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Phase 2a Lecture Notes > Pathology > Flashcards

Pathology Flashcards

1
Q

Thrombosis

A

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

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2
Q

1st stage of thrombosis

A

platelet aggregation. Platelets release chemicals when they aggregate which cause other platelets to stick to them and also which start off the cascade of clotting proteins in the blood

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3
Q

+ive or -ive feeback loop- platelet aggregation

A

postive

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4
Q

2nd stage of thrombosis formation

A

Once the clotting cascade has started there is formation of the large protein molecule fibrin which makes a mesh in which red blood cells can become entrapped

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5
Q

why dont blood clots form all the time

A
  1. Laminar flow - cells travel in the centre of arterial vessels
    and don’t touch the sides
  2. Endothelial cells which line vessels are not ‘sticky’ when healthy
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6
Q

How does smoking cause thrombosis

A

cigarette smoking causing endothelial cell injury (change in vessel wall and change in blood flow over the injured/absent cells)

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7
Q

How to prevent risk of thrombosis in hospital?

A

early mobilisation after operation, low dose subcutaneous heparin

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8
Q

How does aspirin reduce the risk of thrombosis?

A

aspirin inhibits platelet aggregation

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9
Q

How does COVID cause thrombotic events?

A

Causes changes in clotting factors that causes thrombosis, leading to micro-thrombi in vessels

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10
Q

Embolus

A

mass of material in vascular system that becomes stuck in a vessel, blocking it

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11
Q

Most common embolus

A

Thrombus, ie DVT in legs breaking off and embolising through the large veins and right side of the heart to the lungs

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12
Q

Less common causes of embolus

A
  • air (be careful with pressurised systems of intravenous fluids/blood especially in infants and children)
  • cholesterol crystals (from atheromatous plaques)
  • tumour
  • amniotic fluid (rare in pregnant women with precipitate labour)
  • fat (severe trauma with multiple fractures)
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13
Q

Effects of thrombosis or embolus

A

Reduction in blood flow, causing reduction of O2 to surrounding cells, leading to ischemia

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14
Q

Ischaemia

A

a reduction blood flow to a tissue without any other implications

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15
Q

Infacrtion

A

reduced blood flow, leading to cell death

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16
Q

Why are certain organs less prone to infarction

A

dual arterial supply so are much less susceptible to infarction:
liver - with portal venous and hepatic artery supplies,
-lung - with pulmonary venous and bronchial artery supplies,
-brain around the circle of Willis with multiple arterial supplies

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17
Q

Resolution

A
  • initiating factor removed
    -tissue undamaged or able to regenerate
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18
Q

Repair

A
  • initiating factor still present
    -tissue damaged or unable to regenerate
    -replacement of damaged tissue by fibrous tissue
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19
Q

Can the liver regenerate?

A

Yes! as long as not too much liver is removed so the patient dies of liver disease

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20
Q

Why don’t alcoholics livers regenerate?

A

Initiating factor constantly present due to constant alcohol abuse, so repair occurs not resolution

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21
Q

Why can lungs regenerate after lobar pneumonia

A

Pneumocytes can regenerate, no damage to alveoli walls

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22
Q

Does repair or resolution occur after severe COVID?

A

If alveoli walls are damaged as a result severe covid, repair occurs in lungs

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23
Q

Most superficial skin wound

A

Abrasion- only removed top layer of epidermis, basal cells still present

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24
Q

Healing by 1st intention

A

Edges of skins brought together, reduces risk of infection. Fibrinogen first brings skins together, then collogen strengthens and epidermis reforms

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25
Q

Healing by secondary intention

A

sides of the wound are not opposed, therefore healing must occur from the bottom of the wound upwards

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26
Q

Cells that can regenerate

A
  • hepatocytes (liver)
  • pneumocytes (lungs)
  • all blood cells
  • gut epithelium
  • skin epithelium
  • osteocytes (bones)
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27
Q

Cell that don’t regenerate

A
  • myocardial cells
  • neurones
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28
Q

Man aged 30 takes a large overdose paracetamol overdose and doesn’t come to hospital for 2 days. He spends a few days on ITU with liver failure but then recovers.
What will be happening in his liver -
resolution or repair?

