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Medicine > Pathology > Flashcards

Pathology Flashcards

1
Q

What are features of malignant cells?

A 
enlarged cells
High nuclear to cytoplasmic ratio
Variability in size of nucleus and cells
Speckled chromatids
More than 1 nuclei
Hyperchromatism
Mitotic figures - mercedes benz sign
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2
Q

What cells are in carcinoma?

A

All cells that are not epithelial tissue or glandular

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3
Q

What cells are included in sarcoma?

A

Soft tissue

Bone

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4
Q

Histologically what would coeliacs disease look like?

A

Blunting of villi
Decreased goblet cells
Lots of inflammatory cells at top of villi

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5
Q

What is signet ring carcinoma and what causes the characteristic shape?

A

Rare form of highly malignant adenocarcinoma that produces mucin. Epithelial malignancy
The nuclei are pushed towards to the edge of the cell

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6
Q

What would make a benign mole into a malignant mole?

A

Growth in dermis and epidermis

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7
Q

What is adenocarcinoma?

A

glandular lumina surrounded by malignant epithelial cells

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8
Q

What are Reed-Sternberg cells indicative of and what do they look like?

A

Giant cells found in Hodgkins lymphoma. Usually derived from B cells
Owls eyes appearance

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9
Q

What are HER receptors?

A

Human Epideramal Growth Factor Receptor (1 or 2)

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10
Q

What are the 7 stages of producing a slide?

A 
1 - Fixation
2 - Cutting up
3 - Embedding into wax
4 - Microtome cutting
5 - H&E staining (others also available)
6 - Mounting onto slide
7 - Diagnosis
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11
Q

What is autolysis?

A

Tissue autolysis is self digestion that begins when the blood supply is cut off
Cells and tissue architecture is also destroyed

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12
Q

What effects do fixatives have when blocking autolysis?

A

1 - inactivate tissue enzymes and denature proteins
2 - Prevent bacterial growth
3 - Harden tissue

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13
Q

What colour does Haematoxylin stain?

A

Nuclei - Purple

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14
Q

What colour does Eosin stain?

A

Cytoplasm and connective tissue pink

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15
Q

What is the cell injury response pathway to harmful stimuli?

A

Homeostasis -> Cellular adaptation -> Cellular injury -> Cell death

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16
Q

What is the problem with cellular adaptation?

A

Increase in size is the usual adaptation
Increase in size = more nutrients & O2 therefore at risk of cellular damage again which could be reversible or irreversible

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17
Q

What is the difference between hypoxia and ischaemia?

A

Hypoxia - blood has reduced O2

Ischaemia - insufficient blood supply, supplying less O2 to the tissues

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18
Q

What are the 4 types of hypoxia?

A

Hypoxaemic hypoxia
Anaemic hypoxia
Ischaemic hypoxia
Histiocytic hypoxia

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19
Q

What is hypoxaemic hypoxia?

A

Arterial content of O2 is low
Caused by:
Reduced inspired pO2 at altitude
Reduced absorption secondary to lung disease

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20
Q

What is anaemic hypoxia?

A

Decreased ability of Hb to carry O2
Caused by:
Anaemia
CO poisoning

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21
Q

What is ischaemic hypoxia?

A

Interruption to blood supply
Caused by:
Blockage of a vessel
Heart failure

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22
Q

What is histiocytic hypoxia?

A

Inability to utilise oxygen in cells due to disabled oxidative phosphorylation enzymes
Caused by:
Cyanide poisoning

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23
Q

What is anoxia?

A

No O2 in the blood

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24
Q

What happens at the molecular level in hypoxia?

A

Ischaemia -> Decreased mitochondrial OxPhos -> Dec. ATP production -> (1) Dec. Na pumping (2) Inc. Glycolysis (3) Detachment of ribosomes from ER

1) Influx of Ca, H2O, Na. Efflux of K+ -> cellular swelling, blebs
2) Dec pH & glycogen -> Clumping of nuclear chromatin
3) Dec. protein synthesis -> Lipid deposition

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25
Q

What happens in prolonged hypoxia leading to irreversible damage on a cellular molecular level?

A

Ca influx from a variety of sources:
(1) ER (2) External as inc membrane permeability (3) Mitochondrion
Increased calcium activates cytosolic enzymes:
ATPase - dec ATP
Phospholipase - Dec phospholipids
Protease - Disruption of membrane and cytoskeletal proteins
Endonuclease - Nuclear chromatin damage

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26
Q

When are free radicals produced?

A

Normal metabolic reactions - OxPhos
Inflammation - oxidative burst of neutrophils
Radiation - H2O -> OH (free radical)
Contact with unbound metals within the body (iron and copper) - haemachromatosis and Wilson’s disease
Drugs and chemicals - liver during metabolism

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27
Q

How does the body control free radicals?

A

Anti-oxidant scavengers - donate electrons to free radical Vitamins A,C,E
Metal carrier and storage proteins (transferrin, ceruloplasmin): sequester free iron and free copper
Enzymes - Superoxide dismutase, Catalase, Glutathione peroxidase

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28
Q

What is the function of Heat shock proteins?

A

In cell injury heat shock response aims to mend mis-folded proteins and maintain cell viability
Unfoldases or chaperonins are examples

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29
Q

Define oncosis

A

Cell death with swelling, the spectrum of changes that occur in injured cells prior to death

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30
Q

Define Necrosis

A

In a living organism the morphologic changes that occur after a cell has been dead some time - seen after 12-24 hours

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31
Q

What are the two types of necrosis?

A

Coagulative

Liquefactive

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32
Q

What is coagulative necrosis?

A

Cellular death caused by ischaemia or infarction
Injury damages structural proteins and lysosomal proteins thus blocking proteolysis
Protein denaturation > Release of active proteases
-Protein denaturation and clumping
-Tissue becomes firm and cells keep their structure giving them a ghost like appearance
-Occurs in all tissues except brain

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33
Q

What is liquefactive necrosis?

A

Ischaemia in loose tissues: presence of many neutrophils - pus formation
Partial or complete dissolution of dead tissue and transformation into a liquid
Enzyme degradation > Enzyme denaturation
Loss of tissue and cellular profile.
Hydrolytic enzymes cause dissolution of cellular organelles
Occurs in Brain as there is no structural integrity of the tissues

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34
Q

What are two special types of necrosis that aren’t coagulative or liquefactive?

A

Caseous

Fat necrosis

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35
Q

What is caseous necrosis?

A

White, soft, cheese looking material is formed hence name
Contains amorphous (structureless) debris
Microscopically - uniformly eosinophilic centre of necrosis surrounded by a collar of lymphocytes and activated macrophages
Particularly associated with infections: TB is a prime example and granuloma’s

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36
Q

What is fat necrosis?

A

Acute inflammation of adipocytes, could be due to trauma.
Damaged cells release digestive enzymes - lipases, which breaks down lipid -> free fatty acids
Anucleated adipocytes w/ deposits of calcium - saponification

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37
Q

What does gangrene mean?

A

Necrosis visible to the naked eye

An appearance of necrosis (wet and dry)

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38
Q

What does infarction mean?

A

Necrosis caused by reduction in arterial blood flow

- A cause of necrosis -(if untreated)-> Gangrene

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39
Q

What does infarct mean?

A

An area of necrotic tissue which is the result of loss of arterial blood supply
- An area of ischaemic necrosis

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40
Q

What is the difference between wet and dry gangrene?

A

Dry - necrosis modified by exposure to air (coagulative necrosis) - i.e. umbilicus in babies - dry, crisp appearance
Wet - necrosis modified by infection (bacteria, septicaemia) - release proteases which liquify the surrounding area (liquefactive necrosis)

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41
Q

What is gas gangrene?

A

Rapidly spreading gangrene affecting injured tissue infected by bacterium found in soil and accompanied by the production of foul-smelling gas
Form of wet gangrene - anaerobic Clostrium perfringens

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42
Q

What is the difference between thrombosis and embolism?

A

Thrombosis - pathological blood clot abnormally obstructing blood flow
Embolism - is a detached solid (clot), liquid (fat,) or gas (air) carried away from site of origin by blood and causing an obstructing of blood flow

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43
Q

Why are some infarcts white?

A

Solid organs - occlusion of an end artery (sole source of blood to an organ)
Often wedge shaped - blood from lots of vessels merge into 1 vessel = heart, spleen, kidney
Coagulative necrosis

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44
Q

Why are some infarcts red?

A

Haemorrhagic infarct
Loose tissue - poor stromal support
Dual blood supply - 2 arteries supplying organ/ tissue. The blood will fill dead tissue but not enough to reperfuse it and salvage it.
Numerous anatomoses
Prior congestion i.e. haemorrhagic transformation from ischaemic stroke.
Raised venous pressure
Re-perfusion - there are limits of when to reperfuse after which the risk of causing haemorrhaging could lead to a red infarct

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45
Q

What is ischaemic-reperfusion injury?

A

Paradoxically, if blood flow is returned to a damaged but not yet necrotic tissue, damage sustained can be worse than if blood flow hadn’t been returned.
Possible causes:
-Increase production of free radicals
-Inc. no. of neutrophils - inc inflammation and inc tissue damage
-Delivery of complement proteins and activation of complement pathway = inc. inflammation

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46
Q

What are the problems with dying cells for example in tumour lysis syndrome?

