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Principles (Y1) > Pathology > Flashcards

Pathology Flashcards

1
Q

what is a risk factor

A

social or individual factor which increases the risk of development of a disease

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2
Q

what is aetiology

A

cause of a disease

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3
Q

what is pathogenesis

A

sequence of events from a health state to a clinical disease

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4
Q

what causes aging

A
  1. Genetic factors
  2. Environmental factors
  3. Manifestation of age related diseases
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5
Q

For cell integrity what must be highly functioning?

A
  1. DNA
  2. Cell membrane
  3. Energy production
  4. Protein synthesis
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6
Q

What is necrosis

A

Cell death that requires no energy

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7
Q

Patterns of necrosis

A
  1. Coagulative- proteins coagulate to preserve the cell outline
  2. Colliquative- necrotic material becomes sofened and liquefied (PUS), no cell structure remains
  3. caseous- cheese like eg TB
  4. Gangerous- Cell death by necrosis then infection on top of that
  5. Fibrinoid- fibre deposition
  6. Fat necrosis- fat cells die often due to trauma
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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.

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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)
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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

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11
Q

what causes cell aging

A

a progressive decline in the proliferation capacity and lifespan of the cell

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12
Q

biochemical and structural changes in cell aging

A
  1. mitochondrial abnormalities
  2. reduced ER
  3. disorted golgi apparatus
  4. accumualtion of lipofusion
  5. advanced glycation products
  6. abnormally folded proteins
  7. reduced capacity to undertake key biochemical processes
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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

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14
Q

What are telomeres

A

RNA- protein complex (DNA caps at chromosome ends TTAGGG)

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15
Q

What are the functions of teleomeres?

A
  1. ensure complete replication of the genome

2. protect coding sequences at the chromosome ends from damage

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16
Q

What is telomere shortening

A

incomplete replication of chromosome ends which leds to cell cycle arrest

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17
Q

telomere activity is greater in germ cells than in stem cells, why?

A

there is no telomere activity in somatic cells

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18
Q

what type of cells are suceptable to DNA damage?

A
  1. dividing cells
  2. abnormal sequence inherited by daughter cells and so is recognised as normal, so DNA repair mechanisms are by passed
  3. permenant cells are most resistant
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19
Q

what cells are highly succeptable to abnormalities

A

skin and hair cells as they have a high turn over

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20
Q

what cells are at low risk of abnormalities

A

cardiac and adult neurone cells as they have a low turn over

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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
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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)

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23
Q

causes of an inherited metabolic disorder

A

autosomal recessive

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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

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25
Q

Intermediate inflammation

A

eosinophils
Acute–> Chronic
the agent causing inflammation isnt removed, recurrent episodes of acute inflammation

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26
Q

Chronic inflammation

A

macrophages, plasma cells, lymphocytes, fibroblasts

subsequent and ofter prolonged tissue reactions follow initial response. recurrance of acute inflam may lead to chronic

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27
Q

characteristics of inflammation

A

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

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28
Q

what is the exudate fluid

A

a protein containing fluid (including immunoglobins)

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29
Q

What is fribrinogen

A

fibrin on contact with ECM, acutely inflammed organs are commonly covered in fibrin

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30
Q

neutrophil inflammation cascade

A
  1. margination
  2. adhesion
  3. chemotaxis
  4. chemical mediators
  5. recognition of micro-organisms
  6. suppuration
  7. abscess formation
  8. resolution
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31
Q

What occurs in the margination phase?

A

loss of intravascular fluid and increased plasma viscosity, allowing neutrolphils into plasma

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32
Q

What occurs in the adhesion phase?

