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Principles > Pathology > Flashcards

Pathology Flashcards

1
Q

What are the clinical features in response to acute inflammation?

A

Rubor, calor, dolor, tumor, loss of function

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2
Q

What causes calor and rubor?

A

Increased perfusion and permeability, slow blood flow

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3
Q

What causes tumor?

A

Vascular changes

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4
Q

What is dolor mediated by?

A

Prostaglandins and bradykinin

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5
Q

What vascular changes occur in acute inflammation?

A

Vasodilation and increased permeability

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6
Q

What vessels does acute inflammation affect?

A

Arterioles first and then capillary beds

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7
Q

What are vascular changes in acute inflammation mediated by?

A

Histamine and NO

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8
Q

What causes white cell margination?

A

Because of slow blood flow and vasodilation, white blood cells move peripherally

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9
Q

Why is integrin/selectin binding low affinity?

A

So WB cells can quickly bind and unbind to stay attached the the endothelium but also roll along it to the sight of inflammation

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10
Q

What proteins are found on the endothelium?

A

Selectins and ICAMs/VCAMs

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11
Q

What proteins are found on WBCs?

A

Integrins

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12
Q

What increases the expression of selectins?

A

Histamine and thrombin

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13
Q

What increases the expression of ICAM/VCAMS?

A

TNF and IL1

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14
Q

What increases the affinity of ICAMS/VCAMS for Integrins?

A

Chemokines from the site of injury bind to protoglycans on the endothelial cell surface

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15
Q

How does chemotaxis work?

A

Cells follow a chemical gradient

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16
Q

What components can be involved in chemotaxis?

A

Complement, bacterial components, leukotrienes and cytokines

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17
Q

What cell characterises acute inflammation?

A

Neutrophil

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18
Q

What are the 3 stages of phagocytosis?

A

Recognition and attachment, engulfment and killing and degradation

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19
Q

What receptors (which are found on bacterial and not mammalian cells) are used for recognition?

A

Mannose, and sometimes scavenger receptors

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20
Q

What makes bacteria stand out to phagocytes?

A

Protein coating with antibodies and complement

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21
Q

What is the name for the cell arm that incapsulates the bacteria?

A

Pseudopod

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22
Q

What is the vesicles called before and after joining with a lysosome?

A

Phagosome, phagolysosome

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23
Q

What is an important molecule involved in killing and degradation?

A

NADPH oxidase combines with NO to form ONOO

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24
Q

What does the fate of an inflamed tissue depend on?

A

Site of injury, type/severity of injury, duration of injury

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25
Q

Which areas tend to have a better capacity for repair?

A

Those with a good vascular supply

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26
Q

What is resolution?

A

Complete restoration of tissue to normal after removal of inflammatory components

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27
Q

What improves chances of resolution?

A

Tissue with good capacity to repair, good vascular supply, injurious agent easily removed

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28
Q

What is supparation?

A

A collection of pus forming (abscess)

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29
Q

What forms when pus is walled off?

A

Empyema

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30
Q

What is pus described as?

A

A sea of neutrophils

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31
Q

What does pus not have and how is it treated?

A

No blood supply so it has to be drained

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32
Q

When does organisation occur?

A

If the injury produces a lot of necrosis or fibrin that isn’t easily cleared

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33
Q

What type of injury usually results in organisation?

A

When damage goes beyond the basement membrane

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34
Q

What are injuries where the basement membrane is intact known as?

A

Abrasions and erosions

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35
Q

What is the common response to inflammation in all tissues?

A

Formation of granulation tissue

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36
Q

What does scarring/fibrosis result in?

A

Loss of function

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37
Q

What do different forms of repair show on an MI autopsy?

A

Neutrophils (recent), granulation tissue (1-2 weeks), further scarring (6+ weeks)

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38
Q

What signifies acute inflammation?

A

Neutrophils (anything else is chronic)

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39
Q

What is chronic inflammation NOT related with?

A

no acute inflammation needed, not related to time or severity

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40
Q

When is chronic inflammation favoured?

A

Supparation, persistence of injury, infectious injury, autoimmune injury

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41
Q

What are granulomas?

