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Principles - Kate > Pathology > Flashcards

Pathology Flashcards

1
Q

what can inflammation be caused by?

A

injury, infection, trauma, foreign bodies, immune reaction, necrosis

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2
Q

what are the responses to injury?

A

vascular change, cellular change, chemical mediators, morphological patters

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3
Q

what happens during vascular change?

A

change in flow and vessel caliber, vasodilation, blood flow slows, arterioles then capillary beds, mediated by histamine and nitric oxide, white cell margination - rolling - pavementing - migrating, increased calor and rubor, cell adhesion molecules expressed on white and endothelial cells mediate pavementing

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4
Q

what are some cellular changes?

A

stasis, white cell margination (cells drift out), rolling, adhesion, migration

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5
Q

what are some adhesion molecules?

A

integrins (over 30 types, bind to ICAM), selectins (expressed on various cells), VCAM (vascular cell adhesion molecule), ICAM (intercellular adhesion molecule)

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6
Q

what is the intergrin/selectin interaction with their ligand like?

A

of low affinity and binding on is fast as well as binding off

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7
Q

what are the inflammatory cells?

A

histamine and thrombin from inflammatory cells increase selectin expression, tumour necrosis factor (TNFY and interleukin-1 (IL-1) increase endothelial cell expression of VCAM and ICAM

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8
Q

what is avidity?

A

the strength of the total binding

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9
Q

what happens during increased avidity?

A

chemokine from the site of the injury bind to proteoglycans on endothelial cell surfaces, these proteoglycans then increase the affinity of VCAMs and ICAMs for integrins

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10
Q

what happens due to vascular permeability?

A

leaky vessels - loss of proteins, change in osmotic pressure, water flows protein - swelling (tumour)

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11
Q

why are the vessels so leaky?

A

endothelial contraction - histamine, bradykinin substance P, leukotrienes, if its direct injury, toxins and burns. VEGF makes new vessels but also increase leakiness

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12
Q

what is chemotaxis?

A

when cells follow a chemical gradient and move along it , bacterial components, complement to help find the injury, leukotrienes, cytokines (interleukins)

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13
Q

what are the three stages of phagocytosis?

A

recognition and attachment, engulfment, killing and degradation

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14
Q

what happens during recognition and attachment?

A

mannose receptors, bacterial surface glycoproteins and glycolipids contain terminator mannose residues, scavenger receptors, similar to mechanism that phagocytes recognise low density lipoprotein, opsonins (peptides that attach to antigens) include components of the complement cascade as well as IgG

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15
Q

what happens during engulfment?

A

pseudopods, vesicle formation (phagosome) joins with lysosome (phagolysosome)

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16
Q

what happens during killing and degradation?

A

reactive oxygen species (ROS), NADPH oxidase (oxygen gains an electron from NAGPH and become superoxide), reactive nitrogen species, nitric oxide synthase (combines NO with superoxide and produces ONOO) many other cytotoxic granules

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17
Q

what does rubor mean?

A

redness - increased perfusion, slow flow, increased permeability of vessels

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18
Q

what does calor mean?

A

heat, increased perfusion, slow flow rate, increased vascular permeability

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19
Q

what does tumour mean?

A

swelling, due to vascular changes

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20
Q

what does dolar mean?

A

pain, mediated by prostaglandins and bradykinin

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21
Q

what does function lease?

A

loss of function

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22
Q

what’s the microscopic appearance of an acute infection?

A

the cell that characterises acute inflammation is the neutrophil, polymorph, many lobes to the nucleus, granulocyte, phagocytic and cytotoxic abilities

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23
Q

how long to neutrophils survive for?

A

only a couple of hours one outside of the blood vessel

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24
Q

what does inflammation repair depend on?

A

site if injury, type of injury and duration of injury (can it be removed)

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25
Q

what does resolution mean?

A

complete restoration of the tissue to normal after removal of inflammatory components , minimal cell death, tissue has capacity to repair. good vascular supply, injurious agent easily removed

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26
Q

what is suppuration?

A

formation of pus (pis contains living, dying and dead cells, neutrophils, bacteria, inflammatory debris), may be termed abscess, when a space is filled by puss and walled off it may be called empyema

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27
Q

what is organisation and repair?

A

essentially scarring, the the injury produces lots of necrosis, and lots of fibrin that isn’t easily cleared, poor blood supply and tissue type. mucosa where damage goes beyond the basement membrane favours healing by organisation and repair

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28
Q

what do erosions and abrasions describe?

A

injury with basement membrane intact, heal rapidly with complete resolution

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29
Q

what is a common healing response in all tissues?

