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Phase 2a > ICS Pathology > Flashcards

ICS Pathology Flashcards

1
Q

What are the two categories of autopsy?

A

Hospital and Medico-legal

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2
Q

What are hospital autopsies used for?

A

Teaching, audit, research

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3
Q

Which type of autopsy is most common?

A

Medico-legal autopsies= over 90% of UK autopsies

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4
Q

What are the two types of medico-legal autopsy?

A

Coronial autopsies (where death is not due to unlawful action), and forensic autopsies (where death is thought to be unlawful)

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5
Q

What are the 4 questions to answer during a coronial autopsy?

A
  • Who is the deceased?
  • When did they die?
  • Where did they die?
  • What brought about their death?
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6
Q

What are the three categories for when deaths are referred to the coroner?

A
  • Presumed natural but death is unknown and patient hasn’t seen doctor in 14 days prior
  • Presumed iatrogenic such as peri/postoperative death, anesthetic deaths, complications of therapy etc
  • Presumed unnatural such as accidents, suicide, unlawful killing, neglect, custody death etc
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7
Q

What do histopathologists do?

A

Perform hospital autopsies and some coronial autopsies including natural deaths, suicide, accidents, road traffic deaths, peri/post-operative deaths

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8
Q

What do forensic pathologists do?

A

Perform autopsies where the death could be due to the action of a third party such as homicide, death in custody or neglect

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9
Q

What are the parts of the coroners rules of 1984?

A
  • Autopsy as soon as possible
  • By a pathologist of suitable qualification
  • Report findings promptly and only to coroner
  • Autopsy only on appropriate premises
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10
Q

What are the rules of the coroners act of 1988?

A
  • Allows coroner to order an autopsy where death is likely due to natural causes to obliviate need for inquest.
  • Allows coroner to order an autopsy where death is clearly unnatural and inquest will be needed
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11
Q

What are the rules of the coronial legislation of 2005?

A

Pathologist must tell coroner precisely what material have been retained, coroner authorizes retention and sets disposal date. Coroner must inform family of retention. The family then has choices either to return material, retain for research/teaching or to respectfully dispose of.

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12
Q

What are the rules of the coroners and justice act of 2009?

A

Coroner can now defer opening the inquest and instead launch an investigation

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13
Q

What can be used to identify a body?

A

Formal identifies, body habitus, jewelry, body modification or clothing

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14
Q

What is inflammation?

A

A local physiological response to tissue injury that is either acute or chronic

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15
Q

List some benefits of inflammation

A

Destruction of invading microorganisms and walling off an abscess cavity to prevent the spread of infection

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16
Q

List some negatives of inflammation

A

Disease will compress surounding structures, Fibrosis may distort the surrounding tissues, digestion of normal tissues, swelling in dangerous places, inappropriate inflammatory responses

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17
Q

Give an example of acute inflammation?

A

Acute appendicitis

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18
Q

What are the 4 stages of acute inflammation?

A
  1. Changes in vessel calibre
  2. Fluid exudate
  3. Cellular exudate
  4. Chemotaxis
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19
Q

What is cellular exudate?

A

An accumulation of neutrophil polymorphs in the extracellular space

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20
Q

What causes the fluid exudate in acute inflammation?

A
  1. Sphincters in arteriolar walls relax thereby increasing blood flow into capillaries
  2. Capillary hydrostatic pressure is increased and there is escape of plasma proteins, increasing osmotic pressure in extravascular space
  3. Therefore more fluid leaves the vessels = fluid exudate
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21
Q

What are the 4 steps of neutrophil extravasation?

A
  1. Margination of neutrophils
  2. Pavementing of neutrophils
  3. Pass between endothelial cells
  4. Pass through basal lamina and migrate into adventitia
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22
Q

What is neutrophil extravasation?

A

The leakage of neutrophils from capillaries into the surrounding tissues during acute inflammation

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23
Q

What is neutrophil margination?

A

When neutrophils begin to flow at the peripheral zone of capillaries, near the endothelium, due to a loss of intravascular fluid and increase in plasma viscosity with slowing of flow at site of inflammation

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24
Q

What is pavementing of neutrophils?

A

At the site of acute inflammation, neutrophils begin to adhere to endothelium of venules due to its “sticky” wall

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25
Q

What is diapedesis?

A

When erythrocytes escape through the vessel walls passively during acute inflammation

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26
Q

What does large numbers of RBC in the extracellular space during inflammation imply?

A

Severe vascular injury

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27
Q

List some chemical mediators during acute inflammation

A

Histamine and Thrombin

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28
Q

What cells release histamine?

A

Mast cells, and basophil&eosinophil leucocytes

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29
Q

What are some effects of histamine?

A

Contraction of smooth muscle in the lungs, uterus and stomach, dilation of blood vessels thus lowering of blood pressure, gastric acid secretion etc.

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30
Q

What are the 4 enzymatic cascade systems in plasma?

A

Complement system
Kinin System
Coagulation factors
Fibrinolytic system

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31
Q

What is the purpose of the complement system?

A

To remove or destroy antigens either by lysis or oponization

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32
Q

What can activate the complement system?

A

Enzymes released from dying cells, endotoxins of bacterias etc.

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33
Q

What chemical mediators are secreted by tissue macrophages?

A

Interleukin-1 and TNF-alpha

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34
Q

Why do lymphatic channels become dilated in acute inflammation?

A

They drain away oedematous fluid of the inflammatory exudate

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35
Q

What is opsonization?

A

Making microorganisms more amenable to phagocytosis by either immunoglobulins of complement components

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36
Q

What are phagolysosomes?

A

When a particle is ingested by a phagocyte into a phagosome, which then fuses with a lysosome

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37
Q

What are the steps of phagocytosis?

