Pathology Flashcards
(131 cards)
1
Q
What does VINDICATE stand for?
A
- Vascular
- Infectious/Inflammatory
- Neoplastic
- Drugs/toxins
- Interventions/Iatrogenic
- Congenital/developmental
- Autoimmune
- Trauma
- Endocrine/metabolic
2
Q
What are the main categories for response to injury?
A
- vascular changes
- cellular changes
- chemical mediators
- morphological patterns
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
4
Q
What are the cellular changes that can happen in response to injury?
A
stasis whit cell margination rollin adhesions migration
5
Q
What does vasodilation do to normal blood flow?
A
causes white cell margination as blood no longer flows centrally
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
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
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
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
10
Q
What is chemotaxis?
A
cells following a chemical gradient and moving along it
11
Q
What are the steps of phagocytosis?
A
- recognition and attachment
- engulfment
- killing and degradation
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)
13
Q
What happens in the engulfment has of phagocytosis?
A
- arms are pseudopods
- phagosome forms and joins with lysosome to make phagolysosome
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)
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
16
Q
What cell is also called a polymorph?
A
neutrophil due to many lobes
these are granulocytes with phagocytic and cytotoxic abilities
17
Q
What is the major cell involved in acute inflammation?
A
neutrophil
18
Q
What are the factors that determine what happens after acute inflammation?
A
- site of injury
- type of injury
- duration of injury
19
Q
What is resolution?
A
- complete restoration of tissue to normal after removal of inflammatory components
- minimal cell death
20
Q
What does the tissue need to have resolution after inflammation?
A
- fast delivery of white cells
- removal of injurious agent
21
Q
What is suppuration?
A
pus neutrophils bacteria inflammatory debris abcsess
22
Q
When does organisation happen?
A
if there is necrosis, fibrin, poor blood supply or damage beyond the basement membrane
23
Q
How do erosions and abrasions heal?
A
there is an intact basement membrane so it will heal with complete resolution
24
Q
What is granulation tissue?
A
hole is infiltration by capillaries then myofibroblasts which deposit collagen and smooth muscle cells
25
What does scarring and fibrosis cause?
patch job with loss of function
| skin will be less mobile and stretchy
26
What happens when the liver gets overwhelmed by fibrosis?
cirrhosis leading to liver failure
27
Who is chronic inflammation favoured?
suppuration, scarring, empyema, persistence of injury so foreign material, infectious agent so virus or autoimmune such as transplant rejection
28
What are the cells of chronic inflammation?
- lymphocytes (small round blue cell)
| - macrophages
29
What are granulomas?
balls of macrophages including foreign bodies that can be endogenous (keratin, bone, crystals) or exogenous (talc, asbestos, suture) eg TB mycobacterium
30
What is caseous necrosis from?
tuberculous granulomas
31
What happens when they is no ATP?
increased K+ (causes swelling), Ca2+ pump fails so increased Ca2+
32
What does increased Ca2+ cause?
- ATPase
- phopholipase (membrane damage)
- proteases (membrane and cytoskeleton damage)
- endonuclease (DNA damage/breakdown)
- mitochondrial permeability (release pro death factors)
33
After how long does cell death occur?
20 minutes
34
What happens when cell begin to die?
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
35
What is coagulative necrosis and where does it occur?
happens in cardiac tissue
| ghost outline before neutrophils can remove them
36
What is restitution?
gradual progressive scarring as macrophages are replaced by fibroblasts that lay down collagen, this is complete at 6 weeks
37
What is hyperplasia?
enlargement of an organ caused by an increase in reproduction rate of cells
38
What is hypertrophy?
enlargement of an organ due to an increased size of cell
39
What is atrophy?
decrease in the size of cell
40
What is metaplasia?
reversible transformation of one differentiated cell type to another
41
What is cell division caused by?
production of more growth factors or more growth factor receptors
42
What actions can growth receptors have?
- intrinsic tyrosine kinase activity
- 7 transmembrane G-protein-coupled receptors
- receptors without intrinsic kinase activity
43
What controls each stage of the cell cycle?
cyclin dependent kinases which are activated by cyclins A, B, D and E
44
What happens in G1?
