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MCD Year 1 > Cell Pathology > Flashcards

Cell Pathology Flashcards

1
Q

Why would a death need to be reported to the coroner?

A 
Is the cause of death is:
Unknown
Not seen a doctor in >14 days
Violent/ suspicious
Accidental (even if years later)
Due to neglect by others
Due to industrial disease
Due to abortion
During operation
Suicide (even if suspicious)
During/ after police detention
Poisoning
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2
Q

What are the reasons for conducting a hospital autopsy?

A

1) Audit major discrepancies between stated COD and actual COD
2) Monitoring effects of new treatments
3) Teaching
4) Research

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3
Q

What consent is needed for a hospital autopsy?

A

Consent of next of kin.

With consent, tissue can be taken and used from the body for research etc

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4
Q

What consent is needed for a coroner’s autopsy?

A

No consent needed (although families wishes considered)

Material can only be taken if coroner gives permission and it is needed to establish cause of death.

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5
Q

List 4 causes of sudden unexpected death in the community

A

1) Cardiovascular disease
2) Vascular system (e.g. ruptured aortic aneurism)
3) Central nervous system (e.g. Berry aneurism, intracerebral haemorrhage (stroke) or epilepsy)
4) Respiratory system (e.g. Pulmonary embolus, asthma, bleeding ulcers or pancreatitis)
5) Not natural (e.g. drugs, alcohol or trauma)

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6
Q

What is a contusion? What would cause one?

A

A bruise.
It is an extravasated collection of blood which has leaked from small arteries, venules and veins but not capillaries. Takes hours-days to form. May be patterned or deep. Caused by a blunt trauma injury.
Cannot age a bruise as can bruise after death

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7
Q

What is an abrasion? What mechanism of injury would cause an abrasion?

A

A graze/scratch.
Superficial blunt trauma confined to the epidermis (may extend to superficial dermis). can occur before or after death.
Due to tangential force (distal skin tag occurs) or vertical force (no tag)
e.g. friction burn, car radiator, flooring, whip, stamp

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8
Q

What is a laceration? What mechanism of injury would cause an abrasion?

A

Split to skin (caused by blunt force trauma over stretching the skin).
Deep (full thickness). Bleeds. Margins ragged and crushed/ bruised.
Common where skin can be compressed between force and bone (scalp, elbow, shin). Rare over soft fleshy areas (buttocks, breasts)
Flaying- tangentially applied force → horizontal laceration (difficult to identify the object causing it)

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9
Q

What are the causes of cell injury? (8)

A

1) Oxygen deprivation
2) Chemical agents
3) Infectious agents
4) Immunological reactions
5) Genetic defects
6) Nutritional imbalances
7) Physical agents
8) Ageing

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10
Q

What is lethal injury?

A

Causes cell death

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11
Q

What is sub-lethal injury?

A

Produces injury not amounting to cell death. It may be reversible or progress to cell death

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12
Q

What does cellular response to an injurious stimuli depend on? (3)

A

1) The type of injury
2) It’s duration
3) It’s severity

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13
Q

What four intracellular systems are particularly vulnerable to cell injury?

A

1) Cell membrane integrity
2) ATP generation
3) Protein synthesis
4) Integrity of the genetic apparatus

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14
Q

What is atrophy? Give an example

A

Shrinkage in the size of the cell (or organ) by the loss of cell substance
e.g. dementia

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15
Q

What is hypertrophy?

A

An increase in the size of cells and consequently an increase in the size of the organ.
It can by physiological or pathological. Caused either by increased functional demand or by specific hormone stimulation

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16
Q

What is hyperplasia?

A

An increase in the number of cells in an organ. Can be physiological or pathological.
Physiological hyperplasia can be either hormonal or compensatory
Pathological hyperplasia is usually due to excessive hormonal or growth factor stimulation

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17
Q

What is metaplasia?

A

The reversible replacement of one differentiated cell type with another differentiated cell type

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18
Q

What is dysplasia?