A

A sudden release of potassium can potentially be pro-arrhythmic
Sudden release of urea - cause confusion, kidneys not able to handle this amount of urea
(also hyperphosphataemia and hypocalcaemia are features of TLS)

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47
Q

What enzyme is measured during/ after MI and why?

A

Troponin

1st enzyme to leave and longest half life

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48
Q

Define apoptosis

A

Cell death with shrinkage, induced by a regulated intracellular program where a cell activates enzymes that degrade its own nuclear DNA and proteins
The process requires ATP (whereas necrosis doesn’t)
Pathological and/or physiological

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49
Q

When does apoptosis occur pathologically?

A

Cytotoxic T cell killing of virus-infected or neoplastic cells
When cells are damaged, particularly with damaged DNA
Graft vs host

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50
Q

What are the 3 stages of apoptosis?

A

Normal cell -> Condensation -> Fragmentation -> Apoptotic bodies

Initiation -> Execution -> Degradation & phagocytosis

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51
Q

What are the two mechanisms that cause initiation and execution of apoptosis?

A

Intrinsic and extrinsic
Both result in activation of caspases:
Enzymes that control and mediate apoptosis
Cause cleavage of DNA and proteins of the cytoskeleton

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52
Q

How is the intrinsic pathway of apoptosis initiated?

A

Initiation comes from within the cell

Triggers: -cellular stress -Irreparable DNA damage - Withdrawal of growth factors or hormones

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53
Q

How is the intrinsic pathway of apoptosis carried out?

A

p53 protein is activated and this results in the outer mitochondrial membrane becoming leaky
Cytochrome C is released from the mitochondria and this causes activation of caspases

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54
Q

How is the extrinsic pathway of apoptosis initiated?

A

Signals from other cells

Triggers: -cells that a danger, e.g. tumour cells, virus-infected cells

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55
Q

How is the extrinsic pathway of apoptosis carried out?

A

One of the signals if TNFalpha

  • Secreted by T-killer cells
  • Binds to cell membrane receptor (death receptor)
  • Results in activation of caspases
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56
Q

Why are apoptotic bodies phagocytosed?

A

Cells shrink -> apoptotic bodies -> proteins expressed on the surface -> phagocytes and neighbouring cells recognition -> degradation within phagocyte/ neighbour

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57
Q

What are the 3 stages of necrosis of the nucleus in greek and what do they mean?

A

Pyknosis - condensation of chromatin
Karyorrhexis - fragmentation of the nucleus
Karyolysis - dissolution of cell nucleus

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58
Q

What are the 5 main groups of intracellular accumulations?

A 
Water and electrolytes
Lipids
Carbohydrates
Proteins
Pigments - exogenous and endogenous
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59
Q

When is hydropic swelling seen?

A

Intracellular oedema seen with viral infections

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60
Q

Why does hypoxia cause fluid to accumulate in cells?

A

Hypoxia -> No OxPhos -> reduced ATP production -> Na/K ATPase does function to remove Na -> Water follows Na and so cells swell

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61
Q

When do lipids accumulate in cells?

A

Often seen in the liver - due to major organ of fat metabolism. Causes: Alcohol, Diabetes mellitus, Obesity, Toxins
Cholesterol: cannot be broke down and is insoluble, elimination through the liver (bile), excess stores in cell in vesicles. Accumulation in smooth muscle cells and macrophages in atherosclerotic plaques - foam cells.
Present in macrophages in skin and tendons of people with hereditary hyperlipiaemias = xanthomas

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62
Q

In what 2 conditions do proteins accumulate (hepatic)?

A

Alcoholic liver disease - Mallory’s hyaline (damaged keratin filaments which are intracytoplasmic proteins)
Alpha1-antitrypsin deficiency - liver produces incorrectly folded A1-antitrypsin

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63
Q

When do pigments accumulate in cells?

A

Carbon/coal dust/soot - urban air pollution
Inhaled and phagocytes by alveolar macrophages
Anthracosis and blackened peribronchial lymph nodes
Usually harmless unless in large amounts
Tattooing - phagocytosed by macrophages in dermis but remains there - some pigment reaches draining lymph nodes
Haemosiderin: iron storage molecule - derived from Hb. Systemic iron overloading - haemosiderin is deposited= haemosiderosis - haemolytic anaemias, blood transfusions and hereditary haemochromatosis

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64
Q

What are the 4 mechanisms of intracellular accumulations?

A

1 - abnormal metabolism
2 - alterations in protein folding and transport
3 - deficiency of critical enzyme
4 - inability to degrade phagocytosed particles

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65
Q

Why does calcification occur in metastatic disease?

A

Due to hypercalcaemia secondary to disturbances in Ca metabolism
Hydroxyapatite crystals are deposits in normal tissues throughout the body
Usually asymptomatic but it can be lethal
Can regress if the cause of hypercalcaemia is corrected

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66
Q

What causes hypercalcaemia?

A

Increased secretion of PTH resulting in bone resorption:
Primary - parathyroid hyperplasia/ tumour
Secondary - renal failure and retention of phosphate
Ectopic - secretion of PTH-related protein by malignant tumours (e.g. carcinoma of the lung)

Destruction of bone:
Primary tumours of bone marrow e.g. leukaemia, multiple myeloma
Diffuse skeletal mets
Paget’s disease of bone - accelerated bone turnover
Immobilisation

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67
Q

What is pepper pot skull and hypercalcaemia indicative of?

A

Multiple myeloma

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68
Q

What enzyme do germ cells and stem cells have that regular cells don’t that allows them to technically become immortal?

A

Telomerase - maintains length of the telomeres which usually prevent further cell division

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69
Q

What do Mallory’s hyaline look like under microscope when stained with H&E?

A

Pink filaments in hepatocyte cytoplasm

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70
Q

What are neutrophils also known as?

A

Polymorphs

Polylobated nucleus is the cause

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71
Q

What is diapedesis?

A

The movement of cells in the blood passing through an intact blood vessel typically during inflammation

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72
Q

Microscopically describe what a macrophage would look like

A

Eccentric nucleus which can be round, kidney shaped or slipper shaped
Often lots of cytoplasm which can appear vacuolated

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73
Q

Describe what a eosinophil would look like microscopically

A

Granular red cytoplasm

Bilobed nucleus

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74
Q

Describe what a granuloma would look like microscopically and what causes it?

A 
Langerhans type giant cell
Epithelioid histiocytes (modified, immobile macrophages)
Cellular attempt to remove offending agent - T-lymphocytes strongly activated/ activating macrophages - persistent antigen presentation low level
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75
Q

What cells would line the outside of a foreign body?

A

Foreign body giant cell

Multinucleated cell that surround the foreign body

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76
Q

What does petechiae look like?

A

Tiny haemorrhages that can be seen on the skin (<3mm)

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77
Q

What are lines of Zahn?

A

A thrombus that has lines of zahn is caused by layers of red blood cells and fibrin and other layers of platelets
Characteristic of thrombi that form particularly in the aorta

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78
Q

What are the layers of an atherosclerotic plaque?

A

Fibrous cap
Necrotic core with cholesterol clefts
Calcification

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79
Q

What are foam cells and where are they usually found?

A

Type of macrophage that takes up LDL’s into itself and lives primarily in blood vessels. With all the lipids it takes on a foam appearance.

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80
Q

What is the difference between metaplasia and dysplasia?

A 
Metaplasia:
Change of one epithelium to another type
Reversible once the stimulus has ceased
Adaptive process
Dysplasia:
Development of abnormal cell types - usually in the epithelium
Irreversible
Alteration of genetic material therefore phenotype also changes
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81
Q

What is transcoelomic spread?

A

Spread of a malignancy into a cavity that occurs by penetrating the surface of the space. E.g. peritoneum, pericardium, pleural cavity

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82
Q

What type of cancer is most common with asbestos fibres in the lung?

A

Malignant mesothelioma

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83
Q

What is Kaposi’s sarcoma?

A

Disease of the endothelial cells and blood vessels that causes masses on the skin
Form of cancer associated with HIV and also classic Kaposi’s is associated with diabetes

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84
Q

What does pleomorphic mean?

A

Variability in size, shape and staining of cells and/or their nuclei

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85
Q

What does nuclear hyperchromasia mean and what does it indicate?

A

Nucleus is darker in colour

Associated with malignant cells

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86
Q

What does the tumour marker CA 27.29 indicate?

A

Breast cancer

Associated also with colon, gastric, hepatic, lung, pancreatic, ovarian, prostate

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87
Q

What does the tumour marker CEA indicate?

A

Colorectal cancer

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88
Q

What does the tumour marker CA 19.9 indicate?

A

Pancreatic cancer, biliary tract cancer

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89
Q

What are 5 features of acute inflammation (not cardinal signs)?

A 
Immediate
Short duration
Innate
Stereotyped (same response every time)
Limits damage
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90
Q

What is inflammation?

A

Vascular and cellular response - accumulation of exudate and neutrophils in tissue
Controlled by a variety of mediators - (derived from plasma or cells
Protective - cause local and systemic complications sometimes

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91
Q

What are the clinical cardinal signs of inflammation?

A 
Rubour - redness
Calor - heat
Tumour - oedema
Loss of function
Dolor - Pain
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92
Q

What changes occur in vessels and surrounding tissues in acute inflammation?