- cell gets bigger with increased protein synthesis
- CDK4 activated by cyclin D
- CDK4 phosphorylates Rb (retinoblastoma protein)
45
What does Rb do in G1?
binds to E2F to stop cell division but when it is phosphorlyated by CDK4 cell division occurs readily
46
What happens in the synthesis phase?
- 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
47
What happens in G2?
second growth phase so cell gets bigger and there is more protein synthesis
48
What does p53 do?
checks cell for mistakes, pauses, repairs and then progressed or causes the cell to commit suicide
(cancer avoids these checks)
49
What are telomeres?
TTAGGG repeats at the end of chromosomes that limit divisions
50
What causes hyperplasia?
- an external stimulus which will stop when stimulus does
| - can be physiological or pathological (by hormones)
51
What is hyperplastic tissue at risk of?
development of cancer
52
What is the mechanism of atrophy?
- reduced cellular component
- protein degradation
- digested in lysosomes
53
What substances increase or decrease atrophy?
glucocorticoids and thyroid increase atrophy
| insulin decreases atrophy
54
What is cancer?
uncontrolled cell proliferation and growth that can invade other tissues
55
What is neoplasia?
new growth that is not is response to a stimulus- it can be benign, premalignant or malignant
56
Where does malignancy occur in relation to the epithelium?
the malignancy goes beyond the basement membrane
57
What is metaplasia?
the reversible change from one mature cell type to another mature cell type
58
How does metaplasia occur?
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
What does thermal or chemical injury do to the bronchial epithelial surface?
changes it to squamous epithelium
60
What is the epithelium in the bladder?
transitional but changes to squamous with injury
61
What is metaplastic tissue at risk of?
becoming cancerous
62
What does hyperplasia need to occur?
can be autonomous and not need a stimulus
63
What is dysplasia?
disordered growth with abnormal cells where growth is not in response to a stimulus and there is no invasion beyond the basement membrane
64
What is carcinoma in situ?
dysplasia affecting the whole epithelium which is the last stage before invasion
65
What are the Weinberg hallmarks of cancer?
- metastasis
- replicative immortality
- angiogenesis
- resist cell death
- sustained proliferative signalling
- evade growth suppressors
66
What is BRCA?
mutations in a tumour suppressor gene
67
What is the double hit hypothesis?
one working gene is enough and two are needed to be faulty for a problem to occur
68
What are initiators?
initiators cause long lasting genetic damage but must be followed by a promoter
69
What are promoters?
there require initiators to cause damage
70
What cancers does smoking cause?
small cell lung
head and neck
bladder
cervical
71
What are aflatoxins?
cause a p53 mutation
72
What does radiation cause?
pyrimidine dimers in DNA
73
How can chronic inflammation cause cancer?
causes lymphomas as so much replication can cause errors
74
What must a cancer cell do to sustain growth signals?
- 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
What must a cancer cell do to have a loss of growth inhibition?
- stops tumour suppressors
| - stopping p53 checking for mistakes
76
How does p53 check for mistakes?
- senses DNA abnormality at G1
- pauses cell cycle
- increases levels of p21 (CDK inhibitors)
- repair or apoptosis
77
How do cancer cells have unlimited replicate potential?
reactivate telomerase to get more telomeres
78
How do cancer cells resist apoptosis?
bcl-2 binds Bak/Bax so stops death
79
How do cancer cells induce angiogenesis?
upregulation of vascular endothelial growth factor
80
How do cancer cells evade inflammatory response?
over expression of PD-L1 which inhibits T cell proliferation
81
What does an inflammatory response do the cancer?
helps body fight it
82
How do cancer cells activate invasion and metastases?
chew up surrounding tissue
| increase expression of matrix metalloproteinases
83
What is atrophy?
physiological or pathological reduction in cell size
84
What is necrosis?
always pathological death that requires no energy
85
What is coagulative necrosis?
preserves cell outline and dead cells are consumed by enzymes eg cardiac muscle
86
What is liquefactive necrosis?
leaves no cell structure, pus, associated with localised infections eg in the brain
87
What is caseous necrosis?
