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Jack 2a > Pathology > Flashcards

Pathology Flashcards

1
Q

Characteristic cell in acute inflammation?

A

Neutrophil polymorph initially

Also monocytes later (become macrophages)

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2
Q

Characteristic cell(s) in chronic inflammation?

A

Lymphocytes, plasma cells and macrophages

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3
Q

Essential macroscopic appearances of acute inflammation

A

Rubor/Redness (dilation of blood vessels)
Calor/Hotness (hyperaemia form dilation +systemic fever)
Tumor/Swelling (from oedema/exudate)
Dolor/Pain (pressure from chemical mediators)
Loss of function

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4
Q

3 processes in acute inflammatory response:

A

Changes in vessel calibre and flow
Increase vascular permeability (contraction of endothelium)
Formation of fluid exudate (emigration of neutrophil polymorphs)

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5
Q

In formation of cellular exudate, explain the 4 stages of neutrophil emigration

A

Margination - the process just before neutrophils adhere to vessel wall (requires slow of fluid etc.)
Adhesion - also called pavementing
Emigration - migrate through endothelium using amoeboid movement
Diapedesis - where RBCs also escape - passive and implies more severe inflammation

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6
Q

Role of macrophage in acute inflammation

A

Secrete inflammatory mediators, proliferate, phagocytose, discharge lysosomal enzymes.
They have a longer life than neutrophils (weeks to months)

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7
Q

Role of neutrophil polymorph in acute inflammation

A

Short lived cells, first on the scene (usually die there). They phagocytose, release inflammatory mediators

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8
Q

Role of endothelial cells in acute inflammation

A

Become sticky so inflammatory cells can adhere, become porous, grow into areas, open capillaries

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9
Q

What are the 4 outcomes of acute inflammation

A

Resolution
Suppuration
Organisation
Progression to chronic inflammation

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10
Q

Describe resolution as the outcome of acute inflammation (and what 3 conditions it requires)

A

Resolution - complete restoration of tissues, it requires minimal cell death, regenerative capacity of tissue (liver) and destruction of causal agent

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11
Q

Describe suppuration as the outcome of acute inflammation

A

The formation of pus (dead neutrophils, bacteria, debris and lipid). Almost always caused by infection.
This can form an abscess

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12
Q

Describe an abscess

A

Pus accumulates, it is surrounded by a pyogenic membrane consisting of sprouting capillaries, neutrophils and fibroblasts. bacteria within are inaccessible to antibodies/antibiotics

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13
Q

Desribe organisation as an outcome of acute inflammation

A

The replacement of tissue by granulation tissue as part of the process of repair. Occurs if lots of fibrin is formed which cannot be removed, lots of tissue is necrotic or exudate cannot be removed
New capillaries grow into material and macrophages follow. Fibroblasts proliferate resulting in fibrosis.

The exudate is “organised”

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14
Q

Describe the progression to chronic inflammation as an outcome of acute inflammation

A

Occurs if chronic agent is not removed, the character of exudate changes with lymphocytes, macrophages, plasma cells and giant cells predominating. Also accompanies organisation

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15
Q

What are some systemic effects of acute inflammation?

A 
Pyrexia
Weight loss
Reactive hyperplasia of reticuloendothelial system
Haematological changes
Amyloidosis
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16
Q

How to treat acute inflammation (for 1. sports injury, 2. mosquito bite, 3. skin rash)

A

Depends on cause:

1) RICE
2) Antihistamine, NSAIDs, Hydrocortisone
3) Steroid cream (only if bacterial infection is not present otherwise you dampen immune response)

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17
Q

What 2 ways can you define chronic inflammation?

A

Over a prolonged time

Different cells invovled (lymphocytes, plasma cells, macrophages)

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18
Q

List some causes of chronic inflammation

A

Resistance to infective agent - TB, leprosy
Endogenous material - uric acid crystals
Exogenous material - silica, asbestos
Primary granulomatous disease - Crohn’s, Sarcoidosis
Transplant rejection

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19
Q

List 4 macroscopic appearances of chronic inflammation

A

1) Chronic ulcer
2) Chronic abscess cavity
3) Granulomatous inflammation
4) Fibrosis

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20
Q

List 4 microscopic appearances of chronic inflammation

A

1) Characteristically lymphocytes, plasma cells and macrophages
2) Exudation is not a common feature
3) Evience of continuing destruction
4) Possible tissue necrosis

