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Pathology Flashcards

1
Q

3 types of growth receptors

A

Receptors with intrinsic tyrosine kinase activity
7 transmembrane GPCR
Receptors without intrinsice tyrosine kinase activity

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2
Q

What controls progression through the cell cycle

A

Cyclin dependant kinases (CDK) activate each other and other enzymes. CDKs are activated by cyclins D, E, A, B

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3
Q

What happens in G1 phase of cell cycle

A

Growth, cell gets bigger with increased protein synthesis, CDK4 is activated by cyclin D. CDK 4 activates retinoblastoma protein

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4
Q

How does retinoblastoma protein (Rb) regulate cell growth

A

E2F is responsible for cell division but is stopped from doing so by Rb. When CDK4 phosphorylates Rb, E2F starts cell division

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5
Q

What happens in S phase of cell cycle

A

Synthesis phase, E2F initiates DNA replication, increases levels of cyclin A. Cyclin A activates CDK2; this promotes DNA replication. Two copies of genome

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6
Q

What happens at G2

A

Second growth phase, cells get bigger and more protein synthesis. p53 is main checkpoint at end G2

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7
Q

What are TAG repeats

A

Chromosomes are capped with TTAGGG repeats called Telomeres. This gets smaller with every division

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8
Q

Physiological hyperplasia

A

Breast tissue formation during puberty

Hyperplasia of endometrial lining of uterus - Pregnancy

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9
Q

Pathological hyperplasia

A

Excess oestrogen leads to endometrial hyperplasia and abnormal menstrual bleeding, often post menopausal

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10
Q

Lymph nodal swelling is due to hyperplasia or trophy?

A

Hyperplasia

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11
Q

Physiological atrophy

A

Uterus after parturition, certain embryological structures

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12
Q

Pathological atrophy

A

Brain during ischaemia, muscles with reduced workload

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13
Q

Main cell of acute inflammation

A

Neutrophils

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14
Q

What mediates vasodilation after injury

A

Histamine and Nitric Oxide

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15
Q

Major cellular changes after injury

A 
Vasodilation - Stasis 
White cell margination
Rolling
Adhesion
Migration
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16
Q

What is white cell margination

A

Blood flow slows with vasodilation, hence white cells are able to move along the periphery

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17
Q

What do vessel walls express that bind to white cells

A

Vascular Cell Adhesion Molecules - VCAM

Intercellular Cell Adhesion Molecule - ICAM

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18
Q

What’s expressed on white cells that bind to vessel walls

A

Selectins which bind CAMs on endothelial surface

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19
Q

What increase carbohydrate expression on WBCs for selections in endothelial cells

A

Histamine and Thrombin from inflammatory cells

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20
Q

What increases endothelial expression of ICAM and VCAM

A

Tumour necrosis factor - TNF and Interleukin 1 - IL1

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21
Q

What increases affinity of VCAM and ICAM for Integrins

A

Chemokines from site on injury bind to proteoglycans

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22
Q

How do WBCs recognise bacterial/pathogen

A

Bacteria have terminal mannose residues, WBCs have mannose receptors

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23
Q

What are opsonins

A

An antibody or other substance which binds to foreign microorganisms or cells making them more susceptible to phagocytosis

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24
Q

How does killing and degradation occur in the phagolysosome

A

Reactive oxygen species-NADPH oxidase; oxygen gains an electron from NADPH and becomes superoxide
Reactive Nitrogen Species-Nitric Oxide Synthase combines NO with superoxide and produces ONOO

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25
Q

Clinical features of inflammation

A

Rubor, Calor, Tumor and Dolor

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26
Q

What causes redness and heat in inflammation

A

Vasodilation leading to increased permeability of vessel

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27
Q

What causes dolor - pain in inflammation

A

Prostaglandins and Bradykinins

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28
Q

What is resolution of tissue

A

Complete restoration of tissue to normal after removal of inflammatory components

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29
Q

What is required for resolution

A

Capacity to regenerate
Good vascular supply
Injurious agent easily removed

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30
Q

What is suppuration

A

Formation of pus

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31
Q

What is empyema

A

Collection of pus within an existing anatomical cavity

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32
Q

What is organisation

A

When the basal membrane is affected, scarring happens. Injuries with basement membrane intact heal rapidly with resolution