A

resolution, Only overdose once, so provided he doesn’t die of liver damage, his liver should regenerate

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29
Q

A child aged 3 falls off a climbing
frame onto his hand, he fractures his
clavicle. He has his arm in a sling for
4 weeks and is very good about
keeping it in the sling
What will be happening in his
clavicle - resolution or repair?

A

Resolution- provide child keeps arms in sling as osteocytes regenerate

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30
Q

Atherosclerosis

A

accumulation of fibrolipid plaques in systemic (as opposed to pulmonary) arteries

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31
Q

Risk of Atherosclerosis

A

narrowing of arteries reduces the blood flow to important areas e.g. myocardial infarction in the heart

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32
Q

Risk factors of atherosclerosis

A
  • hypertension
  • hyperlipidaemia (too many lipids (fats) in your blood)
  • cigarette smoking
  • poorly-controlled diabetes mellitus
    higher in more social deprived areas
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33
Q

Do you find atheroslcerosis in the pulmonary arteries

A

No, blood pressure is lower

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34
Q

Current atherosclerosis theory

A

Endothelial cell damage theory
* endothelial cells are delicate
* easily damaged by cigarette smoke, shearing forces at
arterial divisions, hyperlipidaemia, glycosylation products
* cumulative damage leads to endothelial ulceration, microthrombi, eventual development of established atherosclerotic plaques

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35
Q

How does hypertension lead to atherosclerosis

A

Shearing forces on endothelial cells

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36
Q

How does smoking lead to atherosclerosis

A

Free radicals, nicotine and CO damage endothelial cells

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37
Q

How does diabetes lead to atherosclerosis

A

Superoxide anions and glycosylation products damage endothelial cells

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38
Q

How does hyperlipidaemia lead to atherosclerosis

A

direct damage to endothelial cells

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39
Q

Atherosclerosis feedback loop

A

Positive feedback loop. Damage to endothelium, leads to thrombi healing over, causes increased narrowing, higher BP, causes more damage…

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39
Q

Complications of atherosclerosis

A

Consequences of blocked pluming, occlusion of blood vessel leading to ischemia and possibly infarction

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40
Q

Apoptosis

A

Programmed individual cell death.

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41
Q

What causes apoptosis?

A

DNA damage detected, cell triggers a series of proteins which lead to the release of enzymes (caspases) that auto digest the cell

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42
Q

Importance of apoptosis for healthy function

A
  • Development - removal of cells during development e.g. interdigital webs
  • Cell turnover - removal of cells during normal turnover e.g. cells in the intestinal villi at the tips, to be replaced by cells from below
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43
Q

Apoptosis in disease

A
  • Cancer - cells in tumours often don’t apoptose when they would have been expected to which results in increase in the tumour size and accumulation of genetic mutations. Often this is due to mutations in the P53 gene so the p53 protein can no longer detect DNA damage and instigate apoptosis.
  • HIV - the HIV virus can induce apoptosis. It can induce apoptosis in CD4 helper cells which reduces their numbers enormously to produce an immunodeficient state.
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44
Q

Necrosis

A

Traumatic cell death- wholesale destruction of large numbers of cells by some external factor

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45
Q

Apoptosis vs Necrosis

A

Apoptosis is programmed cell death. Necrosis is traumatic cell death by external factor

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46
Q

Clinical Example of Necrosis

A
  • Infarction due to loss of blood supply e.g. myocardial infarction, cerebral infarction, avascular necrosis of bone
  • Frostbite
  • Toxic venom from reptiles and insects
  • Pancreatitis
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47
Q

Spina bifida occulta

A

Missing a spinus process, wouldn’t notice unless CT scan performed

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48
Q

Meningocele

A

Outpouring sac filled with fluid, n can need to be fixed by surgery, minor disability can occur

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49
Q

Myelomeningocele

A

Outpouring sac containing spinal cord, leads to paralysis

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50
Q

Congenital

A

Present at birth, not always genetic ie club foot

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51
Q

Inherited

A

Caused by an inherited genetic abnormality

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52
Q

Chromosomal Abnormalities

A

Incorrect number of chromosomes inherited, ie downs syndrome, 3 chromosome 21’s inherited

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53
Q

Medellin Inheritance

A

Single gene mutation causes problem

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54
Q

Autosomal inheritance

A

On paired chromosome except sex chromosomes

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55
Q

Autosomal dominace

A

Only one dominant allele needed to express problem

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56
Q

Autosomal recessive

A

2 recessives alleles needed to express problem

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57
Q

Polygenetic Inheritance

A

Variation in several genes lead to increased risk of problem

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58
Q

Acquired

A

Caused by non-genetic environmental factors

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59
Q

Are inherited diseases always congenital?

