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Osha 2a > Pathology > Flashcards

Pathology Flashcards

1
Q

When is inflammation good?

A

During infection or injury

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2
Q

When is inflammation bad?

A

In autoimmunity, due to an overreaction to a stimulus

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3
Q

What is acute inflammation (cells, duration, resolution?

A
  • Lots of neutrophils
  • Sudden onset and short duration
  • Usually resolves
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4
Q

What is chronic inflammation (cells, duration, resolution)?

A
  • Lots of lymphocytes and macrophages
  • Slow onset or occurs after acute
  • Long duration and may never resolve
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5
Q

What are the characteristics of neutrophil polymorphs?

A
  • Filled with cytoplasmic granules that kill bacteria
  • Short lived cells that die at the scene
  • Release chemicals attracting other immune cells
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6
Q

What are the characteristics of macrophages?

A
  • Last weeks to months
  • Phagocytic properties, ingest bacteria and debris
  • Can antigen present to lymphocytes
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7
Q

What are the characteristics of mature lymphocytes?

A
  • Last several years
  • Produce chemicals to attract other inflammatory cells
  • Immunological memory
  • Large nucleus, little cytoplasm and little ER as they don’t really produce proteins
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8
Q

What are the characteristics of plasma cells?

A
  • Only antibody producing
  • Have a lot of ER for antibody production
  • Smaller nucleus
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9
Q

How do endothelial cells work?

A
  • Produce nitric oxide to stop things sticking
  • Line capillaries in inflammation
  • Become sticky to allow inflammatory cells to adhere
  • Become porous to allow inflammatory cells to pass into tissues
  • Grow into areas of damage to form new vessels
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10
Q

What happens to fluid in acute inflammation?

A
  • More fluid leaking out of tissues, even at venous ends of capillaries
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11
Q

What are the characteristics of fibroblasts?

A
  • Lots of ER
  • Produce collagen in areas of chronic inflammation and repair
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12
Q

What are the characteristics of acute appendicitis?

A
  • Unknown precipitating factor
  • Neutrophils appear
  • Blood vessels dilate
  • Inflammation of serous surface
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13
Q

What is the sequence of acute inflammation?

A
  • injury or infection
  • neutrophils arrive and phagocytose and release enzymes
  • macrophages arrive and phagocytose
  • either resolution with clearance of inflammation or progression to chronic inflammation
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14
Q

What is the sequence of chronic inflammation?

A
  • either progression from acute inflammation or starts as ‘chronic’ inflammation
  • no or very few neutrophils
  • macrophages and lymphocytes, then usually fibroblasts
  • can resolve if no tissue damage (e.g. viral infection like glandular fever) but often ends up with repair and for- mation of scar tissue
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15
Q

What is a granuloma?

A
  • Particular type of chronic inflammation: collections of macrophages surrounded by lymphocytes
  • Significance: due to mycobacterial infection
  • May be seen around foreign material in tissue
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16
Q

What is resolution?

A
  • initiating factor removed
  • tissue undamaged or able to regenerate
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17
Q

What is repair?

A
  • initiating factor still present
  • tissue damaged or unable to regenerate
  • Can lead to replacement of damaged tissue by fibrous tissue
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18
Q

What types of cells can’t regenerate?

A

myocardial cells and neurones

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19
Q

What is thrombosis?

A

The formation of a solid mass from blood constituents in an intact vessel in a living person

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20
Q

What is an embolism?

A

Anything that moves through the blood vessels and when it reaches an area too small to pass through, blocks the blood flow.

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21
Q

What is ischaemia?

A

A reduction in blood flow to a tissue without any other implications

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22
Q

What is an infarction?

A

Reduction in blood flow to a tissue so reduced that it cannot support the maintenance of cells in the tissue so they die. Organs with end arterial supply are more prone to this

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23
Q

What is the implication of an embolus entering the venous system?

A
  • Travels through vena cava > RHS of heart > lodges in pulmonary arteries >
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24
Q

What are the 3 factors of Virchow’s triad?

A

Causes of thrombosis:
- Change in vessel wall
- Change in blood flow
- Change in blood constituents

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25
Q

What are the possible causes of embolus?

