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Pathology Flashcards

1
Q

What is the important nemonic for pathology?

A 
V -vascular
I - infection /inflammation 
N -neoplasia =new 
D -drugs/ toxins
I - iatrogenic = diseased caused by medical means
C - congenital / developmental
A - autoimmune
T - trauma
E - endocrine / metabolic
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2
Q

What causes acute inflammation?

A

Injury
Vascular changes
Cellular changes

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3
Q

How long do mediators last?

A

Only as long as the stimulus exists

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4
Q

How long do neutrophils last outside blood vessels?

A

Only a few hours

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5
Q

What are the stages of inflammation?

A

Resolution
Suppuration
Repair, organisation and fibrosis
Chronic inflammation

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6
Q

What is the progression of inflammation dependant on?

A

The site of the injury
The type of injury
The duration of injury

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7
Q

What is required for resolution from injury?

A

Minimal cell death
Tissue has the capacity to repair
Good vascular supply
Injurious agent easily removed

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8
Q

What is suppuration?

A

The formation of pus in inflammatory response.
Pus contains living, dying and dead cells and if it’s collected may be termed an abscess
A walled off space filled with pus may be called an empyema

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9
Q

What is repair, organisation and fibrosis to do with?

A

Scarring

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10
Q

When is organisation/ repair not good?

A

If an injury produces lots of necrosis
If an injury produces lots of fibrin that isn’t easily cleared
If it has a poor blood supply
If it’s a particular tissue type

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11
Q

What happens when damage goes beyond the basement membrane?

A

Healing by organisation and repair is favoured over resolution
This requires a scaffold for resolution to occur around
Erosions/ abrasions = injury with the basement membrane intact

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12
Q

What is a common response of the mucosa when injury is severe and it can’t be easily rebuilt?

A

Granulation tissue formation.
The defect is slowly infiltrated by capillaries and then myofibroblasts which deposit collagen and smooth muscle cell leaving it looking very red.
The tissue is replaced by scar tissue which is not particularly functional and can lead to loss of function.

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13
Q

What is scarring and fibrosis in the liver?

A

Cirrhosis

Results in liver failure and vascular disturbances

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14
Q

Describe chronic inflammation.

A

It isn’t related to time or severity and can occur without preceding acute inflammation.
Favoured if there is suppuration, persistency of injury, infectious agents, or autoimmune injuries.
Characterised by lymphocytes and macrophages.

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15
Q

What are granulomas?

A

Aggregate epithelial hystocytes
(Collection of inflammatory cells)
Can be caused by foreign bodies, endogenous substances (keratin, bone, crystals) and exogenous substances (talc, asbestos, suture material, oil)
Can also be caused by specific infections (worms, parasites, syphilis, mycobacterium- TB)

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16
Q

What occurs with tuberculosis granulomas?

A

Caseous necrosis

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17
Q

How does hypoxia cause cell injury and then acute inflammation?

A

No oxygen = no ATP > Na/K ATPase fails > increases potassium > swelling > calcium pump fails > increased intracellular calcium > stimulates a number of things which make it worse (ATPases, phosphlipase, proteases, endonucleas, mitochondrial permeability)

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18
Q

How do phospholipases make cell injury worse in hypoxia?

A

They cause membrane damage

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19
Q

How do proteases make cell injury worse in hypoxia?

A

They cause membrane and cytoskeleton damage

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20
Q

How do endonucleases make cell injury worse in hypoxia?

A

They damage DNA and break it down

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21
Q

What does mitochondrial permeability do that worsens cell injury in hypoxia?

A

Released pro death factors

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22
Q

What is the window of time in which clot busting drugs can be used to prevent cell death?

A

20 minutes, after 30 mins the cells will certainly die

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23
Q

What can be seen in the first 20 minutes of myocardial infarction?

A

Nothing to see
Changes on an ECG
At autopsy there would be no macroscopic changes
There would also be no changes under a microscope

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24
Q

What happens to cells in the first 20 mins hypoxia?

A

Cells shrink (pyknotic), becomes red, nucleus shrinks and becomes dark, marginal contraction bands appear

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25
Q

What happens to cells 24 hours after hypoxia?

A

Cell contents leak
Complement cascade initates
Acute inflammation
Vascular changes (vasodilation, slowing of flow, margination, rolling, pavementing, diapedesis, chemists is, phagocytosis)

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26
Q

When is the risk of cardiac rupture greatest?