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21
Q

Describe a granuloma

cells, causes, stain

A

This is an aggregate of epitheloid histocytes (a type of macrophage), some of which fuse to form giant cells and organise to wall of infection, sometimes necrosis centrally. Other cells such as lymphocytes, neutrophils etc. also present. Seen in TB, leprosy, Chron’s and sarcoidosis.
They can be stained using Ziehl-Neelsen

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22
Q

What happens to B, T and macrophages in chronic inflammation? (cellular cooperation)

A

B => Plasma cells to produce antibodies
T => cause cell-mediated immunity
Macrophages respond to chemotactic stimuli and produce cytokines such as IFa, TNFa and others

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23
Q

What are the 2 outcomes of injury (RR) and briefly describe what each needs

A

Resolution – initiating factor removed, tissue not permenantly damaged (can regenerate)
Repair - initiating factor still present, tissue cannot repair

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24
Q

3 types of cells based on their potential for renewal

A

Labile cells - good capacity to regenerate (some epithelium)
Stable cell populations (hepatocytes)
Permenant populations (nerve cells)

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25
Q

When considering tissue repair, describe organisation

A

the REPAIR of tissue by production of granulation tissue and a fibrous scar. dead tissue is removed by phagocytes.

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26
Q

Describe how granulation tissue forms (a form of repair)

A

Capillaries proliferate and grow into the area as loops
Simultaneously, fibroblasts divide and secrete collagen and other matrix
Myofibroblasts secrete collagen and cause wound contraction.

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27
Q

Describe stages of apoptosis

A

Healthy cell, nucleus condenses (pyknosis), cytoplasmic blebs form, cell breaks up into apoptotic bodies (each containing 1 or 2 organelles), these are often phagocytosed

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28
Q

What is the main enzyme which carries out apoptosis?

A

Caspase enzymes (the executioner)

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29
Q

Describe the internal signalling which regulates caspases and apoptosis

A 
BcL2 proteins act as the internal trigger:
Bcl2 protein inhibits caspases
Bax protein (also a member of Bcl2 family) activates caspases

p53 can upregulate Bax as this detects DNA damage

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30
Q

Describe the external signalling which regulates caspases and apoptosis

A

Fas receptor acts as an external trigger. Fas ligand from outside the cell binds to this receptor and activates caspases

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31
Q

When is apoptosis useful?

A

In development
Get rid of dysfunctional cells (in the gut)
Get rid of cells with DNA problems

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32
Q

What is autophagy?

A

Where due to stress, cell components are isolated into vacuoles and prevents cell death

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33
Q

What are some characteristic features of necrosis?

A

Mutliple cells die
Not programmed
Due to external stimulus

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34
Q

What is hypertrophy?

Give example

A

Cells increase in size, not in number (bigger muscle)

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35
Q

What is hyperplasia?

Give example

A

An increase in cell number but not size

Benign hyerplasia of the prostate

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36
Q

What is atrophy?

A

A decrease in size of a tissue either by decreased size or number of cells

Muscle atrophy in ALS

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37
Q

What is metaplasia?

example

A

change in differentiation of a cell from one fully-differentiated type to a different fully differentiated type. (functional plasticity).
(squamous to columnar in barrett’s oesophagus)

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38
Q

What is Dysplasia?

example

A

Imprecise term for the morphological changes seen in cells in the progression to becoming cancer (cells are growing but not quite right).

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39
Q

What is a homeobox gene?

A

A gene who’s prodcut controls function and migration of cells through development

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40
Q

How do telomeres work and how do they cause aging?

A

Telomeres help unwrap DNA but get shorter each time they help. They cannot help at the Hayflick limit (shortess a cell can be).

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41
Q

What is atherosclerosis?

A

Atherosclerosis is the hardening of plaques in the arterial walls

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42
Q

What is an atheroma?

A

Atheroma is like a lipidy plaque on the inside of blood vessels. Accumulation of these can lead to atherosclerosis (hardening).

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43
Q

What is the best theory to describe atherosclerosis and describe it?