A
  • thrombus
  • air
  • cholesterol crystals
  • tumour
  • amniotic fluid
  • fat
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26
Q

What are some differences between arterial and venous thromboses?

A
  • Arterial occurs over decades, venous is rapid.
  • Arterial circulation: platelet rich
  • Venous circulation: fibrin rich
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27
Q

What are risk factors for venous thrombosis?

A

Major surgery, infection, inflammation

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28
Q

What are risk factors for arterial thrombosis?

A

smoking, diabetes, high BP, high cholesterol, lack of activity, poor diet, family history

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29
Q

What is apoptosis?

A

Programmed cell death in single cells

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30
Q

What protein triggers programmed cell death?

A

p53

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31
Q

What is apoptosis important for?

A
  • Development: removal of cells e.g. interdigital webs
  • Cell turnover: removal during normal turnover e.g. in intestinal villi
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32
Q

What is the role of apoptosis in cancer?

A
  • Cells don’t apoptose when they should leading to increase in tumour size and accumulation of genetic mutations.
  • Mutations in the p53 protein mean DNA damage lies undetected and apoptosis can’t be initiated
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33
Q

What is the role of apoptosis in HIV?

A

HIV induces apoptosis in CD4 helper cells, reducing their number and causing immunodeficiency

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34
Q

What is necrosis?

A

Traumatic cell death due to external factors. It occurs in a large number of cells

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35
Q

What are clinical examples of necrosis?

A
  • Infarction
  • Frostbite
  • Toxic venom
  • Pancreatitis
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36
Q

What is atherosclerosis?

A

The accumulation of fibrolipid plaques in the intima of systemic arteries. It reduces blood flow to important areas

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37
Q

Describe the time course of atherosclerosis?

A
  • birth: no atherosclerosis
  • late teens/20s: fatty streaks form
  • 30s-50s: development of established plaques
  • 40s-80s: complications of plaques e.g. thrombosis, haemorrhage
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38
Q

What are risk factors for atherosclerosis?

A
  • hypertension
  • hyperlipidaemia
  • cigarette smoking
  • diabetes mellitus
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39
Q

What are some complications of atherosclerosis?

A

Organ death if it is an end arterial supply/ reduced blood supply. Could cause embolism.

40
Q

What is endothelial damage theory?

A
  • Endothelial cells are easily damaged.
  • Smoking: free radicals, nicotine and CO damage
  • High BP: more pressure on side of blood vessels particularly in bifurcation
  • Hyperlipidaemia: damages endothelial cells (is cholesterol synthesised by body, not from food)
41
Q

What is hyperplasia and where does it occur?

A

Increase in the tissue size caused by increase in the number of constituent cells. Occurs in tissue where cells can’t divide e.g. skeletal muscle in bodybuilders

42
Q

What is hypertrophy?

A

Increase in tissue size caused by increase in size of cells e.g. uterine hypertrophy

43
Q

What is atrophy?

A

Decrease in the size of tissue caused by decrease in size of cells/decrease in constituent number e.g. Alzheimer’s

44
Q

What is metaplasia?

A

Change in differentiation of a cell from one fully-differentiated type to a different fully-differentiated type e.g. Barrett’s oesophagus (squamous > columnar due to stomach acid)

45
Q

What is the cause of metaplasia and give an example?

A

A consistent change in the environment of an epithelial surface e.g. bronchial epithelium from ciliated columnar > squamous due to cigarette smoke

46
Q

What is dysplasia?

A

Imprecise term for the morphological changes seen in cells in the progression to becoming cancer

47
Q

How can be dysplasia be investigated?

A

H&E staining is cheap and easy

48
Q

When do most chromosomal abnormalities occur?

A

Within the first month after conception

49
Q

What are the different stages of spina bifida?

A
  • initial epithelium formation
  • columnar base forms
  • invagination
  • tube formation and closure
50
Q

What does congenital mean?

A

Present at birth

51
Q

What is genetic disease?

A

Caused by a DNA mutation

52
Q

What is acquired disease?

A

Caused by non-genetic environmental factors but may still be congenital

53
Q

What is an effect of Down’s syndrome?