A

Changes in blood flow - temperatures - Transient vasoconstriction (seconds) then vasodilation (inc overall blood flow)
Vascular phase- Movement of fluid into tissues - oedema - inc. hydrostatic pressure reduced oncotic pressure (in blood vessels)
Cellular phase - Inflation of inflammatory cells into tissue

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93
Q

What is the problem with movement of fluid out of the vessel but you also want this in acute inflammation?

A

Stasis
Increased viscosity of the blood -> reduced flow through vessel -> stasis -> inc contact time with bacteria/ causative agent of acute inflammation

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94
Q

What are the types of interstitial fluid and what are their causes?

A

Exudate - occurs in inflammation, protein rich - don’t contain fibrinogen, increased vascular permeability
Transudate - fluid loss due to increased capillary hydrostatic pressure or reduced oncotic pressure, no change of vascular permeability, occurs in heart failure/ hepatic failure/ renal failure (damaged tubules-protein loss - red. oncotic pressure)

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95
Q

What are mechanisms of increasing vascular permeability?

A

Endothelial contraction - histamine and leukotrienes
Endothelial cytoskeleton reorganisation - Cytokines, IL-1 TNF
Direct injury - chemical and toxic burns
Leukocyte dependent injury - enzymes and toxic oxygen species from leukocytes

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96
Q

What is the primary WBC involved in acute inflammation?

A

Neutrophil

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97
Q

What are some features of a neutrophil?

A

Trilbed nucleus
A granulocyte
Part of innate immune system

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98
Q

How do neutrophils escape vessels?

A

Margination= Stasis causes neutrophils to line up at edge of blood vessels along the endothelium
Rolling = neutrophils roll along endothelium sticking to it intermittently
Adhesion = Neutrophils stick more avidly to the site of injury - increasing affinity as gets closer to site of injury
Emigration (diapedesis) = Neutrophils follow through the blood vessel wall

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99
Q

What are the 2 adhesion molecules used by neutrophils to bind to the endothelium?

A 
Selectins = endothelial cell surface (ICAM-1) unregulated by chemical mediators
Integrins = On neutrophil cell surface (Integrins B2 on leukocytes) binds to endothelial surface
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100
Q

How do neutrophils move through the interstitium?

A

Chemotaxis -
Movement along a chemical gradient of chemoattractants
Rearrangement of neutrophil cytoskeleton
Pseudopods formed which help it move along endothelium and then emigrate

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101
Q

What do neutrophils do in acute inflammation?

A

Opsonisation - facilitates recognition of toxin
Toxin covered in C3b and Fc (Fc domain on antibodies - IgG is the most important - only if a bacteria has been encountered before) - opsonins
Receptors for C3b and Fc on neutrophil surface triggers phagocytosis

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102
Q

What are 2 killing mechanisms of neutrophils?

A

Oxygen dependent - ROS and RNS

Oxygen independent - Lysozyme, Hydrolytic enzymes, Defensins (punch holes in bacterial cell membranes)

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103
Q

What are the 2 phases of acute inflammation?

A

Vascular phase - exudation of fluid into interstitium

Cellular phase - infiltration of neutrophils

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104
Q

How does oedema limit damage?

A 
Dilutes toxins (exudate)
Delivers plasma proteins to area of injury - fibrin mesh limits spread of toxin, inflammatory mediators and immunoglobulins
Increased lymphatic drainage from area (more extracellular fluid) - delivers antigens to lymph nodes (inducing adaptive immune response)
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105
Q

How do inflammatory cells limit damage?

A

Removal of toxins and pathogenic organisms
Removal of necrotic tissue
Release of chemical mediators that stimulate and regulates further inflammation
Stimulates pain - encourages rest and limits risk of further damage

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106
Q

What are chemical mediators released by?

A

Activated inflammatory cells
Platelets
Endothelial cells

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107
Q

What chemical mediators cause vasodilation?

A

Histamine
Serotonin
Prostaglandins - pyrogens = inc fever and pain
Nitric oxide

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108
Q

What chemical mediators increase vascular permeability?

A

Histamine
Bradykinins
Leukotrienes
C3a and C5a

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109
Q

What chemical mediators cause chemotaxis?

A

C5a, LTB4, TNF-alpha, IL-1, Bacterial peptides

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110
Q

What chemical mediators cause fever?

A

Prostaglandins
IL-1
TNF-alpha
IL-6

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111
Q

What chemical mediators cause pain?

A

Bradykinin
Substance P
Prostaglandins

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112
Q

What is one local complication of swelling?

A

Blockage of nearby tubes and ducts

e.g. bile duct/ intestines

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113
Q

What is one local complication of exudate production?

A

Compression of organs

e.g. cardiac tamponade

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114
Q

What is one local complication of pain and loss of function?

A

Muscle atrophy - disuse contractures

Psycho-social consequences of chronic pain

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115
Q

What cells increase in number with bacterial infections?

A

Neutrophils

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116
Q

What cells increase in number with viral infections?

A

Lymphocytes

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117
Q

What chemical mediators cause the bone marrow to increase production of lymphocytes?

A

IL-1

TNF

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118
Q

What are acute phase proteins?

A

C-reactive protein (commonly used blood marker)
A1-antitrypsin
Haptoglobin - binds free Hb - inhibits oxidative activity
Fibrinogen
Serum amyloid A protein - transport cholesterol to liver. Recuits immune cells to inflammation site - induces proteases etc to degrade extracellular matrix

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119
Q

What are 4 acute phase responses that are universal for inflammation?

A

Malaise
Reduced appetite
Altered sleep
Tachycardia

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120
Q

What are the features of septic shock?

A 
Overwhelming infection
Huge release of chemical mediators
Widespread vasodilation
Hypotension, tachycardia
Multi-organ failure
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121
Q

What are the 4 sequelae of acute inflammation?

A

1 - complete resolution
2 - continued acute inflammation with chronic inflammation -> ABSCESS
3 - chronic inflammation and FIBROUS REPAIR, with some tissue regeneration
4 - death

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122
Q

What is important in allowing damaged tissues to regenerate?

A

Architecture preservation

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123
Q

What is an abscess?

A

Accumulation of dead and dying neutrophils

Associated liquefactive necrosis

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124
Q

What are 4 non-ischaemic and non-inflammatory causes of cardiomyopathy?

A

Hypertrophic
Arrhythmogenic right ventricular cardiomyopathy
Obstructive
Dilated (post viral from inflammation)

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125
Q

What are causes of acute inflammation?

A 
Microbial infections - e.g. pyogenic organisms
Hypersensitivity reactions (acute phase)
Physical agents
Chemicals
Tissue necrosis
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126
Q

What is the response of Histamine in acute inflammation?

A

Immediate early response
Released from mast cells, basophils and platelets
In response to physical damage, immunologic reactions, C3a, C5a, IL-1

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127
Q

What is a systemic effect of acute inflammation that is severe?

A

In the acute phase response
SHOCK is a response that is severe
A clinical circulatory failure

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128
Q

Microscopically what do neutrophils look like?

A

Multilobed nucleus
Few organelles
Light pink coloured cytoplasm

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129
Q

Microscopically what do eosinophils look like?

A

They take up a large amount of eosin inside their cytoplasm.
Eosin is acidic and is attracted to basic components - cytoplasm
As lots of basic products inside the cytoplasm it stains the cytoplasm in deep pink

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130
Q

Microscopically what do macrophages look like?

A

Large eccentrically placed nucleus, which is kidney bean shaped
Abundant cytoplasm some pink granules in the cytoplasm

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131
Q

What is the difference between leiomyosarcoma and leiomyoma?

A

Leiomyosarcoma - soft tissue cancer - develop in muscle, fat, blood vessel etc.
Leiomyoma - aka fibroids - benign smooth muscle tumour. Can occur in any organ. Most common place is uterus, small bowel and the oesophagus.

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132
Q

Define chronic inflammation

A

Chronic response to injury with associated fibrosis

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133
Q

How does acute inflammation become chronic inflammation?

A

Damage is too severe to be resolved in a few days

Chronic inflammatory cells will be recruited

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134
Q

How does chronic inflammation arise?

A

May arise de novo e.g.
-some autoimmune conditions e.g. RA
-some chronic infections e.g. viral hepatitis
-chronic low-level irritation
Develop alongside acute inflammation - severe or repeated irritation

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135
Q

What are the major differences between neutrophils and macrophages?

A

Neutrophils - found in blood, macrophages found in tissues
Neutrophils - granulocytes and macrophages - agranulocytes
Neutrophils - multilobated nucleus, macrophages - spherical nucleus

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136
Q

What is the other name of macrophages?

A

Blood monocytes

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137
Q

What are the functions of macrophages?

A

Phagocytosis and destruction of debris and bacteria
Processing and presentation of antigen to immune system
Synthesis of not only cytokines, but also complement components, blood clotting factors and proteases
Control of other cells by cytokine release
Stimulation of angiogenesis
Inducing fibrosis
Inducing fever, acute phase reactions and cachexia

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138
Q

What are the main cell type causing chronic inflammation?

A

Lymphocytes

Don’t normally cause fibrosis but does in chronic inflammation

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139
Q

What are the basic functions of lymphocytes?

A

Complex, mainly immunological
B lymphocytes differentiate to produce antibodies
T lymphocytes involved in control (T-helper) and some cytotoxic (CTL) functions

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140
Q

What is characteristic of the nucleus of plasma cells (B-cells)

A

Clock like morphology of chromatin

Eccentrically placed

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141
Q

What are 2 characteristics of eosinophils?