A

Endothelial damage theory
The delicate endothelium are damaged by free radicals, nicotine and CO which causes damage, platelet adheration fibirn etc. LDL moves into intima and is oxidised causing damage, monocytes move in and become macrophages then foam cells there is inflammation. Smooth muscle from tunica media proliferates and endothelium grows over the top making the lumen slightly narrower

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44
Q

What are the risk factors for atherosclerosis and explain the pathophysiology behind each of them

A

Using the endothelial damage theory:
Smoking, free radicals, nicotine, CO, hypertension, uncontrolled diabetes (high levels of free radicals, superoxide anions/glycosylation), hyperlipidaemia all damage endothelium. Free radicals also cause increased oxidation of LDLs
Obesity causes more pro-inflammatory cytokines, women have more oestrogen receptors which protects against vascular injury

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45
Q

What are the 2 (4) types of autopsy and what are they/what is the difference?

A

Hospital autopsy (<10%) - requested by consultant to confirm cause of death (must be pretty much known).
Medico-legal autopsies (>90%) - occur in medico-legal centre at the request of the coroner. These can be divided into 2:
1)Coronial - routine, confirm cause of death if unkown
2)Forensic - clarify suspected crime

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46
Q

Give 3 reasons why a death may be referred to the coroner for autopsy

A

1) cause of death is unknown (no chronic conditions, not seen doctor in 14days)
2) Presumed iatrogenic cause - usually to prove the doctor did not kill the patient
3) Presumed unnatural - due to road traffic accidents, suicide, murder, industrial death

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47
Q

Who can refer a death to a coroner?

A

Doctors, registrar of BDM, properly interest parties (relatives, police, technicians etc.)

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48
Q

What is the difference between the 2 different people who perform autopsies? (histopathologists/forensic pathologists)

A

Histopathologists do all hospital autopsies and some coronial autopsies, while forensic pathologists do some coronial autopsies.

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49
Q

What 4 questions does an autopsy try to answer?

A

Who was the deceased?
When did they die?
Where did they die?
How did they die?

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50
Q

Describe the 5 general parts to an autopsy

A 
History/scene of death (sometimes)
External examination - identification/injuries/clothing
Evisceration/disembowelment
Internal examination (in situ first)
Reconstruction for funeral
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51
Q

What 2 mechanisms prevent blood clotting constantly?

A

Laminar flow - cells travel in centre of vessel

Endothelial cells are not “sticky” when healthy

52
Q

What is a clot and how does it differ to thrombosis?

A

Clotting is when blod stagnates in a test tube/dead body and becomes solid, while a thrombosis is in living blood vessels

53
Q

Briefly describe 3 stages of clotting

A

1) Endothelium is damaged, disrupting laminar flow and exposing “sticky” collagen beneath
2) Platelets activate and adhere/aggregate to the damage
3) The clotting cascade ensues causing fibrin deposition trapping platelets and red blood cells
This can totally occlude a blood vessel

54
Q

What is the “proper” definition of thrombosis?

A

the formation of a solid mass of blood constituents formed within an intact vascular system during life

55
Q

What are the 3 corners of Virchow’s triangle?

A

Change in vessel wall
Change in blood flow
Change in blood constituents

A thrombosis is usually owed to 2 of these factors

56
Q

What is the main reasons we get venous thrombosis and why?

What can it cause?

A

Stasis - blood is moving slower in veins relies on muscle contraction. There is low pressure and no laminar flow.
It can cause oedema and DVT

57
Q

What drugs can prevent thrombosis?

A

Anti-platelet therapy such as clopidogrel and aspirin

58
Q

Name 4 things which can embolise

A 
Thrombosus
Embolic atheroma (plaque falls off)
Gas emboli (often iatrogenic)
Permissible liquid (fat emboli)
Infective emboli (infective endocarditis)
Amniotic embolism
Tumour embolism
Embolism of foreign matter
59
Q

Why is pulmonary embolism so common?

A

Any embolus formed in the veins travels in larger and larger vessels until through the right side of the heart. Then pulmonary arteries get smaller and form a capillary bed which filters the embolism

60
Q

What are signs/symptoms of a PE?

A

Chest pain, shortness of breath (lack of oxygen due to occulded area of lung),
ecg; deep S in lead 1, Q waves inverted in lead 3

61
Q

What is ischaemia?

A

A reduction in blood flow, can be caused by thrombosis or embolism

62
Q

What is infarction?

A

Ischaemic death (necrosis of tissue). Can cause gangrene - infarction of mixed tissues in bulk.