A
  1. Neutrophil ingests bacterium
  2. Bacterium lies within a phagosome
  3. Lysosome fuses with phagosome (phagolysosome), and digests the bacterium
  4. Bacterial debris is released
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38
Q

List some causes of acute inflammation

A
  • Microbial infection
  • Hypersensitivity reaction
  • Physical agents
  • Tissue Necrosis
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39
Q

How does tissue necrosis cause acute inflammation?

A

Peptides are released from the dead tissues which trigger inflammation

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40
Q

What are the 5 signs of acute inflammation?

A

Tumor (Swelling), Rubor (Redness), Calor (Heat), Dolor (Pain), loss of function

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41
Q

What causes swelling in acute inflammation?

A

Oedema, and formation of new connective tissue

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42
Q

What causes redness in acute inflammation?

A

Dilation of small blood vessels

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43
Q

What causes heat in acute inflammation?

A

Increased blood flow (Hyperaemia) and systemic fever

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44
Q

What causes pain in acute inflammation?

A

Stretching and distribution of the tissues to inflammatory oedema. Some chemical mediators also induce pain

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45
Q

What are the possible outcomes of acute inflammation?

A
  • Resolution
  • Suppuration
  • Organisation
  • Progression to chronic inflammation
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46
Q

What conditions favor resolution?

A

Minimal cell death and damage, in tissues capable of regeneration, rapid destruction of causal agent

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47
Q

What is suppuration?

A

Formation of pus

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48
Q

What conditions favour suppuration?

A

Persistant causative stimulus, and normally an infective agent, usually pyogenic bacteria

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49
Q

What is organisation?

A

When tissue is replaced with granulation tissue as part of the healing process - healing by fibrosis where there is substantial damage to connective tissue framework with excessive necrosis

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50
Q

When will acute inflammation progress onto chronic inflammation?

A

If the causative agent is not removed

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51
Q

What is pyrexia and how does it happen?

A

Fever= Neutrophils and macrophages produce endogenous pyrogens which act on the hypothalamus to set the thermoregulatory mechanisms at a higher temperature

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52
Q

List some systemic effects of inflammation

A

Pyrexia, malaise, anorexia, nausea, splenomegaly, weight loss, lymph node enlargement, anaemia

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53
Q

What is primary chronic inflammation?

A

Where there is no initial phase of acute inflammation

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54
Q

What are the histological features of chronic inflammation?

A

Cellular infiltrate consisting of lymphocytes, plasma cells and macrophages

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55
Q

Name an example of chronic inflammation

A

Tuberculosis

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56
Q

What is resolution?

A

Healing where the initiating factor is removed. Generally one single large injury such as a single fracture, liver damage through paracetamol overdose etc which is then left to repair. Can fully repair if in a cell population which can do so.

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57
Q

What is repair?

A

Healing where the initiating factor is still present. Generally a recurring injury/ disease such as fracture that it frequently moved, liver damage through recurrent alcohol intake etc. Won’t fully repair as there will be scar tissue

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58
Q

What is the role of B lymphocytes?

A

Production of antibodies

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59
Q

What is the role of T lymphocytes?

A

Cell-mediated immunity

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60
Q

What is a granuloma?

A

An aggregate of epithelioid histocytes- Part of type IV hypersensitivity

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61
Q

List some systemic granulomatosis diseases

A

TB, Sarcoidosis, Crohn’s disease, Leprosy, Schistosomiasis

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62
Q

How can you identify tuberculosis?

A

Use ziehl-neelsen stain, will get a bright red result if TB

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63
Q

What are the histological features of epithelioid histocytes?

A

Large vesticular nuclei
Plentiful eosinophilic cytoplasm
Elongated
Arranged in clusters

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64
Q

What are langerhans giant cells?

A

Giant cells with a horseshoe arrangement of peripheral nuclei at one pole. It is characteristically seen in TB.

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65
Q

What are foreign body giant cells?

A

Large cells with nuclei randomly scattered throughout their cytoplasm

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66
Q

What are touton giant cells?

A

Large cells with a central ring of nuclei, peripheral to which there is lipid material

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67
Q

What cells are involved in acute inflammation?

A

Neutrophils and macrophages

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68
Q

What cells are involved in chronic inflammation?

A

Lymphocytes, macrophages and plasma cells

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69
Q

What are labile cells?

A

Cells with a good capacity to regenerate e.g. epithelial cells

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70
Q

What are stable cell populations?

A

Cells that divide at a very slow rate normally, and still retain their capacity to divide when necessary. E.g. hepatocytes

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71
Q

What are permanent cells?

A

Cells with no effective regeneration

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72
Q

How does organisation occur?

A

Granulation tissue is formed in the early stages, which then contracts and gradually accumulates collagen. Granulation tissue is the combination of capillary loops and myofibroblasts. The organized area is firmer than normal

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73
Q

How do abrasions heal?

A

Scab forms over surface
Epidermis grows out from adnexa, protected by scam
Leads to a thin confluent epidermis
Final epidermal regrowth leading back to normal skin

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74
Q

What is healing by first intension?

A
  • Fibrin deposited locally will weakly bind the two sides of the wound
  • Coagulated blood on the surface will form a scab
  • Capillaries then proliferate sufficiently to bridge the gap, and fibroblasts secrete collagen as they migrate into the fibrin network to form a strong collagen join
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75
Q

When can healing by first intension occur?

A

If there is a small incision with little damage to tissue either side of the cut.

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76
Q

What is healing by second intension?

A
  • When there is tissue loss so the wound margins are not apposed.
  • There is first phagocytosis to remove any debris
  • Granulation tissue to fill in defects and repair specialised tissue lost
  • There is finally epithelial regeneration to cover the surface
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77
Q

List some cells that can regenerate

A

Hepatocytes, Pneumocytes, all blood cells, epithelia, osteocytes

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78
Q

What cells cannot regenerate?

A

Myocardial cells, neurones

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79
Q

How is local inflammation due to injury (e.g. banging the ankle) treated?

A

RICE

Rest, Ice, Compression, Elevation

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80
Q

How are bites treated?