A

Abundant in parasitic infections and IgE hypersensitivity reactions - allergies
Morphologically - sunglasses on with pinky cytoplasm

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142
Q

What is a giant cell?

A

Multinucleated cell made by fusion of macrophages

Frustrated phagocytosis

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143
Q

What are the 5 main types of giant cells?

A 
Langhans - TB
Foreign body
Touton - fat necrosis
Giant-cell arteritis
Reed-Sternberg cell - Hodgkins lymphoma
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144
Q

What chronic inflammatory cells are mainly found in rheumatoid arthritis?

A

Plasma cells

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145
Q

What chronic inflammatory cells are mainly found in chronic gastritis?

A

Lymphocytes

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146
Q

What chronic inflammatory cells are mainly found in Leishmaniasis?

A

Macrophages

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147
Q

What are the 4 stages of chronic inflammation that lead to a cycle?

A

Fibrosis -> Impaired function -> Atrophy -> Stimulation of immune response -> back to fibrosis

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148
Q

How do you get impaired function in IBD?

A

UC - superficial - local effects of inflammation

Crohn’s - transmural - strictures and fistulae -

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149
Q

What does thyrotoxicosis look like microscopically?

A

Grave’s disease - hyperthyroidism -> decreased colloid and increased fat

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150
Q

What is the basic principle of wound healing?

A

Close the gap

Replace lost tissue with new functioning tissue or replace it with a scar

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151
Q

What is the mnemonic involved in wound healing?

A 
HIMRES:
Haemostasis
Inflammation
Migration
Regeneration
Early scar
Mature scar
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152
Q

What is regeneration?

A

Regrowth with no or minimal evidence that there was a previous injury
Healing by primary intention in the skin

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153
Q

What is healing by primary intention?

A

Healing that occurs when a clean laceration or a surgical incision is closed - margins bought together
Disruption of basement membrane continuity but death of only small number of epithelial and connective tissue cells
Used when little tissue loss

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154
Q

What is healing by secondary intention?

A

Extensive skin and tissue loss - edges not able to be bought together
e.g. pressure sore

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155
Q

Which cells replicate in regeneration?

A

Stem cells

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156
Q

Where are the stem cells in the skin, intestines and liver?

A

Skin - basal layer adjacent to basement membrane
Intestines - mucosa - bottom of crypts
Liver - between hepatocytes and bile ducts

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157
Q

What are the 3 lineages of stem cells in their ability to divide?

A

Unipotent - only produce one differentiated cell e.g. epithelia
Multipotent - produce several differentiated cells e.g. haematopoietic stem cells
Totipotent - embryonic stem cells - produce any tissue

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158
Q

What are the 3 groups of tissues based on their proliferative activity?

A

Labile tissues
Stable tissues
Permanent tisses

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159
Q

What are labile tissues?

A

Short lived cells that are replaced from cells derived from stem cells
E.g. surface epithelia, haematopoietic tissues

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160
Q

What are stable tissues?

A

Normally low level of replication - can undergo rapid proliferation
Both stem cells and mature cells proliferate
e.g. liver parenchyma, bone, fibrous tissue, endothelium

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161
Q

What are permanent tissues?

A

Mature cells can’t undergo mitosis and no or only a few stem cells present
e.g. neural tissue, skeletal muscle, cardiac muscle

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162
Q

What one thing does regeneration require in order to occur?

A

Intact basement membrane

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163
Q

When does regeneration or fibrous repair take place?

A

Regeneration= collagen framework

Fibrous repair = collagen framework destroyed, on-going chronic inflammation or necrosis of permanent tissues

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164
Q

How does scar formation progress from minutes to years duration?

A 
Seconds-minutes = haemostasis
Minutes-hours = acute inflammation
1-2days = chronic inflammation
3 days = granulation tissue forms
7-10days = early scar
weeks - 2 years = scar maturation
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165
Q

What is granulation tissue?

A

New connective tissue + microscopic blood vessels. Typically goes from the base of a wound upwards
Complex of fibroblasts (collagen deposition and myofibroblasts contract), vascular endothelial cells (angiogenesis) and macrophages (removal of dead tissue debris) within a mix of collagen

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166
Q

What is the function of granulation tissue?

A

Fills the gap
Capillaries supply oxygen, nutrients and cells
Contracts and closes the hole by myofibroblasts

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167
Q

What occurs in tissue regeneration maturation?

A

Long lasting process - collagen deposition matures and remodels
Myofibroblasts contract and reduces volume of defect
Vessels differentiate and are reduced if not used
Left with a fibrous scar

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168
Q

Which cells are involved in fibrous repair and what is their function?

A

Phagocytosis of debris - neutrophils and macrophages
Production of chemical mediators - lymphocytes and macrophages
Endothelial cells - proliferation results in angiogenesis (stable tissue type)
Fibroblasts and myofibroblasts - produce extracellular matrix (collagen), responsible for wound contraction

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169
Q

What are 4 growth factors needed in wound repair/ healing?

A

1 - epidermal growth factor
2 - vascular endothelial growth factor
3 - platelet derived growth factor
4 - tumour necrosis factor

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170
Q

What is the role of cell-cell and cell-stomal contact in wound repair and healing?

A

Contact inhibition:
- signalling through adhesion molecules - catherine bind cells together and interns bind cells to the extracellular matrix
- inhibits proliferation in intact tissues, promotes proliferation in damaged tissues
If cells have contact in all directions they sense that the tissue is grown and so no need to grow anymore

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171
Q

What occurs in healing by primary intention?

A

Epidermis regenerates - basal epidermal cells move 0.5mm/day - > deposition of basement membrane -> fuse in midline beneath scab
Dermis undergoes fibrous repair

172
Q

What occurs in healing by secondary intention?

A

Epidermis regenerates - deposition of basement membrane
+
Considerable wound contraction required - 1 week later myofibroblasts appear and contract
Substantial scar formation
New epidermis grows from edges to cover the defect

173
Q

What is the difference between split thickness and full thickness in skin grafts

A

Split thickness - above the hair bud follicle

Full thickness - below the hair bud follicle

174
Q

What is the process of bone healing?

A 
1 - haematoma
2 - granulation tissue forms
3 - soft callus
4 - hard callous
5 - lamellar bone
175
Q

What 5 local factors influence wound healing?

A 
1 - type, size, location of wound
2 - mechanical stress
3 - blood supply
4 - local infection
5 - foreign bodies
176
Q

What 8 factors influence wound healing?

A 
1- age
2- anaemia, hypoxia, hypovolaemia
3- obesity
4- diabetes
5- genetic disorders
6- drugs- anticoagulants, antimicrobials, anti-rheumatoid drugs, aspirin, NSAIDs
7- vitamin deficiency
8- malnutrition
177
Q

What are 5 complications of fibrous repair?

A

Formation of adhesions - compromising organ function or blocking tubes
Loss of function - replacement of specialised functional parenchymal cells by scar tissue (e.g. MI non-contracting tissue)
Disruption of complex tissue - distortion of architecture interfering with normal function
Overproduction of fibrous scar tissue - keloid scar
Excessive scar contraction - obstruction of tubes, disfiguring scars - fixed flexures

178
Q

What cell produces platelets in the bone marrow?

A

Megakaryocytes

179
Q

What factors cause platelet adhesion?

A

Damage to vessel wall
Exposure of underlying tissues
Platelets adhere to collagen via vWF/ receptor

180
Q

What substances to platelets release when they are activated?

A

ADP
Thromboxane
Serotonin

181
Q

What are natural anticoagulants?

A

Antithrombin
Tissue factor pathway inhibition
Antithrombin
Activated protein C and protein S

182
Q

What causes fibrinolysis?

A

Plaminogen activator activates plasminogen -> plasmin -> breaks down the fibrin clot -> D-dimers

183
Q

What clotting factors are in the intrinsic pathway?

A

VIII, IX, X, XI, XII

184
Q

What clotting factors are in the extrinsic pathway?

A

VII

185
Q

What clotting factors are in the common pathway?

A

V, X, prothrombin (FII)

186
Q

How would you measure clotting?

A

Prothrombin time

Activated partial thromboplastin time

187
Q

What pathways does prothrombin time measure?

A

Extrinsic and common pathways

188
Q

What pathways does activated partial thromboplastin time?

A

Intrinsic and common pathways

189
Q

What is the function of von Willebrand factor?

A

Platelet adhesion to the vessel wall
Platelet aggregation
Carries FVIII

190
Q

In simple terms how does haemophilia A present and what is the clotting factor that is deficient?

A

X-linked recessive
Congenital lack of FVIII
Diagnosed pre-natally
Bleeding into muscles and joints and post-operatively
Treatment with recombinant factor VIII or desmopressin

191
Q

In simple terms how does haemophilia B present and what is the clotting factor that is deficient?

A

Similar presentation to Haemophilia A

Congenital reduction in factor IX

192
Q

What is von Willebrand’s disease?

A 
Common
autosomal dominant
Abnormal platelet adhesion to vessel wall
Reduced FVIII amount/ activity
Quantitative - not enough produced
Qualitative - reduced activity/ function
193
Q

What is hereditary haemorrhagic telangiectasia?

