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MCD > Cell Pathology > Flashcards

Cell Pathology Flashcards

1
Q

Define atrophy

A
  • Shrinkage in the size of a cell and consequently the size of a whole organ, by the loss of cell substance
  • We see a decrease in weight of an atrophic organ
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2
Q

Define hypertrophy

A
  • Increase in the size of a cell and consequently the size of a whole organ
  • Physiological or pathological
  • important because muscle cells (skeletal and cardiac) cannot divide so an increase in cell size is the only way in which an organ can get bigger
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3
Q

Define hyperplasia

A
  • Increase in the number of cells in an organ

- Physiological or pathological

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4
Q

Define metaplasia

A
  • Reversible change in which one normal adult cell type (mature cell) is replaced by another (normal adult cell replacement)
  • Physiological or pathological
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5
Q

Define dysplasia

A
  • Precancerous cells which show the genetic and cytological features of malignancy but do not invade the underlying tissue (does not invade through the basal lamina)
  • bridge between normality and cancer
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6
Q

Examples of atrophy

A
  • Gastric atrophy causing pernicious anaemia (anaemia resulting from vitamin B12 deficiency)
  • Posterior cortical atrophy from the loss of neurones in Alzheimer’s disease
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7
Q

Examples of hypertrophy

A

Physiological: muscle hypertrophy in the uterus during pregnancy
Pathological: left ventricular hypertrophy in response to hypertension

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8
Q

Examples of hyperplasia

A

Physiological: oestrogen-induced endometrial hyperplasia
Pathological: benign prostatic hyperplasia, carcinoma

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9
Q

Examples of metaplasia

A

Physiological: metaplasia in the cervix
Pathological: Barrett’s Oesophagus (columnar lined oesophagus)

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10
Q

Examples of dysplasia

A
  • Cervical intraepithelial neoplasia
  • Patients with Barrett’s oesophagus are associated with a much greater oesophageal cancer risk because metaplasia is typically followed by dysplasia
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11
Q

Light microscopic changes associated with reversible cell injury

A
  • fatty changes (fat accumulation in cells=fatty globules)

- cellular swelling (ballooning)

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12
Q

Light microscopic changes associated with irreversible cell injury

A

-The different types of necrosis

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13
Q

Define coagulative necrosis

A
  • substance changes but the shape of the molecule does not change
  • tissue retains structure after coagulation and can be recognised (nuclei gone and inflammatory cells present)
  • myocardial infarction example
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14
Q

Define liquefactive necrosis

A
  • tissue broken down leaving empty space which fills with fluid (tissue is totally liquefied)
  • identification only from cells surrounding it (empty space)
  • old cerebral brain infarct example
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15
Q

Define caseous necrosis

A

-form of granulomatous inflammation
-characteristic ‘cheesy’ appearance where
necrotic area becomes granular
-tissue cannot be recognised from structure
-associated with pulmonary tuberculosis

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16
Q

Define fat necrosis

A
  • breakdown of fat cells by lipase release or trauma (significantly severe fat trauma)
  • release of lipases digests the fat and hydrolyses the triglycerides into free fatty acids and glycerol
  • free fatty acids combine with calcium in ECF forming calcium fat salts which deposit themselves
  • associated with acute pancreatitis
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17
Q

Define necrosis

A

Confluent cell death associated with inflammation

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18
Q

Define apoptosis

A

Programmed cell death of single cells, not associated with inflammation
-normal in organism’s growth and development

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19
Q

Features of apoptosis

A
  • active (energy dependent=requires ATP hydrolysis)
  • physiological and pathological
  • not associated with inflammation (no bystander damage to healthy tissue)
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20
Q

Features of necrosis

A
  • cellular reaction of inflammation
  • not just single cells (areas)
  • not energy dependent
  • always pathological
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21
Q

