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GRACE Phase 2a Medicine > ICS - Pathology > Flashcards

ICS - Pathology Flashcards

1
Q

Two different types of autopsy? % of all autopsies in UK

A

Hospital 10% , medico-legal 90%

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2
Q

Two types of medico-legal autopsies?

A

coronial (standard), forensic (deaths involving crime)

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3
Q

What are hospital autopsies used for?

A

teaching, research, governance

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4
Q

Types of death referred to coroners?

A
  1. Presumed natural (cause of death not known)
  2. Presumed iatrogenic (anaesthetic deaths, abortion, etc.)
  3. Presumed unnatural (accidents, suicide, neglect, unlawful killing, etc.)
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5
Q

Who refers death to coroners?

A

Doctors (GMC guidance, no statutory duty), registrar of BDM, relatives, police

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6
Q

Laws related to autopsies?

A

Coroners Act 1988, Coroners Rules 1984, Amendment Rules 2005, Coroners and Justice Act 2009, Human Tissue Act 2004

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7
Q

Define inflammation

A

the local physiological response to tissue injury

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8
Q

Benefits of inflammation?

A

destruction of invading microorganisms, walling off an abscess cavity (thus preventing the spread of infection)

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9
Q

Problems of inflammation?

A
  • an abscess in the brain would lead to compression of vital surrounding structures
  • fibrosis resulting from chronic inflammation may distort tissues and alter their function
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10
Q

5 different cells involved in inflammation?

A

neutrophil polymorphs, macrophages, lymphocytes, endothelial cells, fibroblasts

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11
Q

What is acute inflammation?

A

initial and often transient series of tissue reactions to injury

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12
Q

Acute inflammation steps (I’VE NO Really Sick Opening Pick-ups)

A

Initial reaction to tissue injury
Vascular component - dilation of vessels
Exudative component - vascular leakage of protein-rich fluid
Neutrophil polymorph - characteristic cell recruited to the tissue
Outcome(s)- (1) Resolution, (2) Suppuration (pus formation), (3) Organisation (tissue replacement by granulation tissue), (4) Progression to chronic inflammation

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13
Q

Causes of acute inflammation (My Hairy Backside Cannot Poo Today)

A 
Microbial infections
Hypersensitivity reactions
Bacterial toxins
Chemicals 
Physical agents (e.g. trauma, radiation)
Tissue necrosis
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14
Q

Signs of acute inflammation? (Some People Really Hate Leicester)

A 
Swelling (tumor)
Pain (dolor)
Redness (rubor)
Heat (calor)
Loss of function
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15
Q

Chemical mediators of acute inflammation inducing pain?

A

Bradykinin, prostaglandins, serotonin

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16
Q

In the early stages of acute inflammation, what accumulates in the extracellular spaces of damaged tissue?

A

Oedema fluid, fibrin, neutrophil polymorphs

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17
Q

Acute inflammation involves which 3 response processes?

A
  1. Vessels get wider, increased flow
  2. Increased vascular permeability and formation of fluid exudate
  3. Formation of cellular exudate, emigration of neutrophil polymorphs into the extravascular space
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18
Q

Diagnostic histological feature of acute inflammation?

A

Accumulation of neutrophil polymorphs in the extracellular space

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19
Q

Chemical mediators in acute inflammation?

A

Histamine, serotonin, prostaglandins

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20
Q

Large source of histamine in acute inflammation?

A

Mast cells

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21
Q

Define chronic inflammation?

A

subsequent and prolonged tissue reactions to injury following the initial response

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22
Q

4 causes of chronic inflammation?

A
  1. primary chronic inflammation
  2. transplant rejection
  3. progression from acute inflammation
  4. recurrent episodes of acute inflammation
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23
Q

What are granulomas?

A

Collection of macrophages, structure found during inflammation

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24
Q

granulation tissue?

A

important component of healing and comprises small blood vessels in a connective tissue matrix with myofibroblasts

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25
Q

In chronic inflammation what type of cells are typically in the cellular infiltrate?

A

Lymphocytes, plasma cells, macrophages

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26
Q

Most common form of granuloma?

A

tuberculosis

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27
Q

What is lobar pneumonia?