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33
Q

Response in most tissues when injury is severe and can’t be rebuilt easily

A

Granulation tissue formation

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34
Q

What is scarring and fibrosis in the liver known as

A

Cirrhosis

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35
Q

What are histiocytes

A

Histiocytes are tissue macrophages or dendritic cells

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36
Q

What are granulomas

A

Granulomas are a collection of histiocytes or tissue macrophages where the immune system attempts to wall off the substance

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37
Q

What can cause granulomas

A

Specific infections, parasites, worms, eggs, syphilis, mycobacterium

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38
Q

What is caseous necrosis

A

Cell death in which the tissue maintain a cheese-like appearance

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39
Q

Consequences of no ATP

A

Na/K ATPase fails, leads to increase K, swelling
Calcium pump fails, increase intracellular Ca stimulates ATPase, Phospholipase, Protease, Endonuclease Mitochondrial permeability

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40
Q

How long are clot busting drugs viable for

A

30 mins

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41
Q

Pyknosis

A

Irreversible condensation of chromatin in the nucleus of the cell undergoing necrosis or apoptosis. Followed by Karyorrhexis or fragmentation of nucleus

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42
Q

What is coagulative necrosis

A

Cell death due to ischaemia or infarction leaving a ghost outline before complete phagocytosis of the cell

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43
Q

When is risk of cardiac rupture the greatest

A

3-7 days

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44
Q

What replaces macrophage after MI

A

Fibroblasts; finish laying collagen 6 weeks

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45
Q

What cells have a central role in matrix formation after an injury

A

Myofibroblasts

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46
Q

When is necrosis physiological

A

Never

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47
Q

What kind of necrosis is found in the brain

A

Liquefactive necrosis

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48
Q

What kind of necrosis is found in TB

A

Caseous necrosis

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49
Q

Example of physiological apoptosis

A

Removal of self reactive lymphocytes
Embryological growth
Hormonal induced involution

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50
Q

Causes of pathological apoptosis

A

Injury, radiation, chemotherapy, cancer, graft vs host disease, viral infection

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51
Q

What is the extrinsic pathway for apoptosis

A

Death receptor initiated pathway: Tumour Necrosis Factor, Fas

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52
Q

What is Fas ligand

A

Fas ligand belongs to the Tumour Necrosis Factor family. It’s binding with receptor induces apoptosis

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53
Q

What is intrinsic pathway of apoptosis

A

Mitochondrial pathway

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54
Q

What is the BAX protein

A

Functions as an anti or pro apoptotic regulator. Increases permeability of mitochondria and release of cytochrome C

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55
Q

What ligands are involved in extrinsic and intrinsic pathway

A

Fas and Bax ligand

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56
Q

What protein is a checkpoint in cell cycle

A

p53, can induce apoptosis

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57
Q

What is lipofuscin

A

Fine yellow-brown pigment granules composed of lipid-containing residues of lysosomal digestion. Sign of wear and tear and ageing

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58
Q

What is cancer

A

Uncontrolled cell proliferation and growth that can invade other tissues

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59
Q

What is neoplasia

A

New and abnormal growth of tissue in body

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60
Q

Benign or malignant

A

If the cancerous cells chew up the basement membrane

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61
Q

What is metaplasia

A

Change in form, reversible substitution of a kind of cell with another mature cell of another differentiated kind

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62
Q

What causes metaplasia

A

Change in signals delivered to stem cells causing them to differentiate down a different line, due to cytokines, growth factors or chemicals in cells

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63
Q

What metaplastic change can occur in the lungs due to thermal/chemical injury

A

Squamous metaplasia - Usual bronchial epithelium turns to squamous epithelium

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64
Q

What metaplastic change can occur in the bladder due to catheter inflammation

A

Usual transitional epithelium changes to squamous epithelium

65
Q

How is metaplastic tissue at risk of cancer development

A

No squamous cells in lungs but thermal/chemical injury can cause squamous metaplasia. This can become cancerous leading to lung squamous cell cancer

66
Q

What is dysplasia

A

Bad form, cell maturation is hindered in tissue and not in response to a stimuli, basement membrane intact