A

No, ie Huntington’s disease

60
Q

Can acquired disease be congenital?

A

Yes, ie fetal alcohol syndrome

61
Q

hypertrophy

A

increase in size of a tissue caused by increase in size of the constituent cells, usually occurs organs when cells cannot divide, ie skeletal and cardiac muscle

62
Q

hyperplasia

A

increase in size of a tissue caused by an increase in number of constituent cells, usually occurs in organs that can regenerate, ie gut, skin, smooth muscle ect

63
Q

Common conditions caused by hyperplasia

A

prostate enlargement as a result of smooth muscle hyperplasia
endometrial hyperplasia, often as a result of hormone imbalance

64
Q

Atrophy

A

decrease in size of a tissue by a decrease in number of constituent cells and/or a decrease in their size

65
Q

Common atrophy conditions

A

Cerebral atrophy can be a result of Alzheimer’s
Muscle atrophy, can be a result of lack of use after immobilization
Optic atrophy

66
Q

Metaplasia

A

change in differentiation of a cell from one fully-differentiated type to another fully-differentiated cell

67
Q

Common metaplasia condtions

A

Bronchi of smokers, ciliated columnar epithelium to squamous epithelium
Barrett’s oesophagus, squamous epithelium to columnar epithelium as result of regular stomach acid exposure

68
Q

Dysplasia

A

imprecise term for the morphological change seen in cell in the progression of becoming cancer, can be used to refer to a developmental abnormality

69
Q

What is found at the end of chromosomes?

A

Telomeres, region of repetitive DNA

70
Q

Common conditions associated with aging

A

Dermal elastosis, osteoporosis, cataracts, dementia, sarcopenia, deafness

71
Q

Dermal elastosis

A

Skin aging, wrinkling, due to cross linking of proteins

72
Q

Cataracts

A

Protein cross linking in eye lens leading to them becoming opaque

73
Q

Osteoporosis

A

Increased bone reabsorption, leading to weaker, more brittle bones, more common in woman after the menopause due to hormone imbalance

74
Q

Sarcopenia

A

Decrease in muscle mass with age, mobility problems (falls, getting up and around) after after losing a lot muscle

75
Q

Deafness

A

Loss of hair cells in cochlea, these cells do not regenerate

76
Q

Features of acute inflammation

A

Redness, heat, swelling, pain, loss of function

77
Q

Key cells involved in acute inflammatory process

A

Neutrophils, multi-lobular nuclease

78
Q

NSAIDS

A

Non-steroidal anti-inflammatory drugs

79
Q

Common side effect of chronic NSAID use

A

Gastritis. NSAIDs diminish protective mucin secretions. They also cause exfoliation of the surface epithelium. This results in damage to the surface epithelium, eliciting an acute inflammatory response

80
Q

Most common Bacteria that causes gastritis

A

Helicobacter pylori

81
Q

Common signs of sepsis

A

High temp, HR is fast, BP is low, Confusion

82
Q

Chronic inflammation, causes and cells associated

A

May be a progression from acute inflammation. May represent a primary disease process. Lymphocytes, macrophages, plasma cells and eosinophils are associated with chronic inflammation

83
Q

Granuloma

A

Aggregate around cause of inflammation of epithelioid histocytes (tissue resident macrophages)

84
Q

How does chronic inflammation lead to cancer?

A

Chronic inflammation> Metaplasia> Dysplasia> Carcinoma in situ> Invasive Carcinoma

85
Q

Why does chronic inflammation cause cancer?