A

affects a lobe of the lung rather than the whole thing, characterised by inflammatory exudate (neutrophil polymorphs) within the intra-alveolar space (Streptococcus pneumoniae)

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28
Q

What is granulation tissue?

A

New connective tissue and microscopic blood vessels that form on the surfaces of wounds during the healing process (combination of myofibroblasts and capillary loops)

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29
Q

define organisation?

A

repair of specialised tissues by the formation of a fibrous scar

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30
Q

What is wound contraction?

A

reduces the volume of tissue repair due to contraction of myofibroblasts

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31
Q

Incised skin wounds - healing by 1st intention

A
  1. Incision (e.g. by surgical scalpel) causes minimal tissue damage either side of cut
  2. Blood vessels occluded by thrombosis
  3. Exudation of fibrinogen, forms weak fibrin join to bind two sides
  4. Collagen synthesis and epidermal re-growth
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32
Q

Tissue loss - healing by 2nd intention

A

A tissue loss injury/ other reason meaning the wound margins are not aligned, requiring another mechanism for repair:

  1. Loss of tissue, formation of granulation tissue
  2. Organisation - early fibrous scar
  3. Scar contraction
  4. Phagocytosis to remove any debris
  5. Granulation tissue fills in defects
  6. Epithelial regeneration to cover surface
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33
Q

Cells that regenerate?

A

hepatocytes, pneumocytes, all blood cells, gut epithelium, skin epithelium, osteocytes

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34
Q

Cells that DON’T regenerate?

A

myocardial cells, neurones

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35
Q

Repair - when tissue is damaged and unable to…? Damaged tissue is replaced by…? examples?

A

Regenerate, fibrous tissue, heart after myocardial infarction, spinal cord after trauma

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36
Q

Cell renewal

A
  1. Labile cells - good capacity to regenerate, e.g. surface epithelial cells
  2. Stable cell populations - divide at slow rate, e.g. hepatocytes
  3. Permanent cells - no regeneration, e.g. nerve cells
  4. Stem cells
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37
Q

Hepatocytes have excellent regenerative capacity, they are part of which cell population?

A

Stable

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38
Q

Define thrombosis

A

solidification of blood contents that forms WITHIN the vascular system during LIFE

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39
Q

How is a CLOT different from thrombosis? A clot is

A

Blood coagulated OUTSIDE the vascular system or after DEATH

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40
Q

Why doesn’t thrombosis occur all the time? (2)

A
  1. Laminar flow - cells travel in the centre of vessels

2. Endothelial cells (healthy) are not ‘sticky’

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41
Q

Platelets are derived from cells in the bone marrow called?

A

megakaryocytes

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42
Q

Granules within platelets?

A

Alpha - structural components e.g. fibrinogen

Electron dense - e.g. ADP, TxA2 which cause platelets to aggregate

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43
Q

When are platelets activated and subsequently release the contents of their granules?

A

When they come into contact with exposed collagen in the damaged endothelium

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44
Q

Shape change of platelets?

A

Smooth discoid –> spiculated, develop pseudopodia

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45
Q

Action of TxA2 in platelet aggregation?

A

Stimulates platelet binding and causes contraction of action and myosin to condense aggregation

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46
Q

Platelets bind to collagen via?

A

vWF

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47
Q

Thrombosis may be caused by 3 factors?

A
  1. Changes in vessel wall
  2. Changes in blood flow
  3. Changes in blood constitutents
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48
Q

How do lose does of aspirin inhibit thrombosis?

A

Inhibit COX-1 enzyme which is required for the formation of thromboxane A2 which stimulates platelet aggregation

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49
Q

Atheroma?

A

degeneration of the walls of the arteries caused by accumulated fatty deposits and scar tissue, thus leading to restricted circulation and risk of thrombosis

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50
Q

Where do most venous thrombi begin? Why?

A

Valves, induce a degree of turbulence

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51
Q

Why does immobilisation increase the risk of deep vein thrombosis?

A

Venous return from the legs is very reliant upon calf and muscle contraction and relaxation

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52
Q

How does warfarin prevent clot formation (in severe cases)?

A

Blocks the liver from using vitamin K to produce clotting factors (inhibits vitamin K epoxide reductase complex 1 which activates vitamin K int he body)

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53
Q

What is an embolus?

