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2A content- Sameera > 1. PATHOLOGY > Flashcards

1. PATHOLOGY Flashcards

1
Q

define inflammation

A

local physiological response to tissue injury

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2
Q

give two examples of acute inflammation causes

A

infections and hypersensitivity

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3
Q

give two examples of chronic inflammation causes

A

autoimmunity, chronic infection

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4
Q

what does a polymorph have

A

many lobes

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5
Q

what r Barr bodies and why do they form

A

in female neutrophils
due to visible silenced x chromosomes due to lyonisation

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6
Q

what is the histological diagnosis for acute inflammation (3 parts, 1 point)

A

presence of neutrophil polymorphs in extravascular space as part of cellular exudate

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7
Q

what is acute inflammation

A

initial response of a tissue to an injury

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8
Q

6 causes of acute inflammation

A

microbial infections: bacteria and viruses
hypersensitivity reactions: parasites
physical agents: trauma, heat, cold
chemicals: corrosives, acid
bacterial toxins
tissue necrosis: ischaemic infarction

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9
Q

what causes dolor in acute inflammation

A

inflammatory mediators such as secretins, bradykinin and prostaGLANDIN which increase sensitivity to pain

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10
Q

5 macroscopic/ cardinal acute signs of inflammation

A

rubor: redness
dolor: pain
calor: heat
tumor: swelling
loss of function

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11
Q

explain how acute inflammation occurs (3 steps)

A
  1. increase in vessel calibre:
    -inflammatory cytokines eg bradykinin, NO and prostacyclin cause vasodilation and increase in permeability
  2. fluid exudate:
    -vessel becomes leaky and protein rich fluid is forced out of the vessel
  3. cellular exudate:
    -neutrophil polymorphs recruited to the tissue and become abundant in cellular exudate
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12
Q

4 steps of neutrophil migration in acute inflammation

A

margination: neutrophils migrate to edge of blood vessel due to increase plasma viscosity and slower flow
adhesion: selections binds to neutrophils, causing rolling along BV margin (called pavementing)
emigration and diapedesis: movement of neutrophils out of BV though endothelium and other inflammatory cells follow
chemotaxis: movement of cells towards the site of inflammation via a chemical gradient (often done by cytokines like C5a)

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13
Q

what is the difference between emigration and diapedesis

A

diapedesis: process of other inflammatory cells and RBCs pass through the endothelium with the neutrophils
emigration: neutrophils passing through endothelium via endothelial cells then basal lamina then vessel wall

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14
Q

3 steps of action of immune cells at site of infection

A

identification and cytokine release
phagocytosis/ bacterial killing
macrophages clear debris

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15
Q

why is suppuration in acute inflammation significant regarding treatment with drugs

A

bacteria is located within abscess which in inaccessible to antibiotics

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16
Q

give an example of resolution, organisation and progression to chronic inflammation

A

acute liver injury, MI/stroke, chronic cholecystitis

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17
Q

4 outcomes of acute inflammation

A

resolution: normal restoration of tissues
suppuration: pus formation (causing pyogenic membrane= scarring)
organisation: fibrotic tissue replaces normal tissue, loss of function
progression: recurrent inflammation which becomes chronic and fibrotic tissue

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18
Q

example of a acute condition that can become chronic

A

pnuemonia

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19
Q

onset, duration and 2 cells involved in acute inflammation

A

fast, short, neutrophils and monocytes

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20
Q

onset, duration and 3 cells involved in chronic inflammation

A

slower, long, lymphocytes and macrophages and plasma cells

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21
Q

1 macroscopic feature of chronic inflammation

A

fibrotic tissue

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22
Q

2 histological hallmarks of acute inflammation

A

neutrophil EXTRAVASATION
presence of neutrophil polymorphs

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23
Q

2 HISTOLOGICAL HALLMARKS of chronic inflammation

A

cellular infiltrate of lymphocytes, macrophages and plasma cells
possible granulomas (epitheliod histiocytes)