A

-Inflammation causes cellular changes and immune responses to repair damaged tissue → cell proliferation @ site of injury
-Inflammatory response becomes chronic → ↑ cell proliferation and ↑ risk of the development of mutations
-Chronic inflammatory cells (especially macrophages) generate high levels of reactive oxygen and nitrogen species to fight infection → release of mutagenic agents
-Inflammatory cells also release factors that interfere with regulation of cell replication exacerbating tumourgenesis

86
Q

Conditions when chronic inflammation plays a key role

A

-Myocardial fibrosis (post MI)
-Atheroma development
-Multiple sclerosis (macrophages break down myelin)

87
Q

Is osteoarthritis an inflammatory disease?

A

NO, inflammation plays a small role in disease pathogenesis. Primarily degenerative disease

88
Q

Can basal cell carcinomas of the skin metastases?

A

No

89
Q

Name of a malignant tumour of striated muscle

A

Rhabdo myo sarcoma

90
Q

Is it common for liposarcomas to metastasise to bone?

A

No

91
Q

Common bone metastases

A

Breast, lung, prostate, renal cell and thyroid cancer

92
Q

Name of benign tumour of glandular epithelium

A

Adenoma

93
Q

UK screening programs, types of cancer

A

Breast cancer, colorectal cancer and cervical cancer

94
Q

Name of benign tumour of fat

A

Lipoma

95
Q

Name of malignant tumour of glandular epithelium

A

Adenocarcinoma

96
Q

Can ovarian cancer spread in the peritoneum

A

Yes, if it breaches the ovarian cavity

97
Q

Why does leukemia cause a large range of symptoms?

A

WBC circulate round the body and so will any tumour of WBC, hence can spread easily causing many symptoms

98
Q

Why do lymph nodes need to be removed when treating certain carcinomas?

A

Carcinomas can spread to the lymph nodes that drain the site of carcinomas so need to be removed to ensure as many tumours as possible have been taken out

99
Q

Ways carcinomas can spread

A

-Invade nearby structures
-Through lymph nodes
-Through blood to bone

100
Q

Steps for breast cancer treatment

A
  1. Diagnosis breast cancer
  2. Check has it spread to the axilla via lymph nodes, if yes axillary node need to be removed with breast cancer
  3. Check has it spread to the rest of the body ie bone scan or CT scan, if yes systemic treatment needed (chemo)
  4. If no to 3, Surgery need to remove breast cancer either with or without axillary clearance
  5. Radiotherapy to remove any remaining micro metastases
  6. Further adjuvant treatment depending on breast cancer pathology
101
Q

Is a patient definitely cured if a tumour has been completely excised?

A

No, micro metastases could still be present

102
Q

Adjuvant treatment

A

Extra treatment given after surgery

103
Q

Tumour

A

Any abnormal swelling ie neoplasm, inflammation. Hypertrophy and hyperplasia

104
Q

Neoplasm

A

A lesion resulting from the autonomous or relatively autonomous abnormal growth of cells with persists after the initiating stimulus has been removed

105
Q

Lesion

A

area of abnormal tissue

106
Q

Malignant-benign spectrum

A

Not always binary, some neoplasms are borderline so can present as benign or malignant but act as the opposite

107
Q

Structure of neoplasms

A

Neoplastic cell (derived from nucleated cells) are supported by a stroma (a connective tissue framework which provides mechanical support and nutrition)

108
Q

What does central necrosis of neoplasm show?

A

Neoplasm is growing so quickly that blood supply is unable to provide nutrients to the centre of the neoplasm

109
Q

Tumour angiogenesis

A

Essential to growth, how a tumour forms a blood supply to provide its self with nutrients, tumour unable to grow via simple diffusion

110
Q

Classification of neoplasms

A

Benign, borderline and malignant

111
Q

Benign neoplasms

A

-Localised, non-invasive
-Slow growth rate
-Low mitotic activity
-Close resemblance to normal tissue
-Circumscribed or encapsulated, well defined

112
Q

Histology of benign neoplasms

A

-Nuclear morphometry (shape) often normal
-Necrosis rare
-Ulceration rare
-Growth on mucosal surface usually exophytic (grow outward beyond the surface epithelium from which it originates)

113
Q

Can benign neoplasms be harmful?