A

granulation tissue formation:
defect is slowly infiltrated by capillaries and then by myofibroblasts, deposit collagen and smooth muscle cells, given constituents it looks very red

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30
Q

how does the liver heal after infection?

A

has some regenerative capacity, undergoes scarring and fibrosis, known as cirrhosis in the liver, results in liver failure, can’t remove toxins and can’t make proteins, large volume of blood flows through liver - vascular disturbance

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31
Q

what happens during chronic inflammation?

A

favoured if: suppuration, walled off pus and scarring, persistence of injury, infectious agents and if the injury is autoimmune or a transplant rejection, characterised by lymphocytes and macrocytes/monocyte

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32
Q

what are macrophages?

A

they are specific immune cells, granulomas, aggregate of epithelioid histiocytes

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33
Q

what are the TB granulomas?

A

caseous necrosis

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34
Q

what are granulomas?

A

a structure formed during infection found in many diseases, a collection of immune cells (macrophages)

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35
Q

what is a myocardial infarction?

A

a heart attack

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36
Q

what is a hypoxic injury to the heart?

A

no oxygen resulting in no ATP resulting in cell injury and acute inflammation

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37
Q

what happens in there is no ATP?

A

Na/K ATPase fails, increased K, giving swelling, calcium pump fails, increased intracellular calcium which stimulates:
ATPase, phospholipase, proteases, endonuclease, mitochondrial permeability

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38
Q

what happens during a heat attack after the first 20 minutes?

A

cell death, die via apoptosis or necrosis, cells shrink and become red, nucleus shrinks and becomes darker and marginal contraction band appears

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39
Q

what happens during the first 24 hours of a heart attack?

A

cell contents leaked, compliment cascade initiated, acute inflammation, necrosis and neutrophils may be all that is holding it together - risk of cardiac rupture, soon neutrophils fade and are replaced by macrophages

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40
Q

what happens after necrosis?

A

the cells are dead and neutrophils mop them up

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41
Q

what are the three types of necrosis?

A

caseous (TB), liquefactive, coagulative - cell death with some structure of cells left as ghost outline before complete phagocytosis of material

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42
Q

is resolution likely after necrosis of the heart?

A

no more likely restitution which is a gradual process, progressive scarring macrophages fade away and are replaced by fibroblasts

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43
Q

what do fibroblasts do?

A

gradually lay down collagen complete after 6 weeks

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44
Q

what is hypertrophy?

A

increase in cell size, often occurs in conjunction with hyperplasia, often in isolation in non-dividing cells, often in response to mechanical stress

45
Q

what is hyperplasia?

A

increased number of cells, must be in response to an external stimulus, will regress on withdrawal of stimulus, usually results in increased organ volume, can be physiological and pathological, occurs during puberty and pregnancy

46
Q

what is atrophy?

A

decreased cell size, physiological (embryological structures) or pathological (decreased workload) due to loss of innervation, loss of function after nerve supply is removed, blocked blood supply, loss of hormonal stimulation

47
Q

what is metaplasia?

A

when a cell differentiated into a different cell

48
Q

what can we do if we receive growth factors in order to set of a chain of events to lead to cell division?

A

produce more growth factors and produce more growth factor receptors

49
Q

what are the three categories of growth receptors?

A

receptors with intrinsic tyrosine kinase activity,

7 membrane G protein-coupled receptors, receptors without intrinsic tyrosine kinase activity

50
Q

what is the cell cycle?

A

tightly controlled process, stepwise progression through a series of stages, domino like effect, various check points, faulty cells may not perform the desired function, faulty cells may predispose to cancers, 4 main stages, G1, S, G2, M

51
Q

what do CDKs and cyclins do in the cell cycle?

A

each controlled by a series of cyclin dependent kinases (CDKs) that activate each other and other enzymes on a step-wise fashion, each CDK is activated by a specific cyclin, each cyclins vary in concentration throughout cell cycle. cyclin D, E, A and B

52
Q

what happens during G1?

A

growth 1, cells get bigger with increased protein synthesis, during G1 CDK4 is activated by cyclin D, CDK4 phosphorylates (i.e. activates) the retinoblastoma protein

53
Q

what is the retinoblastoma protein?

A

(Rb) is important in normal cell growth and in malignancy . normally Rb is bounciest to E2F, E2F kicks off the cell division but is stopped from doing so by Rb. when phosphorylated by CDK4, Rb can’t bind to E2F and therefore E2F is free to give a green light tp cell division

54
Q

what happens during S phase?

