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Pathology Flashcards

1
Q

what 3 factors are involved in the process of aging? (ie how well you age?)

A

genetic factors
environmental factors
manifestation of age related disease

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2
Q

why does cellular aging occur?

A

progressive decline in the proliferation capacity and life span of the cell

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3
Q

what 7 biochemical and structural changes occur with cellular aging?

A 
mitochondria abnormalities
reduced ER
distorted Golgi appartus
accumulation of lipofusin
advanced glycation end products
abnormally folded  proteins
reduced capacity to undertake key biochemical process
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4
Q

what 3 key biochemical processes become less effective with cellular aging?

A

decreased oxidative phosphorylation
decreased synthesis of key nucleic acids and proteins/enzymes
reduced capacity for nutrient uptake

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5
Q

what causes accumulation of lipofuscin in a cell?

A

episodes of oxidative damage

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6
Q

describe the life span and metabolic rate of small animals?

A

shorter life span

high metabolic rate

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7
Q

how are free radicals usually formed?

A

by-products of oxidative phosphrylation

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8
Q

what is the term used to describe the non-dividing state a cell goes into after a fixed number of cell divisions?

A

senescence

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9
Q

what happens to Hayflicks number as you get older?

A

Hayflicks number decreases?

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10
Q

what genetic abnormality is associated with defective DNA helicase and so has a much reduced capacity for rounds of cell division?

A

Werner’s Syndrome

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11
Q

What are Telomeres?

A

DNA caps at chromosome ends

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12
Q

what is the DNA sequence of telomeres?

A

repeated sequences of TTAGGG

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13
Q

what are the 2 functions of telomeres?

A
  1. ensure complete replication of genome

2. protect coding sequences at the chromosome ends from damage

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14
Q

what happens in telomere shortening?

A

incomplete replication of chromosome ends which leads to cell cycle arrest

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15
Q

What is the function of Telomerase?

A

maintains the telomere length

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16
Q

what is Telomerase made out of?

A

a RNA-protein complex

the RNA provides the template for telomere maintenance

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17
Q

compare Telomerase activity in germ cells, stem cells and somatic cells?
(germ cells = sperm/egg, somatic cells = every other cell in the body)

A

telomerase activity is greater in germ cells than stem cells but there is no telomerase activity in somatic cells

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18
Q

what is enzyme is up-regulated in immortalised cells?

A

telomerase

allows maintenance of telomere length therefore cell cycle will never arrest

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19
Q

where do the genes for longevity in families come from?

A

mirochondria

maternal inheritance

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20
Q

what is Progeria?

A

a rare genetic condition causing growth retardation in infancy with macrocephaly and fast developing signs of old age

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21
Q

what causes Progeria?

A

usually a spontaneous mutation

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22
Q

why do children with Progeria have a life expectancy of late teens to 30?

A

they develop atherosclerosis very early and die of its consequences eg MI, CVA, heart failure

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23
Q

what occurs in neurogenerative disease? (such as alzheimer type dementia)

A

frontal and temporal lobe atrophy and compensatory ventricular dilation
formation of senile plaques and neurofibrillary tangles
all causing acceleration of normal aging process

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24
Q

what is osteoporosis?

A

when bones decline in density causing the patient to become prone to fractures, even with minimal stress

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25
Q

what is osteoarthritis?

A

degeneration of articular surfaces (“wear and tear”)

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26
Q

what are the 4 factors must be highly functioning to ensure cell integrity?

A

DNA
Cell membrane
Energy production
Protein synthesis

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27
Q

what type of cells are more susceptible to DNA damages and why?

A

dividing cells
abnormal (but non-lethal) sequence is inherited by daughter cells and so is recognised as normal, DNA repair mechanisms are by passed
(pemanent cells are more resistant)

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28
Q

what type of turnover do skin and hair cells have?

and what does this mean in regards to acquiring abnormalities?

A

high cell turnover

highly susceptible to abnormalities

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29
Q

what type of turnover do cardiac cells and adult neurones have?
and what does this mean in regards to acquiring abnormalities?

A

low cell turnover

resistant to abnormalities

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30
Q

what is the role of p53 genes?

A

makes a protein that causes apoptosis in cells with DNA damage

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31
Q

if p53 is lost what is more likely to happen?

A

obtain a malignancy

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32
Q

if a cancer is due to a loss of p53 function how affected is it by drugs?

A

more likely chemotherapy/drug resistant because many drugs use p53’s apoptosis ability

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33
Q

what 2 major things can cause failure of ion pumps and therefore disruption of ionic concentrations and osmolarity?