A

Congenital autosomal dominant disease
Dilated microvascular swellings increasing with time
Abnormal blood vessel formation in skin, mucous membranes, brain, liver etc
Can form abnormal arteriovenous malformations

194
Q

What is an acquired vessel wall abnormality causing bleeding?

A

Senile purpura
Steroids
Infection e.d. measles, meningococcal infection
Scurvy - Vit C deficiency

195
Q

What is DIC and what the 4 pathways of each outcome?

A

Pathological activation of coagulation - loss of appropriate localisation/ limitation/ fibrinolysis
Risk of bleeding and thrombosis together
(1) Fibrin formation + (2) inhibited fibrinolysis -> microvascular thrombosis -> organ failure
(3a) - Consumption of haemostatic factors -> reduced anticoagulant effect -> microvascular thrombosis
(3b) - Consumption of haemostatic factors -> reduced clotting factors + platelets ->haemorrhagic tendencies -> bleeding
(4) Fibrinolysis activated -> reduced clotting factors + platelets -> haemorrhagic tendencies -> bleeding

196
Q

With DIC what are the triggers causing it to happen?

A 
Malignancy
Massive tissue injury
Infections - gram negative sepsis
Massive haemorrhage and transfusion
ABO transfusion reaction
Obstetric causes - placental abruption, pre-eclampsia, amniotic fluid embolism
197
Q

What are the components to Virchow’s triad?

A

Abnormal clotting
Abnormal vessel wall
Abnormal blood flow

198
Q

What is the appearance of an arterial and venous thrombus?

A

Arterial: pale, granular, lines of Zahn, lower cell content
Venous: soft, gelatinous, deep red, higher cell content

199
Q

What are the 3 outcomes of thrombosis and what happens in each stage?

A

Propagation - progressive spread of thrombosis, distally in arteries, proximally in veins (direction of blood flow)
Organisation - reparative process, fibroblasts and capillaries, lumen remains obstructed - scar tissue forms
Recanalisation - bloodflow re-establised, one or more channels formed through thrombus
Embolism - part breaks off - travels through bloodstream - lodges at distant site

200
Q

What are the effects of thrombi in arteries and veins?

A

Arteries: ischaemia, infarction, depends on site and collateral circulation
Veins: congestion, oedema, ischaemia, infarction

201
Q

Define embolism

A

Embolism is a blockage of a blood vessel by a soli

202
Q

What % level of blood flow obstruction is enough to call a massive PE?

A

> 60% - rapidly fatal

203
Q

What are the simple constituents of a primary haemostatic plug?

A

Platelets

Fibrin

204
Q

What are 4 key steps to clot formation?

A

1 - initiation
2 - amplification
3 - propagation
4 - termination

205
Q

What is thrombin time?

A

Fibrinogen -> fibrin

Raised TT - heparin, fibrinogen deficiency or abnormality

206
Q

Define atherosclerosis

A

Accumulation of intracellular and extracellular lipid in the intimacy and media of large and medium sized arteries
The thickening and hardening of arterial walls as a consequence of atherosclerosis

207
Q

What are 3 macroscopic features of atherosclerosis?

A

Fatty streak
Simple plaque
Complicated plaque

208
Q

What is a fatty streak?

A

Lipid deposits in intima

Yellow, slightly raised

209
Q

What is a simple plaque?

A

Raised yellow/ white plaque
Irregular outline
Widely distributed
Enlarge and the coalesce

210
Q

What is a complicated plaque?

A

Thrombosis
Haemorrhage into plaque
Calcification
Aneurysm formation - tunica media involved and loss of elasticity

211
Q

What are early changes that occur in atherosclerosis?

A

Proliferation of smooth muscle cells - tunica media
Accumulation of foam cells
Extracellular lipid

212
Q

What are later changes that occur in atherosclerosis?

A

Fibrosis + Necrosis, Cholesterol clefts + Inflammatory cells
Disruption of internal elastic lamina extending into media
Ingrowth of blood vessels
Plaque fissuring

213
Q

Why is plaque fissuring a problem in atherosclerosis?

A

Link between atherosclerosis and thrombosis is through the fibrous cap
The cap will crack or fall off and will expose collage, VWF, tissue factor -> platelet aggregation

214
Q

What is a clinical effect of atherosclerosis in the peripheries?

A

Peripheral vascular disease:
Intermittent claudication - pain in the periphery for example calves when exercising that gets gradually worse due to inadequate O2 supply

215
Q

What is ischaemic rest pain?

A

Continuous burning pain of the lower leg or feet
Begins or aggrevated after reaching or elevating the limb
Relieved by sitting or standing
More severe than intermittent claudication

216
Q

What are polymorphisms in the genes affecting Apo E useful for detecting and why?

A

Polymorphisms can be used as risk markers for atherosclerosis
Genetic variations in Apo E are associated with changes in LDL levels

217
Q

What 3 signs are indicative of familiar hyperlipidaemia?

A

Corneal arcus
Tendon xanthoma
Xanthelasma

218
Q

What are immediate, early and late complications of splenectomy?

A

Immediate - haemorrhage
Early - Haemorrhage, infection, raised platelets (thrombosis)
Late - Infections - prophylactic Abx

219
Q

What are the cell cycle steps in mitosis?

A

G1 , S , G2 , Mitosis + cytokinesis (M phase)

Can leave the cell cycle and enter G0

220
Q

What are the 2 cell cycle check points?

A

End of G1 and G2

221
Q

What is the R point of the cell cycle?

A

R point= restriction point
This is the most critical checkpoint
Majority of cells will pass R point and complete cell cycle - point of no return

222
Q

By what process does cell checkpoint activation alter the fate of the cells?

A

If activated - DNA repair mechanisms OR apoptosis via p53

223
Q

What is p53?

A

The protein which leads to tumour suppression - discouraging of cell proliferation

224
Q

What are cyclins and CDK function in the cell cycle?

A

Cyclin A,B,D,E

CDK - Cyclin Dependent Kinase

225
Q

What cyclins and CKD’s are functioning at different points of the cell cycle?

A

G1 -Cyclin D/ CDK2
S - Cyclin E/CDK2
G2 - Cyclin A/CDK2
M - Cyclin B/CDK1

226
Q

What is the retinoblastoma protein?

A

Retinoblastoma is a cancer of the retina - red eye and white eye are seen on pictures
Usually acts to prevent DNA replication - tumour suppressor protein
Most common primary malignancy in children - almost exclusively found in young children

227
Q

What factors affect cell population?

A

Balance of cell proliferation and death
Excessive physiological stimulation can become pathological e.g. prostatic hypertrophy
Proto-oncogenes regulate normal cell proliferation
Proliferation stimulated by growth factors, injury, cell death, mechanical deformation of cells

228
Q

What are the two types of cellular adaptation response?

A

Adaptations - reversible changes in number/size/phenotype/function
Physiologic - response to normal stimulation by hormones or chemical mediators
Pathologic - response to stress that allow cells to escape injury

229
Q

How do cells adapt to stress?

A 
Hypertrophy
Atrophy
Hyperplasia
Metaplasia
Dysplasia
230
Q

Define hyperplasia

A

Increase in tissue or organ size due to increased cell numbers

231
Q

Which two cell types does hyperplasia occur in?

A

Labile and stable tissues - constant regrowth and cells not replaced but can increase cell turnover if required respectively

232
Q

What are two main causes of hyperplasia?

A

Hormonal - e.g. oestrogen causing endometrial hyperplasia

Compensatory - e.g. following injury

233
Q

What is the risk with repeated hyperplasia?

A

Repeated cell divisions expose the cell to risk of mutations and neoplasia

234
Q

Name an example of pathological and physiological hyperplasia

A

Pathological - goitre - thyroid disease

Physiological - proliferation in endometrium by oestrogen or bone marrow - erythrocytes - hypoxia

235
Q

Define hypertrophy

A

Increase in tissue or organ size due to increased cell size

236
Q

In which tissues does hypertrophy occur?

A

All types but especially in permanent (doesn’t have capacity for hyperplasia)

237
Q

What factors cause hypertrophy?

A

Increased functional demand or hormonal stimulation

238
Q

What are 2 examples where physiological hypertrophy occurs

A

Skeletal muscle

Pregnant uterus

239
Q

What is an example of pathological hypertrophy

A

Cardiomegaly due to increased work load of the heart in IHD/ peripheral vascular disease
Urinary bladder hypertrophy

240
Q

Define atrophy

A

Shrinkage of a tissue or organ due to an acquired decrease in size and/or number of cells

241
Q

Why do tissues atrophy?

A

Shrink to a size where the cell can still try and survive

242
Q

Which cells die first parenchymal or stromal in atrophy?

A

Parenchymal because stroma has stem cells inside still that can potentially be used

243
Q

Name 4 examples of physiological atrophy

A

Reduced functional demand/workload = atrophy of disuse - reversible with activity
Loss of innevation = denervation atrophy
Inadequate blood supply - thinning of skin on legs with peripheral vascular disease
Inadequate nutrition - wasting of muscles with malnutrition

244
Q

Name 4 examples of pathological atrophy

A

Loss of endocrine stimuli - breast, reproductive organs
Persistent injury - polymyositis
Ageing - senile atrophy - brain and heart
Pressure - tissues around an enlarging being tumour (secondary to ischaemia)

245
Q

Define metaplasia

A

Reversible change of one differentiated cell type to another

Phenotypic change of the cells

246
Q

What causes metaplasia?

