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Biomedical Sciences > Cell And Tissue Pathology > Flashcards

Cell And Tissue Pathology Flashcards

1
Q

Which types of cells are present in granulomatus inflammation?

A

Macrophages, T cells, epitheloid cells (large macrophages) and giant cells (fused macrophages)

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2
Q

What are the two types of granulomas?

A

Foreign body granules and immune granules

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3
Q

What is an epitheloid cell?

A

A macrophage with an abundant cytoplasm

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4
Q

What is a giant cell?

A

A multinucleated cell formed by fusion of active macrophages

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5
Q

What are the inciting agents of immune granulomas?

A

Persistent microbe or self antigen

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6
Q

How do immune granulomas form?

A

Macrophages activate T cells, which produce IL-2, which activate more T cells, which produce IFN-gamma which activates more macrophages. IL-4 or IFN-gamma transform macrophages into epitheloid and giant cells

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7
Q

What causes crohns disease?

A

Intestinal bacteria and possibly self antigens

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8
Q

What is the tissue reaction in crohns disease?

A

Occasional noncaseating granulomas form in the intestine wall

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9
Q

What are the 4 characteristics of inflammation?

A

Calor
Rubour
Dolor
Tumour

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10
Q

What are the 4 stages of inflammation?

A

Vascular response
Inflammation
Cell proliferation
Remodelling

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11
Q

What are 3 types of inflammatory muscle disease?

A

Temporal arteritis
Dermatomyositis
Polymyositis

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12
Q

Which arteries are affected by giant cell arteritis?

A

Temporal arteries
Opthalmic arteries
Vertebral arteries
Aorta

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13
Q

What is the pathogenesis of temporal arteritis?

A

T cell mediated immune response against vessel wall antigens
Cytokine production
Anti-endothelial cell antibodies and anti-smooth muscle cell antibodies - causative or consequence of?

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14
Q

What is the morphology of temporal arteritis?

A

Intimal thickening that reduces laminal diameter

Granulomas form on internal elastic lamina causing elastic lamina fragmentation

Inflammatory lesions are focally distributed

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15
Q

What are the symptoms of temporal arteritis?

A

Headache, fever, fatigue, weight loss, ocular symptoms

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16
Q

What is the pathogenesis of dermatomyositis?

A

Components of the MAC are found in the capillary beds in muscle and skin

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17
Q

What are the symptoms of dermatomyositis?

A 
Rash
Proximal muscle weakness
Myalgia
Dysphagia
Elevated serum creatine kinase levels
Interstitial lung disease
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18
Q

What is the pathogenesis of polymyositis?

A

CD8+ cytotoxic T cells infiltrate muscle cells

Vascular injury has no major role

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19
Q

What are the symptoms of polymyositis?

A

Proximal muscle weakness

No cutaneous features

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20
Q

What are the 2 types of inflammatory bowl disease? What are the differences between them?

A

Ulcerative colitis and crohns disease. Ulcerative colitis is characterised by continuous lesions of the bowl whereas crohns is characterised by skip lesions and mouth ulcers

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21
Q

Which diseases are associated with inflammatory bowl disease?

A

Ankylosing spondylitis and uveitis

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22
Q

Ulcerative colitis increases the risk of which two diseases?

A

Anaemia and bowel carcinoma

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23
Q

What causes gastric ulceration?

A

Excess stomach acid

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24
Q

Which bacteria is associated with gastric ulceration?

A

H. Pylori

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25
Q

How is gastric ulceration treated?

A

Proton pump inhibitors and antibiotics if have H. Pylori infection

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26
Q

Which tracts are affected by cystic fibrosis?

A

Respiratory tract
GI tract
Reproductive tract

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27
Q

What are the symptoms of CF?

A

Finger clubbing

Cough

Recurrent lung infections

Reduced FEV1

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28
Q

Where is the CFTR gene found?

A

7q31.2

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29
Q

What is the most common CFTR mutation?

A

DeltaF508 (60 %)

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30
Q

What inheritance is associated with Cystic fibrosis?

A

Autosomal recessive

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31
Q

How common is cystic fibrosis?

A

1 in 2000 have CF
1 in 20 are carriers
(In caucasian population)

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32
Q

What is the CFTR structure?