A

Mass material in the vascular system able to lodge in a vessel and block the lumen (usually caused by part of a thrombus that has broken off)

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54
Q

What is meant by embolism?

A

The process of a solid mass in the blood being carried through the circulation to a place where it gets stuck and blocks the vessel

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55
Q

Venous embolism –> pulmonary embolism?

A

If an embolus enters the venous system it will enter the R atrium via the vena cava and will lodge somewhere in the pulmonary arteries resulting in a pulmonary embolism

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56
Q

Why can’t a pulmonary embolism –> arterial circulation?

A

Vessels in the lung split down to capillary size, thus the lungs act as a filter for any venous emboli

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57
Q

Ischaemia?

A

Reduction of blood flow to a tissue without any other implications

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58
Q

Infarction?

A

reduction of blood flow to a tissue that is so reduced that it cannot even support mere maintenance of the cells in the tissue so they die

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59
Q

End arterial supply

A

Organ which only receives its arterial supply from one artery

60
Q

Organs with dual arterial supply and therefore less susceptible to infarction?

A
  1. Liver (hepatic artery and portal vein)
  2. Brain (vertebral and common carotid)
  3. Lung (pulmonary venous and bronchial artery)
61
Q

Gangrene

A

When whole 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

62
Q

What is atherosclerosis?

A

Disease characterised by the formation of atherosclerotic plaques in the intima of large and medium sized arteries (e.g. aorta, coronary arteries)

63
Q

Atherosclerotic plaques alone are NOT life threatening - when do they become so?

A

When an occlusive thrombosis forms on a spontaneously disrupted plaque

64
Q

Risk factors for atherosclerotic plaques

A

Hypercholesterolaemia (most important risk factor), smoking, hypertension, diabetes, male gender, increasing age

65
Q

What is an aneurysm?

A

Enlargement of an artery caused by weakness in the arterial wall

66
Q

Types of stroke?

A
  1. Transient ischaemic attack (< 24 hours)
  2. Cerebral infarction (occur within internal carotid territory)
  3. Intracranial haemorrhage (intracerebral and subarachnoid)
67
Q

Apoptosis?

A

programmed cell death

68
Q

Apoptosis differs from necrosis?

A

Necrosis is the unintended cell death in response to cellular injury. The mechanisms of apoptosis act to suppress the inflammatory response triggered by necrosis

69
Q

Cancer and apoptosis?

A

Lack of apoptosis, cells live longer and proliferate

70
Q

AIDS and apoptosis?

A

HIV proteins may activate CD4+ on T helper cells inducing apoptosis

71
Q

Apoptosis can be triggered by?

A

DNA damage

72
Q

Necrosis

A

Death of most or all the cells in an organ or tissue due to disease, injury or failure of the blood supply, inducing inflammation and repair

73
Q

Clinical examples of necrosis?

A

Toxic spider venom, frostbite, cerebral infarction

74
Q

Congenital disease?

A

Disease someone is born with, can be genetic (cystic fibrosis, sickle cell anaemia), spontaneous (Down’s syndrome), or environmental (fetal alcohol syndrome)

75
Q

Polygenic gene disorder

A

Genetic disease which is a result of the interaction of several different genes e.g. breast cancer

76
Q

Hypertrophy

A

Increase in size of a tissue without an increase in the number of cells

77
Q

Hyperplasia

A

Increase in the size of a tissue caused by an increase in the number of constituent cells

78
Q

Atrophy

A

Decrease in the size of a tissue due to a decrease in a number or cells OR size

79
Q

Metaplasia

A

Change in differentiation of a cell from one fully-differentiated type to a different fully-differentiated type (e.g. ciliated respiratory epithelium in smokers –> squamous epithelium)

80
Q

Dysplasia

A

Imprecise term for the morphological changes seen in cells in the progression to becoming cancer (i.e. not quite cancer but could be heading that way)

81
Q

What happens to telomeres are each cell division?

A

They get shorter, limiting the amount of division that can occur (hence ageing)

82
Q

What is a telomere?

A

Non-coding random repetitive DNA sequence at the tip of each chromosome, adds stability

83
Q

Why do telomeres get shorter?

A

Not fully copied in to DNA synthesis prior to mitosis, single strand at the tip is cut off and thus with each cell division the telomeres decrease in length

84
Q

Telomere length is inherited from which parent?

