Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 3 > Week 2 > Flashcards

Week 2 Flashcards

1
Q

What is pathology?

A

the study of disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is disease?

A

abnormality of cell / tissue structure and/or function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is meant by general pathology?

A

disease causes and processes in general. e.g. inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is meant by systemic pathology?

A

general processes occurring in each system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

WHat are the levels of magnification?

A

gross
light microscopy
electron microscopu
molecular cell biology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the broad tissue types?

A 
epithelial
connective tissue
haematology-lymphoid
neuro-glial
melanocytic
germ cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What types of environmental changes (stresses) are there?

A

external and internal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Give examples of external stresses

A

physical factors
chemical factors
infection
nutrition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Give examples of internal stresses

A

more or less functional demand
hormones/metabolic
immune response etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What can happen to a cell when the stress is too great to be dealt with by homeostasis?

A 
atrophy
hyperplasia
hypertrophy
metaplasia
dysplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are examples of categories of disease?

A

developmental
inflammatory
neoplastic
degenerative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are examples of causes of disease?

A 
congenital vs acquired
physical agents
chemicals 
drugs
infections
hypoxia/ischaemia
immunoligical reactions
nutritional
endocrine / metabolic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Give examples of physical agents that cause disease

A

mechanical trauma - stricture, adhesions, hernia, criminal
temperature extremes
ionising radiation
electric shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is hypoxia?

A

deficiency of oxygen
Causes - anaemia, respiratory failure
disrupts oxidative respiratory processes in cell so decreases ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is ischaemia?

A

reduction in blood supply to tissue.
Caused by blockage of arterial supply or venous drainage
depletion of not just oxygen but also nutrients
more severe and rapid damage than hypoxia alone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

describe reversible cell damage

A

changes due to stress in environment

return to normal once stimulus removed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe irreversible cell damage

A

permanent

cell death, usually necrosis follows

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe the pathogenesis of cell injury

A

damage to mitochondria -
cell membrane - disrupted ion concentrations, esp .Ca2+
Cytoplasmm
nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe oxidative stress

A

caused by reactive oxygen species
normal by-product of respiration in small amounts
formed pathologically by absorption of radiation, toxic chemicals, hypoxia etc
lack of antioxidants makes damage more likely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

WHat are the changes mainly seen in reversible injury?

A

“cloudy swelling” osmotic disturbance: loss of energy dependent Na pump leads to Na build up of intracellular metabolites
Cytoplasmic blebs, disrupted microvilli, swollen mitochondria
“fatty change” accumulation of lipid vacuoles in cytoplasm causes by disruption of fatty acid metabolism, especially in the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is meant by necrosis?

A

unprogrammed cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is infarction?

A

necrosis caused by loss of blood supply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the histological changes seen in necrosis?

A

cell swelling, vacuolation and disruption of membranes od cell and its organelles
release of cell contents including enzymes causes adjacent damage and acute inflammation
DNA disruption and hydrolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

WHat can happen to the nucleus in necrosis?

A

nuclear fading
shrinkage
fragmentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is coagulative necrosis?

A

firm, tissue outline retained.
Haemorrhagic - blockage of venous drainage
Gangrenous - larger area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is colliquitive necrosis?

A

tissue becomes liquid and its structure is lost e.g. infective abscess, cerebral infarct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

WHat is caseous necrosis?

A

combination of coagulative and colliquitive, appearing cheese-like: classical for granulomatous inflammation - especially TB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is fatty necrosis?

A

Due to action of lipase on fatty tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

In what normal situations does apoptosis occur?

A

embryogenesis
hormone dependent involution; uterus, breast, ovary
cell deletion in proliferating cell populations to maintain constant number
deletion of inflammatory cells after response
deletion of self-reactive lymphocytes in thymus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Describe the morphology of apoptosis

A

cell shrinkage
chromatin condensation: packing up of nucleus
membrane of cell and mitochondria remain in tact
cytoplasmic blebs form and break off to form apoptotic bodies which are phagocytosed by macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Describe amyloid

A

organisation of soluble protein fibrils into specific abnormal, insoluble aggregates
resembles fibrosis without prior inflammation
can be stained by congo red

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How can amyloid occur?