A

An abnormality of development; in pathology, alteration in size, shape and organisation of adult cells.
Precancerous cells which show the genetic and cytological features of malignancy but not invading the underlying tissue

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19
Q

What types of cell adaptation are reversible?

A
  • Hypertrophy and hyperplasia
  • Atrophy and involution
  • Metaplasia
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20
Q

What types of cell adaptation are irreversible?

A
  • Apoptosis

- Necrosis

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21
Q

What is apoptosis?

A

A process of programmed cell death that occurs in multicellular organisms. Biochemical events lead to characteristic cell changes (morphology) and death

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22
Q

What is necrosis?

A

A form of cell injury which results in the premature death of cells in living tissue by autolysis

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23
Q

What is necroptosis?

A

A programmed execution of cell death. It is favoured in certain circumstances, such as aiding targeting of pathogens by the immune system

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24
Q

What is acute inflammation?

A

Transient and early response. Release of chemical mediators. Typical vascular and leucocyte response.
NOT the same as infection

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25
Q

What is chronic inflammation?

A

Inflammation of prolonged duration (weeks to years). usually due to persistence of injury-causing agent.
Active inflammation, tissue destruction and attempts at repair occur simultaneously

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26
Q

What is granulomatous inflammation?

A

A specialised form of chronic inflammation

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27
Q

What are the cardinal signs of inflammation?

A

1) Rubor (redness)
2) Calor (heat)
3) Tumor (swelling)
4) Dolor (pain)
5) Loss of function

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28
Q

What causes calor in inflammation?

A

Histamine-mediated vasodilation

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29
Q

What causes tumor in inflammation?

A

Oedema and histamine

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30
Q

What is histamine?

A

A vasoactive amine produced by mast cells.
Pre-formed and released cell degranulates. Degranulation triggered by cell surface IgE antibody interactions with antigen
Leads to vasodilation and increased vascular permeability
Dysregulation in allergy (Type 1 hypersensitivity)

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31
Q

What cells are predominant in acute phase inflammation?

A

Neutrophils

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32
Q

What are the three phases of an inflammatory response? Which cells are present in each phase?

A 
Acute phase (neutrophils)
Chronic phase (monocytes/ macrophages/ lymphocytes/ plasma cells)
Resolution/ Repair (macrophages/ fibroblasts)
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33
Q

What causes chronic inflammation?

A 
Persistent infection (HCV, TB)
Prolonged exposure to toxic agent (uric acid)
Autoimmunity
Foreign body (splinter)
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34
Q

What is the basic pathology of granulomatous inflammation?

A

Cluster of macrophages

Involves specific immune reaction T cells

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35
Q

What are the causes of granulomatous inflammation?

A

Infection (TB, fungal)
Foreign material
reaction to tumours
Immune diseases (sarcoid, Crohn’s)

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36
Q

What are the benefits of an inflammatory response?

A

Removal of causative agent
Cessation of the inflammatory reaction
Healing of tissue damage to preserve integrity and function (resolution)

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37
Q

What are the negative local effects of inflammation?

A

Can cause excess local tissue damage and scarring

Secondary effects on nearby tissue (e.g. bronchoconstriction in asthma)

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38
Q

What are the negative systemic effects of inflammation?

A

Can evolve into systemic inflammatory reaction and secondary multi-organ failure (e.g. septic shock, amyloid)

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39
Q

What is wound healing?

A

Parenchymal cell regeneration and resolution

repair by connective tissue and scar tissue formation

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40
Q

What is resolution in terms of wound healing? When does it occur?

A

Tissue architecture returns to normal
Only occurs if:
- Tissue contains cells able to regenerate to replace lost cells (e.g. liver)
- Little structural damage is done- cells need a framework to build on (basement membrane e.g. lung in lobar pneumonia)

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41
Q

What is repair in terms of wound healing? What are the important components of repair?

A

If tissue loss is too great and cells are unable to regenerate normal tissue is replaced with scar tissue
Fibroblasts- produce collagen
Collagen- strong “scar” type collagen
Remodelling- reorientation of collagen fibres for maximal tensile strength

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42
Q

What general and local factors hinder repair?