Define necroptosis

A

Programmed cell death associated with inflammation

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22
Q

Features of necroptosis

A
  • energy dependent
  • halfway between apoptosis and necrosis
  • many causes including viral infection
  • generally occurs in pathological circumstances
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23
Q

Causes of cell injury

A

G=genetic defects
I=infectious agents (bacteria, viruses, multicellular parasites)
N=nutritional imbalances
C=chemical agents (includes iatrogenic injury resulting from the drugs/medication doctors give)
H=hypoxia
A=aging
P=physical agents (eg: gunshot wound, trauma etc)
I=immunological reactions (autoimmune disease where the body attacks itself=conditions include rheumatoid arthritis)

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24
Q

What causes cell adaptation?

A
  • stress on cells of increased demand/load

- cell remains in equilibrium but works in newly adapted state

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25
Q

What causes cell injury?

A
  • respond to injurious stimuli (stress which is harmful)

- stress exceeds the cell’s adaptive capability

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26
Q

Define lethal cell injury

A

Produces cell death

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27
Q

Define sublethal cell injury

A

Injury does not amount to cell death(injury does not kill the cell/organism)

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28
Q

Define reversible cell injury

A

Within certain limits, the cell can return back to normal

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29
Q

Define irreversible cell injury

A

Progresses to cell death

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30
Q

Intracellular mechanisms/systems vulnerable to cell injury (linked systems so damage to one will impact the others)

A
  • cell membrane integrity
  • ATP generation
  • protein synthesis
  • integrity of the genetic apparatus
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31
Q

List the 5 adaptive responses of cells

A
  • Atrophy (growth)
  • Hypertrophy (growth)
  • Hyperplasia (development)
  • Metaplasia (development)
  • Dysplasia (development)
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32
Q

Define degenerative

A

Change to a tissue to a lower or less functionally active form

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33
Q

Define ulcer

A

Local defect or excavation of the surface of an organ or tissue, produced by the sloughing of necrotic inflammatory tissues

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34
Q

Explain Barrett’s Oesophagus

A

Normal epithelial tissue lining of the oesophagus converts from stratified squamous to columnar (resembles the lining of the small intestine)

  • Cause: acid reflux
  • Reversal: PPI’s to inhibit acid production (Proton Pump Inhibitors)
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35
Q

Explain metaplasia in the cervix

A

-Endocervix is lined with columnar epithelium
-Ectocervix is lined with stratified squamous epithelium
-Columnar of endocervix is converted to stratified squamous
Cause:At puberty/during pregnancy, the cervix expands and fragile columnar epithelial lining of the endocervical canal is exposed to harsher more acidic environments in the vagina
Reversal: cervix contracts and closes up

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36
Q

Factors affecting the cellular response to injurious stimuli

A
  • type of injury
  • duration of the injury
  • severity of the injury
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37
Q

Factors affecting the consequences of an injurious stimuli

A
  • type of cell (some cell types are naturally more resistant to injury than others=example of bone, fat, brain and heart to oxygen deprivation)
  • Cell status (more vulnerable to various agents if dividing)
  • adaptability of the cell
  • genetic makeup of the cell
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38
Q

Define infarction

A

Tissue death due to ischaemia

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39
Q

Causes of cell death

A
  • Stress is too severe

- Prolonged/persistent stress

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40
Q

Physiological effects

A

-result of a normal stressor (healthy people)

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41
Q

Pathological effects

A

-result of an abnormal stressor (diseased state)

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42
Q

Hypertrophy causes

A
  • Increased functional demand

- Specific hormonal stimulation (seen in pregnancy)

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43
Q

Physiological hyperplasia causes

A
  • Hormonal(eg: Oestrogen causes wave of proliferation of the endometrium=inner lining of the uterus)
  • Compensatory (tissue previously lost)
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44
Q

Pathological hyperplasia causes

A
  • excessive hormonal or growth factor stimulation

- observed in cancer (high cell proliferation)