63
Q

Desrcibe reperfusion injury

A

Dead tissue has calcium transporters damaged. When oxygen re-arrives at the area this forms “oxygen-dependent free radicals”. Macrophages and polymorphs migrate to aid in debris clearing also contributing thier own free radicals - causing damage. Anti-oxidants can help.

64
Q

What are in alpha granules in platelets?

A

Molecules involved in platelet adhesion - fibrinogen

65
Q

What are in dense granules in platelets?

A

Molecules involved in platelet aggregation - ADP

66
Q

Describe approximately 8 stages of arterial thrombosis due to an atheromatous plaque

A

1) An atheromatous plaque will result in a change in the vessel wall - seen as fatty streak
2) Over time, the plaque grows and protrudes into the lumen causing turbulence in blood flow
3) Turbulence causes rubbing away of intimal cells
4) Fibrin deposition and platelet clumping occurs. LDL is deposited
5) Process is self-perpetuating, leading to formation of platelet layer (first stage)
6) This layer allows for the precipitation of a fibrin meshowrk in which RBCs get trapped
7) the structure protrudes further into the lumen causing more tuberbulence and platelet deposition

67
Q

How do atheroma form?

A

Due to endothelial damage, LDL is deposited and endothelium grows over the top

68
Q

Do veins form atheroma? why?

A

No - there is lower pressure, but they can form at valves as valves produce turbulence which can be damaged (trauma/stasis)

69
Q

What are the 4 fates of thrombi?

A

1) Resolve - body dissolves and clears it
2) Organised - becomes a scar and causes slight narrowing of the vessel lumen
3) Recanalisation - intimal cells proliferate, capillaries grow into it
4) Embolus - fragments of thrombus leak into circulation

70
Q

What are the clinical features of:

1) Arterial thrombus
2) Venous thrombus

A

1) Loss of pulse distal to thrombus, area becomes cold, pale and painful, possible gangrene
2) Tender, area becomes reddened and swollen

71
Q

How would you treat/prevent a:

1) arterial thrombus
2) venous thrombus?

A

1) Arterial T - antiplatelets (aspirin)

2) Venous T - anticoagulants (warfarin)

72
Q

What commonly causes:

1) Arterial thrombosis
2) Venous thrombosis

A

1) Commonly caused by atheroma (high pressure)

2) Commonly caused by stasis (low pressure)

73
Q

How can we prevent atherosclerosis?

A 
Smoking cessation
Blood pressure control
Weight reduction
Low dose aspirin (inhibits platelets)
Statins (cholesterol reducing drug)
74
Q

What is the difference between a tumour and neoplasm?

A

A tumour is any abnormal swelling and refers to both inflammatory and neoplastic disease processes (and hypertrophy and hyperplasia)

75
Q

What are 4 characteristics common to any neoplasm?

A

Autonomous - growth is not regulated by normal homeostatic feedback loops
Abnormal always
Persistent - continued growing after stimulus has gone
A new growth

76
Q

Neoplasms are constructed of neoplastic cells and stroma. Describe neoplastic cells

A

1) Always derived from nucleated cells
2) Usually monoclonal, but become polyclonal with growth
3) Growth pattern related to parent cell
4) Synthetic activity of neoplasm is related to the parent (can secrete hormones/collagen etc.)

77
Q

Which growth factor promotes angiogenesis in tumours

A

Vascular endothelial growth factor (VEGF)

This action is opposed by factors such as angiostatin, and endostatin (therapeutic)

78
Q

How do neoplasms differ histologically from their normal tissue?

A

Loss of differentiation
Less cellular cohesion
Nuclear enlargement
Increased mitotic activity

79
Q

What are the 2 ways we can classify neoplasms?

A

Behavioural - benign/malignant (+borderline)

Histogenetic - cell of origin

80
Q

Describe some features of benign neoplasms
Growth rate, Mitoses, Histological resemblance to normal tissue, Nuclear morphology, Invasion, Metastases, Border, Necrosis, Ulceration, Direction of growth on skin or mucosal surfaces

A 
Slow growth rate
Infrequent mitoses
Good resemblence to normal tissue
No invasion
Never metastases
Often encapsulated
Rare necrosis/ulceration
Direction of growth is often exophytic (into a lumen)
81
Q

Describe some features of malignant tumours

Mitoses, Histological resemblance to normal tissue, Nuclear morphology, Invasion, Metastases, Border, Necrosis, Ulceration, Direction of growth on skin or mucosal surfaces

A 
Rapid growth
Frequent/aytpical mitoses
Variable resemblence to normal tissue, often poor
Invasion yes, metastasis frequent
Poor border
Necrosis and ulceration common
Often endophytic growth
82
Q

What are the 3 broad groups in histogenetic classification?