A

Antihistamines, NSAIDs

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81
Q

How are chronic rashes treated?

A

Steroid creams

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82
Q

How do steroid creams work?

A

They bind to DNA and up regulate inhibitors of inflammation and down regulates chemical mediators of inflammation

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83
Q

What is an abscess?

A

A localized collection of inflammatory cells with a fibrotic wall

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84
Q

List two ways of investigating inflammation

A
  • Localised aspiration

- Blood cultures

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85
Q

What is a thrombus?

A

The solidification of blood contents that forms within the vascular system during life

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86
Q

What are the three components of Virchow’s triad?

A
  • Stasis of blood flow
  • Endothelial injury
  • Hypercoagulability
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87
Q

What is Virchow’s triad?

A

3 elements that predispose to thrombosis

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88
Q

What mechanisms prevent thrombus formation?

A
  • Laminar flow (where cells travel in the centre of arterial vessels and don’t touch the sides)
  • Endothelial cells which line vessels are not “sticky” when healthy
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89
Q

What are contained within alpha granules of platelets?

A

Platelet adhesion molecules such as fibrinogen, fibronectin and platelet growth factor

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90
Q

What are contained within the dense granules of platelets?

A

Adenosine diphosphate that cause platelets to aggregate

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91
Q

What is platelet aggregation?

A

Platelets release chemicals which cause other platelets to stick, and starts the cascade of clotting proteins

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92
Q

What is the process of arterial thrombosis formation?

A
  1. A fatty streak forms, which protrudes into the lumen causing turbulence in blood flow
  2. This turbulence eventually results in the loss of intimal cells and the exposed plaque surface is presented to the blood cells
  3. This results in fibrin deposition and platelet clumping due to exposed collagen
  4. This process may be self perpetuating, causing thrombi to grow
  5. This disrupts laminar flow
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93
Q

What is a fatty streak?

A

An early atheromatous plaque which is a slightly raised area on the luminal surface of an artery

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94
Q

What does arterial thrombus result in?

A
  • Loss of pulse distal to thrombus
  • Area becomes cold, painful and pale
  • Eventually tissue dies and gangrene results
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95
Q

Does atheroma normally occur in arteries or veins?

A

Arteries, as veins are low pressure

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96
Q

How do venous thrombi normally occur?

A

Normally due to stasis

  • At valves are there is a natural degree of turbulence here
  • Or if blood pressure falls during surgery or following a MI
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97
Q

Where do venous thrombi normally occur?

A

95% occur in leg veins

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98
Q

What does a venous thrombus result in?

A
  • Area becomes tender and causes general ischaemic pain
  • Area becomes reddened
  • Area becomes swollen
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99
Q

What are arterial thrombosis made up of?

A

Blood clot- Many platelets (White thrombus)

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100
Q

What are venous thrombosis made up of?

A

Blood clot- Mainly coagulation factors (Red thrombus)

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101
Q

What can arterial thrombosis lead to?

A

MI/Stroke

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102
Q

What can venous thrombosis lead to?

A

Deep vein thrombosis/ Pulmonary embolism

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103
Q

What is the treatment for arterial thrombosis?

A

Anti-platelets e.g. aspirin, clopidogerel

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104
Q

What is the treatment for venous thrombosis?

A

Anti-coagulants e.g. warfarin, heparin, NOACs

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105
Q

What is the commonest cause of arterial thrombosis?

A

Most commonly due to atheroma

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106
Q

What is the commonest cause of venous thrombosis?

A

Stasis- slowing of blood flow in veins

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107
Q

What is an embolus?

A

A mass of material in the vascular system able to lodge in a vessel and block its lumen

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108
Q

What things can cause an embolus?

A

Thrombus, air, cholesterol crystals from plaques, tumour amniotic fluid, fat after severe trauma etc.

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109
Q

Where will a venous embolism occur?

A

It will travel to the vena cava, then lodge somewhere in the pulmonary arteries causing a pulmonary embolism

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110
Q

What will be the outcome of a pulmonary embolism?

A

Small embolism= May be lysed in lung or remain unnoticed
Large embolism= Acute respiratory and cardiac problems (chest pain, shortness of breath)
Massive embolism= Sudden death

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111
Q

Where do arterial emboli normally occur?

A

Either from the heart on areas of damaged cardiac muscle, or from an atheromatous plaque

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112
Q

What is ischaemia?

A

A reduction in blood flow to a tissue or part of the body caused by constriction or blockage of the blood vessels supplying it

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113
Q

What is infarction?

A

The necrosis of part or whole of an organ that occurs when the artery supplying it becomes obstructed

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114
Q

Why are the liver, lung and brain less susceptible to infarction?

A

Dual blood supply

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115
Q

What is reperfusion injury?

A

When blood flow returns to an ischaemic area, there is removal of dead cells and activation of oxygen-dependent free radical systems. There are also intrinsic oxygen free radicals brought by WBC, resulting in more damage.

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116
Q

What is gangrene?

A

When areas of a limb or a region of the gut have their arterial supply cut off, and large areas of mixed tissue die in bulk

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117
Q

What is wet gangrene?

A

Where bacterial infection supervenes as a secondary complication and patient becomes septic

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118
Q

What is disseminated intravascular coagulation (DIC)?

A

Where there is minute thrombi and bleeding at multiple sites due to the consumption of clotting factors

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119
Q

What are causes of ischaemia?

A 
Thrombi
Spasms in smooth muscle in the vessel wall
External compression of veins
Hyperviscosity of blood
Vasculitis
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120
Q

What is atherosclerosis?

A

An accumulation of lipid, macrophages and smooth muscle cells in intimal plaques in arteries

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121
Q

Do plaques occur in mainly high or low pressure systems?

A

Only occurs in high pressure systems

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122
Q

What can occlusive atheroma cause?