A

synthesis phase, E2F initiated DNA replication, increases levels of cyclin A, which activated CDK2 which also promotes DNA replication. by the end of S phase the cell should contain two copies of the genome

55
Q

what happens during G2?

A

second growth factor, cell gets bigger and more protein synthesis, main checkpoint occurs and the end of G2, main checkpoint is p53

56
Q

what does p53 do?

A

check cells for mistakes, if mistakes are found cell cycle is paused, repair is then attempted, if successful cell can progress if not cell is instructed to carryout apoptosis, important step in cancer if they can avoid being checked by p53

57
Q

what do telomeres do?

A

chromosome are capped - provide protection and stops chromosome ends from degradation and fusion, consists of TTAGGG repeats, with every division the number of repeats gets smaller, stem cells can switch on and off telomerase

58
Q

what is a compensatory mechanism?

A

action taken by the body to continue physiological function, occurs after loss of tissue, not common in many tissues, liver and bone marrow are examples

59
Q

what is pathological hyperplasia?

A

hormonal induced, will regress on withdrawal of stimulus, lymph nodes contain machinery for fighting infection, areas in lymph node will undergo hyperplasia in response to infection, hyperplasia is reversible growth, cancers keep growing in the absence of stimulus

60
Q

what are the mechanism of atrophy?

A

reduced cellular components, protein degradation, digested in lysosomes and degraded in many cases by ubiquitin proteasome pathway, some hormones promote degradation and atrophy and some oppose atrophy and promote growth, a balance of growth and atrophy remains homeostasis

61
Q

how do cells cope with stress?

A

hypertrophy, atrophy, hyperplasia

62
Q

what happens when stress becomes too much?

A

necrosis or apoptosis

63
Q

is necrosis pathological or physiological?

A

always pathological

64
Q

what is coagulative necrosis?

A

preservation of cell outline, dead cells are consumed by various enzymatic processes and cells, microenvironment too toxic for proteolysis, often seen in myocardial infarction

65
Q

what is liquefactive necrosis?

A

liquid viscous mass - no cell structure remains, pus, associated with localised bacterial and fungal infections, necrosis within the brain

66
Q

what is caseous necrosis?

A

cheesy necrosis, microscopic, granulomatous inflammation with central necrosis, associated with TB, stain using Ziehl Neelson stain

67
Q

what is apoptosis?

A

programmed cell death in response to specific signals, requires energy

68
Q

what is physiological apoptosis?

A

sometimes cell death is physiological and we need cells to die off, may be part of normal growth, removal of self-reactive lymphocytes, hormonal-dependent involution

69
Q

what is pathological apoptosis?

A

in response to injury, radiation, chemotherapy, viral infection (hepatitis), cancers

70
Q

what do all mechanisms rely on activating ?

A

capases

71
Q

what are the two mechanism pathways

A

extrinsic and intrinsic

72
Q

what happens in the extrinsic pathway?

A

death receptor-initiated pathway, cell membrane receptors with death domain, death receptors (tumour necrosis factor, TNF), Fas - recognition of self, apoptosis in lymphocytes, people with Fas mutations often get autoimmune diseases. TNF - complex but does not induce apoptosis in association with inflammatory conditions

73
Q

what happens in the intrinsic pathway?

A

mitochondrial pathway, growth signal promote anti-apoptotic molecules in mitochondrial membrane, when removed replaced by Bax, Bak, increase permeability of mitochondria, release of proteins that stimulate caspases, cytochrome C

74
Q

what is pyknosis?

A

when a cell shrinks

75
Q

what is chromatin condensation?

A

when nucleus clumps and breaks up

76
Q

what are cytoplasmic blebs?

A

when cytoplasm breaks up

77
Q

what is cancer?

A

uncontrolled cell proliferation and growth that can invade other tissues

78
Q

what is neoplasia?

A

new growth, not in response to a stimulus, can begin as premalignant or malignant, can occur is any cell of any organ, clinician code for cancer

79
Q

how can you tell if a tumour is benign or malignant?

A

malignant has metastatic potential (spreads to other sites), epithelium has a basement membrane, malignancy goes beyond basement membrane, there are precursor stages, precursor lesions are dysplasia, metaplasia and hyperplasia

80
Q

what is metaplasia?

A

reversible change from one mature cell type to another, associated with stress, not reversal in appearance of an adult cell, represents a change in signals delivered to stem cells causing them to differentiate, may be in response to cytokines (chemical messengers), growth factors, occur commonly is response to a noxious stimulus

81
Q

what does bronchial epithelium in the lung differentiate to often in response to thermal and chemical injury?