A

Stressed cells are replaced by different types - to try to preserve the tissue

247
Q

Can mucosal tissue become bone tissue in metaplasia?

A

No

There is no metaplasia across germ layers

248
Q

What tissue type can metaplasia occur across?

A

Labile or stable tissue types

249
Q

Name 2 examples of metaplasia

A

Bronchial pseudo stratified ciliated epithelium -> stratified squamous epithelium
Stratified squamous epithelium in oesophagus -> glandular epithelium

250
Q

What is aplasia and what are examples of aplasia?

A

Pathological failure to completely develop - organ, tissue
Thymic aplasia - infections and auto-immune problems
Aplasia of kidney
Also used to describe organs whose cells have ceased to proliferate e.g. aplasia of bone marrow in aplastic anaemia

251
Q

What is hypoplasia and what are examples of tissues that may have hypoplasia?

A

Underdevelopment of incomplete development of tissue or organ at embryonic stage due to inadequate number of cells
Not opposite of hyperplasia as it is a congenital condition
Examples - Renal, Breast, Testicles in Klinefelter’s syndrome, chambers of the heart

252
Q

What is involution

A

Overlap with atrophy but normal programmes shrinkage of an organ
Uterus after childbirth, thymus in early life, pro and mesonephros

253
Q

What is reconstitution?

A

Replacement of a lost part of the body

254
Q

What is atresia and give 4 examples?

A

No orifice
Congenital imperforation of an opening
E.g. pulmonary valve, anus, vagina, small bowel

255
Q

What is dysplasia and what is a problem with it?

A

Abnormal maturation of cells within a tissue
Potentially reversible
Often pre-cancerous condition

256
Q

What is a neoplasm?

A

Abnormal growth of cells that persists after the initial stimulus is removed

257
Q

What is a malignant neoplasm?

A

Abnormal growth of cells that persists after the initial stimulus is removed AND invades surrounding tissue with potential to spread to distant sites

258
Q

What is a tumour?

A

A clinically detectable lump or swelling

259
Q

What are 2 subsections of tumours?

A

Non-neoplastic

Neoplastic

260
Q

What are 2 subsections of neoplastic tumours?

A

Benign

Malignant - Primary or secondary carcinomas

261
Q

What do neoplasms look like under the microscope in terms of differentiation?

A

Benign - resemble parent tissue - well differentiated
Malignant - Poorly differentiated
Anaplastic - no resemblance to any tissue

262
Q

What causes neoplasia?

A

Accumulated mutations in somatic cells

263
Q

What is the name given to mutation causers?

A

Initiators

264
Q

What is the name given to mutations that induce cell proliferation?

A

Promoters

265
Q

What does progression refer to in neoplasia?

A

A neoplasm emerging from a monoclonal population occurs from a process called progression, characterised by the accumulation of yet more mutations

266
Q

How do inherited mutations affect progression in neoplasms?

A

Head start as the tissues already have the initiator required to start the process of neoplasia formation and also promoters. All of the cells in the monoclonal population will have the same features together

267
Q

What are the two genes that are involved in controlling the cell proliferation into neoplasms?

A

Proto-oncogene and tumour suppressor gene

268
Q

How do proto-oncogenes lead to neoplasms?

A

Proto-oncogenes become oncogenes when they are abnormally activated, favouring neoplasm formation
Only 1 is needed to be altered to lead to neoplasm formation

269
Q

How do tumour suppressor genes lead to neoplasms?

A

Tumour suppressor genes normally suppress neoplasm formation become inactivated
These act as a brake to cell proliferation
2 have to be altered to form a neoplasm

270
Q

What is the nomenclature for benign neoplasms

A

Benign - ending is oma

271
Q

What is the nomenclature for malignant neoplasms?

A

Epithelial origin - carcinoma

Stromal origin - sarcoma

272
Q

What is a neoplasm referred to if it has penetrated through the basement membrane or not?

A

Invasion - invasive

No invasion - in-situ

273
Q

What cell lineage is referred to in leukaemia and lymphoma?

A

Leukaemia - malignant neoplasm of blood-forming cells arising in the bone marrow
Lymphoma - malignant neoplasm of lymphocytes, mainly affecting lymph nodes

274
Q

What type of cell is referred to as myeloma?

A

Malignant neoplasm of plasma cells

275
Q

What is the name of a neoplasm that originates from the testis/ ovaries?

A

Germ cell neoplasms

276
Q

What is the name of the tumour that arises from cells distributed throughout the body?

A

Neuroendocrine

277
Q

Why is blastoma used to describe neoplasms?

A

Occur mainly in children
Formed from immature precursor cells
e.g. nephroblastoma

278
Q

When is the term adenoma used?

A

A neoplasm of glandular epithelial origin

279
Q

What is the term used to describe neoplasms that are putting pressure on the body systems?

A

Tumour burden

280
Q

What are the 3 steps for a malignant cell to get from a primary to a secondary site?

A

1 - grow and invade at the primary site
2 - enter a transport system and lodge at a secondary site
3 - grow at the secondary site to form a new tumour (colonisation)

281
Q

Why is metastasising of cells difficult?

A

The whole process is inefficient-
Evasion of the immune system is tough when metastasising
Cells destroyed by the process - unstable cells in general

282
Q

What 3 alterations are required for invasion?

A

Adhesion
Stromal proteolysis
Motility

283
Q

How do malignant cells alter their adhesion?

A

Cell to cell adhesion - reduction in E-cadherin expression

Cell to matrix adhesion - reduction in Integrin expression

284
Q

How do malignant cells cause stromal proteolysis?

A

Altered expression of proteases e.g. Matrix Metalloproteinases

285
Q

What is epithelial-to-mesenchymal transition?

A

Adhesion, proteolysis and motility create a carcinoma cell phenotype that sometimes appears more like a mesenchymal cell than an epithelial cell

286
Q

What are the 3 ways of transport to distant sites via three routes?

A

1 - blood vessels via capillaries and venules
2 - lymphatic drainage
3 - fluid in body cavities (pleura, peritoneal, pericardial and brain ventricles), Transcoelomic spread

287
Q

What is colonisation in reference to malignancy?

A

Secondary sites malignant cells must grow - colonisation

Failed colonisation - greatest barrier to successful metastasis

288
Q

What are micrometastases?

A

Surviving microscopic deposits that fail to grow

289
Q

What is the phenomenon called where a person has many micromets?

A

Tumour dormancy

290
Q

What are 3 routes leading to tumour dormancy?

A

1 - Immune attack
2 - Reduced angiogenesis
3 - Hostile secondary site

291
Q

What determines the site of a secondary tumour?

A

1 - regional drainage of blood, lymph or coelomic fluid

2 - ‘seed and soil’ phenomenon

292
Q

What is a cancer niche?

A

Malignant cells take advantage of nearby non-neoplastic cells which together form a cancer niche

293
Q

How do carcinomas and sarcomas typically spread?

A

Carcinomas -> first to draining lymph nodes -> blood-borne distant sites
Sarcomas -> blood stream

294
Q

What are effects of neoplasms?

A

Direct local effects = primary neoplasm and secondary neoplasm
Indirect systemic effects = increasing tumour burden - secreted hormones + things that will affect conginition/ personality e.g. in brain tumours

295
Q

What is a paraneoplastic syndrome?

A

Side effects of a cancer when the immune system starts attacking normal cells
For benign neoplasms, local effects from the primary and hormonal effects

296
Q

What are local effects of primary and secondary neoplasms?

A

1 - direct invasion and destruction of normal tissue
2 - ulceration (discontinuity or break in a membrane) at a surface leading to bleeding
3 - compression of adjacent structures
4 - blocking tubes and orifices

297
Q

What are systemic effects of neoplasms?

A

Sarcopenia - loss of muscle mass
Reduced appetite and weight loss (cachexia), malaise, immunosuppression (direct bone marrow destruction), thrombosis (platelet aggregation)

298
Q

What are 2 ways of carcinogenesis?

A

Intrinsic factors - heredity, age, sex (hormonal)

Extrinsic factors - environment and behaviour

299
Q

What are the 5 leading behavioural and dietary risks for neoplasm?

A 
High BMI
Low fruit and veg intake
Lack of physical activity
Tobacco use
Alcohol use
300
Q

What are the 3 categories of extrinsic carcinogens?

A

Chemicals,
Radiation
Infections

301
Q

What is a risk of industrial dyes in carcinogenesis?

A

2-napthylamine an industrial carcinogen used in the dye manufacturing industry -> bladder cancer

302
Q

What is the effect of tropisms in carcinogenesis?

A

Certain carcinogens have a tropism where they predominantly affect certain parts of the body

303
Q

What 3 factors increase the risk of getting a malignant neoplasm caused by a carcinogen?

A

1 - Long delay between carcinogen exposure and malignant neoplasm onset
2 - Risk of cancer depends on total carcinogen dosage
3 - Organ specificity for particular carcinogens

304
Q

What is a pro-carcinogen?

A

Pro-carcinogen -CYP450-> carcinogen

Non-carcinogenic till metabolised

305
Q

What are carcinogens that act as both initiators and promoters called?

A

Complete carcinogens e.g. cigarette smoke

306
Q

What type of radiation is bad for us and why is ultrasound not mutagenic?

A

Ionising is bad for us
Ionising and non-ionising radiation
Ionising - Radon, medical test
Non-ionising radiation - UV, Ultrasound

307
Q

What infection is carcinogenic and relies upon mutations in the tumour suppressor genes?