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24
Q

give 4 examples of an autoimmune disease

A

T1DM, Grave’s, Hashimoto’s, SLE

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25
Q

what is an ulcer and why

A

a break in the skin that is slow to heal due to poor blood supply

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26
Q

macroscopic appearance of chronic inflammation (4)

A

chronic ulcer
chronic abscess cavity
granulomatous inflammation
fibrosis

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27
Q

4 causes of chronic inflammation

A

primary chronic inflammation
primary granulomatous disease
transplant rejection
progression from acute inflammation (due to a persistent agent)

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28
Q

3 causes of primary chronic inflammation

A

resistance of infective agent
endogenous/ exogenous materials
autoimmune conditions

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29
Q

chronic inflammation microscopic appearance (3)

A

lymphocytes, plasma cells and macrophages present
continuous destruction of tissue
NO EXUDATION

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30
Q

2 things formed in chronic inflammation

A

formation of granulation tissue
formation of a fibrous scar

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31
Q

what is ischaemia and is it caused by (2)

A

reduction in blood flow to a tissue caused by constriction/ blockage of the vessels suppling it

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32
Q

what is infarction

A

death of tissue due to severe/ prolonged ischaemia

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33
Q

what is a re-perfusion injury

A

damage to tissue during re-oxygenation

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34
Q

what three organs r less susceptible to infarction and why

A

liver, brain and lungs have dual supply so less susceptible

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35
Q

what is a thrombi

A

solidification of blood contents that form within the vascular system during life

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36
Q

4 stages of thrombus formation

A

vasospasm
primary platelet plug forms
coagulation cascade occurs
formation of secondary platelet

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37
Q

3 steps of primary plug formation

A

platelet adhesion: platelets bind to vwf via gp1b which attaches to exposed collagen
platelet activation: conformational shape from discoid to pseudopoid because of gp1b binding
aggregation: platelets bind to each other via gp2a/3b

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38
Q

recall coagulation cascade

A

intrinsic pathway: 12>11>9>8>10
extrinsic pathway: 3>7>10
common pathway: 10>2>1 (10-> 2 with help of 5)

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39
Q

medical definition of granulomas

A

aggregates of epitheliod histiocytes (essentially macrophages)

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40
Q

explain the types necrosis in granulatomas (2) and example diseases for each (1, 3)

A

central necrosis (classical TB)
no central necrosis (sarcoidosis, leprosy, vasculitis, Crohn’s)

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41
Q

what do granulomas secrete? why is this useful?

A

ACE
blood marker- increases in patients with granulomatous disease eg sarcoidosis

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42
Q

what three things suggest a parasite infection

A

granulomas, high serum ACE and raised eosinophils

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43
Q

what is arterial thrombi and the main cause

A

blood clot blocks an artery
main cause= when an artery is damaged by atherosclerosis

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44
Q

what r the complications of a small, moderate and large PE

A

small-idiopathic hypertension
moderate- chest pain and dyspnoea
large-death

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45
Q

what can DVT lead to and how

A

pulmonary embolism
IVC-> RA-> RV-> pulmonary arteries

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46
Q

what is the treatment for arterial thrombi (3) and give examples for each and how each works

A

anti-platelets eg aspirin (inhibit platelet activation)
thrombolytic therapy eg tissue plasminogen activator like alteplase (activates plasmin which breaks down fibrin, causing breakdown of the clot)
P2Y12 inhibitor eg clopidogrel (inhibits platelet aggregation)

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47
Q

what is venous thrombi and the two main types

A

blood clot blocks a vein
main types= DVT or pulmonary embolism (in right side of heart)

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48
Q

3 arterial thrombi symptoms

A

symptoms: cold, pale, loss of pulse to skin

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49
Q

the cause of venous thrombi

A

due to venous stasis (area of turbulence or potential damage of stasis valves)