A

father

85
Q

Sarcopenia?

A

Condition characterised by muscle loss due to ageing (decreased growth hormone, testosterone, etc)

86
Q

Deafness in elderly?

A

loss of hair cells in ear

87
Q

Senile dementia

A

due to brain atrophy since nerve cells cannot regenerate

88
Q

Cataracts

A

Caused by UV light damage resulting in cross-linking proteins in the eye

89
Q

Osteoporosis

A

Due to lack of oestrogen as well as vitamin D and calcium in earlier life

90
Q

Neoplasm

A

Abnormal growth of cells which persists even after the initiating stimulus is removed, neoplastic diseases are conditions that cause tumour growth

91
Q

Carcinogenesis

A

Transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations

92
Q

Why does the incidence of cancer increase with age?

A

The probability of neoplastic transformation increases with the number of cell divisions experience by a cell

93
Q

Carcinogens increase the…

A

probability of mutational events

94
Q

Contents of a plaque

A

fibrous tissue, smooth muscle cells, lipids, macrophages, lymphocytes, cell debris, calcium

95
Q

Process of plaque development

A
  1. Endothelial cell dysfunction (lots of cholesterol damages wall)
  2. High levels of LDL begins to accumulate in the arterial wall
  3. Macrophages are attracted to site of damage and take up lipids
  4. Formation of a fatty streak
  5. Activated macrophages release their own products e.g. cytokines, growth factors
  6. Smooth muscle proliferation to around the lipid cord and formation of a fibrous collagen cap
96
Q

Tumour

A

any abnormal swelling:

  • neoplasm
  • inflammation
  • hypertrophy
  • hyperplasia
97
Q

Solid tumours consist of

A

neoplastic cells embedded in the connective tissue framework, the stroma

98
Q

Process essential to neoplasm growth?

A

Angiogenesis (development of blood supply)

99
Q

The stroma of a neoplasm provides what?

A

mechanical support, intracellular signalling, nutrition to the neoplastic cells

100
Q

Prominent within the neoplasm stroma are?

A

Fibroblasts and collagen

101
Q

What is secreted by tumour cells to induce angiogenesis?

A

Vascular endothelial growth factor (VEGF)

102
Q

Behavioural classifications of tumours?

A

Malignant –> borderline –> benign

103
Q

Benign neoplasms

A
  • Localised
  • Slow growth rate
  • Non-invasive
  • Do not spread
  • Close resemblance to normal tissue
  • Exophytic (outward) growth
  • Ulceration and necrosis both rare
104
Q

How do benign tumours cause morbidity and mortality?

A
  • Pressure on vital organs
  • Obstruction to fluid flow
  • Transformation to a malignant neoplasm
  • Induces anxiety
105
Q

What is ulceration of a neoplasm?

A

Breach of the mucosal surface

106
Q

Malignant neoplasms

A
  • Invasive
  • Metastisise - invade tissue and spread, forming secondary tumours
  • Rapid growth
  • Endophytic growth - invasive inward growth
  • Hyperchromatic nuclei - dark staining
  • Necrosis and ulceration are common
107
Q

How do malignant tumours cause morbidity and mortality?

A
  • Pressure on and destruction of adjacent tissue
  • Blood loss from ulcerated surfaces
  • Secondary tumours
  • Obstruction of flow
  • Anxiety and pain
108
Q

Most important criteria for malignancy

A

tumour invasion

109
Q

Histological appearance of malignant tumours

A
  • High mitotic activity
  • Pleomorphism
  • Hyperchromatic nuclei
  • Poorly defined border
110
Q

Possible physical signs of metastasis?

A

Bone pain, palpable lump

111
Q

How are malignant tumours histologically graded?

A

poorly –> moderately –> well differentiated

112
Q

What is meant by a poorly differentiated malignant tumour?

A

More closely resembles parent tissue

113
Q

Which are the more aggressive tumours?

A

Well differentiated

114
Q

Papilloma

A

benign tumour of NON-GLANDULAR, NON-SECRETORY epithelium

115
Q

Adenoma

A

benign tumour of GLANDULAR or SECRETORY epithelium

116
Q

Carcinoma

A

Malignant tumour of epithelial cells

117
Q

Adenocarcinoma

A

Malignant tumour of glandular epithelium

118
Q

Sarcomas

A

Malignancies of connective tissue

119
Q

What suffix denotes neoplasm

A

-oma

120
Q

Why do neoplastic cells show uncontrolled proliferation with a prolonged/ indefinite lifespan?