A

Direct carcinogen
Human papilloma virus - cervical carcinoma link
E6 and E7 proteins that inhibit p53 and pRB - mutated

308
Q

What malfunctioning proteins cause an increases in cervical cancer risk ?

A

E6 and E7 proteins are produced by the virus but they also inhibit p53 and pRB

309
Q

Through what basic mechanism does hepatitis B virus infection cause cancer?

A

Indirect cause
HBV causes chronic inflammation and regeneration
The chronic inflammation itself leads to mutations

310
Q

What is the 2 hit hypothesis?

A

For example: first hit delivered through germline in familial cancers and affected all the cells in the body
Second hit is a somatic mutation in one of the cells already having a mutation
The two hits refers to the tumour suppressor genes - both are required to be mutated

311
Q

Why if a child has retinoblastoma cancer would it be bilateral and in an adult it would likely be unilateral?

A

Bilateral as this is genetic and all the cells would have a mutation - inherited pattern
Unilateral in adults because this mutation occurred after birth and so only one cell is required to have the mutation in an eye

312
Q

What is RAS in pathology?

A

Human oncogene -> mutated in 1/3 of all malignant neoplasms
RAS proto-oncogene encodes a small G protein that relays to the cell to put it past the restriction point in the cell cycle

313
Q

What type of repair is defective in Xeroderma pigmentosa?

A

Nucleotide excision repair

Skin is very sensitive to UV damage - develop skin cancer at young age

314
Q

What type of repair is defective in Hereditary non-polyposis colon cancer (HNPCC)?

A

Mismatch repair
Autosomal dominant
Germ line mutation

315
Q

What type of repair is defective in BRCA1 or 2?

A

Double stranded breaks

BRCA1/2 - tumour suppressor proteins

316
Q

Why does genetic instability occur in malignant neoplasms?

A

Chromosome segregation is abnormal

+ whatever the original problem/ mutation = accelerated mutation rate = genetic instability

317
Q

What are the genes that maintain genetic stability called?

A

Caretaker genes - class of tumour suppressor gene

318
Q

Describe the term cancer progression?

A

Step-wise accumulation of mutations that is steadily increase

319
Q

What are 6 hallmarks of cancer?

A

1 - self-sufficiency in growth signals
2 - resistance to growth stop signals
3 - no limit on the number of times a cell can divide
4 - sustained ability to induce new blood vessels
5 - resistance to apoptosis
6 - the ability to invade and produce mets

320
Q

How do we stage lymphoma?

A

Ann Arbour staging 1 - 4 depending on diaphragm nodes
Stage 1 - single node region
S2 - two separate regions on one side of the diaphragm
S3 - Spread to both sides of the diaphragm
S4 - Diffuse or disseminated involvement of one or more extra-lymphatic organs

321
Q

How do we stage colon cancer?

A 
Dukes staging A-D
Depending on depth through GI wall, lymph nodes and mets
A - Invasion but not through the bowel
B - invasion through the bowel wall
C - Involvement of lymph nodes
D - Distant mets
322
Q

How do we stage breast cancer?

A

Richardson

Grading 1-3 depending on tubule involvement, mitoses, nuclear pleomorphism

323
Q

What is adjuvant therapy?

A

Treatment given after surgical resection of a primary tumour to eliminate subclinical disease

324
Q

What is neoadjuvant therapy?

A

Treatment given before surgery to reduce the size of a primary tumour

325
Q

In what phase of the cell cycle does radiotherapy best kill rapidly dividing cells?

A

G2 phase

326
Q

What is the principal of giving fractional radiotherapy rather than one big dose?

A

The smaller doses allows normal tissues to recover and but the cancer won’t be able to recover as quickly
Over time the multiple smaller doses is more effective at removing more cells than one big dose

327
Q

What are the 4 main ways of chemotherapy treatment?

A

1 - antimetabolites = mimic normal substrates in DNA replication - Fluouracil
2 - Alkylating and platinum based = cross-link the DNA strands together - Cyclophosphamide and Cisplatin
3 - Antibiotics = Inhibit DNA topoisomerase - Doxorubicin or Double-stranded DNA breaks - Bleomycin
4 - Plant-derived = Block microtubule assembly and interfere with mitotic spindle formation - Vincristine

328
Q

Give an example of hormone based treatment for malignant tumours?

A

Selective oestrogen receptor modulators - Tamoxifen
Bind to oestrogen receptors - preventing oestrogen binding
TX hormone receptor positive breast cancer
Androgen blockade is used for prostate cancer

329
Q

How does transtuzumab work?

A

HER-2 gene -> HER-2 receptor blocking by drug

1/4 of all breast cancers have gross over-expression of HER-2 receptors

330
Q

How does Imatinib work?

A

CML shows chromosomal re-arrangement creating an abnormal chromosome in which an oncogenic fusion protein is encoded (BCR-ABL).
Imatinib inhibits this fusion protein

331
Q

How do nivolumab and ipilimumab work?

A

Immune checkpoint blockers
Ipilimumab - priming and activation of APC’s and T-cells
Nivolumab - enhances killing of cancer cells by immune system

332
Q

What hormone is released by testicular tumours that can be tested for?

A

Human Chorionic Gonadotrophin

333
Q

What are tumour markers useful for?

A

Monitoring tumour burden during treatment and follow up

334
Q

What oncofoetal antigen is released by hepatocellular carcinoma?

A

Alpha fetoprotein

335
Q

What specific protein is released in prostate tumours?

A

Prostate-specific antigen

336
Q

What is released by ovarian cancer?

A

Mucin/ glycoprotein CA-125

337
Q

When are free radicals produced the most?

A

Chemical and radiation injury
Ischaemia-reperfusion injury
Cellular ageing
High oxygen concentrations

338
Q

What are the 3 free radicals of importance?

A

OH- (hydroxyl - most dangerous)
O2- (superoxide)
H2O2 (hydrogen peroxide)

339
Q

What 3 enzymes remove free radicals

A

Catalases
Superoxide dismutase
Peroxidases

340
Q

What is the term used to describe the maximum number of divisions of a cell?

A

Replicative senescence

341
Q

Which area of the liver lobule is most susceptible to paracetamol damage and what CYP enzyme breaks it down?

A

Zone 3

CYP2E1

342
Q

What is a basic difference between apoptosis and necrosis in terms of local microscopic changes seen?

A

Apoptosis - no inflammation, single cell dying, intact plasma membrane, apoptotic bodies seen
Necrosis - cells swell before dying but apoptosis shrink only

343
Q

What do opsonins do?

A

Coat foreign materials and make them easy to phagocytose

344
Q

What is complement?

A

A group of proteins that are assembled locally to produce a bacteria-perforating structure

345
Q

What are the two subtypes of exudate?

A

Serous exudate and fibrous exudate

346
Q

What is serous exudate?

A

Plasma proteins mostly
Few leucocytes - suggesting no infection by micro-organisms
Clear (no colour)
Contain proteins - no fibrinogen

347
Q

What is fibrinous exudate?

A

Significant deposition of fibrin (i.e. a blood clot without RBC)
Fibrin deposited in the space e.g. pleural/ pericardial

348
Q

What cancer are eosinophils most abundantly present?

A

Hodgkin’s lymphoma

349
Q

Why are myofibroblasts bad in hepatic cirrhosis?

A

Contraction of cirrhotic liver impairs blood flow of portal blood resulting in ascites

350
Q

What are 2 subcategories of granulomas?

A

Foreign body granuloma

Hypersensitivity of immune type granuloma

351
Q

What is sarcoidosis?

A

A disease with unknown cause in which granulomas are seen in organs throughout the body

352
Q

Apart from sarcoidosis which gastric condition also produces granulomas?

A

Crohn’s disease

353
Q

What cells are primarily seen in rheumatoid arthritis?

A

Lymphocytes, macrophages and plasma cells

354
Q

What factors contribute to cellular regeneration in simple terms?

A

Growth factors in the microenvironment
Cell - to - cell communication
Electric currents and nervous stimuli

355
Q

What is asymmetric replication?

A

One daughter cell remains as a stem cell that is totipotent

356
Q

What nerves can regenerate?

A

Peripheral nerves

CNS can not regenerate

357
Q

What muscle type has good regenerative capacity?

A

Smooth muscle

Striated muscle is limited

358
Q

How do striated muscle’s regenerate?

A

From satellite cells - muscle stem cells

359
Q

What epithelia are exceptions to having very good regenerative capacity?

A

Lens of the eye

Renal podocytes

360
Q

What is alport syndrome?

A

X - linked disease
Type IV collagen abnormal
Glomerular basement membrane, cochlea of the ear and lens of the eye dysfunction

361
Q

What is autocrine cell communication?

A

Cells respond to signalling molecules they produced themselves

362
Q

What is paracrine communication?

A

Cell produces signalling molecules hat act on adjacent cells

Cells responding are close in proximity but different type

363
Q

What growth factors are important in wound healing?

A

Epidermal growth factor - mitogenic for epithelial cells, fibroblasts
Vascular endothelial growth factor - potent inducer of blood vessel development
Platelet derived growth factor - migration and proliferation of fibroblasts
Tumour necrosis factor - induces fibroblast migration proliferation and collagenase secretion

364
Q

In basics what is the difference between a hypertrophic and a keloid scar?