A

squamous epithelium

82
Q

what does transitional epithelium often differentiate to in the bladder after use of a catheter?

A

epithelium changes to squamous

83
Q

what is dysplasia?

A

disordered growth, abnormal cells, growth is not in response to stimulus, no invasion - growth beyond basement membrane, low graded is the most normal, high grade is the most abnormal and closest to become cancer

84
Q

what is CIS?

A

carcinoma in-situ, dysplasia affecting the whole of the epithelium, applies to non-glandular epithelium

85
Q

what are some causes of cancer?

A

genes, smoking, alcohol, UV radiation, drugs, infections, obesity

86
Q

what are Weinberg’s hallmarks of cancer?

A

increased growth signals, Remove growth suppression, avoid apoptosis, achieve immortality, become invasive, angiogenesis (makes its own blood supply), loss of spell DNA checks, avoid the immune system

87
Q

what are the three categories of growth receptors?

A

receptors with intrinsic tyrosine kinase activity, 7 transmembrane G protein-coupled receptors, receptors without intrinsic tyrosine kinase activity

88
Q

what is Myc?

A

Myc is a nuclear transcription factor that promotes growth -DNA replication etc., common in lymphoma. Myc translocation which is diagnostic

89
Q

what is PI3K?

A

most commonly mutated kinase in caner, targeted at haematological malignancies, may be used in combination with receptor inhibitors (Wnt/ACP/beta catenin) ACP mutations are one of the earliest mutations in colorectal cancer, can occur as a gremlin mutation causing an inherited condition - adenomatous polyposis and Gardner’s syndrome

90
Q

what is a tumour suppressor?

A

stop growth, cells with malignant ambitions must remove them to survive and proliferate, tumour suppressor genes, lots of proteins that inhibit the cell cycle (often fixed p, p52 most commonly mutated protein across all cancers)

91
Q

what is PTEN?

A

increases transcription of p27, p27 block CDKs and cell cycle proliferation, CDKs are activated by cyclins, inhibits P13K/AKT pathway we saw earlier, without PTEN and therefore p27 cells can proliferate in an uncontrolled fashion

92
Q

in malignancy what often happens to telomerase?

A

it is reactivated

93
Q

what is angiogenesis?

A

cancers grow fast, increased demand for oxygen etc., outgrow blood supply, successful cancers will create their own blood supply. VEGF - vascular endothelial growth factor, frequently up-regulated in some malignancies

94
Q

what is BRCA?

A

it is the breast cancer gene, breast ovarian and pancreatic tumours, complex role in ER and AR regulation

95
Q

what are the mismatch repair proteins?

A

family of proteins responsible for identifying faults in the code - mismatched sequences, MLH1, MLH3, MSH2, MSH3, PMS1, PMS2, abnormal in Lynch syndrome

96
Q

how do malignancies evade the immune system?

A

we do react to our own malignancy, malignant cells may express foreign proteins or expose proteins to the immune system that aren’t normally exposed, cancers with a pronounced inflammatory response do better, some melanomas even regress

97
Q

what is PD-L1?

A

programmed death - ligand 1, inhibits T-cell proliferation through apoptosis, tumours can over express PD-L1 and avoid the immune system, can block PD-L1 as a form of targeted treatment

98
Q

what does metastatic mean?

A

ability to spread to other organs, must grow uncontrollably and survive, avoid own immune system, chew basement membrane, extend through connective tissue, break and enter through vessel walls, survive in the vessel, aggregate and adhere to vessel wall, anchor in new organ, develop a new vascular system and survive and grow

99
Q

are slow growing lesions usually malignant or benign?

A

benign

100
Q

what do malignant lesions look like?

A

nasty, don’t look natural, irregular, infiltrative, destructive

101
Q

if a cell is poorly differentiated what does that mean?

A

difficult to tell what the cell of origin is, higher grade cancer

102
Q

where is neoplasia always malignant?

A

the blood

103
Q

is melanoma malignant or benign?

A

malignant, doesn’t follow the same pattern as the others

104
Q

what do the different stages of cancer mean?

A

how far the tumour has grown

105
Q

what do the different grades of cancer mean?

A

if the cell is well (low) or poorly (high) differentiated

106
Q

what does sarcoma mean?

A

malignant growth of connective tissue e.g. bone, smooth and skeletal muscle, fat, fibrous tissue

107
Q

what does adenoma mean?

A

is a benign growth of glandular tissue

108
Q

what does papilloma mean?

A

is a benign growth of squamous cells

109
Q

what does carcinoma mean?

A

malignant growth of epithelium

Principles - Kate (10 decks)

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