A 
Cerebral infarction
MI
Aortic aneurysm
Peripheral vascular disease
Gangrene
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123
Q

What are the five types of arteries where atherosclerosis occurs?

A 
Aorta (Normally descending)
Cerebral arteries
Common iliac arteries/ Femoral arteries
Coronary arteries
Carotid
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124
Q

What are the contents of a plaque?

A

Fibrous tissue cap with macrophages and lymphocytes
Central lipid core
Smooth muscle cells, cell debris, calcium, connective tissues, foam cells

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125
Q

What are foam cells?

A

Macrophages that have phagocytosed oxidised lipoproteins = appear foamy. Often at the border of a thrombogenic lesion

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126
Q

What are the risk factors for plaque formation?

A
  • Hypercholesterolaemia
  • Hyperlipidaemia
  • Hypertension
  • Smoking
  • Poorly controlled diabetes
  • Male gender
  • Increasing age
  • Social deprivation
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127
Q

How do atherosclerotic plaques form?

A
  1. Endothelial cell dysfunction
  2. High levels of LDL in the blood begin to accumulate
  3. Macrophages are attracted to the site of damage and take up lipid to form foam cells
  4. Formation of a fatty streak
  5. The activated macrophages release their own products- cytokines and growth factors
  6. Smooth muscle proliferation around the lipid core and formation of a fibrous cap
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128
Q

What things can damage endothelial cells?

A
  • High cholesterol
  • Smoking
  • Hypertension
  • Poorly controlled diabetes
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129
Q

How can someone prevent atherosclerosis?

A 
Smoking cessation
Control of blood pressure
Weight reduction
Low dose aspirin
Statins
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130
Q

How does aspirin prevent thrombosis and atherosclerosis?

A

Inhibits platelet aggregation

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131
Q

What is the difference between atherosclerotic plaque and thrombi?

A
  • Plaques= mainly lipid, macrophages, cholesterol etc

- Thrombi= Blood clot

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132
Q

What is an aneurysm?

A

A localised permanent dilation of part of the vascular tree

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133
Q

What is an aortic dissection?

A

Where blood is forced through a tear in the aortic intima to create a blood-filled space in the media

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134
Q

What is a berry aneurysm?

A

An aneurysm in the circle of willis causing a subarachnoid haemorrhage

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135
Q

What is a TIA?

A

A stroke that lasts for less than 24 hrs and is associated with complete clinical recovery

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136
Q

What is the normal cause of a intracerebral haemorrhage?

A

A rupture of the middle cerebral artery

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137
Q

What is the normal cause of a subarachnoid haemorrhage?

A

A rupture of a saccular aneurysm of the circle of willis

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138
Q

Define hypertrophy

A

An increase in size of organ or tissue due to an increase in the size of the cells

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139
Q

Give an example of hypertrophy

A

Example-Increase in skeletal muscle mass during exercise

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140
Q

Define hyperplasia

A

An increase in the size of an organ or tissue due to an increase in the number of cells

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141
Q

Give an example of hyperplasia

A

Benign prostatic hyperplasia

142
Q

Define atrophy

A

Decrease in the size of an organ or tissue and results from a decrease in the mass of pre-existing cells, either by decrease in cell size or decrease in numbers of cells.

143
Q

Give an example of atrophy

A

Atrophy of the endometrium

144
Q

Define metaplasia

A

Replacement of one differentiated cell type by a different differentiated cell type

145
Q

Give an example of metaplasia

A

Barretts oesophagus

146
Q

Define dysplasia

A

Increased cell growth and decreased differentiation. Pathological a variation in size and shape of cells, with a high nuclear/cytoplasmic ration, and increased nuclear DNA

147
Q

Give an example of dysplasia

A

Pre-cancerous state

148
Q

Define apoptosis

A

Programmed cell death. Pathologically death of scattered single cells forming membrane-bound bodies eventually phagocytosed and broken down by adjacent unaffected cells

149
Q

Give an example of apoptosis

A

Apoptosis between digits in utero

150
Q

Define necrosis

A

Traumatic cell death which induces inflammation and repair

151
Q

Give an example of necrosis

A

Gangrene

152
Q

Do cells swell in apoptosis or necrosis?

A

Swell in necrosis, shrink in apoptosis

153
Q

Are organelles damaged in apoptosis or necrosis?

A

Damaged in necrosis, undamaged in apoptosis

154
Q

Is there inflammation in necrosis or apoptosis?

A

Inflammation in necrosis

155
Q

Is apoptosis energy dependent or independent?

A

Energy dependent

156
Q

What inhibits apoptosis?

A

Growth factors, extracellular cell matrix, sex steroids and some viral proteins

157
Q

What induces apoptosis?

A

Growth factor withdrawal, glucocorticoids, some viruses, free radicals, ionising radiation, DNA damage, ligand-binding at death receptors

158
Q

Briefly describe the intrinsic apoptotic pathway

A
  1. BCL2 proteins inhibit apoptosis, and Bax proteins enhance apoptosis
  2. Their ratio determines cell’s susceptibility to apoptotic stimuli
  3. The cell responds to stimuli
  4. P53 can then induce cell cycle arrest, or if there is severe damage in the cell, it can induce apoptosis
159
Q

Briefly describe the extrinsic apoptotic pathway

A
  1. There are specific mechanisms for the activation of apoptosis characterised by ligand-binding at death receptors
  2. Receptors include members of the tumour necrosis factor receptor family
  3. Fas ligands bind to Fas receptors on the cell surface, which sends a signal into the cell and switches on caspases
160
Q

Briefly describe the execution phase of apoptosis

A
  1. Caspases are activated by either the intrinsic or extrinsic pathway (Either by Fas binding, Bax, or by lower Bcl-2)
  2. This therefore induced degradation of the cytoskeletal framework and nuclear proteins
  3. This is then phagocytosed
161
Q

How does necrosis induce inflammation?