A

General
- Poor nutrition (require protein for collagen production and energy for cell function)
- Vitamin deficiency (Vit C- needed by fibroblasts to make collagen. Vit A- required for epithelial regeneration)
- Mineral deficiency (e.g. zinc)
- Suppressed inflammation (e.g. by steroids, old age, diabetes)
Local
- Poor blood supply (e.g. ischaemic leg ulcers)
- Persistent foreign body (e.g. splinter)
- Movement (e.g. across a fracture site- need for a cast)

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43
Q

What complications can occur in wound healing?

A
  • Keloid formation (excess collagen deposition)
  • Contractures (fibrous scar tissue contracts as it matures. If scarring occurs across a joint it can cause poor joint mobility
  • Impaired organ function (e.g. fibrous scars in the myocardium after a heart attack)
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44
Q

What is a neoplasm?

A

A new growth
“Abnormal mass of tissue, the growth of which is virtually autonomous and exceeds that of normal tissue. The growth is uncoordinated and persists after the cessation of the stimuli that initiated the change”

45
Q

What are the basic components of a neoplasm?

A

Parenchyma- transformed parenchymal cells

Stroma- without ‘stromal’ blood vessels. tumour cannot grow.

46
Q

What is a tumour?

A

A swelling of part of the body, without inflammation, caused by an abnormal growth of tissue. Can be benign of malignant

47
Q

What is a carcinogen?

A

Any substance, radionuclide, or radiation that is an agent directly involved in causing cancer. This may be due to the ability to damage the genome or to the disruption of cellular metabolic processes.

48
Q

What is a benign tumour? (4)

A

1) ‘Well’ differentiated
2) Usually slow growing
3) Rarely invade locally (cohesive, expansile, encapsulated mass)
4) Seldom metastasize

49
Q

What is a malignant tumour? (4)

A

1) Anaplasia (complete lack of differentiation)
2) Rapid turnover (‘chemo targets’)
3) ‘Infiltrative’ margins
4) Metastasize (except 2 tumours)

50
Q

What are the four mechanisms of metastases?

A
  • Lymphatic
  • Haematogenous
  • Body cavities
  • Contiguous
51
Q

What effect does age have on cancer?

A

Higher incidence >55 years
Some cancers specifically affect the young (e.g. leukaemias, neuroblastomas, Wilm’s tumour, retinoblastoma, primary bone sarcomas)

52
Q

Give examples of the effect geography has on cancer

A

Stomach cancer higher (7x) in Japan than USA but colon cancer lower
Melanoma higher in NZ and Australia than Scandinavia
HCC more common in Uganda
Oesophageal cancer higher in China and Iran (nitrates in soil, abrasives in diet)

53
Q

What environment factors effect cancer?

A
  • UV light
  • Occupational agents (asbestos, alcohol, smoking)
  • Infections notably viruses (HPV, HBV, EBV etc)
54
Q

What are the three categories of genetic factors affecting cancer?

A

1) Autosomal dominant (retinoblastoma, FAP)
2) Autosomal recessive ( Xeroderma)
3) Unknown (Familial cancer syndromes e.g. BRCA)

55
Q

What are the different classes of carcinogens? (6)

A

1) Chemicals
2) Viruses
3) Ionising/ non-ionising radiation
4) Hormones
5) Bacteria, fungi, parasites
6) Miscellaneous

56
Q

What are chemical carcinogens? Give examples

A

No common structural features
Need metabolic conversion (procarcinogen) to active peptide (ultimate carcinogen)
Some act directly without conversion
If enzyme present within tissues, tumour occurs at the site (e.g. skin and lung cancer with aromatic hydrocarbons)
Others may require metabolic conversion in the liver (e.g. aromatic amines causing UB cancer)
E.g. Alkylating agents (cyclophoshamide and busulphan)
Polycyclic aromatic hydrocarbons (cigarette smoking in lung cancers)
Aromatic amines and azo dyes (b-napthalene dyes in bladder cancer)

57
Q

Where do oncogenic viruses cause cancer? Give examples

A

Generally in the young and immunosuppressed

EBV (BL) and HPV (CC). HBV and HCV hepatic cancers

58
Q

What is the mechanism for oncogenic viruses?