A

excessive production / accumulation of a normal protein or

production/accumulation of an abnormal protein and tendency to misfiled

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

describe AL amyloid

A

immunoglobulin light chain

produced by B-ce neoplasms e.g. multiple myeloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Describe AA amyloid

A

serum amyloid associated protein (normal AP protein_ produced in liver
produced in prolonged chronic inflammation e.e.g RA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the 2 types of calcification?

A

dystrophic and metastatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Describe dystrophic calcification

A

deposition in abnormal tissue with normal serum calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Describe metastatic calcification

A

deposition in normal, living tissue with raised serum calcium
often in connective tissue of blood vessels
can compromise tissue function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is inflammation?

A

a physiological response to tissue injury
vascular and cellular components
can be acute or chronic
terminates in resolution, repair or continues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are some causes of inflammation?

A

infection
tissue necrosis(burn, radiation, injury, trauma)
foreign material
immune reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the 5 cardinal signs?

A 
redness
heat 
swelling
pain
loss of function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What vascular changes occur in inflammation?

A

vasodilation
increased vascular permeability
vascular congestion/stasis
Endothelial activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Describe vasodilation in inflammation

A

transient vasoconstriction then vasodilation
starts in arterioles
increased blood flow
due to histamine, NO on vascular smooth muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Describe increased vascular permeability

A 
contraction of endothelial cells
increased interendothelial spaces
mediated by histamine, bradykinin, substance P
endothelial injury in severe injuries 
injury can be caused by neutrophils 
increased transcytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the steps that WBCs migrate to the site of inflammation?

A 
margination
rolling
adhesion
migration (diapedesis)
CHemotaxis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Describe margination

A

white cells more peripheral due to stasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Describe rolling

A 
white cells stick and detach from wall
mediated by selecting
upregulated by IL!, and TNF
histamine, thrombin, PAF,
Binds L-selectin on leukocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Describe adhesion

A

mediated by interns
stimulated by IL1 and TNF
chemokines also facilitate binding
reorganisation of cytoskeleton

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Describe diapedesis

A

chemokines act on leukocytes to stimulate migration across the endothelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Describe chemotaxis

A 
travel along a chemical gradient
bacterial products 
cytokines IL8
complement
leukotriene (from arachidonic acid)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are involved in the activation of leukocytes and recognition of microbes?

A

toll like receptors
g-protein coupled receptors onPMNs and macrophages
Receptors for opsonins on surface of leukocytes
receptors for cytokines on surface of leukocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Describe the roll of toll-like recptors

A

receptors for microbial products on the surface of leukocytes
stimulate microbe killing and cytokine production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Describe G protein coupled receptors on PMNs and macrophages

A

Recognise products of short bacterial peptides, complement, prostaglandinds
induce migration of cells and production of respiratory burst

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Describe the roll of receptors for opsonins on surface of leukocytes

A

coating a particle target for ingestion

coating includes antibodies and complement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Describe phagocytosis

A

opsonisation
engulfment using pseudopodia
formation of phagosomes
fusion with lysosomes containing enzymes to form phagolysososmes
material destroyed and removed from cell by pinocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Describe termination of the acute response

A 
removal of stimulus
neutrophils have short half life
variation in cytokine stimuli
neural impulses
macrophages are activated to perform different functions
56
Q

Give examples of cellular derived mediators of inflammation

A

vasoactive amines (histamine and serotonin)
arachidonic acid metabolites
nitric oxide
cytokines

57
Q

Give examples of plasma protein derived mediators of inflammation

A

complement

coagulation and kinin systems

58
Q

What is the role of histamine?

A

from mast cells, basophils and platelets

vasodilation, increased vascular permeability, endothelial activation

59
Q

What is the role of serotonin?

A

from platelets
vasodilation
increased vascular permeabiltiy

60
Q

What is the role of prostaglandin?

A

from mast cells and leukocytes

vasodilation, pain, fever

61
Q

What is the role of leukotriene?

A

from mast cells, leukocytes

increased vascular permeability, chemotaxis, leukocyte adhesion and activation

62
Q

What is the role of platelet activating factor

A

from leukocytes, mast cells.

vasodilation, increased vascular permeability, leukocyte adhesion, degranulation, oxidative burst

63
Q

What is exudate?