A

Yes, they can put pressure on adjacent structures, obstruct flow, produce hormones, transform to malignant neoplasm and anxiety for patient

114
Q

Malignant neoplasms

A

-Invasive
-Metastases
-Rapid growth rate
-Variable resemblance to normal tissue
-Poorly defined or irregular border

115
Q

Histology of malignant neoplasms

A

-Hyperchromatic (stain more deeply than normal) and pleomorphic (changes shape) nuclei
-Increased mitotic activity
-Necrosis and ulceration common
-Growth on mucosal surfaces and skin often endophytic (tending to grow inward into tissues in fingerlike projections from a superficial site of origin)

116
Q

Why are malignant neoplasms harmful?

A

-destruction of adjacent tissue
-mets
-Blood loss from ulcers
-obstruct flow
-produce hormones
-paraneoplastic effects (disorders that occur when the immune system has a reaction to a cancerous tumour)
-anxiety and pain

117
Q

Papilloma

A

Benign neoplasm of non-glandular non-secretory epithelium, prefix with cell type origin

118
Q

Carcinoma

A

-Malignant epithelial neoplasm
-Prefix with epithelial cell type e.g. urothelial carcinoma
-Carcinomas of glandular epithelium are adenocarcinomas

119
Q

Adenoma

A

-Benign neoplasm of glandular or secretory epithelium
-Prefix with cell type of origin, e.g. colonic adenoma, thyroid adenoma

120
Q

Anaplastic neoplasm

A

Cell type of origin cannot be determined, typically poor prognosis

121
Q

Teratoma

A

congenital (present prior to birth) tumor formed by different types of tissue. Teratomas in newborns are generally benign

122
Q

Papilloma

A

Benign neoplasm of non-glandular non-secretory epithelium

123
Q

How do decided a prefix for a neoplasm?

A

Depends on behavioural classification and cell type

124
Q

Adenocarcinomas

A

Carcinomas of glandular epithelium

125
Q

What is cell type origin of Lipoma?

A

adipocytes

126
Q

What is cell type origin of Chondroma

A

cartilage

127
Q

What is cell type origin of Osteoma

A

Bone

128
Q

What is cell type origin of Angioma

A

Vascular

129
Q

What is cell type origin of Rhabdomyoma

A

striated muscle

130
Q

What is cell type origin of Leiomyoma

A

smooth muscle

131
Q

What is cell type origin of Neuroma

A

nerves

132
Q

What is cell type origin of Liposarcoma

A

adipose tissue

133
Q

What is cell type origin of Rhabdomyosarcoma

A

striated muscle

134
Q

What is cell type origin of Leiomyosarcoma

A

smooth muscle

135
Q

What is cell type origin of Chrondrosarcoma

A

cartilage

136
Q

What is cell type origin of Osteosarcoma

A

bone

137
Q

What is cell type origin of Angiosarcoma

A

blood vessels

138
Q

Carcinogenesis

A

The transformation of normal cells to neoplastic cells though permanent genetic alterations or mutations
Applies to malignant neoplasms

139
Q

Carcinogenic vs Oncogenic

A

Both agents known or suspected to cause tumours
Carcinogenic = cancer causing
Oncogenic = tumour causing

140
Q

Classes of carcinogens

A

Chemical, Viral, Ionising and non-ionising radiation, Hormones, parasites and mycotoxins, Miscellaneous

141
Q

Host Factors

A

Ethnicity, Diet / Lifestyle, Constitutional factors (age, gender etc), Premalignant lesions, Transplacental exposure

142
Q

conventional chemotherapy

A
  • not selective for tumour cells
    – except that they might be dividing faster
  • usually hits normal cells which are dividing
    – myelosuppression
    – hair loss
    – diarrhoea
143
Q

What type of tumour is conventional chemotherapy most effective for treating

A

good for fast dividing tumours
– germ cell tumours of testis
– acute leukaemias
– lymphomas
– embryonal paediatric tumours
– choriocarcinoma

144
Q

What type of tumour is conventional chemotherapy less effective for treating

A

not so good for slower dividing tumours
– most other tumours

145
Q

targeted chemotherapy

A

exploits some difference between cancer cells
and normal cells to target drugs to the cancer
cells
– more effective
– less side effects

146
Q

Methods for differentiating tumours

A

Gene arrays, proteomics, tissue microarrays

147
Q
A

Phase 2a Lecture Notes (14 decks)

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