A

3-7 days
At this point the wall of the heart is weakest. Necrosis and neutrophils may be all that’s is holding it together if the full thickness is affected.

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27
Q

What happens 48 hours after hypoxia?

A

-as time progresses, neutrophils fade away and are gradually replaced by macrophages
Definite changes can be seen at autopsy -macrophages have a yellow appearance
Macrophages can also be seen down the microscope

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28
Q

What restitution happens after myocardial infarction?

A
  • gradual process
  • progressive scarring
  • macrophages fade away and are replaced by fibroblasts
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29
Q

What do fibroblasts do?

A

Gradually lay down collagen
Occurs progressively after 2 weeks
Complete at 6 weeks (if an MI occurred more than 6 weeks ago it can’t be dated)

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30
Q

What is scarring after an MI a problem?

A

(Depends in amount of damage)
Scar tissue has replaced an area of muscle so the muscle can’t pump as well > weak heart
Nerve bundles may also be damaged and so the pace of the heart isn’t kept properly

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31
Q

What are the adaptive responses to stress?

A

Hypertrophy (more work)
Hyperplasia (more work)
Atrophy (less work) -reduction in size, physiological or pathological
Metaplasia (different work)

These only work to a point and then stress is too much (cell death)

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32
Q

Describe necrosis.

A

Requires no energy
Not normal, always pathological
Three types - coagulative, liquefactive and caseous

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33
Q

What is coagulative necrosis ?

A

Necrosis which preserves cell outlines
Dead cells are consumed by various enzymatic processes and cells
Occurs when the micro environment is too toxic for proteolysis
Common types
Seen in cardiac muscle (myocardial infarction)

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34
Q

What is liquefactive necrosis ?

A

Involved a liquid viscous mass where no cell structure remains
Pus formed
Associated with localised bacterial and fungal infections
Necrosis within the brain

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35
Q

What is caseous necrosis?

A

(Cheesy necrosis)
Associated with TB
Microscopic
Granulomatous inflammation with central necrosis
To test - ask for culture, PCR and a ziehl neelson stain

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36
Q

Describe apoptosis.

A

Programmed cell death in response to specific signals
Requires energy
Can be physiological, part of normal growth
Involved in removal of self reactive lymphocytes
Hormone dependant involution (how tissues that grow as a result of hormonal changes are removed after the hormone is removed)
Can also be pathological-in response to injury, radiation, chemotherapy, graft vs bone disease etc
All mechanisms rely on activating caspases (intrinsic or extrinsic)

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37
Q

Describe the extrinsic pathway.

A

Death receptor initiates pathway
Cell membrane receptors with “death domain”
Death receptors - tumour necrosis factor (TNF) and fas
Fas is involved in recognition of self (preventing autoimmune disease)
TNF - induces apoptosis in association with inflammatory conditions

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38
Q

Describe the intrinsic pathway

A

Mitochondrial pathway
Growth signals promote anti-apoptotic molecules in mitochondrial membrane
When these are removed they are replaced by Bax and Bak which increase the permeability of mitochondria
This results in the release of proteins that stimulate caspases and cytochrome C

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39
Q

What does p53 do?

A

Asses DNA damage, halts cells cycle and if DNA cannot be repaired then p53 stimulated caspases and induced apoptosis

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40
Q

What is the morphology of apoptosis?

A

Cells shrink
Chromatin condensed
Cytoplasmic blend are formed by breakdown of the cytoplasm
Macrophages hoover everything up

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41
Q

What are the signs of cellular aging?

A

Oxidative stress - free radical damage
Accumulation of metabolism by products
Lipofuscin

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42
Q

How do we slow aging?

A

Low calories reduced IGF signalling which silences specific genes

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43
Q

what is hyperplasia?

A

increase in cell number in response to an external stimuli. it will regress onwithdrwl of stimulus and usually increases organ volume. can be physiological or pathological.

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44
Q

what is hypertrophy?

A

increase in cell size not number.

often occurs with hyperplasia or can be in isolation. response to mechanical stress.

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45
Q

what is atrophy?

A

reduction in cell size which can be physiological or pathological.

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46
Q

what happens in response to stress?