A

The rupture of the plasma membrane and spillage of cell contents, with some being immunostimulatory, which provokes an inflammatory response

162
Q

What is caseous necrosis?

A

A pattern of necrosis where the dead tissue is structureless almost like soft cheese. It is characteristic of tuberculosis

163
Q

What is gangrene?

A

A type of necrosis with the rotting of tissues, sometimes as a result of certain bacteria particularly clostridia. Affected tissue appears black

164
Q

Why does gangrenous tissue appear black?

A

Deposition of iron sulphide from degraded haemoglobin

165
Q

What is a congenital disease?

A

A disease present at birth and includes chromosomal disorders, hereditary and spontaneous genetic diseases etc.

166
Q

What is a genetic disease?

A

Inherited diseases such as cystic fibrosis, such as sickle cell anaemia, or spontaneous such as Down’s syndrome

167
Q

What is trisomy 21?

A

Down’s syndrome

168
Q

What is acquired disease?

A

A disease caused by non-genetic environmental factors, such as TB, lung cancer, AIDS

169
Q

What is multifactorial disease?

A

A disease due to many different factors, such as spina bifida. A common example is cleft palate

170
Q

What is a homeobox gene?

A

A group of genes that control mutations

171
Q

What is mendelian inheritance?

A

Single gene inheritance

172
Q

What is autosomal inheritance?

A

Non-sex linked inheritance

173
Q

What is polygenic disease?

A

Disease caused by multiple genes

174
Q

What is acromegaly?

A

Excess growth hormone leading to increasing bone sizes mainly in hands, feet and face

175
Q

What is the normal cause of acromegaly?

A

Pituitary tumour leading to growth hormone excess

176
Q

What is achondroplasia?

A

A disorder of bone growth that prevents the changing of cartilage in bone. It is characterized by dwarfism, large head size, small fingers

177
Q

Describe telomere length in aging

A

The telomere is the region at the end of each DNA sequence. They are not fully copied on division, thus gradually get shortened. Eventually they become so short that DNA polymerase cannot bind and thus the cell can’t replicate again.

178
Q

What is sarcopaenia?

A

Muscle loss due to aging caused by decreased growth hormone, decreased testosterone, and icnreased acatabolic cytokines

179
Q

How does deafness occur?

A

Loss of hair cells

180
Q

How do cataracts form in aging?

A

UV damage results in cross-linking proteins in the eye

181
Q

What causes osteoporosis in aging?

A

Oestrogen loss

182
Q

What is dermal elastosis?

A

Wrinkling

183
Q

What causes wrinkling?

A

UV damage resulting in less collagen and less elastin within the skin

184
Q

What is progeria?

A

A disease of rapid aging in children.

185
Q

Which cells produce collagen?

A

Fibroblasts

186
Q

What is the main effector cell in acute inflammation?

A

Neutrophil Polymorphs

187
Q

Give an example of primary chronic inflammation?

A

Transplant rejection

188
Q

Name a drug that inhibits platelet aggregation

A

Aspirin

189
Q

How can you cure basal cell carcinoma?

A

Complete local excision - basal cell carcinoma never metastasises

190
Q

Where do sarcomas normally metastases to?

A

The lung

191
Q

What is metastasis?

A

When tumours spread from their site of origin to tumours at distant sites

192
Q

What are the possible routes of metastasis?

A

Haematogenous
Lymphatic
Transcoelomic

193
Q

Where do breast cancers normally metastasis to?

A

Axillary lymph node then bone

194
Q

What is haematogenous spread?

A

Via the blood stream

195
Q

What carcinomas favour bone haematogenous metastasis?

A 
Lung
Breast
Kidney
Thyroid
Prostate
196
Q

What is lymphatic spread?

A

Via the lymph nodes

197
Q

What is the most common route of spread for carcinomas?

A

Lymphatic spread

198
Q

What is transcoelomic spread?

A

Via the peroneal cavitys

199
Q

How is leukaemia treated and why?

A

Leukaemia is a cancer of bone marrow and thus white blood cells are affected. This means that the cancer is circulating, so would have to treat systemically (Chemotherapy)

200
Q

What are some generalised cancer symptoms?

A

Weight loss, fever, frequent infections, easy shortness of breath, weakness, pain, fatigue, splenomegaly, night sweats

201
Q

How is a breast carcinoma diagnosis confirmed?

A

Biopsy using a core biopsy needle. Can confirm if it has spread using ultrasound and core biopsy needle at lymph nodes and using full body scans

202
Q

How is breast carcinoma normally treated?

A

Surgery with or without axillary lymph node clearance to remove the tumor. Radiotherapy to destroy microtumors. Chemotherapy if the cancer has spread further

203
Q

What is carcinogenesis?

A

The transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations

204
Q

What is a carcinogen?

A

An environmental agent participating in the causation of tumours

205
Q

What percentage of cancer risk is environmental?

A

85%

206
Q

What are some problems with identifying carcinogens?

A
  • Latent period may be decades
  • Complexity of environment
  • Ethical constraints
207
Q

Where is hepatocellular carcinoma common and why?

A

Uncommon in UK/USA. Common in areas with high hep B and C (South Africa)

208
Q

Where is oesophageal carcinoma common and why?

A

Japan and china due to consumption of carcinogenic chicken

Turkey and Iran due to drinking extremely hot coffee

209
Q

What is the biggest risk for lung cancer?

A

Smoking

210
Q

What population has increased risk of bladder cancer?

A

Those who have worked with aniline dye and rubber

211
Q

What population has increased risk of scrotal carcinoma?

A

Chimney sweeps due to soot exposure

212
Q

What are the categories of carcinogen?

A
  • Chemical
  • Viral
  • Radiation
  • Hormones, mycotoxins and parasites
  • Misc
213
Q

What are pro-carcinogens?

A

The pre-carcinogenic state of chemical carcinogens, which then require metabolic conversion into ultimate carcinogens

214
Q

What viruses are associated with cancer?

