _______ removed
  2. Inflammatory mediators and _______ die
  3. ________ are activated to release anti-inflammatory products
  4. ______ release anti-inflammatory products known as lipoxins.
A
  1. Stimulus removed
  2. Inflammatory mediators and neutrophils die
  3. M2 macrophages are activated to release anti-inflammatory products
  4. Mast cells release anti-inflammatory products known as lipoxins.
103
Q

There are 4 consequences to acute inflammation:

A
  1. Complete healing
  2. Healing by fibrosis
  3. Chronic inflammation
  4. Abscess formation
104
Q

Histamine is a soluble factor (vasoactive amine) that is released from _________, ________ and _______.
It has 3 main functions:

A

Released from mast cells, basophils and plasma cells

3 functions:

  1. Allergy (IgE)
  2. Vasodilation
  3. Increase vascular permeability
105
Q

Prostaglandins act as (vasodilators/vasocontrictors).

A

vasodilators

106
Q

There are two types of conditions which are abnormal due to excessive unchecked acute inflammation:

A
  1. Local acute respiratory distress syndrome (ARDS) in the lungs
  2. Systemic septic shock
107
Q

4 stages of lobar pnemonia:

A
  1. Congestion
  2. Red Hepatisation
  3. Grey Hepatisation
  4. Resolution
108
Q

There are two types of conditions that might cause excessive unchecked acute inflammation:

A
  1. Local acute respiratory distress syndrome (ARDS) in the lungs
  2. Systemic septic shock
109
Q

The predominant immune cells in chronic inflammation are:

A

Macrophages, lymphocytes and plasma cells

110
Q

NO exudate is seen in chronic inflammation.

True or False.

A

True

111
Q

________ inflammation is a particular form of chronic inflammation showing granuloma formation.

A

Granulomatous inflammation

112
Q

What are granulomas?

A

Granulomas are clusters of activated, epithelioid macrophages which aggregate to form giant cells, some may fuse to form multi-nucleated giant cells.

113
Q

Tuberculosis causes granulomatous inflammation, and it forms ________ type giant cells.

A

Langerhans - larger cells are observed as multi-nucleated giant cells, with nuclei arranged at the periphery.

114
Q

___________ disease is a genetic disease where there is a defect in the microbicidal activity of macrophages, so that when the bacteria are engulfed, they cannot be killed due to enzyme deficiency.
To control the infection, the cells may become surrounded by activated macrophages to form the _______.

A

Chronic granulomatous disease;

form granuloma

115
Q

_________ deficiencies is an inherited condition where the patient does not have regulatory proteins which control the complement system, resulting in a state of overactivation with damaging inflammatory effects => Chronic inflammation.

A

Complement deficiencies

116
Q

There are 3 main complications to tissue repair using collagen:

  1. ______ formation - excess _______ deposition
  2. Contractures
  3. Impaired organ function
A
  1. Keloid formation - excess collagen deposition
  2. Contractures - scar forms over time; scar contracts => joint mobility severely impaired
  3. Impaired organ function - functional cells are replaced with fibrous scar tissue
117
Q

Acute calculous cholecystitis is the acute inflammation of the ________.

A

gall bladder

118
Q

__________ is the chronic inflammation of the gall bladder.

A

Chronic calculous cholecystitis

foundations of medicine (21 decks)

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