A

extra-cellular fluid with a high protein and cellular content

64
Q

What types of exudate are there?

A 
serous
fibrinous
suppurative
haemorrhage
mebranous
pseudomembranous
necrotising
65
Q

Describe the action of neutrophil polymorphs

A 
opsonisation
phagocytosis
intra-cellular killing of microorganisms
oxygen dependent / independent 
release lysosomal products, propagating the response
66
Q

Describe the actions of mast cells

A

reside in tissues
contain histamine and heparin in preformed granules
stimulates to release contents by injury, complement, IgE
role in allergy
also make eicosanoids to propagate immune response

67
Q

What are the beneficial effects of acute inflammation?

A

dilution of toxins by oedema fluid
increased entry of antibodies and drug transport
fibrin traps micro-organisms
stimulation of immune response

68
Q

What are the detrimental effects of acute inflammation?

A

digestion of normal tissues
swelling (epiglottis)
inappropriate response

69
Q

What are the 4 key clinical features on systemic inflammatory response?

A

increased RR
Increased HR
high or low temp
low or raise WCC

70
Q

Describe resolution of acute inflammation

A 
tissue restores back to normal if;
minimal tissue damage
occurs in tissue with regenerative capacity
cause is rapidly removed or destroyed
there is good vascular drainage
71
Q

Describe healing by fibrosis

A

after substantial tissue damage
tissue incapable of regeneration
abundant fibrin exudate

72
Q

Describe progression to chronic inflammation

A

persistent stimulus

tissue destruction leading to ongoing inflammation n

73
Q

When is inflammation defined as chronic?

A

when it is persistent and lacks resolution when the inflamed tissue is unable to overcome the effects of the injurous agent
it persists weeks, months or years
it is characterised by infiltrates of lymphocytes, plasma cells and macrophages

74
Q

What are the factors which are imporant in whether inflammation becomes chronic?

A 
site affected
type of wound
presence of infection and the type of organism involved
presence of indigestible material
treatment given
background disease
75
Q

What types of cells are involved in chronic inflammation?

A

macrophages
plasma cells
lymphocytes

76
Q

what are the activated macrophage products involved in tissue destruction?

A 
toxic oxygen metabolites
proteases
neutrophil chemotactic factors
coagulation factors 
arachidonic acid metabolites
nitric oxide
77
Q

What are the activated macrophage products involved in fibrosis?

A 
growth factors (PDGF, FGF)
fibrogenic cytokines (TGF beta)
angiogenesis factors
remodelling collagenases
78
Q

What are the predominant cell types in granulomatous inflammation?

A

activated macrophages with a modified appearance (epithelia macrophages)
and giant cells (formed from fused epitheloid macrophages)
lymphocytes

79
Q

What is caseous necrosis characteristic of?

A

tuberculosis

80
Q

What are some causes of chronic granulomatous inflammation?

A

TB, leprsoy, toxoplasmosis
foreign materal
sarcoidosis, crown’s disease
response to tumour (e.g. hodgkin lymphoma)

81
Q

Describe epithelia macrophages

A

modified macrophages arranged in small nodules or clusters
have a mainly secretory role rather than phagocytosis
multinucleate giant cells form where material is difficult to digest

82
Q

What is formation of granulomas a manifestation of?

A

T cell mediated immune reaction (delayed type hypersensitivity)
the antigen is presented to CD4+T cells which in turn produce IFN gamma and other cytokines resulting in macrophage activation

83
Q

Describe atherosclerosis and inflammation

A

macrophage key role
endothelial injury (sheer stress, smoking etc)
recruitment of macrophages, become foam cells,
lymphocytes release chemical mediators

84
Q

Describe chronic granulomatous disease

A

defect in NADPH oxidase system within phagocytes
heterogenous, usually x linked
inability to kill intracellular organisms by respiratory burst
patients have repeated and recurrent infections
patients develop granulomata of lymph nodes, skin lungs liver and GI tract

85
Q

What are the three phases of cutaneous wound healing?

A

inflammation
proliferation
maturation

86
Q

How do wounds heal?