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50
Q

3 risk factors of venous thrombi

A

history of DVT and pulmonary embolism and then being inactive for long periods of time can cause venous thrombi

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51
Q

treatment for venous thrombi

A

treatment: anticoagulants- DOACs, warfarin

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52
Q

4 symptoms of venous thrombi

A

symptoms: tender, swollen, red, one side of the leg affected

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53
Q

what is the rule of virchow’s triad

A

typically 2 factors out of the 3 r required for thrombosis

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54
Q

factors affecting thrombosis and what causes them (5,3,4)

A

endothelial injury: due to trauma, surgery, myocardial infarction/ HYPERTENSION or smoking
abnormal blood flow: usually a decrease in blood
stasis (change in blood flow)- due to IMMOBILISATION, ATRIAL FIBRILLATION and varicose veins
hyper coagulability: due to ATHEROSCLEROSIS, sepsis, malignancy, pregnancy

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55
Q

why is smoking signficant in the virchow’s triad and explain the mechanisms of how?

A

causes a change in blood flow and endothelial damage (affects 2 factors)
nicotine increases HR and BP which increase force on endothelium (can cause endothelial damage)
free radicals damage the endothelium, causing atherosclerotic plaques which increase turbulence

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56
Q

what is the definition of hypercoagulability

A

change in blood constituents

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57
Q

what r the 4 fates of thrombi

A

resolution: fibrinolysis of thrombi (normal response)
organisation: leaves fibrotic scar tissue behind
recanalisation: returned blood flow to obstructed area through growth of new capillaries
embolism: fragments of thrombi break off and lodge in the distal circulation

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58
Q

what is an emboli

A

mass of material in vascular system able to lodge in vessel and block its lumen

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59
Q

what is a arterial emboli and what is the composition of the emboli

A

thrombi formed in artery, higher amounts of platelets making up the clot

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60
Q

what is a venous emboli and what is the composition of the emboli

A

thrombi formed in vein, higher amounts of fibrin making up the clot

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61
Q

where do arterial emboli lodge and travel and cause (3)

A

lodges in systemic circulation (thrombi is from from left side of heart)
travels to heart/ brain/ peripheries to cause heart attack/ stroke/ gangrene

62
Q

where do venous emboli lodge and travel (2)

A

lodges in pulmonary circulation (thrombi is from right side of heart)

lodges in pulmonary arteries= PE

lodges in peripheries= DVT

this can break off and cause pulmonary embolism

(PE is normally secondary to DVT)

63
Q

what r arterial ulcers caused by and their appearance

A

caused by lack of blood supply to a tissue which causes tissue to die due to lack of oxygen and leaves a open wound

PUNCHED OUT HOLES with little exudate

64
Q

what r venous ulcers caused by and their appearance

A

problem with circulation usually caused by faulty valves. This leads to high blood pressure which damage small blood vessels and makes them fragile. As a result, skin can break easily and form an ulcer
less markated with lots of exudate

65
Q

location of arterial ulcers

A

on tips of toes and lateral malleolus

66
Q

presentation of arterial ulcers (3)

A

pale, cool skin with low distal pulse

67
Q

location of venous ulcers

A

on medial malleolus and inner calf

68
Q

DVT presentation on skin (1)

A

have erythematous skin (for DVT)

69
Q

what is an atherosclerosis

A

plaques that form in intima and media of arteries

70
Q

6 risk factors of atherosclerosis

A

diabetes mellitus, hypertension, smoking, obesity, old age, male

71
Q

atherosclerotic plaque composition (6)

A

lipids, smooth muscle, MACROPHAGES, FOAM CELLS (macrophages that phagocytose LDLs), platelets, fibroblasts