A

Epstein-Barr

Human Papillomavirus

215
Q

What type of cancers are associated with UVA and UVB?

A

Basal cell carcinoma and squamous cell carcinoma

216
Q

Why are Ukranian children more prone to thyroid cancer?

A

Chernobyl caused excess ionising Iodine which is taken up by the thyroid to form thyroxine

217
Q

What types of cancers is oestrogen associated with?

A

Mammary and endometrial cancer

218
Q

What type of cancer is associated with steroids?

A

Hepatocellular carcinoma

219
Q

What type of cancer is associated with Schistosoma?

A

Bladder cancer

220
Q

How can race affect cancers?

A

Darker skinned people have more melanin and thus are more protected from the carcinogenic effect of UV

221
Q

What is the most common cancer in males?

A

Prostate

222
Q

What is the most common cancer in women?

A

Breast cancer

223
Q

What premalignant lesions give a predisposition for cancer?

A

Colonic polyps
Cervical dysplasia
Undescended testicles

224
Q

What dietary factors are linked to cancer?

A 
Fat= Colorectal cancers
Alcohol= breast and oesophageal cancer
225
Q

What is a neoplasm?

A

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

226
Q

Where does colon cancer normally metastasise to and why?

A

It invades the veins and travels through the portal system into the liver

227
Q

Can neoplasms arise form erythrocytes?

A

No- they don’t have a nucleus

228
Q

How do neoplastic cells relate to their parent cells?

A

Their synthetic activity is related (if parent cells produce hormones they will too), their growth patterns are also related to the parent cell

229
Q

What are the types of tumours?

A

Neoplasm, inflammation, hypertrophy, hyperplasia

230
Q

What is angiogenesis?

A

The ability of a tumour to induce blood vessels. It is induced by factors secreted by tumour cells such as vascular endothelial growth factor

231
Q

What things promote angiogenesis?

A

Vascular endothelial growth factor, basic fibroblast growth factor

232
Q

What things inhibit angiogenesis?

A

Angiostatin, endostatin, vasculostatin

233
Q

Why is abnormal coagulation common in patients with hepatitis?

A

Hepatitis damages the liver, which means it cannot produce clotting factors.

234
Q

What coagulation products does the liver produce?

A

Factor I, II, VII, IX
Proteins C and S for inhibition of coagulation
Anti-thrombin III which impairs coagulation

235
Q

What is a prothrombotic state?

A

A state of abnormal coagulation that increases the chances of thrombosis

236
Q

How can drug use cause embolism?

A

Filler material can build up in the venous system, normally in very small fragments

237
Q

How can DVT be avoided post-surgery?

A

TED stockings
Anti-coagulants
If very high risk- can have a IVC cage and anticoagulants

238
Q

What are the three main coagulation tests?

A

APTT
PT
TT

239
Q

What is an APTT test?

A

Activated partial thromboplasmin time

Uses contact activation which provides a large surface area for plasma contact. Extra phosopholipid is added.

240
Q

What does an APTT measure?

A

Activated partial thromboplasmin time

Measures all clotting factors except VII and XIII

241
Q

What is a PT test?

A

Prothrombin time

Tissue factor and phospholipid are added to patient serum

242
Q

What does PT measure?

A

Prothrombin time

Assesses factor II, V, VII, X, and fibrinogen

243
Q

What is a TT test?

A

Thrombin time
Blood test to measure the time for clot formation. An excess of thrombin is added directly to blood to measure the speed of coagulation.

244
Q

What are the three steps of carginogenesis?

A
  1. Initiation= Carcinogen induces genetic change
  2. Promotion= Stimulation of clonal proliferation of the transformed cell
  3. Progression= The process culminating in malignant behaviour, characterised by invasion
245
Q

What genetic alterations are needed to transform a cell into a neoplastic cell?

A
  • Expression of telomerase leading to immortalisation
  • Loss or inactivation of tumour suppressor genes
  • Activation or abnormal expression of oncogenes
246
Q

Why do mutations occur in cells?

A
  • By chance mutations
  • By direct inheritance of faulty genes from parents
  • As a consequence of toxic insult delivered to the cell
247
Q

What is a gatekeeper gene?

A

A gene that inhibits the proliferation or promote the death of cells with damaged DNA e.g. P53

248
Q

What is the HER2 gene?

A

A gene that can play a role in the development of breast cancer

249
Q

What is a caretaker gene?

A

A gene that repairs DNA damage e.g. BRCA1

250
Q

What is a MDT meeting?

A

Multidisciplinary team meeting - where cases are discussed with various staff members

251
Q

What is P53?

A

A caretaker gene on chromosome 17 which is the most frequently mutated. It normally repairs damaged DNA before S phase by arresting the cell cycle in G1 until the damage is repaired, or will cause cell death if there is extensive damage

252
Q

What are oncogenes?

A

Genes driving the neoplastic behaviour of cells

253
Q

What is the mechanism of activation of oncogenes?

A

A) Translocation= The oncogene is translocated to an actively transcribed gene
B) Point mutations= A specific base is translated into an oncogene to make it hyperactive
C) Amplification= Insertion of multiple copies of the oncogene

254
Q

Describe benign tumours

A

They do not invade the basement membrane, and are often exophytic (Grows outwards). They have a low mitotic activity, and are well circumscribed. Necrosis/ulceration is rare. They bare a close resemblance to normal tissue.

255
Q

What are the risks of benign tumours?

A
  • Can cause pressure on adjacent structures
  • Obstruct flow
  • Produce hormones
  • Can cause anxiety
  • Can possibly transform into malignant tumours
256
Q

Describe malignant tumours

A

They invade the basement membrane, and are often endophytic (grows inwards). They have a high mitotic activity, and are poorly circumscribed. Necrosis/ ulceration is common. They have pleomorphic nuclei (vary in size and shape), and do not resemble the parent cell.