A

we produce more growth factors or growth factor receptors

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47
Q

what are the 3 categories of growth receptor?

A

1- receptors with intrinsic tyrosine kinase activity
2- 7 transmembrane G protein coupled receptors
3- receptors without intrinsic tyrosine kinase activity

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48
Q

what are the stages of the cell cycle?

A

G1, S, G2, M

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49
Q

what are cyclins and CDKs?

A

each step in the cell cycle is controlled by a series of cyclin dependant kinases that activate each other and other enzymes. each CDK is activated by a specific cyclin and these vary in concentration throughout the cell cycle.
cyclins D, E, A and B (D= highest conc., B= lowest conc.)

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50
Q

what happens in G1?

A

the cell gets bigger with increased protein synthesis and CDK4 is activated by cyclin D.
CDK4 phosphorylates the Rb (retinoblastoma protein)

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51
Q

describe the Rb protein.

A
  • important in normal cell growth and malignancy
  • is bound to E2F normally, which prevents the beginning of cell division
  • when phosphorylated by CDK4, Rb can,t bind to E2F and therefore cell division occurs.
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52
Q

describe the S phase

A

E2F initiates DNA replication and increases the levels of cyclin A which goes on to activate CDK2. CDK2 also promotes DNA replication.

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53
Q

Describe G2 phase

A

second growth phase where the cell gets bigger and there is more protein synthesis.
the main checkpoint occurs at the end of G2 and is checked by p53.

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54
Q

what does p53 do?

A

checks cell for mistakes and if they are found the cell cycle is paused and a repair attempt is made. if the repair is successful it will progress, if not it will undergo apoptosis. (via BAX pathway)

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55
Q

what are telomeres?

A

capped ends of chromosomes that provide protection and stop degradation. consists of TTAGGG repeats and with every division the number of repeats gets smaller
stem cells can switch them off

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56
Q

what examples of hyperplasia?

A

-breast tissue at puberty
-endometrial lining of uterus in pregnancy
can occur after loss of tissue e.g liver

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57
Q

what are examples of pathological hyperplasia?

A
  • hormonally induced - excess oestrogen
  • hormonally induced prostatic hyperplasia - enlarged prostate
  • as a result of infection
  • hyperplastic tissue is at risk of development of cancer.
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58
Q

when does hypertrophy become pathological?

A

when the heart can no longer function, may result in heart failure.

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59
Q

what are the causes of atrophy?

A

-decreased workload
-loss of innervation = loss of function after a nerve supply is removed
- blocked blood supply
-loss of hormonal stimulation
-inadequate nutrition
ageing
-pressure atrophy (tissue adjacent to tumours)

60
Q

Describe the mechanism of atrophy.

A

Reduced cellular components > protein degradation> “digested by lysosome
-some hormones promote degradation and atrophy (glucocortids and thyroid) and some oppose it (insulin) - a balance keeps homeostasis.

61
Q

what is cancer?

A

uncontrolled cell proliferation and growth that can invade other tissues

62
Q

what does tumour mean?

A

=swelling

can be benign, malignant, inflammatory or a foreign body.

63
Q

what is neoplasia?

A

new growth not in response to a stimuli. can be benign, premalignant or malignant.

64
Q

what is malignancy?

A

a tumour with metastatic potential.

In epithelial cells it must have gone beyond the basement membrane.

65
Q

what are metastases?

A

when the cells have spread to other sites

66
Q

what are screening programmes?

A

looking for the precursor stages of malignancy in order to prevent it.
often looks for dysplasia.

67
Q

what is metaplasia?

A

reversible change from one mature cell type to another mature cell type.
Not reversible in adult cells.
This may be in response to cytokines.
It commonly occurs due to cell damage in which normal cells are swapped for squamous epithelial cells which are resistant to this type of injury (noxious stimuli).
Metaplastic tissue is at risk of cancer.

68
Q

how can hyperplasia cause cancers?

A

it can become autonomous and no longer require stimulus which leads to uncontrolled growth.

69
Q

what is dysplasia?

A

disordered growth leading to abnormal cells growing without a stimuli. this can lead to invasion of the basement membrane and in high grade dysplasia, cancer.
Can cause cervical cancer.

70
Q

what is carcinoma in-situ ?

A

High grade pre-malignancy.
It is the last stage before coming invasive.
e.g Dysplasia affecting the whole of the epithelium

71
Q

what must cancers do to be successful?