67
Q

What is cervical screening based on

A

Catching dysplasia before it becomes cancerous

68
Q

What is carcinoma in situ

A

Means cancer in place, dysplasia affecting entire non-glandular epithelium, localized and not past basement membrane

69
Q

Most potent cancer in men and women

A

Lung cancer

70
Q

Causes of cancer

A

Smoking,genes,alcohol,radiation,drugs,infection,weight

71
Q

What are BRCA 1 and BRCA 2 genes

A

Produce tumour suppressor proteins that help repair DNA. When these genes are mutated, there is genetic instability causing lack of DNA repair

72
Q

Example of autosomal dominant cancer causing genes

A

Retinoblastoma mutation

Familial Adenomatous Polyposis

73
Q

What is the double hit hypothesis

A

Knudson hypothesis states that mutation in both alleles of tumour suppressor genes is required to have a phenotypical problem. Those with one inherited faulty copy are at increased risk

74
Q

Two steps towards chemical carcinogenesis

A

Initiaters - Cause long lasting genetic damage

Promoter - Require initiator to have caused damage

75
Q

What is Ames test

A

Biological assay to assess the mutagenic potential of chemical compounds

76
Q

What can Aflatoxin (fungus on peanuts) cause

A

p53 mutation

77
Q

What cancers can Human Papillomavirus cause

A

Cervical cancer

78
Q

What cancer can Beta Naphthylamine cause

A

Bladder cancer. Liver deactivates Naphthylamine to Glucuronic acid. This is re-activated by glucuronidase leading to bladder cancer

79
Q

How does radiation affect the body

A

Radiation causes formation of pyrimidine dimers in DNA. Nucleotide excision repair helps remove DNA damage induced by UV light, however this is eventually overwhelmed.

80
Q

What is Xeroderma pigmentosa

A

Genetic defect in nucleotide excision repair (NER) and suffer from numerous skin cancers

81
Q

Example of not direct genetic mutation

A

Oncogenic virus - During viral replication, certains virus DNA/RNA can affect host cells genes causing it to become cancerous. Indirectly affects protein translation. HPV has E7 as an oncogenic product which binds to Rb gene. When free of Rb, E2F (initially attached to Rb) promotes transcription

82
Q

What is Schistosomiasis

A

Snail fever caused by parasitic flatworm called Schistosomes. Cause UTI which may develop into liver damage, kidney failure or bladder cancer

83
Q

Common forgotten condition predisposing to malignancy

A

Persistent chronic inflammation, tissue is replicating very often, prone to errors in production

84
Q

Common mutation in Lymphoma, neuroblastoma, small cell carcinoma of lung

A

Myc - Nuclear transcription factor that promotes cell growth

85
Q

Most commonly mutated kinase in cancer

A

PI3K, common target for haematological malignancies

86
Q

Earliest mutations in colorectal cancer

A

APC gene, tumour suppressor gene. Ensures chromosome number through cell division is correct

87
Q

Steps to malignancy

A 
Sustained growth signalling
Loss of growth inhibition
Unlimited replicative potential
Resisting apoptosis
Inducing angiogenesis
Disordered repair mechanisms
Evasion of immune system
Activating invasion and metastasis
88
Q

What are cyclins

A

Cyclins are a family of proteins that control progression through the cell cycle by activating cyclin-dependant kinase enzymes

89
Q

Most commonly mutated protein across all cancer

A

p53

90
Q

von Hippel-Lindau Tumour suppressor

A

Known as VHL, codes for pVHL. Loss of this increases angiogenesis, can be a syndrome

91
Q

Function of PTEN

A

PTEN increases transcription of p27. p27 blocks CDK and cell cycle progression. Mutation and deletion of PTEN leads to uncontrolled cell division

92
Q

What can cause unlimited replicative potential

A

Mutation that reactivates telomerase, this can renew length of telomeres

93
Q

What is upregulated in cancerous cells for angiogenesis

A

Vascular Endothelial Growth Factor

94
Q

Mechanisms for mutation repair (DNA repair)

A

p53, NER, BRCA, mismatch repair proteins

95
Q

Syndrome associated with frequent mismatched microsatellites

A

Lynch Syndrome

96
Q

PD-L1

A

Programmed death - ligand 1. Inhibits T-cell proliferation. Over expressed by malignant cells to avoid apoptosis.

