Pathology Flashcards
(109 cards)
1
Q
what is a risk factor
A
social or individual factor which increases the risk of development of a disease
2
Q
what is aetiology
A
cause of a disease
3
Q
what is pathogenesis
A
sequence of events from a health state to a clinical disease
4
Q
what causes aging
A
- Genetic factors
- Environmental factors
- Manifestation of age related diseases
5
Q
For cell integrity what must be highly functioning?
A
- DNA
- Cell membrane
- Energy production
- Protein synthesis
6
Q
What is necrosis
A
Cell death that requires no energy
7
Q
Patterns of necrosis
A
- Coagulative- proteins coagulate to preserve the cell outline
- Colliquative- necrotic material becomes sofened and liquefied (PUS), no cell structure remains
- caseous- cheese like eg TB
- Gangerous- Cell death by necrosis then infection on top of that
- Fibrinoid- fibre deposition
- Fat necrosis- fat cells die often due to trauma
8
Q
what is apoptosis
A
cell death that requires energy- programmed cell death due to a stimuli. May be physiological or pathological. No inflammation.
9
Q
causes of apoptosis
A
withdrawal of growth factors loss of matrix attachment viruses free radicals ionising radiation DNA damage (AIDs and neurodegenerative disorders increase apoptosis) (Neoplasia and auto-immune diseases decrease apoptosis)
10
Q
what is p53
A
like a spell checker at G1 of the cell cycle, if a mistake is found the cell cycle is paused and p53 repairs it, if it cannot be fixed then p53 stimulates apoptosis
11
Q
what causes cell aging
A
a progressive decline in the proliferation capacity and lifespan of the cell
12
Q
biochemical and structural changes in cell aging
A
- mitochondrial abnormalities
- reduced ER
- disorted golgi apparatus
- accumualtion of lipofusion
- advanced glycation products
- abnormally folded proteins
- reduced capacity to undertake key biochemical processes
13
Q
what happens to biochemical processes with cell aging?
A
they become less effective; decreased oxidative phosphorylation, decreased synthesis of key nucleic acids and proteins/enzymes and reduced capacity for nutrient uptake
14
Q
What are telomeres
A
RNA- protein complex (DNA caps at chromosome ends TTAGGG)
15
Q
What are the functions of teleomeres?
A
- ensure complete replication of the genome
2. protect coding sequences at the chromosome ends from damage
16
Q
What is telomere shortening
A
incomplete replication of chromosome ends which leds to cell cycle arrest
17
Q
telomere activity is greater in germ cells than in stem cells, why?
A
there is no telomere activity in somatic cells
18
Q
what type of cells are suceptable to DNA damage?
A
- dividing cells
- abnormal sequence inherited by daughter cells and so is recognised as normal, so DNA repair mechanisms are by passed
- permenant cells are most resistant
19
Q
what cells are highly succeptable to abnormalities
A
skin and hair cells as they have a high turn over
20
Q
what cells are at low risk of abnormalities
A
cardiac and adult neurone cells as they have a low turn over
21
Q
what can cause loss of membrane integrity
A
- failure of ion pumps
- disruption of membrane
- alteration of lipids
- cross linking of membrane proteins
22
Q
what is a metabolic disorder
A
a defective enzyme leading to an increased substrate metabolite and a decreased product metabolism and therefore the rest of the molecules in the pathway are also decreased (may be inherited or acquired)
23
Q
causes of an inherited metabolic disorder
A
autosomal recessive
24
Q
Acute inflammation
A
neutrophils
vascular phase- dilatation and increased permability of blood vessels
exudative and cellular phase- fluid and cells escape from the permeabily venules
neutrophil accumulation in extracellular space
25
Intermediate inflammation
eosinophils
Acute--> Chronic
the agent causing inflammation isnt removed, recurrent episodes of acute inflammation
26
Chronic inflammation
macrophages, plasma cells, lymphocytes, fibroblasts
| subsequent and ofter prolonged tissue reactions follow initial response. recurrance of acute inflam may lead to chronic
27
characteristics of inflammation
redness (erythema)- due to dilatation of the of blood vessels
Heat (calor)- increased blood flow
swelling- accumulation of fluid in extravascular space
pain- distortion of tissues
loss of function- inhibited by pain of swelling
28
what is the exudate fluid
a protein containing fluid (including immunoglobins)
29
What is fribrinogen
fibrin on contact with ECM, acutely inflammed organs are commonly covered in fibrin
30
neutrophil inflammation cascade
1. margination
2. adhesion
3. chemotaxis
4. chemical mediators
5. recognition of micro-organisms
6. suppuration
7. abscess formation
8. resolution
31
What occurs in the margination phase?
loss of intravascular fluid and increased plasma viscosity, allowing neutrolphils into plasma
32
What occurs in the adhesion phase?
