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My Principles > Pathology > Flashcards

Pathology Flashcards

1
Q

What does VINDICATE stand for?

A
  • Vascular
  • Infectious/Inflammatory
  • Neoplastic
  • Drugs/toxins
  • Interventions/Iatrogenic
  • Congenital/developmental
  • Autoimmune
  • Trauma
  • Endocrine/metabolic
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2
Q

What are the main categories for response to injury?

A
  • vascular changes
  • cellular changes
  • chemical mediators
  • morphological patterns
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3
Q

What are the vascular changes that happen in response to injury?

A

vasodilation in the arterioles then capillary beds which is mediated by histamine and nitric oxide and results in rubor and calor

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4
Q

What are the cellular changes that can happen in response to injury?

A 
stasis
whit cell margination
rollin
adhesions
migration
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5
Q

What does vasodilation do to normal blood flow?

A

causes white cell margination as blood no longer flows centrally

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6
Q

What are the two types of cell adhesion molecule and what do they do?

A

selectins: expressed on endothelial cell surface
integrins: bind to walls, matrix and other cells

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7
Q

What hormones cause the inflammatory response and what do they cause?

A

histamine and thrombin from inflammatory cells increase selection expression, TNF and IL1 which increases endothelial cell expression of VCAM and ICAM

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8
Q

What effect do the chemokine from the injury site have?

A

bind to proteoglycans on cell surface which increases affinity of VCAMs and ICAMs fro integrins

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9
Q

How does swelling happen?

A

leaky vessels leading to loss of protein so change in osmotic pressure so water moves out causing swelling

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10
Q

What is chemotaxis?

A

cells following a chemical gradient and moving along it

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11
Q

What are the steps of phagocytosis?

A
  • recognition and attachment
  • engulfment
  • killing and degradation
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12
Q

What happens in the recognition and attachment phase of phagocytosis?

A
  • bacteria have terminal mannose receptor residues in glycoproteins and glycolipids (mammals don’t)
  • scavenger receptors
  • opsonins (complement and IgG)
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13
Q

What happens in the engulfment has of phagocytosis?

A
  • arms are pseudopods

- phagosome forms and joins with lysosome to make phagolysosome

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14
Q

What components are involved in the killing and degradation phase of phagocytosis?

A

reactive oxygen species (NADPH oxidase)

reactive nitrogen species (nitric oxide synthase)

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15
Q

What are the five pillars of inflammation?

A

rubor- redness with increased perfusion, slow flow and increased vessel permeability
tumor- swelling due to vascular changes
dolor- pain mediated by prostaglandins and bradykinin
calor- heat with increased perfusion, slow flow and increased vessel permeability
functions laesa- loss of function

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16
Q

What cell is also called a polymorph?

A

neutrophil due to many lobes

these are granulocytes with phagocytic and cytotoxic abilities

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17
Q

What is the major cell involved in acute inflammation?

A

neutrophil

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18
Q

What are the factors that determine what happens after acute inflammation?

A
  • site of injury
  • type of injury
  • duration of injury
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19
Q

What is resolution?

A
  • complete restoration of tissue to normal after removal of inflammatory components
  • minimal cell death
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20
Q

What does the tissue need to have resolution after inflammation?

A
  • fast delivery of white cells

- removal of injurious agent

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21
Q

What is suppuration?

A 
pus 
neutrophils 
bacteria
inflammatory debris
abcsess
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22
Q

When does organisation happen?

A

if there is necrosis, fibrin, poor blood supply or damage beyond the basement membrane

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23
Q

How do erosions and abrasions heal?

A

there is an intact basement membrane so it will heal with complete resolution

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24
Q

What is granulation tissue?

A

hole is infiltration by capillaries then myofibroblasts which deposit collagen and smooth muscle cells

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25
Q

What does scarring and fibrosis cause?

A

patch job with loss of function

skin will be less mobile and stretchy

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26
Q

What happens when the liver gets overwhelmed by fibrosis?

A

cirrhosis leading to liver failure

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27
Q

Who is chronic inflammation favoured?