A

Oncogenetic viral DNA genome directly incorporated into host cell DNA
Oncogenic RNA viral genome transcribed into DNA by enzymes prior to incorporation

59
Q

What types of radiation cause cancer?

A 
Ultraviolet (SCC, BCC, MM)
Ionising electromagnetic (i.e. X-rays- cause an increase in leukaemia and solid tumours)
60
Q

Give an example of a type of fungi that causes cancer

A

Naturally occurring carcinogens aspergillus flavus in liver cancers

61
Q

Give an example of a hormone that causes cancer

A

Oestrogens have been linked to breast and endometrial cancer

62
Q

What are the four classes of regulatory gene?

A

1) Growth promoting genes- Proto-oncogenes
2) Growth inhibiting (tumour suppressor)- Anti-oncogenes
3) Genes regulating programmed cell death- Pro-apoptotic genes
4) Genes preventing mutations in the normal cell cycle- DNA repair genes

63
Q

What are oncogenes? Give examples

A

Derived from genes regulating normal cellular growth
e.g. Burkitt lymphoma- Myc
Neuroblastoma- N-Myc
Mantle cell lymphoma- CyclinD1

64
Q

What are tumour suppressor genes? Give examples of their association in cancer

A

Usually regulate normal cell growth
e.g.Rb gene (13q) in genetically inherited retinoblastoma
p53 housekeeper of genome
BRCA-1 and BRCA-2 breast cancers are familial and one of these mutations is present in 80% of breast cancers

65
Q

What laboratory methods are used in cancer diagnosis?

A
  • Cytology FNA ( freehand or USS guided)
  • Histology (core biopsy, incisional or excisional biopsy)
  • Tumour typing
  • Immunocyto/histochemistry
  • Flow cytometry
  • Molecular methods (PRC, FISH, DNA microarrays, spectral karyotyping)
  • Tumour markers (CEA, AFP, Ca125 etc)
66
Q

What is the main staging system for cancer?

A

TNM system

1) TUMOUR- Size of the primary lesion (T1-T4)
2) NODES- Spread to regional lymph nodes (N0, N1-N3)
3) METASTASES- Presence of metastases (M0, M1-M2)

67
Q

What is Duke’s staging of bowel cancer?

A

Stages A (early bowel cancer) to D (advanced)
Stage A→The cancer is only in the innermost lining of the bowel or slightly growing into the muscle layer.
Stage B→The cancer has grown through the muscle layer of the bowel.
Stage C→The cancer has spread to at least one lymph node in the area close to the bowel.
Stage D→The cancer has spread to somewhere else in the body, such as the liver or lungs.

68
Q

What cancer screening programmes are currently used in the UK?

A

Breast screening programme
Cervical screening programme
Bowel screening programme

69
Q

What is oedema?

A

An abnormal increase in interstitial fluid

70
Q

What causes oedema? (4)

A

1) Increased capillary hydrostatic pressure- venous obstruction, congestive cardiac failure
2) Decreased capillary oncotic pressure- renal disease (nephrotic syndrome), liver disease (cirrhosis), malnutrition
3) Increased capillary permeability- severe inflammation, burns
4) Lymphatic obstruction- inflammation, neoplastic, post surgery

71
Q

What is anasarca?

A

Severe generalised oedema
Widespread accumulation of fluid in subcutaneous tissues and serous cavities
Common causes- left ventricular failure, nephrotic syndrome, hepatic failure
Low renal blood flow→ renin→ angiotensin→ aldosterone→ absorption of sodium and water from the kidneys→ generalised oedema

72
Q

What causes pulmonary oedema?