A

Hypertrophic stays within the bounds of the damage and can regress over time. A keloid scar is the opposite.

365
Q

In basics what are the 3 stages of haemostasis?

A

1 - severed artery contacts enough to slow bleeding, veins don’t contract but pressure is much lower
2 - primary haemostat plug of activated platelets forms at the hole in the vessel - seconds to minutes
3 - secondary haemostatic plug forms as fibrin filaments stabilise the platelet plug - 30minutes approx

366
Q

What is clot retraction?

A

Actin and myosin filaments within the platelets contract as the platelets die. Clot retraction then pulls the ends of the wound closer together toughening the clot

367
Q

What activates the function of plasmin?

A

Tissue plasminogen factor

368
Q

Why is streptokinase only given once?

A

Antigenic - formation of antibodies against the drug - risk of immune reaction

369
Q

What sets fibrinolysis in motion?

A

Clotting cascade

As the clotting cascade develops further and further the more the fibrinolysis is activated

370
Q

Why is surgery risky for 7-10days thromboembolism?

A

Fibrinolytic activity drops and remains low for 7-10 days post surgery - time period coincides with increase risk of post-op thrombosis

371
Q

What happens to PT and APTT in thrombocytopenia?

A

Normal as these are clotting cascade function and not platelet function

372
Q

How would you describe the bleeding pattern seen in thrombocytopenia?

A

Petechial

373
Q

What are the 4 classes of causes of thrombocytopenia?

A

Decreased production
Decreased platelet survival
Sequestration
Dilutional

374
Q

What are a few examples of causes of decreased platelet production?

A

Bone marrow infiltrates by malignancy
Drugs
Infections
B12 and folate deficiency

375
Q

What are a few examples of causes of decreased platelet survival?

A

Immunologic destruction - Immune thrombocytopenic purpura (ITP)
Non-immunologic destruction - Disseminated Intravascular Coagulopathy (DIC)

376
Q

What would cause an increased sequestration of platelets?

A

Enlarged spleen

377
Q

What is DIC?

A

Thrombohaemorrhagic disorder occurring as a secondary complication in a variety of conditions
Activator of clotting -> microthrombi formed -> platelets, fibrin, coagulation factors consumed + fibrinolysis activated too -> haemorrhage

378
Q

What are the causes of DIC?

A

Sepsis - gram negative - endotoxin produced which activates the clotting cascade
Severe trauma - especially in brain - large amounts of thromboplastin
Extensive burns
Complications of childbirth -> amniotic fluid embolism, retained dead foetus
Malignancy
Snake bite

379
Q

What is the treatment of DIC?

A

Treat the cause
Transfusion of platelets, fresh frozen plasma, cryoprecipitates, RBC
Heparin if excess clots

380
Q

What is the term used to describe anaemia in DIC?

A

Microangiopathic haemolytic anaemia

381
Q

What is the difference seen in the location of thrombi in the arterial and venous system?

A

Arterial - site of endothelial damage

Venous - areas of stasis

382
Q

Do all 3 factors of Virchow’s triad need to be factors in thrombosis

A

No - only 2 factors are needed

383
Q

What effect does smoking have on clotting?

A

Activates factor 12

384
Q

What is thrombophlebitis?

A

Pain when superficial thrombi form and cause associated inflammation in the wall of the vein

385
Q

What is a thrombus on a cardiac valve called?

A

Vegetation

386
Q

Why are thrombi more common on the left heart?

A

Exposure to greater pressures and therefore micro trauma - exposure to thrombogenic sub endothelial tissues

387
Q

Can embolisation occur in veins?

A

No - blood flow is slower as it goes from smaller to larger vessels

388
Q

What is a paradoxical embolus?

A

Thromboemboli that form in the systemic veins but embolise to the systemic arteries

389
Q

How do paradoxical emboli by-pass the lungs?

A

1 - small emboli pass through arteriovenous anastomoses in pulmonary circulation (also a way that fat droplets pass through the lungs)
2 - larger emboli can only enter the systemic circulation by passing through defects in the interventricular septum or a patent foramen ovale during coughing, lifting or straining

390
Q

Why does coughing, lifting or straining increase the risk of emboli passing through defects in the heart from R -> L heart?

A

Increased pressure in R heart ≥ L heart pushing thrombus through the defect

391
Q

What is the most common emboli that causes TIA?

A

Atheroemboli - coming from carotid arteries

392
Q

Which process can increase the chance of an air emboli?

A

Labour - air enters the uterus and forced into open veins during uterine contractions

393
Q

What procedures increase the risk of fat/ bone marrow emboli?

A

Long bone fractures

Liposuction

394
Q

How do fat emboli cause death?

A

Fat droplets coalesce over few days -> sucked into gaping veins that have been torn by a fracture

395
Q

What are the most common locations of a thrombi occurring that cause a PE?

A

Veins of the thigh and the popliteal vein

396
Q

What causes gas emboli?

A

Trauma to neck/ chest
Negative pressure in veins during inspiration -> Air enters veins -> frothy mass stops circulation

Labour

397
Q

What causes the bends?

A

Underwater diver is under high pressure -> nitrogen dissolves in body fluids and tissues
If diver surfaces too quickly -> gases come out of solution -> bubbles distort tissues -> emboli in blood.
Nitrogen is highly fat soluble -> persistent bubbles and focal ischaemia in lipid-rich tissues i.e. CNS.
+ skeletal muscle, joints, lungs.

398
Q

What are potential sequelae with an amniotic embolus?

A

Causes sudden respiratory distress, hypotension, seizures, loss of consciousness and DIC

399
Q

Define arteriosclerosis

A

Hardening of the arteries

Arteries are thickened and lose their elasticity

400
Q

Define arteriolosclerosis

A

Hardening of the arterioles
Affects all arterioles but particularly the arterioles of the kidneys
Little to no connection with atherosclerosis and usually occurs secondary to severe HTN or in DM

401
Q

By what 3 mechanisms does the endothelium prevent thrombosis?

A

Prostacyclin production
Thrombomodulin production
Expression of heparin-like molecules

402
Q

What is the most common type of cancer to form in the bowel?

A

Adenocarcinoma

403
Q

What is the most common type of cancer to form in the skin?

A

Squamous cell carcinoma, malignant melanoma, basal cell carcinoma

404
Q

What is the most common type of cancer to form in the lung?

A

Adenocarcinoma, squamous cell carcinoma, small cell carcinoma

405
Q

What is the most common type of cancer to form in the Breast?

A

Adenocarcinoma

406
Q

What is the most common type of cancer to form in the prostate?

A

Adenocarcinoma

407
Q

What is the most common type of cancer to form in the Pancreas?

A

Adenocarcinoma

408
Q

What is the most common type of cancer to form in the brain?

A

Astrocytoma

409
Q

What is the most common type of cancer to form in the uterus

A

adenocarcinoma

410
Q

What is the most common type of cancer to form in the oesophagus

A

squamous cell carcinoma, adenocarcinoma

411
Q

What is the most common type of cancer to form in the stomach

A

adenocarcinoma

412
Q

What is the most common type of cancer to form in the thyroid

A

adenocarcinoma

413
Q

What is the most common type of cancer to form in the cervix

A

squamous cell carcinoma

Adenocarcinoma

414
Q

What is the most common type of cancer to form in the bladder

A

transitional cell carcinoma

415
Q

Why can patients get Zollinger-Ellison syndrome from a pancreatic and gastric tumour?

A

Production of excess gastrin causes excess acid production

416
Q

Why can patients get carcinoid syndrome?

A

Metastatic cancer
e.g. Liver mets
Excess production of serotonin and other products which can be detected in the blood and urine
Symptoms of flushing, abdo pain, diarrhoea, nausea and vomiting

417
Q

In the resp system what are the different classifications of neuroendocrine tumours?

A

Low grade malignant (typical and atypical carcinoids)
High grade carcinomas (large cell neuroendocrine and small cell lung carcinomas)
Presence of necrosis and mitotic activity

418
Q

What cancer causes pepper pot skull and also what is the type of lesion present?

A

Myeloma

Osteolytic lesion

419
Q

What primary cancer can metastasise to the bone and what type lesion do they cause?

A

Prostate, breast, transitional cell carcinoma, small cell lung
Sclerotic lesion

420
Q

What is the difference between lytic and sclerosing metastasis?

A

Lytic - destroys bone

Sclerotic - builds bone as part of the mets as a protective process

421
Q

What are the layers of the skin?

A

Stratum corneum -> lucid -> granulosum -> spinosum -> basale

Cute Ladies Get Smart Boys

422
Q

What is the clinical and pathological features of familial adenomatous polyposis?

A

Polyps along the whole colon that can become malignant
Tubular adenomas - most common - adenocarcinomas
APC gene which is a tumour suppressor gene is defective
Autosomal dominant

423
Q

What is the adenoma-carcinoma sequence?

A

Stepwise accumulation of mutations both oncogenes and tumour suppressor genes

424
Q

What is pagets disease of the bone?

A

Interference in the bone remodelling process - osteoclasts are more active than osteoblasts
New bone laid down is of poorer quality and more brittle
Predisposes to fractures

425
Q

What type of tumour is most common in the testis and which is likely to be in a young adult?

A

Most common - seminoma and non-seminomatous

Germ cell tumour most likely as young adult

Medicine (15 decks)

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