A 
structural defect of the ion pump
defective mitochondria (energy dependent)
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34
Q

what can happen to the cell membranes of people with high levels of cholesterol?

A

excessive cholesterol can cause the membrane to harden

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35
Q

what are free radicals?

A

highly reactive charges species which are generated by the body in normal metabolism (oxidative phosphorylation) or infection response. They can also be produced by drugs (eg paracetamol)

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36
Q

what can free radicals do to the lipid membrane?

A

bind to and peroxidise and cross link components of the membrane thus damaging membrane integrity

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37
Q

what are anti-oxidants?

A

molecules which scavenge free radicals and prevent damage to cell membrae through lipid perocidation

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38
Q

with regards to number of free radicals, what occurs when oxygen content of the air increases?

A

free radical content increases- this is what is meant by oxygen toxicity

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39
Q

why are anti-oxidation techniques used in reperfusion procedures?

A

as blood rushes back to an area of the body, many free radicals are produced- reperfusion injury

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40
Q

what 5 things determine the severity of tissue injury?

A 
duration of stimuli persistency
nature of stimuli
proportion of cells affected
regenerative capacity
topography
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41
Q

what is topography?

A

the microanatomy of structures affected by an injury

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42
Q

what type of regenerative capacity do hepatocytes and kidney cells have?

A

high regenerative capacity

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43
Q

what type of regenerative capacity do permanent cells such as cardiac cells and adult neurones have?

A

low regenerative capacity

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44
Q

what happens to ATPase pumps and therefore the osmolarity of the cell if the cell is hypoxic?

A

ATPase pumps are shed to reduce ATP consumption rate and therefore ionic concentrations will be altered and cells swell with fluid intake

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45
Q

which 2 ways can cells die?

A

apoptosis

necrosis

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46
Q

in apoptosis how does the cell die?

A

a stimulus causes the cell to die by collapsing and fragmenting

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47
Q

where does normal apoptosis occur?

A

loss of webbed fingers and toes, palate fusion

embryonic development

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48
Q

are apoptosis and necrosis pathological or physiological?

A

apoptosis can be physiological or pathological

necrosis is always pathological

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49
Q

what are the 6 patterns of necrosis?

A 
coagulative
colliquative
caseous
gangrenus
fibrinoid
fat necrosis
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50
Q

what happens in coagulative necrosis?

A

proteins of of cell coagulate

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51
Q

what is a common reason for coagulative necrosis?

A

prolonged cardiac ischaemia

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52
Q

what happens in colliquative necrosis?

A

phosphlipids turn to liquid

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53
Q

where in the body does colliquative necrosis occur?

A

brain

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54
Q

what is caseous necrosis a diagnosis of?

A

TB

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55
Q

what happens in gangrenous necrosis?

A

cell death by apoptosis and then infection caused by anaerobic bacteria

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56
Q

what happens in fat necrosis?

A

fat cells die often due to trauma

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57
Q

what happens in fibrinoid necrosis?

A

necrosis which causes a fibrin and immune complex deposits

58
Q

what are the 2 types of metabolic disorders?

A

inherited

acquire

59
Q

what is usually the pattern of inheritance for inherited metabolic disorders?

A

aotomal recessive

60
Q

what do metabolic disorders usually cause?

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

61
Q

what is phenylketonuria a deficiency of?

A

phenylalanine hydroxylase

62
Q

what does phenylalanine hydroxylase do?

A

converts phenylalanine from dietary protein to tyrosine

63
Q

what is cretinism a deficiency of?

A

the enzyme that converts tyrosine into thyroid hormones

64
Q

what is tyrosinosis a deficiency of?

A

the enzyme that converts tyrosine into homogenitisic acid

65
Q

what is albinism a deficiency of?

A

the enzyme that converts tyrosine what iinto melanin

66
Q

what is alkaptonuria a deficiency of?

A

the enzyme the breaks down homogenitisic acid into carbon dioxide and water

67
Q

what is the main problem that results from phenylketonuria?

A

accumulation of phenylalanine which causes brain toxicity and mental retardation

68
Q

how can phenylketonuria be tested for?

A

guthrie test

69
Q

what is the treatment for phenylketonuria?

A

phenylalanine free diet

70
Q

why do phenylketonuria patients have fair skin and blue eyes?

A

because they cant produce tyrosine and therefore cant produce melanin

71
Q

what are the 2 phases of cellular injury?