45
Q

Necrosis mechanism

A
  • enzymatic digestion
  • leakage of cellular contents
  • dead cells attract inflammatory cells
46
Q

Apoptosis mechanism

A
  • cell implodes on itself (nucleus shrinks and parts of cell break off but cell membrane is never ruptured=no inflammation)
  • Phagocytosis by macrophages on apoptotic cells and fragments
47
Q

Cases reported to the Coroner in England and Wales

A
  • Cause of death is unknown
  • Deceased has not been seen by a certified doctor either after death or 14 hours before death
  • Unnatural, violent or suspicious death (homicide)
  • Due to an accident regardless of when this occurred
  • Due to neglect by self or others (subjective and difficult to define)
  • Due to industrial disease or deceased person’s employment (occupational such as mesothelioma linked to asbestos exposure)
  • Abortion impact on mother
  • During an operation or before recovery from the effects of anaesthetic
  • suicide
  • poisoning
  • Occurred during or shortly after detention in police or prison custody (exception of DoLS=patients lack the capacity to consent to their care and treatment)
48
Q

Purpose of Coroner’s autopsy

A
  • Conducted to establish the cause of death

- Remit over once Coroner determines the cause of death

49
Q

Define coroner

A
  • independent judicial officer of the crown (employed by the queen) who has statutory duty to investigate the circumstance of certain categories of death for the protection of the public
  • investigates death and how it occurred
  • reported by most junior doctor of the firm
  • only in court room with jury if patient died in police custody etc
50
Q

Consent for Hospital autopsy

A
  • obtained from next of kin/relatives

- any material taken from body with relevant consent

51
Q

Consent for Coroner’s autopsy

A
  • None=investigating cause of death
  • family wishes must be considered
  • material only taken if it is needed to find the cause of death
52
Q

Purpose of Hospital’s autopsy

A
  • Allows very thorough examination of the deceased, extent of disease, treatment and its effects
  • Performed in the case of an audit where there is major discrepancy between stated and actual cause of death
  • medical teaching purposes
  • monitor the effectiveness of new treatments
  • medical research (eg: knowledge of variant CJD relies on the study of the post mortem brain tissue)
53
Q

Multiple secondary effects rapidly occur from cell injury to vulnerable systems

A

-structural and biochemical components of a cell are so integrally related

54
Q

Loss of cellular function occurs before?

A
  • cell death and then morphological changes (structure, shape or form)
  • often loss of function kills a patient before the morphological changes take place=no observations on post mortem
55
Q

Define bruise (contusion)

A

-extravasated collection of blood which has leaked from damaged small arteries, venules and veins but not capillaries

56
Q

Define abrasion (graze or scratch)

A
  • most superficial of the blunt trauma injuries

- confined to the epidermis

57
Q

Define laceration

A

-split to the skin as a result of blunt force trauma which overstretches the skin

58
Q

Define cut (slash)

A

-split in the skin where the injury length is longer than its depth

59
Q

Define stab (penetrating injury)

A

-split in the skin where injury depth is greater than the width

60
Q

Define incised wounds

A
  • Term discrepancy

- some means cuts and stabs, others say it means the same as cuts

61
Q

Define cancer

A
  • malignant neoplasm

- abnormal growth of cells which tend to proliferate in an uncontrolled way and in some cases, to metastasise

62
Q

Define neoplasm

A
  • abnormal mass of tissue, whose growth is autonomous (independent) of the body’s normal homeostatic growth-regulating mechanism and escapes the normal constraints on cell proliferation
  • the growth is purposeless, uncoordinated and will continue after the stimulus which initiated the change is removed
63
Q

Define tumour

A
  • any kind of MASS forming lesion
  • any swelling in or on a part of the body
  • may be neoplastic (benign or malignant), hamartomatous or inflammatory
  • example of a non-neoplastic tumour is nasal polyps (chronic inflammatory cause)
64
Q

