PATHOLOGY COPY Flashcards by Laura Stewart

Causes of acute inflammation

Microbial infections 
Hypersensitivity reactions 
Physical agents  
Chemicals
Tissue necrosis

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What makes up the cellular exudate for acute inflammation?

Neutrophil polymorphs
Macrophages
Lymphocytes

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Causes of chronic inflammation

Primary chronic inflammation
Transplant rejection
Progressing from acute inflammation
Recurrent episodes of acute inflammation

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Causes of primary chronic inflammation

Exogenous materials
Endogenous materials
Resistance of infective agent to phagocytosis and intracellular killing – TB
Autoimmune diseases – rheumatoid arthritis
Primary granulomatous diseases – Crohn’s

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What is the cellular exudate in chronic inflammation mainly made of?

Lymphocytes
Plasma cells
Macrophages
Fibroblasts

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How does organisation occur?

Granulation tissue is formed and dead tissue is removed by phagocytosis
Granulation tissue contracts and accumulated collagen to form a scar

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When does an arterial thrombosis normally occur?

When superimposed on atheroma

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How does an arterial thrombus occur?

Vessel wall damage
Laminar flow disruption
Collagen exposed
Platelets stick to collagen and aggregate - positive feedback
Rbc’s can get trapped - thrombus formation and fibrin deposition (fibrinogen –> fibrin by platelet factors)
Fibrin mesh holds it all together
Thrombus can then build up and occlude artery

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What are the outcomes of a thrombus?

Lysis and resolution
Organisation – into a scar
Recanalisation – scar and residual thrombus
Embolism – breaks off

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What are the functions of histamine?

Vasodilation
Emigration of neutrophils (chemotaxis) 
Increase vascular permeability
Pain 
Itching

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Role of plasma factors

Complement system
Kinin system
Coagulation cascade (pro-clotting)
Fibrinolytic system (anti-clotting)

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What is the microscopic appearance of chronic inflammation?

Chronic ulcer
Abscess cavity
Granulatomous inflammation
Fibrosis

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What is a histiocytic giant cell?

Indeigestible foreign material causes macrophages to fuse together - multinucleate giant cells
Can collect and form granulomas

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What is end arterial supply?

Single artery supplies organ - more susceptible to infarction

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What are watershed territories?

Parts of the brain the have a dual blood supply, but low BP can cause ischaemia

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Explain the pathogenesis of atherosclerosis

Endothelial cell damage – see risk factors
Repeated endothelial damage -> multiple thrombi -> aggregation -> atheroma formation
Vascularised plaque can haemorrhage – propagates atheroma formation

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What are the complications of atherosclerosis?

Cerebral/myocardial infarct
AAA –> weakens aorta and leads to aortic rupture
Peripheral vascular disease - gangrene

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What types of DNA damage cause apoptosis to occur?

Single/double stand break
Base alteration
Cross linking

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Explain mechanism of apoptosis

P53 (gatekeeper of genome) detects DNA damage -> acts as switch for apoptosis
Bcl2 and Fas ligand receptor signal for capsases -> apoptosis
Membrane bound cell fragments engulfed by macrophages

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Example of normal apoptosis

Removal of finger webbing during development

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In what is excess apoptosis present?

HIV mediated T cell destruction

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Give examples of necrosis

Myocardial/cerebral infarction
Avascular necrosis of bone - scaphoid or head of femur break
Caseous necrosis - pathological sign of TB

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Define hypertrophy

Increase in size of a tissue caused by an increase in size of the constituent cells (eg skeletal muscle)

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Define hyperplasia

Increase in size of a tissue caused by an increase in number of the constituent cells (eg. enlarged prostate)

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What are other examples of developmental conditions?

Cleft lip/palate - cells fail to migrate and join | Ventricular septal defect (VSD)

What is congenital development?

Present at birth - can be inherited or acquired

Name 5 types of necrosis

``` Caseous necrosis Coagulative necrosis Colliquative necrosis Fibrinoid necrosis Fat necrosis ```

What is coagulative necrosis?

Cells become firm and pale | Seen in most tissues

What is colliquative necrosis?

Dead area is liquefied | Seen in brain

What is fibrinoid necrosis a microscopic feature of?

Malignant hypertension - in arterioles

What can cause necrosis?

Ischaemia Metabolic Trauma

Name 5 cancers that commonly spread to bone

1. Breast 2. Thyroid 3. Kidney 4. Lung 5. Prostate

What does oncogenesis refer to?

Benign and malignant tumours

Define carcinogen

Mutagenic (act on DNA) agents that cause (or are suspected to cause) tumours

Name the carcinogen classes

Chemical Radiation Biological organisms Miscellaneous

Give an example of a mycotoxin carcinogen

Mycotoxin (Aflatoxin B1) --> hepatocellular cancer

Name host factors for carcinogenesis

Race Constitutional Premalignant conditions Transplacental exposure

Define Neoplasm

A lesion resulting from the NEW AUTONOMOUS ABNORMAL growth of cells that PERSISTS after removal of initiating stimulus

What is the structure of a neoplasm?

Neoplastic cells | Stroma - connettive tissue framework

What does the stroma provide of the neoplasm?

Mechanical support Nutrition Intracellular signalling Contains blood vessels which perfuse the tumour

A tumour <2mm is known as a ...?

Avascular nodule

What neoplasms do epithelial cells form?

Carcinomas

What neoplasms do connective tissues form?

Sarcomas

What is a papilloma?

A benign non glandular epithelial neoplasm

What is a carcinoma?

A malignant non glandular epithelial neoplasm

What is a adenocarcinoma?

A malignant glandular epithelial neoplasm

Name some benign connective tissue neoplasms