A

1) Epithelial cell - probobaly commonest
2) Connective tissues
3) Lymphoid/haematopoietic organs

83
Q

Describe grading of tumours

A

Tumour grade relates to how closely abnormal cells resemble normal tissue histologically. Usually 1, 2, 3.

If well differentiated (similar) then the lower the grade (it is less bad) and the better the prognosis.

High grade, poorly differentiated, worse prognosis.

84
Q

What is an anaplastic tumour?

A

This is where cell-type of origin is unknown - very bad.

85
Q

What is a benign tumour of non-glandular, non-secretory epithelium?

A

Papilloma

e.g. squamous cell papilloma

86
Q

What is a benign tumour of glandular/secretory epithelium?

A

Adenoma

E.g. thyroid adenoma

87
Q

What is a malignant tumour of non-glandular, non-secretory endothelium?

A

Carcinoma

E.g. Urothelial carcinoma

88
Q

What is a malignant tumour of secretory/glandular epithelium?

A

Adenocarcinoma

E.g. Adenocarcinoma of the colon

89
Q

How do you name benign connective tissue neoplasms?

A

Cell of origin suffixed by “-oma”.

E.g. lipoma, Chondroma, osteoma, rhabdomyoma (striated muscle), Leiomyoma (smooth muscle), Fibroid (leiomyoma in uterus)

90
Q

How do you name malignant connective tissue neoplasms?

A

Cell or origin suffixed by “-sarcoma”.

E.g. liposarcoma, rhabdomyosarcoma etc.
Note malignant tumours of connective tissue are less common than malignant tumours of epithelia

91
Q

Name 3 exceptions to the rules (malignant tumours suffixed with -oma)

A

Melanoma, Mesothelioma, lymphoma

92
Q

What is a cyst?

A

A fluid filled space lined by endothelium - not necessarily tumours.

93
Q

What is carcinogenesis?

A

The transformation of normal cells to neoplastic cells due to permanent genetic alterations (mutations).

This is cumulative mutational events of a presumed single cell origin (clonal proliferations)

94
Q

What types of tumours does carcinogenesis apply to? (benign/malignant)

A

Strictly malignant tumours

Carcinogenic is cancer causing

95
Q

What types of tumours does oncogenesis apply to? (benign/malignant)

A

Benign or malignant

Oncogenic means tumour causing (includes benign neoplasia)

96
Q

What do we mean when we say that carcinogenesis is a multi-step process?

A

A single cell needs to be hit by more than one carcinogen over a period of time to accumulate mutliple mutations to cause cancer

97
Q

Name 3 reasons why carcinogens are difficult to identify?

A 
Latent interval (can be decades)
Complexity of environment (we encounter many potential carcinogens)
Ethical constraints - cannot do RCT's etc.
98
Q

Name 3 ways to identify carcinogens

A

1) Epidemiological evidence
2) Direct evidence/accidental exposure
3) Experimental evidence (lab animals, tissue cultures etc.)

99
Q

Name the 5 classes of carcinogens

A

Chemical
Oncogenic viruses
Radiant energy (non-ionising/ionising radiation)
Biological agents (hormones/bacteria, fungi, parasites/mycotoxins)
Misc - asbestos, metals

100
Q

Describe how some chemical carcinogens require conversion.

Give an example of a chemical carcinogen

A

Chemial - may require metabolic conversion from pro-carcinogen to ultimate-carcinogen

Aromatic amines

101
Q

Give an oncogenic viruses example

A

Hepatitis B/C, Epstein-Barr virus

102
Q

Give radiant energy carcinogens example (ionising/non-ionising)

A

Non-ionising (UV light)

Ionising (X-rays, Chernobyl)

103
Q

Give examples of biological agents as carcinogens

A

Hormones - increased oestrogen can cause endometrial cancer

Bacteria, parasites, fungus and mycotoxins

104
Q

What percentage of cancer risk is from environmental factors and what is host factors?

