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
Q

What are the benign and malignant lesions on glandular and squamous epitheliums?

A

Glandular: adenoma or adenocarcinoma
Squamous: papilloma or squamous cell carcinoma

26
Q

What is the visible sign of cancer and why is this?

A

Cachexia (weight loss)

Due to tumours being very metabolically active