A

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

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33
Q

Chemotaxis phase:

A

Locomotion oriented along chemical gradient

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34
Q

Chemical mediators:

A

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

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35
Q

Recognition of micro-organism phase:

A

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)
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36
Q

Suppuration phase:

A

formation of pus- living and dead cells- neutrophilsm bacterial and cellular debris

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37
Q

Absecess formation:

A

tissue architecture destruction and abundant neutrophils after an episode of acute inflammation plus pus, surgically removed, unlikely to solve itself

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38
Q

resolution:

A

complete restoration of tissue to normal after episode of acute inflammation

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39
Q

name 2 chronic inflammation pathways:

A
  1. primary chronic inflammation

2. chronic inflammation secondary to acute inflammation

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40
Q

cells of chronic inflammation

A
  • plasma cells
  • lymphocytes
  • macrophages
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41
Q

macroscopic appearance of chronic inflammation

A
  • ulcer
  • abscess cavity
  • thickening of wall by fibrous tissue
  • granulomas
  • fibrosis
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42
Q

on contact with antigens whar do B and T lymphocytes do?

A

B lymphocyte- becomes a plasma cell

T lymphocyte- produces cytokines

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43
Q

What is repair of a cell?

A

angiogenesis followed by fibroblast proliferation and collagen synthesis

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44
Q

what cells have a high regenerative capacity?

A

hepatocytes and kidney cells

45
Q

what cells have a love regenerative capacity?

A

cardiac and adult neurone cells

46
Q

Name some irreversible cell damage:

A
  1. severe damage to cell membranes and mitochondria
  2. leakage of enzymes
  3. nuclear changes- ATP, cell membrane damage
47
Q

Example of labile cell type?

A

In GI tract and bone marrow

these can proliferate to replace lost cells

48
Q

Example of stabe cells?

A

heaptocytes and endothelium

these can proliferate to replace lost cells

49
Q

Examples of permenant cells?

A

Neurones and skeletal cells

regeneration is not possible

50
Q

What is a granuloma?

A

chronic inflammation, collection of macrophages

51
Q

what is wound contraction?

A

when myofibroblasts act to minimise the volume of a wound but this can lead to stenosis or strictures

52
Q

scarring:

A

injury to tissue–> formation of granulation tissue–> organisation (ie fibrosis)–> fibrous scar matures and contracts (collagen)

53
Q

uclerated scar:

A

widely separated, prominent granulation tissue and prominent fibrosis

54
Q

excessice scarring leads to..

A

hypertophic scar and keloid scarring

55
Q

causes of a granulomatous disease:

A
  • specific infections
  • foreign bodies
  • chemicals
  • drugs
  • idiopathic
56
Q

what is differentiation

A

acquisition of a specialised function

57
Q

what is hyperplasia

A

increase in cell number

amlodipine causes gingival hypertrophy

58
Q

what is hyperplasia

A

increase in cell number

amlodipine causes gingival hypertrophy

59
Q

what is hypertrophy

A

increase in cell size

60
Q

what is atrophy

A

reduction in cell size and number in an organ that was normal size

61
Q

what is hypoplasia

A

reduction in size of an organ that never fully developed to normal size

62
Q

what is metaplasia

A

one type of cell becomes another form of cell in response to stress (site at risk of cancer)
eg barratts oesophagus

63
Q

what is neoplasia

A

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
Q

Benign neoplasia:

A
  • no necrosis
  • nucleus: cytoplasm ratio normal
  • minimal pleomorphism
  • diploid
  • adenoma
  • papilloma
65
Q

Malignant neoplasia:

A
  • 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
Q

what is dysplasia

A

disordered growth, pre-malignant process, abnormal cell changes

67
Q

what is angiogenesis

A

formation of new, abnormal blood vessel, sucessfully growing tumours with develop ability to create own blood supply

68
Q

what are metastasis?

A

formation of tumour implants that are discontinuous from primary lesion

routes:
- lymphatic= carcinoma
- haematogenous=sarcoma

69
Q

what is the double hit hypothesis?

A

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
Q

What is stepwise progession?