A 
2 transmembrane domains (containing 6 alpha  helices)
2 nucleotide binding domains
R domain (has protein kinase A and C phosphorylation sites)
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33
Q

How does the CFTR channel work?

A 
Agonist binds epithelial cells
Increase in cAMP
Activates protein kinase A
Phosphorylates R domain using ATP
Channel opens
Cl out of cell
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34
Q

What are ENaC channels responsible for?

A

Na uptake into cells

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35
Q

What is the relationship between CFTR protein and ENaC protein in most parts of the body?

A

Normally functioning CFTR inhibits ENaC uptake of Na into cells

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36
Q

Which tissue is the exception in terms of CFTR and ENaC?

A

Sweat glands. CFTR pumps Cl into cells. In cystic fibrosis patients Cl is not pumped into cells and neither is Na, leading to salty sweat

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37
Q

What is a class 1 CFTR mutation?

A

No CFTR is trafficked to cell surface

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38
Q

What is a class 2 CFTR mutation?

A

DeltaF508 mutation

Some CFTR is trafficked to the cell membrane but none is functional

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39
Q

What is a class 3 CFTR mutation?

A

Normal amount of CFTR at cell surface

None is functional

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40
Q

What is a class 4 CFTR mutation?

A

Normal no of CFTR at cell surface

Some is functional

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41
Q

What is a class 5 CFTR mutation?

A

Some CFTR is trafficked to cell surface

All is functional

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42
Q

What is the chaperone protein that tried to fold CFTR?

A

HSP40

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43
Q

What are the treatments for CF symptoms?

A 
Antibiotics
Bronchodilators
Physiotherapy
DNAse
High calorie diet
Insulin
Lung transplant
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44
Q

What is VX-809

A

A corrector. It increases the no of CFTR molecules which get to the cell surface

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45
Q

What is ivacaftor?

A

Potentiator. Increases CFTR channel opening

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46
Q

What is ataluren?

A

Ribosomal skipping agent. Allows stop codons to be skipped

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47
Q

What treatments are available to address Cl transport?

A

VX-809
Ivacaftor
Ataluren

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48
Q

What is a sarcoma?

A

Tumour of connective tissue or its mesenchymal precursor

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49
Q

What is atrophy?

A

Degeneration

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50
Q

What is dysplasia?

A

Cells that look abnormal but are not cancerous

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51
Q

What is metaplasia?

A

Reversible change where one cell type is replaced by another

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52
Q

What is pleomorphism?

A

Unusual nuclei

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53
Q

What is an adenoma?

A

Benign tumour in the glandular epithelia

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54
Q

What 2 component tissues are all tumours made up of?

A

Parenchyma and stroma

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55
Q

What is a papilloma?

A

Benign epithelial tumour which forms a finger-like or warty projection

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56
Q

What is a cystadenoma?

A

Benign epithelial tumour which forms hollow masses

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57
Q

What is a papillary cystadenoma?

A

Papillary pattern protrudes into a cyst-like space

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58
Q

What is the difference between a fibroma and a fibrosarcoma?

A

A fibroma is a benign fibroblast tumour. A fibrosarcoma is a malignant fibroblast tumour.

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59
Q

What is neoplasia?

A

Uncontrolled cell growth

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60
Q

What is anaplasia?

A

Lack of differentiation

61
Q

What do the T N and M stand for in TNM staging?

A 
T = extent of the primary tumour
N = is there any regional lymph node metastasis
M = is there distant metastasis
62
Q

What is karyolysis?

A

Loss of dna

63
Q

What is pyknosis?

A

Nuclear shrinkage

64
Q

What is karyohexis?

A

Nuclear fragmentation and disappearance

65
Q

What are common causes of panceatitis?

A

Alcohol
Gallstones
Infection
Genetic

66
Q

What are rare causes of pancreatitis?

A

Trauma
Corticosteroids
Hyperlipidaemia

67
Q

How does alcohol causes pancreatitis?

A

It destroys acinar cells

68
Q

How do gallstones causes pancreatitis?

A

If they move into the pancreas

69
Q

What is a symptom of gallstones?

A

Elevated AST levels

70
Q

How are gallstones treated?

A

By removal of the gallbladder

71
Q

What are complications associated with pancreatitis?

A

Infection
Pancreatic necrosis
Pancreatic cysts

72
Q

How is pancreatitis treated?