A

85% - environment

15% - host factors

105
Q

Describe some host factors

A

Race
Diet/culture
Constitutional factors (age, gender, inherited predisposition)
Premalignant lesions (e.g. colonic polyps, ulcerative colitis)
Transplacental exposure

106
Q

How would you treat a basal cell carcinoma of the skin?

A

Local excision if not metastasised.

107
Q

What are the 5 main cancers that spread to bone?

A

Breast, prostate, lung, thyroid and kidney

They usually spread here through bone

108
Q

Which lymph nodes is a carcinoma likely to spread to?

A

Carcinoma spread to the lymph nodes that drain the site of carcinoma.

109
Q

What are the implications of removing lymph nodes?

A

Poor drainage of the arm, lymphoedema

110
Q

Why might a patient experience metastasis after complete excision?

A

Micro-metastasis could be present, almost impossible to detect (less than 0.1mm)

111
Q

What is adjuvant therapy?

Give 2 examples.

A

Extra-treatment given after surgical excision of a malignant neoplasm.

Radiotherapy to breast after lumpectomy
Drugs like oestrogen blockers (Tamoxifen)/Her2 blockers (Herceptin)

112
Q

Which form of metabolism is favoured by tumours?

A

Anaerobic glycolysis but not definitely

113
Q

What is an in-situ neoplasm?

A

The lesion with cytological features of a malignant neoplasm, but the basement membrane is intact. It has potential to spread but cannot currently.

114
Q

What is “invasion” when regarding malignant neoplasms?

A

Where neoplastic cells spread through connective tissues as it grows in size.

115
Q

What 3 factors are required for a neoplasm to invade local tissue?

A

1) Abnormal or increased cell motility
2) Secretion of proteolytic enzymes (to digest through BM and connective tissue)
3) Decreased cellular adhesion

116
Q

What is metastasis?

A

Where a malignant neoplasm spreads to a distance (secondary) site

117
Q

What is carcinomatosis?

A

Where metastasis is very bad and has caused death

118
Q

What are the routes of metasis?

A

Haemotogenous - Blood vessels
Lymphatic
Transcoelomic - in a body cavity
Implantation - accident of surgery

119
Q

Desrcibe all of the steps required for a malignant neoplasm to metastasise (metastatic cascade) to a nearby site using blood vessels

A

1) Detachment of tumour cells from their neighbours (tumour cells have reduced cohesion)
2) Invasion through BM and connective tissue, requires proteolytic enzymes and tumour cell motility
3) Intravasation - usually of veins due to their thin walls
4) Evasion host defence in vessel
5) Extravasation - adherence to endothelium at remote location, requires certain adhesion molecules etc.

120
Q

What mode of spread do carcinomas and sarcomas prefer?

A

Carcinomas prefer lymphatic spread

Sarcomas prefer haematogenous spread

121
Q

Why do tumours in veins metastasise in the lung?

A

Because veins get bigger and bigger, through right side of the heart then caught in the capillary bed of the lungs

122
Q

Which route of tumour spread causes bone metastasis?

A

Through the arteries

123
Q

What are three minimum genetic alterations required to make a neoplastic cell?

A

1) Expression of telomerase to stop telomeric shortening
2) Loss or inactivation of recessive tumour suppressor gene function (to remove the inhibitory control of cellular replication)
3) Enhanced expression of oncogenes - self-stimulating gene growth

124
Q

What are oncogenes?

A

Genes driving neopasltic behaviour of cells, usually highly regulated

125
Q

What are the 3 types of clinical effects of tumours?

A

Local effects - compression, invasion, ulceration
Metabolic effects - creating hormones, weight loss (cahcexia)
Effects due to metastases

126
Q

What 3 pieces of information helps calculate prognosis of a malignant tumour?

A

1) Tumour type (cell of origin)
2) Grade/degree of differentiation
3) Stage or extent of spread (TNM)

All found by histopathological examination

127
Q

Describe the TNM system of determining tumour spread

A

T - refers to size of the primary
N - refers to lymph node status (N1=one or few nodal mets, N2=many nodal mets)
M - refers to the anatomical extent of distant metasis

Note 0 for any means none.

The TNM derives a stage score where stage 1 is confined to organ of origin and stage 4 has disseminated widely

Jack 2a (8 decks)

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