Define metastasis

A

Spread of a malignant tumour from its site of origin

65
Q

Define carcinogen

A

Any substance that, when exposed to living tissue, may cause the production of cancer

66
Q

Define malignant

A
  • neoplasm classification
  • invades local tissues and has the potential to spread to distant sites of the body
  • difficult to remove due to invasion and metastasis=local surgery plus focus on chemotherapy and radiotherapy
67
Q

Define benign

A
  • neoplasm classification
  • remains localised=defined and well demarcated
  • easy to remove by local surgery
68
Q

Features to distinguish between benign tumours and malignant tumours

A
  • invasion
  • metastasis
  • differentiation
  • growth pattern
69
Q

Examples of environmental carcinogens and the cancers they cause

A
  • UV radiation=basal cell carcinoma, squamous cell carcinoma and multiple myeloma
  • ionising electromagnetic radiations (eg: X rays, X ray used in CT scans)=leukaemia and solid tumours
  • asbestos exposure=mesothelioma
70
Q

Aim of cancer screening programmes

A

Detect cancer at the pre-invasive (dysplastic) or early stage

71
Q

Principles of cancer screening programmes

A
  • condition is an important health problem
  • treatment is possible after screening
  • facilities for diagnosis/treatment are available
  • recognisable latent (dormant) or early symptomatic stage
  • suitable test or examination
  • test is acceptable to the population
  • natural history is understood
  • agreed policy on which patients to treat
  • cost-effective
  • case finding should be a continued process in the population
72
Q

Routes which tumours spread

A
  • direct extension
  • haematogenous
  • lymphatic
  • transcoelomic
  • perineural
73
Q

Examples of chemical carcinogens and the cancers they cause

A
  • hydrocarbons
  • amines
  • nitrosamines
  • azo dyes
  • alkylating agents
74
Q

Examples of infectious carcinogens and the cancers they cause

A
  • Epstein-Barr virus (oncogenic virus)=Burkitt’s lymphoma
  • HPV (oncogenic virus)=cervical cancer
  • Hepatitis B virus (oncogenic virus)=hepatocellular carcinoma
  • HHV-8 (oncogenic virus)=Kaposi’s sarcoma
  • Helicobacter pylori (bacterial carcinogen)=gastric carcinoma and lymphoma
75
Q

Explain invasion

A

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76
Q

Explain metastasis

A

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77
Q

Explain differentiation

A

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78
Q

Explain growth pattern

A

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79
Q

Define hamartomas

A

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80
Q

Define heterotopias

A

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81
Q

Primary description of a neoplasm

A

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82
Q

Secondary description of a neoplasm

A

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83
Q

Define tetratomas

A

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84
Q

Suffix ‘oma’ means?

A

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85
Q

Malignant tumours with the suffix ‘oma’

A

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86
Q

Features of tumour cells

A
  • high nuclear-cytoplasmic ratio compared to normal cells
  • more mitoses
  • mitoses present may be abnormal
  • marked nuclear pleomorphism
87
Q

Link between benign and malignant neoplasms

A

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88
Q

Define direct extension

A

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89
Q

Define haematogenous

A

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90
Q

Define lymphatic

A

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91
Q

Define transcoelomic

A

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92
Q

Define perineural

A

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93
Q

Assessing tumour spread

A

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94
Q

TNM staging system

A

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95
Q

Most important factor determining tumour prognosis

A

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96
Q

Define grade

A

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97
Q

Define stage

A

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98
Q

Define shock

A

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99
Q

Define thrombosis

A

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100
Q

Define embolism

A

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101
Q

Define infarction

A

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102
Q

Causes of thromobosis

A

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103
Q

Causes of embolism

A

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104
Q

Causes of infarction

A

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105
Q

Consequences of thrombosis

A

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106
Q

Consequences of embolism

A

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107
Q

Consequences of infarction

A

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108
Q

3 main causes of death in young people

A

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MCD (8 decks)

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