97
Q

What ligand is tested for in all lung cancers

A

PD-L1, Programmed Death Ligand 1

98
Q

Physiological function of PD-L1

A

In pregnancy to suppress immune response

99
Q

What do metastatic cells overexpress to chew up surrounding tissue

A

Matrix Metalloproteinases (MMP)

100
Q

Is cancer clonal?

A

No, individual cells aren’t identical

101
Q

What is cancer recurrence

A

Clonal cells may have a survival advantage over specific treatment. These can remain in the body after treatment, multiply over time and grow large enough to cause symptoms. Some cancers have expected recurrence

102
Q

4 things wanted from a pathologist

A

Is it out, what is it, how far has it gone, how bad is it

103
Q

N:C Ratio

A

Ratio of the size of nucleus of cell to the size of cytoplasm. Nucleus generally decreases as cell matures, increased ratio associated with precancerous dysplasia

104
Q

What is Pleomorphism

A

Change in size, shape and staining of cells/nuclei. Characteristic of malignant neoplasms/dysplasia

105
Q

What is hyperchromasia

A

Increase in chromatin in cell nuclei leading to excessive pigmentation due to increased staining capacity of nuclei for hematoxylin

106
Q

What kind of mitosis is seen in malignant cells

A

Abnormal and lots of mitosis

107
Q

What are epithelial cancers called

A

Carcinomas

108
Q

What are glandular cancers called

A

Adenoma vs Adenocarcinoma

109
Q

What are squamous cancers called

A

Papilloma vs Squamous Cell Carcinoma

110
Q

What are bladder cancers called

A

Transitional cell carcinoma or Urothelial cell carcinoma

111
Q

What is Desmoplasia

A

Growth of fibrous or connective tissue. May occur around a neoplasm cause fibrosis around tumour

112
Q

Malignant messenchymal lesions

A

Sarcoma

113
Q

What are fat cell cancers called

A

Lipoma vs Liposarcoma (rare, deep soft tissue)

114
Q

What are bone cell cancers called

A

Osteoma vs Osteosarcoma (rare, more in growing child)

115
Q

What are cartilage cell cancers called

A

Enchondroma vs Chondrosarcoma

116
Q

What are skeletal muscle cell cancers called

A

Rhabdomyoma (Rare) vs Rhabdomyosarcoma (Rare, eye, bild duct, gynae tract)

117
Q

What are smooth muscle cell cancers called

A

Leiomyoma (Common, uterine fibroids) vs Leiomyosarcoma (Uncommon)

118
Q

What are nerve cell cancers called

A

Neurofibroma, schwannoma vs Malignant peripheral nerve sheath tumour

119
Q

What are blood vessel cancers called

A

Haemangioma vs Angiosarcoma, Kaposi’s sarcoma

120
Q

What is Kaposi’s Sarcoma

A

Cancer causing patches of abnormal tissue growth under skin and other organs. They are made up of cancer cells, blood vessels and blood cells

121
Q

What are melanocyte cancers called

A

Melanoma - Malignant type

122
Q

What are blood cell cancers called

A

Leukaemia and Lymphoma, always metastatic

123
Q

What is karyotyping

A

Culturing cells to find full chromosome complement

124
Q

How can tumours be classfied

A

TNM classification
T - Tumour size
N - Number of lymph nodes affected
M - Metastasis

125
Q

What is tumour staging

A

High stage - Well differentiated tumour, grows slowly but been there for long, hasn’t spread
Low stage - Aggressively growing, poorly differentiated

126
Q

Tumour grading

A

Low grade - Well differentiated, grows slowly and unlikely to spread
High grade - Poorly differentiated, likely to spread
Lower grade tumours have better outlook

127
Q

Early presentation in vocal cord cancer

A

Change in voice

128
Q

What is Cachexia

A

Loss of weight in someone not actively trying to lose weight

129
Q

What can cause increase metabolism by tumour cells

A

Release of Tumour Necrosis Factor (TNF)