257
Q

What are some risks of malignant tumours?

A
  • They can metastasise
  • Can have paraneoplastic effects such as ACTH from small cell lung cancer
  • Can cause anxiety
  • Pain
  • Blood loss
  • Pressure on adjacent tissue
258
Q

What are borderline neoplasms?

A

Fairly rare tumours that defy precise classification- neither benign or malignant

259
Q

What is the histological appearance of malignant tumours?

A
  • High mitotic activity
  • Pleomorphism
  • Hyperchromatic nuclei
  • Poorly defined border
260
Q

Describe the TNM grading system

A 
T= Primary tumour 
N= Lymph node status
M= Anatomical extent of distant metastases
261
Q

What is a carcinoma?

A

A tumour of epithelial cells

262
Q

What is a sarcoma?

A

A tumour of connective tissues

263
Q

What is a lymphoma?

A

A tumour of lymphoid tissues

264
Q

What is a leukaemia?

A

A tumour of haemopoietic organs

265
Q

What is the grading system of malignant tumours?

A

Grade 1= Well differentiated, closely resembles parent tissue
Grade 2= Moderately differentiated
Grade 3= Poorly differentiated, more aggressive
Anaplastic= lack recognisable histogenic features and extremely aggressive

266
Q

What is histogenesis?

A

The specific cell of origin of a tumour

267
Q

What is a papilloma?

A

Benign tumour of non-glandular, non-secretory epithelium, with the prefix of the cell type of origin e.g. squamous cell papilloma

268
Q

What is an adenoma?

A

Benign tumour of glandular or secretory epithelium with the prefix of the cell type of origin e.g. Colonic adenoma

269
Q

What is a carcinoma?

A

Malignant neoplasm of epithelial cells, prefixed with the name of epithelial cell type .e.g transitional cell carcinoma

270
Q

What is an adenocarcinoma?

A

Malignant tumour of glandular epithelium, coupled with the name of the tissue of origin, e.g. adenocarcinoma of the prostate

271
Q

What is a lipoma?

A

Benign tumour of adipocytes

272
Q

What is a rhabdomyoma?

A

Benign tumour of striated muscle

273
Q

What is a leiomyoma?

A

Benign tumour of smooth muscle cells

274
Q

What is a chondroma?

A

Benign tumour of cartilage

275
Q

What is a osteoma?

A

Benign tumour of bone

276
Q

What is an angioma?

A

Benign vascular tumour

277
Q

What is a neuroma?

A

Benign tumour of nerve

278
Q

What is a liposarcoma?

A

Malignant tumour of adipocytes

279
Q

What is a rhabdomyosarcoma?

A

Malignant tumour of striated muscle

280
Q

What is a leiomyosarcoma?

A

Malignant tumour of smooth muscle cells

281
Q

What is a chondrosarcoma?

A

Malignant tumour of cartilage

282
Q

What is an osteosarcoma?

A

Malignant tumour of bone

283
Q

What is an angiosarcoma?

A

Malignant vascular tumour

284
Q

What is a neurosarcoma?

A

Malignant tumour of the nerve

285
Q

What is a melanoma?

A

Malignant neoplasm of melanocytes

286
Q

What is a mesothelioma?

A

Malignant tumour of mesothelial cells

287
Q

What is a lymphoma?

A

Malignant neoplasm of lymphoid cells

288
Q

What is a teratoma?

A

Neoplasm of germ cell origin that forms representing all three germ cell layers of the embryo

289
Q

What is a carcinosarcoma?

A

Mixed malignant tumours showing characteristics of epithelium and connective tissue

290
Q

What is brukitt’s lymphoma?

A

B cell lymphoma caused by epstein Barr virus

291
Q

What is Ewing’s sarcoma?

A

A malignant tumour of bone

292
Q

What is Hodgkins lymphoma?

A

Malignant lymphoma characterised by the presence of Reed-Sternberg cells

293
Q

What is Kaposi’s sarcoma?

A

Malignant neoplasm derived from vascular endothelium, commonly associated with AIDs

294
Q

How is carcinoma in situ treated?

A

Local excision as it isn’t moving so won’t spread

295
Q

Why do cancerous cells produce meltalloprotinases?

A

To digest the basement membrane to allow for invasion

296
Q

What factors influence invasion?

A
  • Decreased cellular adhesion
  • Secretion of proteolytic enzymes
  • Abnormal or increased cellular motility
297
Q

What are collagenases used for in neoplastic cells?

A

Degrade types I, II and III collagen to invade surrounding tissue

298
Q

What are TIMPs?

A

Tissue inhibitors of metalloproteinases (counteracts meltalloprotinases)

299
Q

How do neoplastic cells evade host immune defense?

A
  • Tumour cells aggregate with platelets to surround themselves and thus go under the radar
  • Shedding of surface antigens
  • Adhesion to other tumour cells
300
Q

What is the mechanism of metastasis?

A
  1. Detachment of tumour cells from their neighbours
  2. Invasion of surrounding tissue through basement membrane
  3. Intravasation into the lumen of vessels
  4. Evasion of host defense mechanisms
  5. Adherance to endothelium at a remote location
  6. Extravasation of the cells
301
Q

What are some side effects of chemotherapy?

A
  • Myelosuppression
  • Hair loss
  • Diarrhoea
302
Q

What is targetted chemotherapy?

A

Chemotherapy that exploits some of the difference between cancer cells and normal cells to target the drugs to the cancer cells

303
Q

Briefly describe the adeno-carcinoma sequence in the colorectum

A
  • Mutation in the APC gene= polyposis
  • Oncogenes are altered- normally KRAS and c-MYC
  • Deletion of the accompanying allele results in complete loss of the tumour suppressor function
304
Q

What is a germline mutation?

A

A mutation in sex or germ cells

305
Q

What is a somatic mutation?

A

A spontaneous mutation in body cells. It cannot be passed on

306
Q

What is lead-time bias?