A
  • increase growth signals
  • remove growth suppression
  • avoid apoptosis
  • achieve immortality
  • become invasive
  • make their own blood supply (angiogenesis)
  • loss of DNA spell checks
  • avoid the immune system
72
Q

what are known causes of cancer?

A
  • inherited predisposition
    -chemicals
    -radiations
    infections
    -inflammation
    -lifestyle factors
73
Q

what are autosomal dominant conditions?

A

where you only need one faulty gene to get the effect.

74
Q

what is the double hit hypothesis?

A

one working gene is enough to be functional but those who have only one working copy are already at increased risk.

75
Q

what are examples of chemical carcinogens?

A
  • carcinogens in smoking
  • aflatoxin (fungus on peanuts)
  • beta-naphthylamine (chemical dyes - bladder cancers)
  • nitrosamines (food preservatives)
  • arsenic >skin cancer
76
Q

what are initiators and promoters in relation to chemical carcinogens?

A

initiators - cause long-lasting genetic damage but not sufficient to cause damage, must be followed by a promoter.
promoters - require initiators to have caused damage.

77
Q

how do we know id something is a carcinogen?

A
  • the ames test

- treating cells with a chemical and if they undergo the same mutation every time then they are a carcinogen.

78
Q

what carcinogens are in cigarettes?

A
  • polycyclic aromatic hydrocarbons (worst type)
  • N-nitrosonornicotine
  • polonium
  • various metals
79
Q

what do aflatoxins do?

A

(from fungus)
cause liver cancers.
associated with p53 mutations.

80
Q

how does radiation cause cancers?

A

UVB rays cause the formation of pyrimidine dimers in DNA.
repair mechanisms are overwhelmed (NER) leading to skin cancers.
-can also cause leukemias and thyroid cancers (Chernobyl)

81
Q

how does HPV cause cancers?

A

it has a viral E6 oncogene which destroys p53.
E7 prevents Rb protein from acting.
This causes transcription and translation and leads to increased likelihood of cancer.

82
Q

what is EBV?

A

a virus implicated in several tumours; - Burkitt-lymphoma. B-cell lymphoma. Hodgkin lymphoma. nasopharyngeal carcinoma.

83
Q

how does chronic inflammation cause cancers?

A

constant lymphocyte reproduction leads to errors in production - causes many lymphomas
-other tumours are caused because the tissue is replicating so much it becomes unstable.
(problem in patients with long term catheters)

84
Q

how does obesity increase the likelihood of cancer?

A
  • hyperplasia in the endometrium
  • cholesterol and oestrogen are similar structures
  • leads to risk of renal cell carcinoma.
  • also has association with growth factors, mTOR pathway and others.
85
Q

what tumours do C-KIT, Ras and Braf cause?

A

C-KIT - GI stromal tumours
Ras - colon, lung etc.
Braf - melanomas (treated with vemurafanib)

86
Q

what is Myc?

A

a nuclear transcription factor that promotes growth and is one of the last points in the sequence.
common in lymphoma, neuroblastoma, small cell carcinoma of the lung, Burkitt .

87
Q

what is PI3K?

A

the most commonly mutated kinase in cancer.

88
Q

what is APC?

A

one of the earliest mutations in colorectal cancer. can occur as a germaline condition causing inherited conditions.

89
Q

what are tumour suppressors?

A
  • stop growth and must be removed for cancer cells to be successful
  • there are lots of proteins that inhibit the cell cycle (often prefixed p) e.g p53 (most commonly mutated protein in all cancers)
90
Q

what does loss of VHL lead to?

A

increased levels of angiogenic growth factors and renal cancers.

91
Q

what does PTEN do?

A

-increases transcription of p27 which blockes CDKs and cell cycle progression.
This inhibits the P13K/AKT pathway
Therefore cells can proliferate in an uncontrolled fashion.

92
Q

how is unlimited replicative potential achieved in cancer cells?

A

a mutation is present which reactivates telomeres so the cells don’t die.

93
Q

how can apoptosis be prevented in cancer cells?

A

Bcl-2 is an antiapoptotic molecule which binds to Bax/Bak to stop holes being punched in the mitochondria.
this means no cell suicide and results in lymphomas.

94
Q

how do cancers create their own blood supply?