A

reversible

irreversible

72
Q

what are the 4 characteristics of irreversible damage?

A

severe damage to cell membranes
severe damage to mitochondria
leakage of enzymes
nuclear changes

73
Q

what 4 things can cause cell membrane damage?

A

progressive loss of phospholipids
lipid breakdown products
reactive oxygen species
cytoskeletal abnormalities

74
Q

what are the differences between apoptosis and necrosis in terms of the cells they affect?

A

apoptosis affects scattered cells

necrosis affects sheets of cells

75
Q

what are the differences between apoptosis and necrosis in terms of cell osmolarity?

A

apoptosis causes the cells to shrink

necrosis causes the cells to swell

76
Q

what are the differences between apoptosis and necrosis in terms of inflammation?

A

apoptosis: no inflammtion
necrosis: inflammation

77
Q

which type of cell death is energy dependent?

A

apoptosis

78
Q

what 2 types of molecules are involved in the biochemical regulation of apoptosis?

A

inducers

inhibitors

79
Q

what are the 3 groups of apoptosis inhibitors?

A

growth factors
cell matrix components
viral proteins

80
Q

what are 7 inducing causes of apoptosis?

A 
withdrawal of growth factors
loss of matrix attachment
viruses
free radicals
ionising radiation
DNA damage
Fas ligand/ CD95 interaction
81
Q

what disorders cause increased apoptosis?

A

AIDS
neurodegenerative disorders
reperfusion injury

82
Q

what disorders cause decreased apoptosis?

A

neoplasia

auto-immune disease

83
Q

what is the outcome of incomplete repair?

A

repair: scarring

84
Q

what is the outcome of complete repair?

A

regeneration: restitution

85
Q

what are the 3 cell types?

with regards to the multiplication

A

liable eg GI tract and bone marrow
stable eg hepatocytes and endothelium
permanent eg neurones and skeletal muscle

86
Q

what is the pool of cells which replace any cells that are lost?

A

stem cells

87
Q

where are stem cells located?

A

in discrete compartments

88
Q

what happens when labile and stable cells die?

A

proliferation to replace lost cells

89
Q

what happens when permanent cells die?

A

proliferation to replace lost cells isn;t possible

90
Q

what happens when restitution isnt possible?

A

repair with scarring

91
Q

when is restitution not possible?

A

when the tissue architecture is damaged

92
Q

what needs to be preserved for restitution to occur?

A

tissue architecture

93
Q

describe the repair (with scarring) process?

A

injury to tissue architecture
formution of granulation tissue
organisation (ie fibrosis)
fibrous scar matures and contracts

94
Q

what is the fibrous scar made of?

A

collagen

95
Q

what is the important precursor to repair of damaged tissue?

A

granulation tissue

96
Q

what forms in granulation tissue?

A

fragile vascular channels

97
Q

what type of scar has closely apposed edges, minimal granulation tissue and minimal fibrosis?

A

surgical scar

98
Q

what type of scar has edges that are widely separated, prominent granulation tissue and prominent fibrosis?

A

ulcerated scar

99
Q

why does the wound contract?

A

caused by the myofibroblasts to minimise the volume of the wound

100
Q

what problem can wound contraction cause?

A

stricture or stenosis

ie in GI tract of CBD

101
Q

what are the 2 types of excessive scar formation?

A

hypertrophic scar

keloid

102
Q

what is resolution?

A

the complete restoration of the tissues to normal after an episode of acute inflammation- ideal scenario

103
Q

what type of inflammation can resolution occur after?

A

acute inflammation

NOT chronic

104
Q

what are the 4 factors favouring resolution?

A
  1. minimal cell death (tissue architecture retained)
  2. cells have a regenerative capcity eg hepatocytes
  3. rapid destruction of causal agent
  4. rapid removal of fluid/debris by a good local vascular drainage
105
Q

what is suppuration?

A

the formation of pus

106
Q

what is pus made out of?

A 
living cells
dying cells
dead neutrophils
cellular debris
bacteria
107
Q

what happens when there is tissue archeticture destruction and abundant neutrophils after an episode of acute inflammation?

A 
abscess formation
(tissue destruction plus pus)
108
Q

what needs to be done to an abscess?

A

surgical procedure to remove, otherwise continues to stimulate inflammation and is unlikely to heal on its own

109
Q

what is organisation?

A

replacement of damaged tissue by granulation tissue?

110
Q

what are the 3 factors favouring organisation instead of resolution?