72
Q

5 steps of atherosclerosis

A

fatty streak formation: precursor for plaque
lipid accumulation: increase in LDLs, macrophages recruited to phagocytose this= foam cells
platelet aggregation: plaque protrude into the artery lumen, disrupts laminar flow so platelets accumulate and thinning of the media occurs
FIBRIN MESH AND RBC TRAPPING: platelet plug forms fibrin mesh over itself and a stable secondary platelet plug is formed and RBCs r trapped within this
fibrous cap: fibroblasts from smooth muscle cap over the secondary plug= stable atheroma

73
Q

what is a complication of an unstable atherosclerotic plaque

A

thrombi

74
Q

what is an unstable atheroma and what happens because of this

A

DAMAGED cap means thrombi formation

75
Q

what is apoptosis (5 key things to mention, 1 point/ definition)

A

genetically programmed non-inflammatory controlled cell death of INDIVIDUAL/ SMALL GROUPS OF CELLS

76
Q

what r the 3 mechanisms of apoptosis

A

intrinsic, extrinsic and cytotoxic

77
Q

what r the steps of apoptosis (5)

A

cells shrink, organelles retained, cell surface membrane REMAINS INTACT
CHROMATIN unaltered and is fragmented for easier phagocytosis
phagocytoses

78
Q

What is the BCL 2 and Bax ratio and why is it signifcant

A

ratio that is maintained between an anti-apoptotic (BCL2) and a pro-apoptotic. So when the intrinsic pathway of apoptosis means Bax has a higher proportion, it determines that apoptosis will occur

79
Q

intrinsic pathway for apoptosis

A

Bax (protein) acts on mitochondrial membrane and promotes cytochrome C release
activates caspases to cause apoptosis

80
Q

is necrosis pathological or physiological

A

always pathological

81
Q

what r the two types of apoptosis and give examples for each

A

pathological eg HIV
physiological eg duodenal cell turnover

82
Q

extrinsic pathway for apoptosis

A

FasL or TNF alpha binds to cell surface membrane receptors
this activates caspases which cause apoptosis

83
Q

what is the caspase cascade

A

the common pathway of caspase production in all 3 mechanisms which causes apoptosis

84
Q

cytotoxic pathway for apoptosis

A

CD8+ binding releases granzyme B from CD8+ cells
granzyme B-> perforin-> caspases which causes apoptosis

85
Q

what is necrosis (3) and causes of it (5)

A

traumatic unprogrammed cell death due to an adverse event
causes: INFARCTION, burns, frost bite, infection, trauma

86
Q

what is the main cytokine that causes apoptosis/ necrosis and what it it released by

A

tumor necrosis factor alpha, macrophages

87
Q

what follows necrosis

A

acute inflammation

88
Q

what r the 4 types of necrosis and explain each one

A

coagulative necrosis (cell death due to ischaemia)
liquefactive (cell death caused by mostly infectious agents- brain becomes soup)
caseous (cell death with a soft cheese appearance due to granuloma formation eg TB)
gangrenous (cell death dye to loss of blood supply causing tissue to die and turn black black due to deposits of iron from Hb in the thrombi)

89
Q

what r the 4 steps of necrosis of cells

A

cells burst
organelles splurge
cell surface membrane damaged
chromatin is altered which leads to death of the cell

90
Q

define hypertrophy and give an example

A

cell gets bigger eg muscles

91
Q

define hyperplasia and what cells do they occur in

A

number of cells increases via mitosis
only occurs in cells that divide (so not neurones or myocytes)

92
Q

define atrophy

A

number and/ or size of cells decrease

93
Q

define Metaplasia and give an example

A

change of cell type from one to another eg Barrett’s oesophagus

94
Q

what is dysplasia and what does this indicate

A

change of a differentiated cell type to a poorly differentiated type
mostly indicated pre/cancerous changes

95
Q

define carcinogenesis in terms of cells

A

transformation of normal to neoplastic cells through permanent mutations

96
Q

define a neoplasm (acronym)

A

autonomous, abnormal, persistent new growth (AAPNG- like Bibi vengeance)