A
  1. Abnormal expression of genes
  2. Reduced apoptosis
  3. Telomerase
121
Q

Carcinogens

A

Environmental agents participating in the causation of tumours, either carcinogenic or oncogenic

122
Q

Classes of carcinogens

A

chemical, viral, ionising/non-ionising radiation, hormones, etc

123
Q

Factors influencing tumour invasion?

A
  1. Decreased cellular adhesion
  2. Secretion of proteolytic enzymes (digest surrounding connective tissues)
  3. Abnormal or increased cellular motility
124
Q

In-situ neoplasia

A
  • Only applies to epithelial neoplasms

- Basement membrane is intact

125
Q

Carcinoma in situ

A

malignant epithelial neoplasm that has not yet invaded through the original basement membrane

126
Q

Invasive carcinoma

A

carcinoma that has breached the basement membrane - can now spread elsewhere

127
Q

micro-invasive carcinoma

A

breached the basement membrane, not yet invaded very far from the original carcinoma

128
Q

Metastasis

A

Process by which a malignant tumour spreads from its primary site to produce secondary tumours at distant sites

129
Q

Mechanism of metastasis (DIIE AEV)

A
  1. detachment of tumour cells from neighbour
  2. invasion through basement membrane
  3. intravasation into lumen of vessels
  4. evasion of host defence mechanisms, e.g. natural killer cells in the blood
  5. adherence to endothelium at remote location
  6. extravasation of cells from vessel lumen to surrounding tissue
  7. vascularisation
130
Q

Angiogenesis inhibitors?

A

angiostatin, endostatin, vasculostatin

131
Q

Routes of metastasis

A

Haematogenous - by blood stream, forms secondary tumours in organs perfused by blood that has drained from a tumour

Lymphatic - lymph channels, form in lymph nodes

Trans-coelomic - pericardial and peritoneal cavities where this invariably results in neoplastic effusion

132
Q

Two drugs given to treat breast cancer?

A

Anti-oestrogen and herceptin

133
Q

Types of cancers that commonly spread to bone? (My Pb (lead) KTL (kettle)

A
  1. Myeloma
  2. Prostate
  3. Breast
  4. Kidney
  5. Thyroid
  6. Lung
134
Q

Cancer screening biases

A
  1. Lead time bias - earlier detection does not affect inevitable outcome, just prolongs survival time
  2. Length bias - preferential detection of slow growing tumours, better prognosis
  3. Overdiagnosis bias - diagnosis of lesions that although are histologically malignant, are clinically harmless
  4. Selection bias - volunteers for screening are more at risk of good-prognosis tumours
135
Q

The spread of the acute inflammatory response following injury to a small area of tissue is due to

A

Chemical mediators being released outwards into uninjured areas

136
Q

Overall effect of chemical mediators of acute inflammation?

A

Firm neutrophil adhesion to the endothelial cells

137
Q

What is a histiocyte?

A

Normal immune cell, found in many parts of the body such as bone marrow, the bloodstream, skin, liver, etc.

138
Q

A granuloma is a form of chronic inflammation which is what type of hypersensitivity?

A

4

139
Q

In lobar pneumonia, the alveoli are filled with?

A

neutrophil polymorphs rather than air

140
Q

Repair

A

Replacement of damaged tissue by fibrous tissue

141
Q

Granulation tissue

A

A repair phenomenon, consists of loops of capillaries, supported by myofibroblasts which actively contract to reduce the wound size

142
Q

Organisation is the process whereby

A

Specialised tissues are repaired by the formation of mature fibrovascular connective tissue

143
Q

How does organisation occur?

A

Production of granulation tissue and the removal of dead tissue by phagocytosis

144
Q

Difference between carcinogenesis and oncogenesis?

A

Oncogenesis refers to both benign and malignant tumours, whereas carcinogenesis refers to just malignant tumours

145
Q

difference between carcinogenic and oncogenic?

A

carcinogenic = cancer causing, oncogenic = tumour causing

GRACE Phase 2a Medicine (20 decks)

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