surface adhesion molecules expression increased by:
- Complement C5a
- Leukotriene B2
- TNF
endothelial cell expression of adhesion molecules is increased by:
- IL1
- Endotoxins
- TNF
Transendothelial migration
33
Chemotaxis phase:
Locomotion oriented along chemical gradient
34
Chemical mediators:
Histamine- vascular dilation, released by mast cells, eosinophils, basophils and platelets. Stimulated by C3a, C5a and lysosomal proteins
Seratonin-increased vasular permeability, 5HT present in high concentration in platelets (serotonin receptors)
Chemokines- attract various leukocytes to site of inflammation
leukotrienes- Type 1 hypersensitivity reaction
Protiglandins- increase vascular permeability and stimulate platelet aggregation
35
Recognition of micro-organism phase:
not recognised until coated in opsonins (phagocyte marking)
- C3b (surface of an antigen, it can be recognized by phagocyte receptors that signal for phagocytosis)
- Fc fragment of IgG (This property allows antibodies to activate the immune system.)
- collectins (trigger elimination of a microorganism and activation of phagocytes)
36
Suppuration phase:
formation of pus- living and dead cells- neutrophilsm bacterial and cellular debris
37
Absecess formation:
tissue architecture destruction and abundant neutrophils after an episode of acute inflammation plus pus, surgically removed, unlikely to solve itself
38
resolution:
complete restoration of tissue to normal after episode of acute inflammation
39
name 2 chronic inflammation pathways:
1. primary chronic inflammation
| 2. chronic inflammation secondary to acute inflammation
40
cells of chronic inflammation
- plasma cells
- lymphocytes
- macrophages
41
macroscopic appearance of chronic inflammation
- ulcer
- abscess cavity
- thickening of wall by fibrous tissue
- granulomas
- fibrosis
42
on contact with antigens whar do B and T lymphocytes do?
B lymphocyte- becomes a plasma cell
| T lymphocyte- produces cytokines
43
What is repair of a cell?
angiogenesis followed by fibroblast proliferation and collagen synthesis
44
what cells have a high regenerative capacity?
hepatocytes and kidney cells
45
what cells have a love regenerative capacity?
cardiac and adult neurone cells
46
Name some irreversible cell damage:
1. severe damage to cell membranes and mitochondria
2. leakage of enzymes
3. nuclear changes- ATP, cell membrane damage
47
Example of labile cell type?
In GI tract and bone marrow
| these can proliferate to replace lost cells
48
Example of stabe cells?
heaptocytes and endothelium
| these can proliferate to replace lost cells
49
Examples of permenant cells?
Neurones and skeletal cells
| regeneration is not possible
50
What is a granuloma?
chronic inflammation, collection of macrophages
51
what is wound contraction?
when myofibroblasts act to minimise the volume of a wound but this can lead to stenosis or strictures
52
scarring:
injury to tissue--> formation of granulation tissue--> organisation (ie fibrosis)--> fibrous scar matures and contracts (collagen)
53
uclerated scar:
widely separated, prominent granulation tissue and prominent fibrosis
54
excessice scarring leads to..
hypertophic scar and keloid scarring
55
causes of a granulomatous disease:
- specific infections
- foreign bodies
- chemicals
- drugs
- idiopathic
56
what is differentiation
acquisition of a specialised function
57
what is hyperplasia
increase in cell number
| amlodipine causes gingival hypertrophy
58
what is hyperplasia
increase in cell number
| amlodipine causes gingival hypertrophy
59
what is hypertrophy
increase in cell size
60
what is atrophy
reduction in cell size and number in an organ that was normal size
61
what is hypoplasia
reduction in size of an organ that never fully developed to normal size
62
what is metaplasia
one type of cell becomes another form of cell in response to stress (site at risk of cancer)
eg barratts oesophagus
63
what is neoplasia
new growth, abnormal mass of tissue, growth of which exceeds and is uncoordinated with that of normal tissue
(monoclonal= derived from a single common ancestor)
64
Benign neoplasia:
- no necrosis
- nucleus: cytoplasm ratio normal
- minimal pleomorphism
- diploid
- adenoma
- papilloma
65
Malignant neoplasia:
- necrosis
- N:C ratio increased
- pleomorphic
- aneuploid
- carcinoma (cancer of epithelial cell)
- carcinoma in situ= not invading other tissues
- sarcoma- cancer of mesenchymal cell
66
what is dysplasia
disordered growth, pre-malignant process, abnormal cell changes
67
what is angiogenesis
formation of new, abnormal blood vessel, sucessfully growing tumours with develop ability to create own blood supply
68
what are metastasis?
formation of tumour implants that are discontinuous from primary lesion
routes:
- lymphatic= carcinoma
- haematogenous=sarcoma
69
what is the double hit hypothesis?
one working gene is enough. one faulty gene puts a person at increased risk. two faulty mutated genes will result in a functional problem
70
What is stepwise progession?