97
Q

which malignant neoplasm never metastises

A

basal cell carcinoma

98
Q

why does necrosis occur in neoplasms and what type of neoplasms is this common in

A

neoplasms outgrow their blood supply due to a fast growth rate- malignant neoplasms

99
Q

what happens to neoplasms bigger than 2mm

A

they require blood supply and they start angiogenesis

100
Q

what cells can neoplasms develop from

A

can only arise from nucleated cells (not from erthyrocytes but can come from their precursors)

101
Q

what is a carcinogen

A

cancer causing agent

102
Q

what r the 5 types of carcinogens

A

chemicals eg paints, dyes, rubber, soot
viruses eg epstein barr-> Burkitt’s, human papillomavirus eg cervical cancer
ionising and non-ionising radiation eg UVB in skin cancer, ionising is in lots
hormones and parasites and mycotoxins eg increase in oestrogen implicated in breast cancer
miscellaneous eg asbestos (mineral)

103
Q

what r the 2 types of mutations

A

genuine and somatic

104
Q

what is a genuine mutation and will it pass down to the next generation

A

mutated original germ cell= will pass down onto next generation

105
Q

what is a somatic mutation and will it pass down to the next generation

A

mutated mitotic copy of germ cell -> won’t pass on to the next generation

106
Q

what r the 2 mutations in colorectal cancer

A

FAP: familial adenomatous polyposis
HNPCC: lynch syndrome (non-polyposis)

107
Q

what is the mutation in FAP, what does it lead to and what type of genetic condition is it

A

mutated APC gene (adenometous polyposis coli)= millions of colorectal adenomas
inevitable adenocarcinoma
autosomal dominant

108
Q

what is the mutation in HNPCC, what does it lead to and what type of genetic condition is it

A

mutated MSH gene
lynch syndrome which is non-polyposis
autosomal dominant

109
Q

What r the 5 steps of metastasis

A

detachment (from primary growth)
invasion of tissue (extracellular matrix)
invasion of basement membrane of the blood vessels
evasion of host defence whilst travelling in circulation
extravasation out of blood vessel to distant site
angiogenesis for own blood supply

110
Q

what r the 3 methods of metastasis spread

A

HAEMATOGENOUS, lymphatic and transcolemic

111
Q

what is haematogenous spread and 4 examples of cancers that spread this way

A

metastasis spread via blood
liver, lung, bone, breast

112
Q

what r the 5 carcinomas that metastasise to bone (ACRONYM)

A

breast, lung, thyroid, kidney and prostate (These Kancers Like Peoples Bones)

113
Q

what is lymphatic spread, where r secondary metastasises formed and 1 example

A

via lymphatics with secondary formation in lymph nodes
eg breast carcinoma metastasises to axillary and internal mammary lymph nodes

114
Q

what is transcolemic spread and what three mediums does it spread through

A

via exudative fluid accumulation
spreads through pleural, pericardial and peritoneal effusions

115
Q

what method of spread do sarcomas usually follow

A

haematogenous

116
Q

what method of spread do carcinomas usually follow and what r the 4 exceptions

A

lymphatic
exceptions: follicular thyroid, choriocarcinoma, renal cell carcinoma, hepatocellular carcinoma

117
Q

define tumor

A

defined as any abnormal swelling

118
Q

what 4 things does the TERM tumor encompass

A

includes neoplasm, inflammation, hypertrophy and hyperplasia

119
Q

what two things r tumors classed by and what r they

A

classified by behaviour and histogenesis
behaviour= malignant or benign
histogenesis= origin cell of tumour

120
Q

what is a clot (why is it different to a thrombi)

A

formed outside the blood vessels or after death

121
Q

give 2 examples of an infective agent resistant to phagocytosis

A

mycobacterium tuberculosis (TB)
mycobacterium leprae (leprosy)