A

suppuration, scarring, empyema, persistence of injury so foreign material, infectious agent so virus or autoimmune such as transplant rejection

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28
Q

What are the cells of chronic inflammation?

A
  • lymphocytes (small round blue cell)

- macrophages

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29
Q

What are granulomas?

A

balls of macrophages including foreign bodies that can be endogenous (keratin, bone, crystals) or exogenous (talc, asbestos, suture) eg TB mycobacterium

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30
Q

What is caseous necrosis from?

A

tuberculous granulomas

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31
Q

What happens when they is no ATP?

A

increased K+ (causes swelling), Ca2+ pump fails so increased Ca2+

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32
Q

What does increased Ca2+ cause?

A
  • ATPase
  • phopholipase (membrane damage)
  • proteases (membrane and cytoskeleton damage)
  • endonuclease (DNA damage/breakdown)
  • mitochondrial permeability (release pro death factors)
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33
Q

After how long does cell death occur?

A

20 minutes

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34
Q

What happens when cell begin to die?

A

1) cells shrink (pyknotic), become red, nucleus shrinks and becomes dark and marginal contraction bands appear
2) cell contents leaked, complement cascade and acute inflammation
3) vasodilation, m flow slows, white cell margination, rolling, parementing, diapedesis, chemotaxis and phagocytosis

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35
Q

What is coagulative necrosis and where does it occur?

A

happens in cardiac tissue

ghost outline before neutrophils can remove them

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36
Q

What is restitution?

A

gradual progressive scarring as macrophages are replaced by fibroblasts that lay down collagen, this is complete at 6 weeks

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37
Q

What is hyperplasia?

A

enlargement of an organ caused by an increase in reproduction rate of cells

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38
Q

What is hypertrophy?

A

enlargement of an organ due to an increased size of cell

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39
Q

What is atrophy?

A

decrease in the size of cell

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40
Q

What is metaplasia?

A

reversible transformation of one differentiated cell type to another

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41
Q

What is cell division caused by?

A

production of more growth factors or more growth factor receptors

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42
Q

What actions can growth receptors have?

A
  • intrinsic tyrosine kinase activity
  • 7 transmembrane G-protein-coupled receptors
  • receptors without intrinsic kinase activity
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43
Q

What controls each stage of the cell cycle?

A

cyclin dependent kinases which are activated by cyclins A, B, D and E

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44
Q

What happens in G1?

A
  • cell gets bigger with increased protein synthesis
  • CDK4 activated by cyclin D
  • CDK4 phosphorylates Rb (retinoblastoma protein)
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45
Q

What does Rb do in G1?

A

binds to E2F to stop cell division but when it is phosphorlyated by CDK4 cell division occurs readily

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46
Q

What happens in the synthesis phase?

A
  • E2F initiates DNA replication
  • increases levels of cyclin A which activates CDK2
  • promotes DNA replication
  • after S phase, there will be two copies of every gene
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47
Q

What happens in G2?

A

second growth phase so cell gets bigger and there is more protein synthesis

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48
Q

What does p53 do?

A

checks cell for mistakes, pauses, repairs and then progressed or causes the cell to commit suicide
(cancer avoids these checks)

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49
Q

What are telomeres?

A

TTAGGG repeats at the end of chromosomes that limit divisions

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50
Q

What causes hyperplasia?

A
  • an external stimulus which will stop when stimulus does

- can be physiological or pathological (by hormones)

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51
Q

What is hyperplastic tissue at risk of?

A

development of cancer

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52
Q

What is the mechanism of atrophy?

A
  • reduced cellular component
  • protein degradation
  • digested in lysosomes
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53
Q

What substances increase or decrease atrophy?

A

glucocorticoids and thyroid increase atrophy

insulin decreases atrophy

54
Q

What is cancer?

A

uncontrolled cell proliferation and growth that can invade other tissues

55
Q

What is neoplasia?

A

new growth that is not is response to a stimulus- it can be benign, premalignant or malignant

56
Q

Where does malignancy occur in relation to the epithelium?