130
Q

What is haemorrhage within tumours a sign of

A

Malignancy

131
Q

What is paraneoplastic syndrome

A

Due to cancer in body but not local presence of cancerous cells. These are mediated by humoral factors (hormones and cytokines) excreted by tumour cells. Can lead to osteoarthropathy, neurological symptoms, rash

132
Q

Which has better prognosis, tumours that stimulate a strong or weak immune response

A

Strong immune response. Cancer cells want to avoid the body’s immune system (immunosuppression) and this makes patient prone to infection

133
Q

Blood clot vs thrombus

A

Blood clot may be extra or intravascular. Blood clot consists of RBCs, fibrin, platelets etc. When the blood clot occurs inside a blood vessel, is it a thrombus. This is static and becomes an embolus when dislodged.

134
Q

Where do the intrinsic and extrinsic coagulation cascades meet

A

Intrinsic - Factor IXa, Extrinsic - Factor VIIa
These factors help in formation of XIa which converts Prothrombin to Thrombin. Thrombin helps form fibrin from fibrinogen

135
Q

What does the intrinsic factor start with

A

Factor XII

136
Q

What does the extrinsic factor start with

A

Tissue factor

137
Q

What is meant by a long Activated Partial Thromboplastin Time (APTT)

A

Something wrong with extrinsic pathway. If Prothrombin Time (PT) is long, something wrong with intrinsic

138
Q

What favours thrombosis

A

Virchows Triad -

Endothelial injury, stasis/turbulent blood flow and Hypercoaguable blood

139
Q

Why are athletes prone to thrombosis

A

Due to low heart rate, more stasis of blood

140
Q

What can air embolism result in

A

Decompression sickness, breathing at high pressure results in more dissolved gas in blood. Upon depressurization, gas comes out in bubbles inside the body. This can embolize and cause an obstruction to blood flow

141
Q

Cause of amniotic fluid embolism

A

Tear in placenta or uterine vessels with secondary infusion of amniotic fluid or fetal material. This can be diagnosed by identifying foetal skin (squamous cells) and hair in pulmonary vessels

142
Q

When can fat embolise in the body

A

After a large skeletal injury where the marrow contents are released (mostly adipose cells)

143
Q

What is septic emboli

A

Thrombus forms in association with an infectious agent

144
Q

What can cause septic emboli

A

Mycotic Aneurysm, Infective Endocarditis

145
Q

Are Atheroma and Atherosclerosis the same?

A

Yes

146
Q

Aetiology of Atheroma

A

Smoking, hypertension, hyperlipidemia, diabetes, age, sex, genetics

147
Q

Which vessels commonly affected by Atherosclerosis

A

Branching sites of vessels

148
Q

How does Diabetes cause Atheroma

A

Tissues lose their elasticity in diabetes, become more rigid and prone to endothelial injury

149
Q

Pathogenesis of Atheroma

A

Primary endothelial injury. Accumulation of LDL and macrophage in Tunica Intima. Migration of smooth muscles form Tunica Media. Formation of foam cells (fat laden macrophage). Collagenous fibrous cap increases in size decreasing size of lumen

150
Q

Why causes macrophages to migrate vessel wall

A

Endothelial injury leads to increase permeability which leads to increase VCAM-1. Monocytes attach and migrate into wall

151
Q

Uncomplicated vs complicated plaque

A

Uncomplicated plaque is static whereas complicated plaque has embolized.

152
Q

Progression of atheromatous plaque

A

Fatty streak - Fibrofatty plaque - Complicated plaque

153
Q

Complications of Atheroma

A

Stenosis, aneurysm, dissection, thrombosis/embolism

154
Q

How can arterial stenosis affect Carotids

A

Transient Ischaemic Attack, Stroke, Vascular dementia

155
Q

How can arterial stenosis affect renal arteries

A

Hypertension, renal failure

156
Q

How can arterial stenosis affect peripheral arteries

A

Claudication and foot/leg ischaemia

157
Q

What is an aneurysm

A

Abnormal and persistent dilation of vessel wall due to dilation of an artery due to weakness in its wall

158
Q

What is arterial dissection

A

Splitting of Tunica media by flowing blood

Principles (14 decks)

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