``` Lipoma = adipocytes Chondroma = cartilage Osteoma = bone Angioma = vascular Rhabdomyoma = striated muscle Leiomyoma = smooth muscle Neuroma = nerves ```

Name some malignant connective tissue neoplasms

``` Liposarcoma = adipose tissue Chondrosarcoma = cartilage Osteosarcoma = bone Angiosarcoma = vascular Rhabdomyosarcoma = striated muscle Leiomyosarcoma = smooth muscle ```

What are the types of grade of malignancy?

Low grade – looks like parent tissue (well differentiated) High grade – doesn’t look like parent tissue (poorly differentiated) Anaplastic – unknown origin cell type

What is a carcinoma in situ?

Carcinoma fills cavity but has not invaded any other tissue

What are the 8 stages of metastasis?

1. Detachment 2. Invasion 3. Intravasation 4. Evasion 5. Adherence 6. Extravasation 7. Growth 8. Angiogenesis

Explain invasion

Some cells go through the basement membrane into the extracellular matrix using enzymes (proteases, collagenase, cathepsin D, urokinase-like plasminogen activator)

What is intravasation?

Tumour cells move from ECM to blood/lymph vessels

What is evasion?

Aggregate with platelets, shed surface antigens and stick to other tumour cells

Explain adherence

Adherence of ells to endothelium at a remote location

Explain extravasation

Tumour cells move from vessels to new tissue area

What is angiogenesis?

Formation of blood vessels

Name 3 routes of metastasis

Haematogenous - by blood stream Lymphatic Transoelomic - in pleural, pericardial and peritoneal cavities

What tumours commonly metastasise to the liver?

Colon, stomach, pancreas, intestine (portal system)

Give 2 promoters of tumour angiogenesis

1. Vascular endothelial growth factors | 2. Fibroblast growth factors

Give 3 inhibitors of tumour angiogenesis

1. Angiostatin 2. Endostatin 3. Vasculostatin

Give 3 endogenous chemical mediators of acute inflammation

1. Bradykinin 2. Histamine 3. Nitric Oxide

The activity of what enzyme in the blood can act as a marker for granulomatous disease?

Angiotensin converting enzyme

Define abscess

Acute inflammation with a fibrotic wall

what are the steps of acute inflammation?

- Initial reaction of tissue to injury - Vascular component: dilation of vessels - Exudative component: vascular leakage of protein-rich fluid

what is the role of p53 protein?

p53 protein looks for DNA damage, if damage is present p53 switches on apoptosis.

What protein can switch on apoptosis if DNA damage is present?

p53 protein

Activation of which family of protease enzymes can turn on apoptosis?

Caspases.

Activation of what receptor can activate caspase and therefore apoptosis?

FAS receptor.

What is required for a tumour to enter the blood stream (intravasation)?

1. Collagenases. | 2. Cell motility.

What is required for a tumour to exit the blood stream (extravasation)?

1. Adhesion receptors. 2. Collagenases. 3. Cell motility.

What causes the pain associated with acute inflammation?

1. Stretching and distortion of tissues due to oedema and pus under high pressure in an abscess cavity. 2. Chemical mediators e.g. bradykinin and prostaglandins, are also known to induce pain.

Describe the process of neutrophil polymorph migration into tissues as seen in acute inflammation.

1. Margination of neutrophils. 2. Pavementing of neutrophils. 3. Neutrophils pass between endothelial cells. 4. Neutrophils pass through basal lamina and migrate into adventitia.

Chemical carcinogens: what types of cancer do polycyclic aromatic hydrocarbons cause?

Lung cancer and skin cancer.

Chemical carcinogens: what can expose people to polycyclic aromatic hydrocarbons?

Smoking cigarettes and mineral oils.

Chemical carcinogens: what types of cancer do aromatic amines cause?

Bladder cancer.

Chemical carcinogens: what types of people are more susceptible to bladder cancer caused by aromatic amine exposure?

People who work in the rubber/dye industry.

Chemical carcinogens: what type of cancer do nitrosamines cause?

Gut cancer.

Chemical carcinogens: what type of cancer do alkylating agents cause?

Leukaemia; the risk is small in humans.