A

the malignancy goes beyond the basement membrane

57
Q

What is metaplasia?

A

the reversible change from one mature cell type to another mature cell type

58
Q

How does metaplasia occur?

A

change in signals sent to stem cells so they differentiate down a different line which can be in response to cytokines, growth factors or other chemicals

59
Q

What does thermal or chemical injury do to the bronchial epithelial surface?

A

changes it to squamous epithelium

60
Q

What is the epithelium in the bladder?

A

transitional but changes to squamous with injury

61
Q

What is metaplastic tissue at risk of?

A

becoming cancerous

62
Q

What does hyperplasia need to occur?

A

can be autonomous and not need a stimulus

63
Q

What is dysplasia?

A

disordered growth with abnormal cells where growth is not in response to a stimulus and there is no invasion beyond the basement membrane

64
Q

What is carcinoma in situ?

A

dysplasia affecting the whole epithelium which is the last stage before invasion

65
Q

What are the Weinberg hallmarks of cancer?

A
  • metastasis
  • replicative immortality
  • angiogenesis
  • resist cell death
  • sustained proliferative signalling
  • evade growth suppressors
66
Q

What is BRCA?

A

mutations in a tumour suppressor gene

67
Q

What is the double hit hypothesis?

A

one working gene is enough and two are needed to be faulty for a problem to occur

68
Q

What are initiators?

A

initiators cause long lasting genetic damage but must be followed by a promoter

69
Q

What are promoters?

A

there require initiators to cause damage

70
Q

What cancers does smoking cause?

A

small cell lung
head and neck
bladder
cervical

71
Q

What are aflatoxins?

A

cause a p53 mutation

72
Q

What does radiation cause?

A

pyrimidine dimers in DNA

73
Q

How can chronic inflammation cause cancer?

A

causes lymphomas as so much replication can cause errors

74
Q

What must a cancer cell do to sustain growth signals?

A
  • grow without stopping
  • avoid homeostatic controls
  • growth receptors (with or without intrinsic tyrosine kinase activity and 7 transmembrane G protein-coupled)
  • Myc promotes growth
  • P13K is commonly mutated
75
Q

What must a cancer cell do to have a loss of growth inhibition?

A
  • stops tumour suppressors

- stopping p53 checking for mistakes

76
Q

How does p53 check for mistakes?

A
  • senses DNA abnormality at G1
  • pauses cell cycle
  • increases levels of p21 (CDK inhibitors)
  • repair or apoptosis
77
Q

How do cancer cells have unlimited replicate potential?

A

reactivate telomerase to get more telomeres

78
Q

How do cancer cells resist apoptosis?

A

bcl-2 binds Bak/Bax so stops death

79
Q

How do cancer cells induce angiogenesis?

A

upregulation of vascular endothelial growth factor

80
Q

How do cancer cells evade inflammatory response?

A

over expression of PD-L1 which inhibits T cell proliferation

81
Q

What does an inflammatory response do the cancer?

A

helps body fight it

82
Q

How do cancer cells activate invasion and metastases?

A

chew up surrounding tissue

increase expression of matrix metalloproteinases

83
Q

What is atrophy?

A

physiological or pathological reduction in cell size

84
Q

What is necrosis?

A

always pathological death that requires no energy

85
Q

What is coagulative necrosis?

A

preserves cell outline and dead cells are consumed by enzymes eg cardiac muscle

86
Q

What is liquefactive necrosis?

A

leaves no cell structure, pus, associated with localised infections eg in the brain

87
Q

What is caseous necrosis?

A

TB, granulomas with central necrosis, ZN positive

88
Q

What is apoptosis?

A

programmed cell death in response specific signals
requires energy
can be physiological

89
Q

What is pathological apoptosis due to?

A 
injury
vasodilation
chemotherapy
viral infection
cancer
90
Q

What is the extrinsic pathway for apoptosis?

A
  • death cell receptors initiated
  • TNF or fas
  • Fas recognises self
  • TNF induces apoptosis with inflammation
91
Q

What is the intrinsic pathway for apoptosis?