A

Pain relief, IV fluids, nil by mouth. Treat the complications antibiotics for infection, operative resection for pancreatic necrosis, drainage of pancreatic cysts

73
Q

What genes are responsible for hereditary pancreatitis?

A 
PRSS1 a cationic trypsin gene
SPINK1 a pancreatic trypsin inhibitor
CTRC a chymotrypsin c gene
CASR a g protein coupled receptor
CFTR a chloride ion channel gene
74
Q

Why does the PRSS1 mutation cause pancreatitis?

A

Trypsin is overactive and causes autodigestion

75
Q

What is trypsin?

A

A protease

76
Q

How do SPINK1 and CTRC mutations causes pancreatitis?

A

Disrupt trypsin inhibition leading to autodigestion

77
Q

What does cathepsin B do in the pancreas?

A

Turns trypsinogen into trypsin

78
Q

What is CASR?

A

An extracellular calcium sensing receptor

79
Q

What role does calcium play in the pancreas?

A

It prevents premature zymogen activation

80
Q

How do CFTR mutations cause pancreatitis?

A

Distuption in bicarbonate transport (not chloride)

81
Q

What are symptoms of pancreatitis?

A 
Elevated amylase levels
Abdominal pain
Fever
Nausea
Diarrhoea
82
Q

What causes gallstones?

A

An imbalance of bile salts and cholesterol

83
Q

What do acinar cells do?

A

Store, synthesise, secrete digestive enzymes (exocrine pancreas)

84
Q

What cells make up the islets of langerhans?

A

Alpha, beta, delta and pp cells

85
Q

What do alpha cells secrete?

A

Glucagon

86
Q

What does glucagon do?

A

Converts glycogen to glucose

87
Q

What do beta cells do?

A

Secrete insulin and amylin

88
Q

What does insulin do?

A

Promotes uptake of glucose by liver, fat and muscle cells and converts glucose to glycogen

89
Q

What does amylin do?

A

Promotes satiety

90
Q

What do delta cells secrete?

A

Somatostatin

91
Q

What does somatostatin do?

A

Inhibits release of growth hormone

92
Q

What do pp cells secrete?

A

Pancreatic polypeptide

93
Q

What does pancreatic polypeptide do?

A

Regulates pancreas secretions

94
Q

What is type 1 diabetes?

A

Where T cells attack beta cells in the pancreas

95
Q

What is type 2 diabetes?

A

Reduced levels of insulin are produced or insulin receptors on fat, liver and muscle cells do not work properly so these cells do not take up enough glucose

96
Q

How is insulin synthesised?

A

As pre pro insulin

97
Q

How many amino acids make up insulin?

A

51

98
Q

What chains make up insulin?

A

A B C

99
Q

What happens to the C chain on insulin?

A

Removed in the golgi

100
Q

Name two types of type 1 diabetes

A

Familial hyper pro insulinaemia

Permanent neonatal diabetes mellitus

101
Q

Why do diabetics get foot ulcers?

A

Neuropathy

Impairment of wound healing - blood vessels narrow due to high blood glucose levels

Infection (compromised immune system)

102
Q

What gene is linked to ankylosing spondylitis?

A

HLA-B27*05

103
Q

Is ankylosing spondylitis more common in men or women?

A

Men

104
Q

Are autoimmune diseases more common in men or women?

A

Women

105
Q

What is the median age of onset for ankylosing spondylitis?

A

23

106
Q

What causes the bamboo spine seen in akylosing spondylitis?

A

Damage to the sacro-ileal joint

107
Q

Which type of MHC is HLA-B27 a variant of?

A

MHC 1

108
Q

What is the function of MHC 1?

A

To present cytosolic peptides to CD8+ T cells

109
Q

What is the median age of onset for ankylosing spondylitis?

A

23

110
Q

What causes the bamboo spine seen in akylosing spondylitis?

A

Damage to the sacro-ileal joint

111
Q

Which type of MHC is HLA-B27 a variant of?

A

MHC 1

112
Q

What is the function of MHC 1?

A

To present cytosolic peptides to CD8+ T cells

113
Q

What complications are associated with ankylosing spodylitis?

A

Uveitis
Enthesitis
IBD

114
Q

What are the 4 explanations for why HLA-B27 is linked to AS?