A

Susceptible to bacterial infections, early dementia and cataracts due to chromosome 21 being affected.

54
Q

What is an inherited disease?

A

Caused by an inherited genetic abnormality. Disease may not manifest until later life

55
Q

What is an example of autosomal co-dominance?

A

Mixing blood groups which works in transfusions

56
Q

What is polygenic inheritance?

A

Quantitative inheritance, where multiple independent genes have an additive/similar effect on a single trait

57
Q

What is an example of mixed hypertrophy/hyperplasia?

A

When number and size of constituent cells increases e.g. smooth muscle cells in uterus in pregnancy

58
Q

How does cell division show proof of ageing?

A

There is a limit to the number of times that cells can divide (Hayflick limit). Skin cells from older people divide less times in a culture than cells from younger people

59
Q

How is telomere length related to ageing?

A
  • The telomere region at the end of chromosomes shortens after each division
  • Eventually becomes so short that it isn’t possible for the chromosomes to divide and replicate
  • Cell no longer divides
60
Q

What are some causes of death of non-dividing cells?

A
  • free radical generation
  • accumulation of toxic by-products of metabolism
  • loss of DNA repair mechanisms
  • perioxidation of membranes
  • cross linking of DNA/proteins
61
Q

What is the only definitive mechanism of slowing down ageing and why?

A

Calorie restriction because there is reduction of metabolic products

62
Q

What is adjuvant therapy?

A

Extra treatment given after surgical excision

63
Q

What is carcinogenesis?

A

The transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations

64
Q

What is the difference between carcinogenesis and oncogenesis?

A

Carcinogenesis applies to malignant tumours but oncogenesis applies to malignant and benign

65
Q

What are the 5 classes of carcinogens?

A
  • Chemical
  • Viral
  • ionising/non-ionising radiation
  • hormones, parasites, mycotoxins
  • misc
66
Q

What are the 5 cardinal signs of inflammation?

A
  1. Rubor (redness due to dilation of vessels)
  2. Calor (heat)
  3. Tumour (swelling from oedema)
  4. Dolor (pain)
  5. Loss of function
67
Q

How do atherosclerotic plaques form?

A
  • Endothelial cells damaged
  • Increased permeability for LDL allowing inflammatory cells and lipids to enter
  • Macrophages attracted and take up lipids forming foam cells
  • Foam cells die and spill lipids forming a fatty streak
  • Activated macrophages release cytokines and PDGF causing proliferation of smooth muscle
  • Synthesis of collagen + elastin occurs and formation of a fibrous cap around lipid core
68
Q

What are risk factors for atherosclerosis?

A
  • Smoking: damage to endothelial cells
  • Hypertension
  • High cholesterol
  • Diabetes
  • Male
  • Age
  • Diabetes
  • Sedentary
69
Q

What are some methods of prevention of atherosclerosis?

A
  • Smoking cessation
  • BP control
  • Exercise
  • Low dose aspirin to inhibit platelet aggregation
  • Statins
70
Q

What is the role of platelets in thrombosis?

A
  • Αlpha granules cause platelet adhesion
  • Dense granules cause platelet aggregation
  • Platelets get activated and release granules when coming into contact with collagen
  • Causes thrombus formation in an intact vessel
71
Q

How are arterial thrombi formed?

A
  • Plaque causes turbulent blood flow
  • Intimal cells lost, fibrin deposited and platelet aggregation occurs
  • Positive feedback loop
  • RBC trapped in fibrin mesh
  • More growth, more turbulence, more platelet deposition
72
Q

How are venous thrombi formed?

A
  • Lower pressure in veins, thrombus begins at valves
  • Valves produce turbulence and can be damaged
  • BP falls, flow slows allowing thrombus formation
73
Q

What is a possible effect of venous emboli?

A
  • pulmonary embolism due to emboli travelling to vena cava and lodging in artery
74
Q

How are tumours classified?

A

T: 1-4 (tumour size)
N: 0-2 (lymph nodes affected)
M: 0-2 (metastasis)

75
Q

What are the stages of metastasis and secondary tumour formation?