A
  • mitochondrial
  • anti-apoptic molecules removed form membrane
  • these are replaced with Bax/Bak
  • increased leakiness in mitochondria so caspases so cytochrome C
92
Q

How does apoptosis occur?

A
  • pyknosis
  • chromatin condensation
  • cytoplasmic blebs
  • macrophages
93
Q

What is cellularly ageing caused by?

A
  • oxidative stress due to free radical damage

- accumulation of metabolism by-products

94
Q

What is a polymorph?

A

neutrophil

95
Q

What is a monocyte/histiocyte?

A

macrophage

96
Q

What is suppuration?

A

involves necrosis, phagocytosis, abscess and neutrophils but not lymphocytes

97
Q

What steps of inflammation are the fibroblasts in?

A

the later stage

98
Q

What does homogenous tissue look like?

A

one area that looks the same as another

99
Q

What is the classification of encapsulated slow growing lesions?

A

benign

100
Q

What does heterogenous tissue look like?

A

all areas look different and there is haemorrhage and necrosis

101
Q

What is an ideal nucleus:cytoplasmic ratio?

A

a low ration is good and a high ratio is seen in malignancy

102
Q

What does differentiation say about a cell?

A

well differentiated cells are normal and poorly differentiated cells can be malignant as they look nothing like they are supposed to

103
Q

What is pleomorphism?

A

all cells look different

104
Q

What is hyperchromasia?

A

is dark staining nuclei due to more DNA

105
Q

What is mitoses?

A

a high mitotic count which is common in malignancy

106
Q

What is a tumour of the epithelium called?

A

carcinoma

107
Q

What is mesenchymal related to?

A

connective tissue

108
Q

What is a tumour of the glands called?

A

adenoma or adenocarcinoma

109
Q

What is a tumour of the squamous cells called?

A

papilloma or squamous cell carcinoma

110
Q

What is a tumour of the bladder called?

A

transitional cell carcinoma

111
Q

What is a tumour of the connective tissue called?

A

mesenchyme sarcomas

112
Q

What is a tumour of the fat called?

A

lipoma or liposarcoma

113
Q

What is a tumour of the bone called?

A

osteoma or osteosarcoma

114
Q

What is a tumour of the cartilage called?

A

enchondroma or chondrosarcoma

115
Q

What is a tumour of the skeletal muscle called?

A

rhabdomyoma or rhabdomyosarcoma

116
Q

What is a tumour of the smooth muscle called?

A

leiomyoma or leiomyosarcoma

117
Q

What is a tumour of the nerve called?

A

meurofribome or shwannoma is benign

malignant peripheral nerve sheath tumour

118
Q

What is a tumour of the vessels called?

A

haemangioma or angiosarcoma

119
Q

What is a freckle?

A

ephelis

120
Q

What is a mole?

A

naevus

121
Q

What is a malignant lesion of the skin called?

A

melanoma (exception to the nomenclature rule)

122
Q

What is the word for how far the cancer has spread?

A

stage

123
Q

What is the word for how differentiated the cells are?

A

grade
well differentiated = low grade
poorly differentiated = high grade

124
Q

What is cachexia?

A

weight loss in cancer due to tumour and TNF which increase metabolism

125
Q

What are paraneoplastic syndromes?

A

result from the tumour but aren’t directly related- can be due to increased Ca2+ or decreased Na+

126
Q

What are examples of paraneoplastic syndromes?

A

osteoarthropathy
skin rash
fever (pyrogens)
pyrexia

127
Q

Why are cancer patients susceptible to infection?

A

tumours can evade and suppress immune system

128
Q

What is the difference between blood colts and thrombosis?

A

blood clots are extravascular

thrombosis is intravascular

129
Q

What are the features of the intrinsic coagulation cascade?

A

factor XII activation

measured with PT

130
Q

What are the features of the extrinsic coagulation cascade?

A

starts with tissue factor

measured with APTT

131
Q

What are the consequences of increased calcium ions?

A 
ATPase
phospholipase
proteases
endonuclease
mitochondrial permeability

My Principles (13 decks)

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