A

Caused by increased hydrostatic pressure in the pulmonary capillaries. Most common cause if left ventricular failure.
Fluid accumulates first in the interstitial space and then eventually spills into the alveolar spaces.
Non-cardiogenic pulmonary oedema caused by increased permeability e.g. ARDS
Can be chronic or acute. Dyspnoea (breathlessness) is the main symptom typically made worse when lying flat (orthopnoea)
Fluid in the alveolar spaces predisposes to bacterial infection in the lung (pneumonia)

73
Q

What are the risks of cerebral oedema?

A

Contributes to a rise in intracranial pressure (ICP). high ICP risks brain herniation and death. Different mechanisms.
Generalised- hypoxia, SIADH
Localised- Around tumour, abscess, haemorrhage

74
Q

What is lymphoedema?

A

Abnormal removal of interstitial fluid by lymphatics

75
Q

What is thrombosis?

A

The formation of a solid mass of blood constituents within the circulatory system

76
Q

What 3 main factors predispose to thrombosis?

A

(Virchow’s triad)

1) Vessel wall injury
2) Hypercoagulability
3) Stasis

77
Q

What is an arterial thrombus? What are the risks and associated conditions?

A

Usually related to vessel wall injury/atheroma
Narrowing causes ischaemia; blockage causes infarction
e.g. angina, MI, ischaemic limb

78
Q

What is a venous thrombus? What are the risks and associate conditions?

A

Usually related to stasis/ hypercoagulability
Most form in deep veins
Can cause congestion, oedema, ischaemia, infarction
e.g. DVT

79
Q

Left atrial thrombosis is usually related to what?

A

Atrial fibrillation

80
Q

Left ventricular thrombosis is usually related to what?

A

Prior myocardial infarction

81
Q

What are the possible fates of a thrombus? (4)

A

1) Propagation
2) Embolisation
3) Dissolution
4) Organisation and recanalization

82
Q

What is an embolism?

A

An embolus is a detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from it’s point of origin.
Most are fragments of dislodged thrombus, can (rarer) be fat, air, amniotic fluid, tumour.
Important because they can lodge in vessels and block them off

83
Q

Where do most venous thromboemboli originate? What are the risk factors? What is the most significant consequence?

A

Most originate in DVT
Risk factors: malignancy, pregnancy, immobility, surgery
Most significant consequence: pulmonary (thrombo)embolism→ embolism to the lungs with blokage of a pulmonary artery

84
Q

What is a pulmonary thromboembolism?

A

Embolism to the lungs blocking a pulmonary artery
Lodging in a major pulmonary artery will cause instant death. Medium sized artery= breathlessness. Small arteries= breathlessness, chest pain, dizziness (hardest to diagnose) ∼30% of patients with a pulmonary embolism will die from it.

85
Q

What is a haemorrhage?

A

Escape of blood from a ruptured vessel.
May be due to trauma or an intrinsic disease of the vessel. Can be external or enclosed within tissue (haematoma)
1-2mm haemorrhage = petechiae
>3mm = purpura
1-2cm = ecchymoses
Large accumulations in body cavities e.g. haemothorax
Risks of hypovolaemia, shock and death

86
Q

What is shock?

A

When tissue perfusion is insufficient to meet metabolic requirements. Characterised by hypotension. Circulatory collapse leading to ischaemia of multiple organs (most vulnerable are: kidneys, bowel, brain, lungs and heart)

87
Q

What is the formula for mean arterial pressure?

A

MAP= COxSVR (cardiac output x systemic vascular resistance)

88
Q

What is the formula for cardiac output?

A

CO=HRxSV (heart rate x stroke volume)

89
Q

What are the different types of shock?

A
  • Hypovolaemic (most commonly due to loss of blood volume e.g. trauma/haemorrhage)
  • Cardiogenic (impaired cardiac funtion/pump failure e.g. acute MI, tamponade)
  • Septic (vasodilation due to inflammatory response)
  • Anaphylactic (IgE mediated hypersensitivity = vasodilation and increased permeability)
  • Neurogenic (injury to sympathetic pathways- loss of vasomotor tone)
90
Q

What is infarction?