A

large amounts of fibrin formed
substantial necrosis
exudate and debris cannot be removed or discharged

111
Q

what are the 2 pathways to chronic inflammation?

A
  1. primary chronic inflammation (most common)

2. chronic inflammation secondary to acute inflammation

112
Q

what cells are characteristical of acute inflammation?

A

neutrophil polymorphs

113
Q

what cells are characteristical of chronic inflammation?

A

macrophages, plasma cells, lymphocytes fibroblasts

114
Q

what are the predominant features in repair?

A

angiogenesis followed by fibroblast proliferation and collagen synthesis

115
Q

whate cells are characteristical of the intermediate phase between acute and chronic phases?

A

eosinophils

116
Q

what 3 reasons can be given for the progression from acute to chronic inflammation?

A
  1. indigestible substances (eg glass and suture material) ie causal agent isn’t removed
  2. deep seated supprative inflammation where drainage is delayed of inadequate
  3. recurrent episodes of acute inflammation
117
Q

what happens to deep seated supprative inflammation where drainage is delayed or inadequate?

A

thick abcess walls composed of granulation tissue form which will fail to come together after drainage and eventually a fibrous scar will form

118
Q

what is an osteomyelitis?

A

a chronic abscess which is extremely difficult to eradicate

119
Q

what 5 factors favour primary chronic inflammation?

A
  1. resistance of infective agent to phagocytosis and intracelular killing
  2. foreign body reactions to endogenous materials
  3. foreign body reactions to exogenous materials
  4. some autoimmune diseases
    5 primary granulomatous disease
120
Q

what is an endogenous material?

A

a material that is made in the body but is present in a site it shouldn’t be

121
Q

what are 5 possible macroscopic appearances of chronic inflammation?

A
  1. chronic ulcer
  2. chronic abscess cavity
  3. thickening of the wall of a hollow viscous by fibrous tissue
  4. granulomatous inflammation
  5. fibrosis
122
Q

what is a chronic ulcer?

A

when mucosa is breached, ulcer base lined by grnulation tissue, fibrous tissue extends through muscle layers

123
Q

what is a granuloma?

A

an aggergate of epitheloid histocytes

124
Q

what is a histocyte?

A

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

125
Q

what are the 5 causes of granulomatous disease?

A 
1. specific infections (mycobacteria shistosomiasis)
2, foreign bodies (endo/exogenous)
3. chemicals
4. drugs
5. idiopathic
126
Q

what type of antibodies to patients with Type 1 diabetes contain?
Type 2 dont contain

A

anti-islet antibodies

127
Q

Which type of diabetes is HLA linked?

A

type 1

128
Q

what is the pathogenesis of type 2 diabetes?

A

target cell becomes unresponsive to the insulin being secreted

129
Q

what is the pathogenesis of type 1 diabetes?

A

anti-islet antibodies form imune complexes with islet B cells causing islet cell destruction and failure of insulin secretion

130
Q

what type of disease is obseity?

A

an acquired metabolic disease

131
Q

what are the 9 risk factors for atheroma?

A 
family history
male (or post-menopausal women)
smoking
hypertension
diabetes
plasma lipids
obesity
age
geography
132
Q

what is the progression from fatty streak on the epithelium to complicated atheroma?

A

fatty streak
fibrofatty plaque
proliferative atheroma
complicated atheroma

133
Q

what are the 5 complications of atheroma?

A 
thrombosis
aneurysm
dissection (a tear in the wall)
embolism
ischaemia
134
Q

what is a thrombus?

A

a solid mass of blood constituents formed within the blood vessel?

135
Q

what are virschows triad? (risk factors for a thrombus)

A

damage to the vessel wall
change in blood flow
change in blood constituents

136
Q

what damage to the vessel wall predisposes to a thrombus?

A

loss of endothelial surface

inflammation

137
Q

what change in blood flow predisposes to a thrombus?

A

stasis (ie not moving for a long period of time, long-haul flights, surgery)
turbulence (ie hypertension)

138
Q

what change in blood constituents predisposes to a thrombus?

A

hypercoaguability

caused by smoking, obesity, contraceptive pill use, pregnancy, cancer

139
Q

what is an embolism?

A

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

140
Q

what 7 types of embolism can occur?

A 
thromboembolsim
fat embolism
atheroembolism
tumour embolism
infective 
amniotic fluid
air embolism
141
Q

what is an infarction?

A

zonal necrosis due to sudden occlusion of blood supply (lack of oxygen and nutrients)

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