A

Molecular mimicry

Unfolded protein response (misfolding of B27 heavy chain)

Inappropriate B27 homodimers forming on the cell surface

Deposition of Beta 2 m in joints following disassociation from HLA-B27

115
Q

What suggests HLA-B27 may not be the sole factor in AS?

A

5% of AS patients do not have the HLA-B27 gene

HLA-B2705 is associated with AS but HLA-B2709 is not

HLA-B27 is expressed on all nucleated cells but AS has specific tissue involvement

116
Q

What other genes are linked to AS?

A

ERAP (antigen processing enzyme)

IL23R (cytokine receptor which causes CD4+ t cells to differentiate into inflammatory TH17 cells

117
Q

Which gene is associated with rheumatoid arthritis?

A

HLA-DR4

118
Q

On which chromosome are MHC genes found?

A

Chromosome 6

119
Q

What job do MHC class 2 molecules have?

A

The present exogenous peptides to CD4+ helper T cells

120
Q

What are the tests for rheumatoid arthritis?

A

X ray

Blood tests

121
Q

What are the blood tests for rheumatoid arthritis?

A 
Anaemia
Elevated ESR
Elevated gamma globulin
Elevated C reactive protein
High titre rheumatoid factor
122
Q

What are the treatments for rheumatoid arthritis?

A

NSAIDs
DMARDs (methotrexate targets rapidly dividing cells)
Corticosteroids (prednisolonr inhibit NFkb)
Monoclonal antibodies (against IL1 (anakinra) and TNF alpha)

123
Q

Which molecules help WBC leave blood vessels?

A

Selectins

124
Q

What are the 4 stages of a WBC leaving a blood vessel?

A

Tethering and rolling
Activation
Firm adhesion
Transmigration

125
Q

What is aneuploidy?

A

Unusual chromosome number

126
Q

What does euploid mean?

A

Has normal numbers of chromosomes

127
Q

What are the stages of the cell cycle?

A

G1, S, G2, M

128
Q

Where are the checkpoints in the cell cycle?

A 
G1 check (entering S phase, is environment okay)
G2 check (entering m phase, is dna replicated, is environment okay)
Metaphase check (exit m, are chromosomes attached to spindle)
129
Q

What controls the cell cycle?

A

Cyclins

130
Q

When in the cell cycle do cyclin A levels rise?

A

During the s phase

131
Q

When in the cell cycle do cyclin b levels rise?

A

During the m phase

132
Q

When in the cell cycle do cyclin E levels rise?

A

After the r point and collapse during the s phase

133
Q

When do cyclin D levels rise?

A

During the G1 phase

134
Q

What is anoikis?

A

Apoptosis due to incorrect cell/ECM attachment

135
Q

Why is epithelial to mesenchymal transition required for metastasis?

A

Epithelial cells cannot migrate

Mesenchymal cells can migrate

136
Q

What are the local affects of interleukin 1B?

A

Endothelium activation (expresses e-selectin and ICAM1)
Leukocyte activation
Destroys local tissue

137
Q

What are the local affects of TNF-alpha?

A

Activates endothelium and makes endothelium more permeable. This causes migration of immune cells, IgG, complement. Also allows fluid drainage to lymph nodes

138
Q

What are the local affects of interleukin 6?

A

Activates lymphocytes

Increases antibody production

139
Q

What is the role of CXCL8?

A

Chemotactic. Recruits neutrophils, basophils and T cells

140
Q

What is the role of IL-12?

A

Activates NK cells

Induces differentiation of CD4 T cells to TH1 cells

141
Q

What is expressed on activated endothelium?

A

E-selectin

ICAM-1

142
Q

How do leukocytes bind to e-selectin?

A

S-LEX

143
Q

How do leukocytes bind to ICAM-1?

A

LFA-1

144
Q

What is the function of histamine?

A

Dilates blood vessels

145
Q

How is histamine synthesised?

A

From histidine via histidine decarboxylase

146
Q

Where is histamine found?

A

In secretory vesicles bound to proteoglycan

147
Q

How is CFTR activated?

A

Adrenergic receptor activity

148
Q

How is CFTR inhibited?

A

LPA receptor activity

149
Q

Cystic fibrosis and diabetes

A

Mucus causes scarring of pancreas = less insulin produced

Insulin resistance

Biomedical Sciences (6 decks)

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