A

Groups of macrophages joined together to form one big multi nucleated cells

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42
Q

When do granulomas usually form?

A

Foreign bodies, parasite/worms, eggs, mycobacterium

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43
Q

What do TB granulomas show?

A

Cheesy necrosis

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44
Q

What are some signs of dying cells?

A

Shrink, become red, nucleus shrinks and darkens, marginal contraction bands appear, also vascular changes occur

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45
Q

In necrosis, what are dead cells mopped up by?

A

Neutrophils

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46
Q

What are the two types of necrosis?

A

Caseous and liquefactive

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47
Q

What are neutrophils replaced by in necrosis and what does this cause?

A

Macrophages, a yellow appearance

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48
Q

In terms of adaptation and growth, what does an altered stimulus result in?

A

Metaplasia

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49
Q

In terms of adaptation and growth, what does decreased demand result in?

A

Atrophy

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50
Q

In terms of adaptation and growth, what does increased demand result in?

A

Hyperplasia and hypertrophy

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51
Q

What is hyperplasia?

A

Increase in number of cells

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52
Q

What is hypertrophy?

A

Increase in cell size

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53
Q

What other adaptations can take place when there is increased demand?

A

increased growth factor production, produce more growth factor receptors

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54
Q

What are growth factor receptors?

A

7 transmembrane GPCRs and receptors with or without tyrosine kinase

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55
Q

What are the stages of the cell cycle controlled by?

A

a series of CDKs that activate each other and other enzymes in a stepwise fashion

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56
Q

How are CDKs activated?

A

By a specific cyclin

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57
Q

What happens in G1?

A

Protein synthesis and growth

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58
Q

What CDK is activated in G1 and how?

A

CDK4 by cyclin D

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59
Q

What does CDK4 do?

A

Phosphorylates the Rb protein

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60
Q

What is the Rb protein normally bound to and what does this do?

A

Normally bound to E2F which kicks off cell division but Rb blocks it so there is no cell division

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61
Q

What does phosphorylation of Rb do?

A

It no longer binds to E2F so cell division can occur

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62
Q

What happens in the S phase?

A

DNA replication

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63
Q

What does E2F do in the S phase?

A

Initiates DNA replication and increases cyclin A

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64
Q

What is activated in the S phase and how?

A

CDK2 by cyclin A

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65
Q

What does CDK2 do?

A

Promotes DNA replication

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66
Q

What should cells have by the end of the S phase?

A

2 copies of the genome

67
Q

What happens in G2?

A

More growth and protein synthesis

68
Q

What happens at the end of G2?

A

The main checkpoint involving p53

69
Q

What are telomeres?

A

Chromosomes are capped to provide protection and stop chromosome ends from degradation and fusing. This consists of TTAGGG repeats

70
Q

What must there be for hyperplasia to occur?

A

An external stimulus, hyperplasia will regress with withdrawal of this

71
Q

What are some physiological causes of hyperplasia?

A

Puberty, pregnancy, compensatory after loss of tissue

72
Q

What are pathological causes of hyperplasia?

A

Hormonally induced or infection (lymph nodes)

73
Q

What is hyperplasia tissue at risk for?

A

CANCER- particularly endometrial

74
Q

What are physiological causes of atrophy?

A

Hormonal, uterus, embryological structures

75
Q

How do cells atrophy?

A

Protein degradation and digested in lysosome

76
Q

What hormones oppose atrophy?

A

insulin

77
Q

what hormones promote atrophy?

A

glucocorticoids and thyroid hormones

78
Q

What are pathological causes of atrophy?

A

Pressure, blocked blood supply, inadequate nutrition, loss of innervation, decreased workload

79
Q

What does hypertrophy often occur in response to?

A

Mechanical stress

80
Q

Can necrosis ever be good?

A

No- it is always pathological

81
Q

Does necrosis require energy?

A

No

82
Q

What are some features of coagulative necrosis?

A

Preserved cell outline and dead cells enzymatically consumed

83
Q

What type of necrosis is most common?