A

VEGF (vascular endothelial growth factor) is frequently up regulated in some malignancies and allows the generation of a blood supply.

95
Q

what do the BRCA genes and proteins do?

A

-have a role in DNA repair and cell cycle arrest at G1/S phase.
if it is mutated it can lead to breast, ovarian and pancreatic tumours.

96
Q

what are mismatch repair proteins?

A

proteins responsible for identifying faults in the code
- MLH1 (Main one), MLH3, MSH2, MSH3, PMS1, PMS2.
commonly develop colorectal carcinomas.

97
Q

what is lynch syndrome?

A

abnormal MHL1 proteins and other mismatch repair proteins. 3% of all colorectal cancers.

98
Q

how do tumours avoid the immune system?

A

PD-L1 is a ligand which inhibits T cell proliferation leading to apoptosis. tumours can over express PD-L1 and avoid the immune system.

99
Q

how do cancer cells invade and metastasize ?

A

increase their expression of metalloproteinases (MMP) sand cells can then chew their way through surrounding blood vessels.
-They must then enter through the vessel wall, survive in the vessel, aggregate and adhere to the vessel wall and get back through the vessel wall. after this they must anchor to a new organ and survive and grow again.

100
Q

why are cancer cells not clonal?

A

the faulty repair mechanisms and lack of apoptosis mean that each daughter cell develops new mutations with each division.

101
Q

what do benign tumours usually look like?

A

usually organised, smooth edges, round and all the same.

  • The surface is homogenous (cut is uniform)
  • legion can have a capsule around it as it is slow growing.
102
Q

what do malignant tumours look like?

A

looks nasty, not natural, irregular, infiltrative, destructive.
- are heterogenous (cut surface is not uniform) due to haemorrhage or necrosis

103
Q

what is a N:C ratio?

A

nuclear-cytoplasmic ratio.

an increased N:C ratio suggests malignancy.

104
Q

how does the quality of differentiation affect how cells look?

A

well differentiated stem cells look like they are supposed to.
In poorly differentiated stem cells, it is hard to tell their origin.

105
Q

what is pleomorphism?

A

variability in size, shape and staining of cells.

106
Q

what is hyperchromasia?

A

occurrence of unusual intense coloration.

107
Q

what cancers are found in the epithelium?

A

carcinomas.

108
Q

what are the benign and malignant tumours found in glandular cells?

A 
benign = adenoma
malignant = adenocarcinoma.
109
Q

what are the benign and malignant tumours found in squamous cells?

A 
benign = papilloma 
malignant = SCC (squamous cell carcinoma)
110
Q

what are the malignant tumours found in the bladder?

A

transitional cell carcinomas (TCC)

111
Q

what are tumours of the mesenchyme (connective tissues) called?

A

sarcomas.

112
Q

what are the benign and malignant tumours found in fat?

A 
benign = lipoma
malignant = liposarcoma
113
Q

what are the benign and malignant tumours found in bones?

A

benign - osteoma

malignant - osteosarcoma

114
Q

what are the benign and malignant tumours found in cartilage?

A 
benign = enchondroma
malignant = chondrosarcoma.
115
Q

what are the benign and malignant tumours found in skeletal muscle?

A 
benign = rhabdomyoma
malignant = rhabdomyosarcoma.
116
Q

what are the benign and malignant tumours found in smooth muscle?

A 
benign = leiomyoma
malignant = leiosarcoma.
117
Q

what are the benign and malignant tumours found in blood vessels?

A 
benign = haemangioma
malignant = angiosarcoma
118
Q

how does cancer affect the body?

A
  • local problems due to size
  • compression of adjacent structures
  • anatomically dependant
  • effect on brain
  • blocking of blood vessels
  • blocking of airways
  • blocking of bile ducts
  • uses a lot of energy
119
Q

which cancers present early?

A
  • vocal cord - change in voice
  • skin cancers can be seen
  • breast cancers can be felt
  • testicular cancers.
120
Q

what happens to the colon as a result of tumour formation?

A

obstruction and perforation.

121
Q

what happens to the lungs as a result of tumour formation?

A
  • decreased area of healthy lung
  • decreased O2 consumption
  • often late occurrences
  • often large and multiple tumours.
  • obstruction then infection, water stagnates
122
Q

what happens when the kidney gets tumour formation?