A

Tissue necrosis due to ischaemia
Most due to obstruction of an artery (may be venous obstruction). Heals by repair. Structural integrity if maintained but there is permanent loss of functional tissue

91
Q

What factors influence development of infarction? (4)

A
  • Nature of blood supply
  • Rate of development of occlusions- collaterals
  • Vulnerability to hypoxia
  • Oxygen content of blood “Pale” infarcts
92
Q

What is atherosclerosis?

A

Complex chronic disease. Focal intimal accumulation of lipids and fibrous tissue associated with smooth muscle proliferation affecting medium and large vessels.
Develops from fatty streak intoplaque with intima

93
Q

What are the risk factors for atherosclerosis? (4)

A

Smoking
Diabetes
Hypertension
Hyperlipidaemia

94
Q

What is the mechanism of onset of atherosclerosis?

A

1) Endothelial damage leading to macrophage infiltration and release of cytokines
2) Circulating low-density lipoproteins are trapped in the lesion and oxidised
3) Oxidised LDL is proinflammatory and drives the progression of the atherosclerotic plaque
4) Smooth muscle cells migrate from the media into the lesion and deposit a collagen-rich matrix that forms a protective fibrous cap

95
Q

What is the difference between stable plaques and unstable plaques?

A 
Stable plaques:
- Less inflammation
- Well developed thick fibrous plaque
- Slow growing
- Less likely to rupture
Unstable plaques:
- More inflammation
- Lipid rich necrotic core
- Thin fibrous cap
- More likely to rupture
96
Q

What diseases are caused by stable atherosclerotic plaques?

A
  • Stable angina

- Chronic lower limb ischaemia

97
Q

What diseases are caused by thrombosis overlying an unstable atherosclerotic plaque?

A
  • Unstable angina
  • Myocardial infarction
  • Cerebral infarction
  • Acute lower limb ischaemia
98
Q

What are the effects of a Helicobacter pylori infection on the stomach?

A

1) Inflammation- acute, chronic (including ulcers)
2) Cell damage- atrophy, metaplasia, dysphasia
3) Neoplasia- carcinoma, lymphoma

99
Q

What are the clinical outcomes of a H. pylori infection?

A

> 80% = asymptomatic or chronic gastritis
15-20% = Chronic atrophic gastritis intestinal metaplasia
Gastric or duodenal ulcer

100
Q

What are the causes of gastritis (8)

A

1) Oxygen deprivation
2) Chemical agents = drugs
3) Infectious agents = helicobacter
4) Immunological reactions = autoimmune
5) Genetic defects
6) Nutritional imbalances
7) Physial agents
8) Aging

101
Q

What is an ulcer?

A

An open sore on an external or internal surface of the body, caused by a break in the skin or mucous membrane which fails to heal.
Ulcers range from small, painful sores in the mouth to bedsores and serious lesions of the stomach or intestine

102
Q

What is the key inflammatory cell of acute inflammation?

A

Neutrophils

103
Q

What is the key inflammatory cell of chronic inflammation?

A

Lymphocytes

104
Q

What is the mechanism of healing of an acute or chronic ulcer?

A

Acute gastric ulcer→ parenchymal cell regeneration and resolution
Chronic gastric ulcer→ Repair by connective tissue and scar tissue formation

105
Q

What cellular adaptations are seen in helicobacter gastritis? (5)

A 
Hyperplasia
Hypertrophy
Atrophy
Metaplasia
Dysplasia
106
Q

What is the system for classification of neoplasms?

A
  • According to the cell of origin
  • According to if they are benign or malignant
    e.g.
    Benign tumours from glandular epithelium = adenomas
    Malignant tumours from glandular epithelium = adenocarcinomas
107
Q

What is the difference between grading and staging?

A

Grading is based on the degree of histological differentiation (less useful than staging)
Staging is based on how far the tumour has spread (combination of clinical, radiological and pathological findings)

108
Q

What are common sites of clinically important atheroma?

A
  • Coronary arteries
  • Carotid arteries
  • Aorta and/or iliac arteries

MCD Year 1 (10 decks)

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