A

Coagulative

84
Q

When is coagulative necrosis seen a lot

A

In the heart post MI

85
Q

What are some features of liquefactive necrosis?

A

Liquid viscous mass with no cell structure, pus

86
Q

What is liquefactive necrosis associated with?

A

Bacterial and fungal infections

87
Q

What is the only type of necrosis in the brain?

A

Liquefactive

88
Q

What is caseous necrosis?

A

Granulomas out inflammation with necrosis?

89
Q

When there is caseous necrosis and granulomas what could this be and what should you do?

A

Probably TB- ask for culture, PCR, Zeihl neilson stain

90
Q

What is apoptosis?

A

Programmed cell death in response to specific signals. Requires ATP.

91
Q

What are some physiological causes of apoptosis?

A

Growth, we need cells to die off, removal of self reactive lymphocytes

92
Q

What are pathological causes of apoptosis?

A

Response to injury, radiation, chemotherapy, viral infections or cancer, transplant rejection

93
Q

What do all mechanisms of apoptosis rely on?

A

Activating caspases

94
Q

What initiates the extrinsic pathway?

A

Death receptors e.g. TNF or Fas

95
Q

When is Fas used in apoptosis?

A

Self recognition and apoptosis in lymphocytes

96
Q

When is TNF used in apoptosis?

A

Indices apoptosis in inflammatory conditions

97
Q

What type of pathway is the intrinsic pathway?

A

A mitochondrial pathway involving a balance between anti and pro apoptotic proteins

98
Q

What blocks anti-apoptotic pathways and what does this cause?

A

Bac/Bax- causes pro apoptotic proteins to punch holes in the mitochondrial membrane to increase permeability

99
Q

What does increased permeability of the mitochondrial membrane result in in the intrinsic apoptotic pathway?

A

Release of cytochrome c to stimulate caspases

100
Q

What can too much apoptosis cause?

A

Neurodegenerative diseases

101
Q

What can too little apoptosis result in?

A

Cancers and autoimmune disease

102
Q

What is the morphology of apoptosis?

A

Cells shrink, chromatin condenses the nucleus, cytoplasm breaks up and macrophages digest the debris

103
Q

What is cancer?

A

Uncontrolled cell proliferation and growth that can invade other tissues

104
Q

What is a tumour?

A

a descriptive term- can be benign or malignant, inflammatory or a foreign body

105
Q

What is a neoplasm?

A

New growth not in response to a stimulus

106
Q

Where can neoplasms come from?

A

Any cell or organ (common in epithelium)

107
Q

What do malignant tumours have?

A

Metastatic potential

108
Q

What is classed as metastases in epithelial cells?

A

Once the mass has passed the basement membrane

109
Q

What is metaplasia?

A

A reversible change from one mature cell type to another

110
Q

What can metaplasia be in response to?

A

Cytokines, but usually in response to an injurious or noxious stimulus

111
Q

What type of cell is commonly changed in response to injury?

A

Squamous epithelium

112
Q

What is the relationship between metaplastic tissue and cancer?

A

Metaplastic tissue is an at risk site for cancer but doesn’t always become cancer

113
Q

What is dysplasia?

A

Disordered growth in abnormal cells not in response to a stimulus

114
Q

How is dysplasia graded?

A

From low to high (risk of becoming cancer)

115
Q

What is carcinoma in situ?

A

The very last stage before dysplasia crosses the epithelium and becomes cancer i.e. high grade dysplasia

116
Q

What do oncogenes do?

A

Promote growth of cancer cells

117
Q

What do tumour suppressors do?

A

Turn off any inhibition to grow

118
Q

What are examples of an inherited predisposition to cancer?

A

BRCA gene (one copy needed to increase risk), Rb mutation in children increases chance of retinoblastoma and familial adenomatous polyposis causes bowel cancer before 50

119
Q

What are some examples of chemicals which increase risk of cancer?

A

Smoking, fungus, chemical dye, food preservatives, arsenic

120
Q

How does radiation increase risk of cancer?

A

Causes the formation of pyramidine dimers in DNA- with repeated exposure this cannot be repaired

121
Q

What other factors can increase risk of cancer?

