Pathology Flashcards

1
Q

What is the difference between hyperplasia and hypertrophy?

A
Hyperplasia = increased number of cells
Hypertrophy = increased size of cells
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2
Q

What are the 4 stages of the cell cycle?

A

G1 (increased growth + protein synthesis)
S (DNA synthesis)
G2 (more growth + protein synthesis)
M (mitosis - division of the cell)

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3
Q

What controls progression of the cell cycle?

A

CDKs

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4
Q

What is the main checkpoint protein of G2?

A

P53 - checks the cell for mistakes (initiates apoptosis if not all correct)

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5
Q

Why is there an increase in malignancy in older patients?

A

Telomeres - have caps to protect and prevent degradation of chromosome ends, these get shorter and shorter with each cell division so mutations more likely

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6
Q

What is the process of inflammation to a site of injury?

A

Vasodilation (arterioles and capillary beds) - redness + heat,
White cell margination (due to slower blood flow),
VCAMs/ICAMs (bind to each other),
Rolling,
Pavementing,
Leaky vessels,
Chemotaxis down chemical gradient - swelling,
Phagocytosis

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7
Q

What are the clinical features of infection?

A
Rubor (redness), 
Calor (heat), 
Tumor (swelling), 
Dolor (pain)
Loss of function
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8
Q

What is suppuration?

A

The formation of pus (dead/dying cells, inflammatory debris, neutrophils, bacteria)

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9
Q

What is complete restoration of the tissue to normal after removal of inflammatory components called?

A

Resolution

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10
Q

What is organisation?

A

Fibrin left at site of injury after repair (used as scaffold to repair around)

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11
Q

What type of immune cells are associated with acute and chronic inflammation?

A

Acute - neutrophils

Chronic - lymphocytes and macrophages

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12
Q

What are the different fates of repair of acute inflammation?

A

Resolution,
Organisation,
Suppuration,
Chronic inflammation

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13
Q

Describe necrosis

A

Always pathological

Requires no energy

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14
Q

What are the 3 different types of necrosis (describe each)?

A

Coagulative - preservation of cell outline
Liquefactive - pus
Caseous - granuloma associated with TB

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15
Q

What is apoptosis?

A

Programmed cell death in response to specific signals - requires energy (can be pathological)

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16
Q

What internal pathway must be activated for cell death (either necrosis or apoptosis)

A

Caspase cascade (extrinsic or intrinsic activation)

17
Q

What is the ‘death receptor’?

A

TNF - tumour necrosis factor

18
Q

What is the process of apoptosis?

A
Caspase cascade,
Cells shrink,
Chromatin condensation,
Cytoplasm breaks up,
Macrophages clear the debris
19
Q

What is cancer?

A

Uncontrolled cell proliferation and growth that can invade other tissues

20
Q

What is neoplasia?

A

New growth, not in response to a stimulus (benign, malignant, pre-malignant)

21
Q

What is metaplasia?

A

Reversible change from one cell type to another - usually in response to a toxic stimulus

22
Q

What is dysplasia?

A

Disordered growth

23
Q

What is carcinoma in-situ?

A

Dysplasia affecting the whole epithelium, last stage before becoming invasive

24
Q

What are the hallmarks of cancer?

A
Sustained growth signalling,
Loss of growth inhibition,
Unlimited replicative potential,
Resisting apoptosis,
Activating invasion and metastasis,
Inducing angiogenesis,
Evasion of the immune system, 
Disordered repair mechanisms
25
What are the benign and malignant lesions on glandular and squamous epitheliums?
Glandular: adenoma or adenocarcinoma Squamous: papilloma or squamous cell carcinoma
26
What is the visible sign of cancer and why is this?
Cachexia (weight loss) | Due to tumours being very metabolically active