A
  • Detachment
  • Invasion of connective tissue
  • Intravasation > vessels
  • Circulation + evasion of host defence
  • Adhesion to vessel wall
  • Extravasation
  • Growth of secondary tumour
76
Q

What cancer type is the exception to metastasis?

A

Basal cell carcinoma

77
Q

What is the difference between a neoplasm and a tumour?

A

Neoplasm: A new growth lesion resulting from autonomous abnormal growth of cells persisting after the original stimulus has been removed
- Tumour: any abnormal swelling

78
Q

What is suppuration?

A
  • Formation of pus
  • Becomes surrounded by pyogenic membrane
  • Leads to scarring
79
Q

What is organisation?

A
  • Replacement of acute inflammation by granulation tissue
  • New capillaries form into inflammatory exudate, macrophages migrate, fibrosis occurs
80
Q

Where does cancer most commonly metastasise from?

A

Lung, breast, kidney, thyroid, prostate

81
Q

What are characteristics of benign tumours?

A
  • Doesn’t invade basement membrane
  • Grows outwards (exophytic)
  • Low mitotic activity
  • Defined
  • Necrosis and ulceration rare
82
Q

What are the characteristics of malignant tumours?

A
  • Invade basement membrane
  • Endophytic
  • High mitotic activity
  • Poorly defined
  • Necrosis and ulceration common
83
Q

How can neoplasms cause morbidity and mortality?

A
  • Pressure on adjacent structures
  • Obstruct flow
  • Production of hormones
  • Transformation to malignant neoplasm
84
Q

How can malignant neoplasms cause morbidity and mortality?

A
  • Destruction of adjacent tissue
  • Metastases
  • Blood loss from ulcers
  • Paraneoplastic effects
  • Anxiety and pain
85
Q

What is a sarcoma?

A

Malignant connective tissue neoplasm

86
Q

Describe neutrophil polymorph emigration

A
  1. Migration of neutrophils to plasmatic zone due to slowing plasma flow
  2. Adhesion of neutrophils to endothelium in venues
  3. Neutrophil emigration onto basal lamina then vessel wall
  4. Diapedesis: RBC can also escape
87
Q

From where are neoplastic cells derived?

A
  • Nucleated, usually monoclonal cells
  • Growth pattern and synthetic activity is related to the parent cell
88
Q

What are neoplasms of glandular/secretory epithelium called?

A

Benign: adenoma
Malignant: adenocarcinoma

89
Q

What is a papilloma?

A

Benign tumour of non-glandular, non-secretory epithelium. e.g. squamous cell papilloma

90
Q

What is a carcinoma?

A

Malignant epithelial neoplasm

91
Q

What is a:
1. lipoma
2. chondroma
3. osteoma
4. angioma
5. rhabdomyoma
6. Leiomyoma
7. Neuroma

A
  1. adipocytes
  2. cartilage
  3. bone
  4. blood vessels/vascular
  5. striated muscle
  6. smooth muscle
  7. nerves
92
Q

What are occupational/behavioural causes of these cancers:
1. lung
2. bladder
3. scrotal?

A
  1. smoking
  2. dye/rubber industries: β-naphthylamine
  3. polycyclic aromatic hydrocarbons in chimney sweeps
93
Q

What lifestyle factors can lead to cancers?

A

alcohol: mouth, oesophagus, liver, colon, breast
obesity: breast, oesophagus, colon, kidney
unprotected sex: HPV (cervix, penis, oropharyngeal)

94
Q

How can ethnicity increase cancer risk?

A
  • inc risk of oral cancer from reverse smoking in india
  • decreased risk of skin cancer from increased melanin
95
Q

Which cancers do these viruses lead to:
1. Epstein Barr
2. Hepatitis B/C
3. Merkel cell polyomavirus
4. Human Herpes Virus 8

A
  1. Burkitt lymphoma/nasopharyngeal carcinoma
  2. Hepatocellular carcinoma
  3. Merkel cell carcinoma
  4. Kaposi sarcoma
96
Q

Which cancers commonly metastasise to bone?

A

breast, lung, prostate, renal, thyroid

Osha 2a (15 decks)

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