A

Viruses (HPV), chronic inflammation, constant catheterisation, obesity

122
Q

What are the Weinberg hallmarks of cancer?

A

Increased growth signals, removed growth suppression, avoiding apoptosis, achieve immortality, become invasive, have own blood supply

123
Q

What are common sites of metastases in general?

A

Liver and local lymph nodes

124
Q

What is angiogenesis?

A

Tumours successfully developing their own blood supply

125
Q

As well as oncogenes and tumour suppressors, what other factors can contribute to cancer?

A

Apoptosis (stopping cell death) and breaking spell checker

126
Q

What does breaking the spell checker do?

A

Allows progression through the cell cycle even with mistakes

127
Q

What is the first mutation in cancer known as?

A

Initiation

128
Q

What is needed for cells to proliferate and become cancer?

A

At least another mutation after the first one

129
Q

What is the further accumulation of mutations, resulting in a pre-malignant phase known as?

A

Promotion

130
Q

What is lots of accumulation of cells to become malignant known as?

A

Progression

131
Q

What is cachexia?

A

Weight loss in cancer

132
Q

What are features of benign tumours?

A

Organised, smooth edges and surface, all looks the same, slow growing

133
Q

What are features of malignant tumours?

A

Not natural looking, irregular, infiltrating and destructive

134
Q

What are epithelial tumours known as?

A

Carcinomas

135
Q

What are benign and malignant glandular tumours known as?

A

Adenoma and adenocarcinoma

136
Q

What are benign and malignant squamous cell tumours known as?

A

Papillomas and squamous cell carcinomas

137
Q

What are transitional/uroepithelial cell carcinomas?

A

Bladder tumours

138
Q

What is mesenchyme?

A

Benign tumour of connective tissue

139
Q

What are malignant tumours of connective tissue known as?

A

Sarcomas

140
Q

What are benign and malignant tumours in fat connective tissue?

A

Lipoma and liposarcoma

141
Q

What are benign and malignant tumours in bone connective tissue?

A

Osteoma and osteosarcoma

142
Q

Who and where do osteosarcomas occur in?

A

Rare- in long bones of children

143
Q

What are benign and malignant tumours in cartilage connective tissue?

A

Endroma and chondrosarcoma

144
Q

What is leiomyoma?

A

Benign tumour of the smooth muscle- one of the commonest tumours in the body

145
Q

What is a leiomyosarcoma?

A

Malignant tumour of the smooth muscle- very rare

146
Q

What are benign and malignant tumours in blood vessel connective tissue?

A

Haemangioma and angiosarcoma

147
Q

What is melanoma?

A

Malignant skin tumour

148
Q

What are blood tumours and what are examples?

A

Always malignant e.g. lymphomas or leukaemia

149
Q

What does the stage of a tumour describe?

A

How far it has grown- often depends on the site

150
Q

What does Tis stand for?

A

Tumour in situ- within the lamina propria and not broken through the muscularis mucosae

151
Q

What does T1 mean?

A

Invaded the submucosa but not the muscularis externa

152
Q

What does T2 mean?

A

Invaded the muscularis propria but not beyond it

153
Q

What does T3 mean?

A

Invaded beyond the muscularis propria and into subserosa

154
Q

What does T4 mean?

A

Directly invaded other organs or perforated the visceral peritoneum

155
Q

What does NX mean?

A

Lymph nodes cannot be assessed

156
Q

What does N0 mean?

A

No regional lymph node metastases

157
Q

What does N1 mean?

A

Metastases to 1-3 nearby lymph nodes

158
Q

What does N2 mean?

A

Metastases to 4+ nearby lymph nodes

159
Q

What does M0 mean?

A

No metastases to distant tissues

160
Q

What does M1 mean?

A

Metastases to distal tissues including distal lymph nodes

161
Q

What does the grade of a tumour convey?

A

Concept of differentiation

162
Q

What suggests low grade tumours?

A

Well differentiated- looks like it should

163
Q

What suggests high grade tumours?

A

Poorly differentiated- difficult to tell what type of cell it came from

Principles (11 decks)

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