A
  1. initiation (1st mutation- basically how cancer is caused)
  2. promotion (further accumulation of mutations)
  3. persistence (unregulated abnormal growth, can beome malignant)
71
Q

Malignant mutation examples:

A

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
Q

causes of failure of ion pump…

A

1.structural defects
2. defective mitochondria
(causing disruption of ionic concentration and osmorailty)

73
Q

Tumour suppressor functions

A
  • inhibit cell proliferation

- stimulate cell death

74
Q

What is P53 function

A

makes a protein that causes apoptosis in cells with DNA damage

75
Q

BRCA 1 and 2 mutations

A

Breast cancer

76
Q

cancer of the epithelium

A

carcinomas

77
Q

cancer of the glands

A

adenoma (benign)

adenocarcinoma (malignant)

78
Q

cancer of squamous cells

A

papilloma (benign)

sqaumous cell carcinoma (malignant)

79
Q

Inherited metabolic disorders:

A

-autosomal recessive

80
Q

Inherited metabolic disorders:

A
  • autosomal recessive
  • loss of function mutation
  • gene encodes in metabolic pathway
81
Q

Phenylketonuria:

A

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
Q

Complication of Phenylketonuria:

A

cant produce tyrosine so cant produce melanin so are fair skinned

83
Q

cretinism:

A

deficiency of the enzyme that converts tyrosine into thyroid hormones

84
Q

what is tyrosinosis?

A

the enzyme that converts tyrosine into homogenitisic

85
Q

albinism:

A

deficiency of the enzyme that converts tyrosine into melanin

86
Q

Alkaptonuria:

A

deficiency of the enzyme that breaks down homogenistic acid into carbon dioxide and water

87
Q

Diabetes type 1:

A

insulin dependent: HLA linked. anti-islet antibodies form immune complexes with islet B cells causing islet cell destruction and failure of insulin secretion

88
Q

Diabetes type 2:

A

non insulin dependent: target cell becomes unresponsive to the insulin being secreted

89
Q

Risk factors of atheroma

A
  • fam history
  • male
  • smoker
  • obesity
  • alchohol
  • hypertension
  • age
  • diabetes
90
Q

Pathogenesis of atheroma

A

fatty streak–> fibrofatty plaque–> proliferative atheroma–> complicated atheroma

91
Q

causes of atheroma

A

endothelial injury–> response to injury–> macrophages and platelets agreggate–> lipid accumulation–> smooth uscle proliferation

92
Q

complications of atheroma

A
  • thombosis
  • aneurysm
  • dissection
  • embolism
  • ischaemia
93
Q

Left ventricular hypertrophy

A
  • increase LV load
  • poor perfusion of organs
  • interstitial fibrosis
  • micro infarcts
  • diastolic dysfunction
94
Q

define thombus

A

solid mass of bloof formed in a blood vessel

95
Q

Virchows triad:

A 
vessel wall (loss of endothelial surface, inflammation)
blood flow (stasis, turbulence)
blood constituents (platelets, coagulation proteins, viscosity)
96
Q

what are platelets

A

anucleated cell fragments, adherence properties and growth factors

97
Q

what is an embolism

A

mass of material in vascular system, moving from its site of origin to lodge in the vessel of a distant site

98
Q

Deep vein thrombus

A

Post op, bed bound, travel , unilateral leg swelling, oedema, pain

99
Q

Pulmonary thromboemolism

A

sudden onset, life threatening, haemoptosis, breathlessness, cardiovascular collapse, cardiac arrest

100
Q

Define infarction

A

Zonal necrosis due to sudden occlusion of blood supply, lack of nutrient and oxygen

101
Q

senescence

A

non dividing state a cell goes into after a fixed number of cell divisions

102
Q

Werners syndome

A

genetic abnormality assoc with defective SNA helicase

103
Q

Progeria:

A

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
Q

neurogenerative disease

A

frontal and temporal lobe atrophy and compensatory ventricular dilation, formation of senile plaque and neurofibillary tangles all causing acceleration of normal aging process

105
Q

osteoporosis

A

when bones decline in density

106
Q

osteartheritis

A

degeneration of articular surfaces

107
Q

hypoxic cell

A

ATPase pumps are shed due to reduced ATP consumption and ionic conc will be altered and cells swell with fluid intake

108
Q

osteomyelitis

A

a chronic abscess which is extremely difficult to eradicate

109
Q

histocyte

A

a macrophage present in connective tissue, mainly secretory function , little phagocytic function

Principles (Y1) (9 decks)

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