A

Earlier detection does not affect the inevitable fatal outcome, but prolongs the apparent survival time

307
Q

What is length-bias?

A

Preferential detection of slow growing tumours with intrinsically better prognosis

308
Q

What is overdiagnosis bias?

A

Diagnosis of lesions that, although histologically malignant, are clinically relatively harmless

309
Q

What is selection bias?

A

Volunteers for screening are more at risk of good-prognosis tumours

310
Q

What are the main screening programmes?

A
  • Pregnancy screening
  • Newborn screening
  • Diabetic eye screening
  • Cervical screening
  • Breast screening
  • Bowel cancer screening
  • AAA screening
311
Q

Which of the following tumours never metastasises?

a. Malignant melanoma
b. Small cell carcinoma of the lung
c. Basal carcinoma of the skin
d. Breast cancer

A

Correct answer= C

312
Q

What is the name of a malignant tumour of striated muscle?

A

Rhabdosarcoma

313
Q

Which of the following tumours doesn’t commonly metastasise to bone?

a. Breast
b. Lung
c. Prostate
d. Liposarcoma

A

D

314
Q

What term describes a cancer that has not invaded the basement membrane?

A

Carcinoma in situ

315
Q

What is the name of a benign tumour of glandular epithelium?

A

Adenoma

316
Q

Which one of these tumours does not have a screening programme in the UK?

a. Breast cancer
b. Colorectal
c. Cervical
d. Lung

A

Correct answer= D

317
Q

Which of the following is not known to be a carcinogen in humans?

a. Hepatitis C virus
b. Ionising radiation
c. Aromatic amines
d. Aspergillus niger fungus

A

Correct answer=D

318
Q

What is the name of a benign tumour of fat cells?

A

Lipoma

319
Q

What is the name of a malignant tumour of glandular epithelium?

A

Adenocarcinoma

320
Q

Which one of the following is not a feature of malignant tumours?

a. Vascular invasion
b. Metastasis
c. Increased cell division
d. Growth related to overall body growth

A

Correct answer= D

321
Q

True or false: A transitional cell carcinoma of the bladder is a malignant tumour?

A

True

322
Q

True or false: A leiomyoma is a benign tumour of smooth muscle?

A

True

323
Q

What is the commonest organ in the body that has benign tumours of smooth muscle?

A

Uterus (Fibroids)

324
Q

True or false: Radon gas is a cause of lung cancer?

A

True

325
Q

True or false: Asbestos is a human carcinogen?

A

True

326
Q

What cancer does asbestos normally cause?

A

Mesothelioma

327
Q

Which lifestyle factor is most likely to cause cancer

a. Drinking half a bottle of wine a day
b. Being obese
c. Running for 20 mins twice a week
d. Smoking 20 cigarettes a day

A

Correct answer= D

328
Q

Which tumour has the shortest median survival

a. Basal cell carcinoma of the skin
b. Malignant melanoma of the skin
c. Breast cancer
d. Anaplastic carcinoma of the thyroid

A

Correct answer= D

329
Q

True or false: Ovarian cancer commonly spreads in the peritoneum

A

True

330
Q

What is the predominant inflammatory cell seen in appendicitis?

A

Neutrophil polymorph

331
Q 
A man breaks his leg and it is plastered for 6 weeks. When the plaster is removed, the leg is much thinner than the other leg. What has happened?
a) Atrophy
b) Hyperplasia
c) Hypertrophy
d) Metaplasia
D) Dysplasia
A

Correct answer=A

332
Q 
Acute inflammation actively involves
A) Constriction of arterioles
B) Capillary endothelial cell enlargement
C) Influx of macrophages 
D) Influx of mast cells
E) Influx of neutrophils
A

Correct answer= E

333
Q 
Benign tumour of glandular origin is called:
A) Adenoma
B) Adenocarcinoma
C) Sarcoma
D) Rhabdomyoma
E) Leiomyoma
A

Correct answer= A

334
Q

Aside from increased mitotic activity, give 2 histological findings you might find when examining a malignant tumour (2 marks)

A

Pleomorphism
Hyperchromatic nuclei
Poorly defined border

335
Q

Name 2 routes of metastasis (2 marks)

A

Lymphatic
Haematogenous
Transcoelemic

336
Q

Name two cancer screening programmes in the UK

A

Breast, Bowel, Cervical

337
Q

Name 2 types of cancers which commonly spread to the bone (2 marks)

A

Myeloma

Prostate, Breast, Kidney, Thyroid, Lung

338
Q

You suspect a patient has Sarcoidosis, which blood marker do you investigate?

A

ACE – released by granulomas

339
Q

Give the classes of drug used to treat i) arterial thrombosis ii) venous thrombosis

A

Arterial Thrombosis- Anti-Platelets e.g Aspirin/Clopidogrel

Venous Thrombosis- Anti-Coagulants e.g Warfarin, Heparin, NOAC

340
Q

What is PSA a tumour marker for?

A

Prostate cancer

341
Q

What is calcitonin a tumour marker for?

A

Medullary carcinoma of the thyroid

342
Q

What is CA 15.3 a tumour marker for?

A

Breast cancer

343
Q

What is CA 19.9 a tumour marker for?

A

Colon and pancreatic cancer

344
Q

What is Ann Arbor used to stage?

A

Lymphoma

345
Q

What is Duke’s classification used to stage?

A

Colon cancer

346
Q

What is The Enneking system used to stage?

A

Bone tumour

347
Q

What is the FIGO staging system used to stage?

A

Cervical cancer staging

348
Q

What is alpha-fetoprotein a tumour marker for?

A

Hepatocellular carcinoma and germ cell cancer of the gonads

349
Q

What is CEA a tumour marker for?

A

Colorectal cancer

350
Q

What is beta-hCG a tumour marker for?

A

Choriocarcinomas, germ cell tumours and lung cancer

Phase 2a (31 decks)

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