A

obstruction leads to backward pressure as it is unable to drain urine and the kidney stops functioning. this builds up toxins and abnormal electrolyte balance.

123
Q

describe tumours in the brain.

A
  • no such thing as benign as lots of important functions are in the brain e.g breathing centre, control of heart rate.
    if pressure increases it can cause seizures and it stops breathing.
124
Q

why does cachexia (weight loss) occur in cancer patients?

A

tumours use a lof energy and can produce all sorts of molecules that result in increased metabolism in the body. They mainly produce tissue necrosis factor (TNF)

125
Q

what does infiltration of cancers mean?

A

nerves can lose function, there can be loss of motor function (swallowing, diaphragm) or sensory pain or loss of sensation. -infiltration of larger vessels can be a huge problem and can lead to death.

126
Q

what is paraneoplasia?

A

tumours can produce hormones which result in electrolyte disturbances and leas to osteoarthropathy (big fingers) and unusual neurological symptoms.
- can also cause rashes, fever and pyrexia (leads to increased temp).

127
Q

what does immunosuppression mean for cancer patients?

A

increased risk of infections (can be unusual).

128
Q

what can metastases cause?

A
  • loss of function in lungs, liver tec.

- fractures in bones.

129
Q

what is atheroma?

A
  • hardening of the arteries leading to ischaemic heart/ coronary heart disease.
  • extremely common in the developed world.
130
Q

what causes atheroma?

A
  • cigarette smoking
  • hypertension
  • hyperlipidemia (elevated lipid levels)
  • diabetes
  • elderly age
  • gender (males)
  • genetics
  • endothelial injury
  • viral and infectious agents
  • homocysteine
131
Q

what areas of vessels does atherosclerosis affect?

A
  • sites of turbulent blood flow

- branching sites

132
Q

how does hypertension lead to atherosclerosis ?

A

high blood pressure damages endothelium > atherosclerosis.

133
Q

how does diabetes lead to atherosclerosis?

A

inceased cholesterol levels> advanced glycation end products (AGE) > abnormal cros linking in vessel walls > loss of elasticity and increased endothelial injury > traps cholesterol.

134
Q

how does atherosclerosis occur?

A

primary endothelial injury > accumulation of lipids and macrophages > migration of smooth muscle cells > increase in size.

135
Q

what does endothelial dysfunction cause?

A

increased permeability and white cell adhesion > increased VCAM -1, >monocytes attach and migrate through wall to become macrophages.

136
Q

how is fat involved in the pathogenesis of atherosclerosis ?

A

macrophages gobble up cholesterol > initially cholesterol is low and remains within the cell> traps cell> LDL is deposited > HDL shuttles back to the liver.

137
Q

how is smooth muscle involved in the pathogenesis of atherosclerosis ?

A

smooth muscle migrates from media to intima > gets stuck to cholesterol > produces extracellular matrix > change lesion from fatty streak to fibrofatty plaque.

138
Q

when is atheromatous narrowing of an artery likely to produce critical disease?

A
  • if it is in the only artery supplying an organ or tissue- the artery diameter is small
  • overall blood flow is reduced
139
Q

what are complications of atheroma?

A
  • stenosis (narrowing of lumen, reduced elasticity and systole flow, tissue ischemia)
  • aneurysm
  • dissection
  • thrombosis and embolism
140
Q

what are the clinical effects of cardiac ischaemia?

A
  • reduced exercise tolerance
  • angina
  • MI
  • cardiac failure
141
Q

what is cardiac fibrosis?

A
  • loss of cardiac myocytes
  • replacement by fibrous tissue
  • loss of contractility
  • reduced elasticity and filling
142
Q

why are aneurysms formed?

A

abnormal and persistent dilation of an artery due to weakness in its wall.
- most common in abdominal aorta

143
Q

what are complications of aneurysm?

A
  • rupture
  • thrombosis
  • embolism
  • pressure erosion of adjacent structures
  • infection
144
Q

what is arterial dissection?

A
  • splitting within the media by flowing blood
  • false lumen filled with blood within the media
  • sudden collapse and high mortality.
145
Q

what conditions are associated with aortic dissection?

A
  • atheroma
  • hypertension
  • trauma
  • coarctation
  • marfans
  • pregnancy

Principles (15 decks)

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