122
Q

what r the two types of benign epithelial neoplasms

A

papilloma= benign neoplasm of non-secretory, non-glandular epithelium
adenoma= benign neoplasm of secretory or glandular epithelium eg pituitary gland

123
Q

what r the two types of malignant epithelial neoplasms

A

carcinoma= malignant epithelial neoplasm eg basal cell carcinoma , squamous cell carcinoma
adenocarcinoma= malignant neoplasm of glandular epithelium

124
Q

what is the classification for leukaemias and lymphomas

A

malignant

125
Q

what is advantageous about basal cell carcinoma never metastasising

A

can be surgically excised

126
Q

what is the suffix for benign connective tissue and malignant connective tissue neoplasms

A

oma-benign
sarcoma-malignant

127
Q

name for benign adipose tissue neoplasm

A

lipoma

128
Q

name for malignant adipose tissue neoplasm

A

liposarcoma

129
Q

name for benign blood vessels neoplasm

A

angioma

130
Q

name for malignant blood vessel tissue neoplasm

A

angiosarcoma

131
Q

name for benign nerves neoplasm

A

nueroma

132
Q

name for malignant nerves neoplasm

A

neurosarcoma

133
Q

name for benign smooth tissue neoplasm

A

leiomyoma

134
Q

name for malignant smooth tissue neoplasm

A

leiomyosarcoma

135
Q

name for benign striated tissue neoplasm

A

rhabdomyoma

136
Q

name for malignant striated tissue neoplasm

A

rhabmomyosarcoma

137
Q

name for benign bone neoplasm

A

osteoma

138
Q

name for malignant bone neoplasm

A

osteosarcoma

139
Q

name for benign cartilage neoplasm

A

chondroma

140
Q

name for malignant cartilage neoplasm

A

chrondrosarcoma

141
Q

two methods of measuring tumors and what does each assess

A
  1. tumor staging via TNM classification, assesses spread
  2. tumor grading via resemblance to parent cell of origin (grade 1-3) assesses malignancy
142
Q

how does TNM staging work?

A

T- tumor size (scale of 1-4)- classified by how far it has invaded
N- degree of lymph nodes affects (0-2)
M- extent of distant metastasis (0-2)

143
Q

explain characteristics of benign tumors regarding:
extent of invasion, mitotic growth, circumscription, growth direction, whether it is common to have necrosis and ulceration and its resemblance to normal tissue

A

localised- no BM invasion
slow growing
well circumsized
exophytic growth outwards
rare to have ulceration and necrosis
close resemblands to normal tissue

144
Q

explain characteristics of malignant tumors regarding:
extent of invasion, mitotic growth, circumscription, growth direction, whether it is common to have necrosis and ulceration, nucleus stain and its resemblance to normal tissue

A

BM invading
fast mitotic growth
poor circumscription
endophytic growth inwards
common for necrosis and ulcers
hyper dense dark-staining nucleus
little resemblance to normal tissue due to poor differentiation

145
Q

4 consequences of benign tumors

A

pressure on local structures eg optic chiasm
obstruction
transformation into malignant
hormone secretion eg prolactinoma

146
Q

consequences of malignant tumors (3 points

A

same as benign and:
they form secondary tumors
often painful

147
Q

3 neoplastic cell characteristics

A

AUTOCRINE STIMULATION (stimulates self growth)
evasion of apoptosis
telomerase action

148
Q

explain what neoplastic cell autocrine growth stimulation involves (3)

A

over-expression of growth factors, inhibition of tumor suppressor genes eg p53,under expression of growth inhibitors

149
Q

explain what neoplastic cell telomerase involves (2) and how does this help the neoplasm do (1)?

A

neoplastic cells prevent telomeres shortening with each replication, preventing its growth rate being limited, which gives it an ability to invade the BM

150
Q

what 3 cancers r screened for in the UK and how

A

cervical: cervical swab
breast: mammogram
colon: fecal occult

2A content- Sameera (21 decks)

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