TB, granulomas with central necrosis, ZN positive
88
What is apoptosis?
programmed cell death in response specific signals
requires energy
can be physiological
89
What is pathological apoptosis due to?
```
injury
vasodilation
chemotherapy
viral infection
cancer
```
90
What is the extrinsic pathway for apoptosis?
- death cell receptors initiated
- TNF or fas
- Fas recognises self
- TNF induces apoptosis with inflammation
91
What is the intrinsic pathway for apoptosis?
- mitochondrial
- anti-apoptic molecules removed form membrane
- these are replaced with Bax/Bak
- increased leakiness in mitochondria so caspases so cytochrome C
92
How does apoptosis occur?
- pyknosis
- chromatin condensation
- cytoplasmic blebs
- macrophages
93
What is cellularly ageing caused by?
- oxidative stress due to free radical damage
| - accumulation of metabolism by-products
94
What is a polymorph?
neutrophil
95
What is a monocyte/histiocyte?
macrophage
96
What is suppuration?
involves necrosis, phagocytosis, abscess and neutrophils but not lymphocytes
97
What steps of inflammation are the fibroblasts in?
the later stage
98
What does homogenous tissue look like?
one area that looks the same as another
99
What is the classification of encapsulated slow growing lesions?
benign
100
What does heterogenous tissue look like?
all areas look different and there is haemorrhage and necrosis
101
What is an ideal nucleus:cytoplasmic ratio?
a low ration is good and a high ratio is seen in malignancy
102
What does differentiation say about a cell?
well differentiated cells are normal and poorly differentiated cells can be malignant as they look nothing like they are supposed to
103
What is pleomorphism?
all cells look different
104
What is hyperchromasia?
is dark staining nuclei due to more DNA
105
What is mitoses?
a high mitotic count which is common in malignancy
106
What is a tumour of the epithelium called?
carcinoma
107
What is mesenchymal related to?
connective tissue
108
What is a tumour of the glands called?
adenoma or adenocarcinoma
109
What is a tumour of the squamous cells called?
papilloma or squamous cell carcinoma
110
What is a tumour of the bladder called?
transitional cell carcinoma
111
What is a tumour of the connective tissue called?
mesenchyme sarcomas
112
What is a tumour of the fat called?
lipoma or liposarcoma
113
What is a tumour of the bone called?
osteoma or osteosarcoma
114
What is a tumour of the cartilage called?
enchondroma or chondrosarcoma
115
What is a tumour of the skeletal muscle called?
rhabdomyoma or rhabdomyosarcoma
116
What is a tumour of the smooth muscle called?
leiomyoma or leiomyosarcoma
117
What is a tumour of the nerve called?
meurofribome or shwannoma is benign
| malignant peripheral nerve sheath tumour
118
What is a tumour of the vessels called?
haemangioma or angiosarcoma
119
What is a freckle?
ephelis
120
What is a mole?
naevus
121
What is a malignant lesion of the skin called?
melanoma (exception to the nomenclature rule)
122
What is the word for how far the cancer has spread?
stage
123
What is the word for how differentiated the cells are?
grade
well differentiated = low grade
poorly differentiated = high grade
124
What is cachexia?
weight loss in cancer due to tumour and TNF which increase metabolism
125
What are paraneoplastic syndromes?
result from the tumour but aren't directly related- can be due to increased Ca2+ or decreased Na+
126
What are examples of paraneoplastic syndromes?
osteoarthropathy
skin rash
fever (pyrogens)
pyrexia
127
Why are cancer patients susceptible to infection?
tumours can evade and suppress immune system
128
What is the difference between blood colts and thrombosis?
blood clots are extravascular
| thrombosis is intravascular
129
What are the features of the intrinsic coagulation cascade?
factor XII activation
| measured with PT
130
What are the features of the extrinsic coagulation cascade?
starts with tissue factor
| measured with APTT
131
What are the consequences of increased calcium ions?
```
ATPase
phospholipase
proteases
endonuclease
mitochondrial permeability
```