1. initiation (1st mutation- basically how cancer is caused)
2. promotion (further accumulation of mutations)
3. persistence (unregulated abnormal growth, can beome malignant)
71
Malignant mutation examples:
RAS (GTP binding) eg. colon, pancreatic, bladder, renal and melanoma
Myc (nuclear transcription factor promoting DNA replication) eg. lymphoma, neuroblastoma, small cell carcinoma
P13K (most common mutated kinase in cancer, located in the nucleus at transcription) eg.haematological malignancies
72
causes of failure of ion pump...
1.structural defects
2. defective mitochondria
(causing disruption of ionic concentration and osmorailty)
73
Tumour suppressor functions
- inhibit cell proliferation
| - stimulate cell death
74
What is P53 function
makes a protein that causes apoptosis in cells with DNA damage
75
BRCA 1 and 2 mutations
Breast cancer
76
cancer of the epithelium
carcinomas
77
cancer of the glands
adenoma (benign)
| adenocarcinoma (malignant)
78
cancer of squamous cells
papilloma (benign)
| sqaumous cell carcinoma (malignant)
79
Inherited metabolic disorders:
-autosomal recessive
80
Inherited metabolic disorders:
- autosomal recessive
- loss of function mutation
- gene encodes in metabolic pathway
81
Phenylketonuria:
deficiency of phenylalanine hydroxylase (an enzyme which converts phenylalanine to tyrosine) this then causes a build up of phenylalanine which causes brain toxicity and mental retardation. GUTHRIE TEST (phenylalanine free diet)
82
Complication of Phenylketonuria:
cant produce tyrosine so cant produce melanin so are fair skinned
83
cretinism:
deficiency of the enzyme that converts tyrosine into thyroid hormones
84
what is tyrosinosis?
the enzyme that converts tyrosine into homogenitisic
85
albinism:
deficiency of the enzyme that converts tyrosine into melanin
86
Alkaptonuria:
deficiency of the enzyme that breaks down homogenistic acid into carbon dioxide and water
87
Diabetes type 1:
insulin dependent: HLA linked. anti-islet antibodies form immune complexes with islet B cells causing islet cell destruction and failure of insulin secretion
88
Diabetes type 2:
non insulin dependent: target cell becomes unresponsive to the insulin being secreted
89
Risk factors of atheroma
- fam history
- male
- smoker
- obesity
- alchohol
- hypertension
- age
- diabetes
90
Pathogenesis of atheroma
fatty streak--> fibrofatty plaque--> proliferative atheroma--> complicated atheroma
91
causes of atheroma
endothelial injury--> response to injury--> macrophages and platelets agreggate--> lipid accumulation--> smooth uscle proliferation
92
complications of atheroma
- thombosis
- aneurysm
- dissection
- embolism
- ischaemia
93
Left ventricular hypertrophy
- increase LV load
- poor perfusion of organs
- interstitial fibrosis
- micro infarcts
- diastolic dysfunction
94
define thombus
solid mass of bloof formed in a blood vessel
95
Virchows triad:
```
vessel wall (loss of endothelial surface, inflammation)
blood flow (stasis, turbulence)
blood constituents (platelets, coagulation proteins, viscosity)
```
96
what are platelets
anucleated cell fragments, adherence properties and growth factors
97
what is an embolism
mass of material in vascular system, moving from its site of origin to lodge in the vessel of a distant site
98
Deep vein thrombus
Post op, bed bound, travel , unilateral leg swelling, oedema, pain
99
Pulmonary thromboemolism
sudden onset, life threatening, haemoptosis, breathlessness, cardiovascular collapse, cardiac arrest
100
Define infarction
Zonal necrosis due to sudden occlusion of blood supply, lack of nutrient and oxygen
101
senescence
non dividing state a cell goes into after a fixed number of cell divisions
102
Werners syndome
genetic abnormality assoc with defective SNA helicase
103
Progeria:
a rare genetic condition causing growth retardation in infancy with macrocelphaly and fast developing signs of old age- low life expectancy due to high risk of athersclerosis
104
neurogenerative disease
frontal and temporal lobe atrophy and compensatory ventricular dilation, formation of senile plaque and neurofibillary tangles all causing acceleration of normal aging process
105
osteoporosis
when bones decline in density
106
osteartheritis
degeneration of articular surfaces
107
hypoxic cell
ATPase pumps are shed due to reduced ATP consumption and ionic conc will be altered and cells swell with fluid intake
108
osteomyelitis
a chronic abscess which is extremely difficult to eradicate
109
histocyte
a macrophage present in connective tissue, mainly secretory function , little phagocytic function