A 
formation of blood clot
formation of granulation tissue
cell proliferation and collagen deposition
scar formation
wound contraction 
connective tissue remodelling
recovery of tensile strength
87
Q

Describe the inflammatory phase of fracture healing

A

haematoma forms at site of fracture
prostaglandin recruit neutrophil polymorphs, macrophages, lymphocytes and fibroblasts to the site of injury
granulation tissue, ingrowth of vessels, migration of mesenchymal cells occurs
nutrients and oxygen are supplied by the exposed bone and muscle

88
Q

Describe the repair phase of fracture healing

A

fibroblasts lay down stroma to support ingrowing vessels
collagen matrix is laid down
osteoid is secreted and mineralised leading to soft callous formation
callus ossifies after 4-6 weeks by forming bridge of woven bone between fracture fragments

89
Q

Describe the remodelling phase of fracture healing

A

occurs slowly over months and years
returns bone to its original shape, structure and mechanical strength
facilitated by mechanical stress

90
Q

What are the local factors that influence wound healing?

A 
type, size and location of wound
movement of wound
infection 
presence of foreign / necrotic material
irradiation
poor blood supply
91
Q

What are the systemic factors that influence wound healing?

A 
age
nutrition (vitamin C, zinc)
systemic disease (e.g. renal failure, diabetes)
drugs (esp. steroids)
smoking
92
Q

What is carried out in the external examination in an autopsy?

A

identification of the deceased by the pathologist
height / weight
skin, hair, eye colour
iatrogenic - scars, drains, IV lines
evidence of trauma
jaundice, cyanosis, finger clubbing, oedema, lymphadenopathy

93
Q

What are the outcomes of MI that can cause death?

A

arrhythmia or acute left ventricular failure

cardiac rupture through weakened muscle

94
Q

What is an embolism?

A

a mass of material that can move through the vascular system and is capable of blocking the lumen

95
Q

What can an embolus be?

A

thrombus
air
fat
amniotic fluid

96
Q

What can cause a blood vessel to rupture?

A

high pressure
congenital weakness
weakened by disease
eroded into

97
Q

What are virchow’s triad?

A

hypercoagulable state
vascular wall injury
circulatory stasis

98
Q

describe arterial thrombi

A

“white thrombus” many platelets, small amounts of fibrin

99
Q

Describe venous thrombi

A

“red thrombus” many fibrin with trapped red cells

100
Q

What are the risk factors for DVT?

A

vessel wall - age, varicose veins, surgery
blood flow - obesity, pregnancy, immobilisation, IV catheters, external vein compression
composition of blood - thombophilias
inflammatory conditions, oestrogen hormones

101
Q

How is DVT diagnosed?

A

clinical decision rule
blood tests - fibrin D-dimer
image venous system of leg

102
Q

How is VTE prevented?

A

avoid risk factors if possible
risk assess hospital admission or surgery
provide thrombi-prophylaxis when appropriate
educating patients on risks and avoidance measures - early mobilisation

103
Q

What are the risk factors for arteriosclerotic cardiovascular disease?

A 
smoking
hypertension
hyperlipidaemia
diabetes
obesity
family history
104
Q

What are the visible structures seen in a chest X-ray?

A 
trachea
hilum
lungs
diaphragm
heart
aortic knock;e
ribs
scapulae
breasts
stomach
105
Q

What are important invisible / obscure structures in a chest X-ray?

A 
sternum
oesophagus
spine
fissures
pleura
aorta
106
Q

in which lung is aspiration more common and why?

A

on the right - straight main bronchus

107
Q

What can blunting of the costophrenic recess indicate?

A

collection of fluid, pleural thickening

108
Q

What are emergency indications for CXRs?

A 
acute respiratory symptoms
chest pain
septic screen
acute abdomen
post central line / chest drain insertion
109
Q

What are indications for elective CXRs?

A

persistant/chronic respiratory symptoms
pre-operative work up
metastatic screen
TB contacts

110
Q

Describe imunohistochemistry

A

staining technique which yields brown staining of specific proteins

111
Q

What are the applications of IHC?

A

tumour diagnosis and classification
prediction of prognosis
of treatment efficacy and diagnosis of effective disease

112
Q

What is a developmental anomaly?

A

any congenital defect that occurs when normal growth and differentiation of the foetus is disturbed

113
Q

What can cause developmental anomalies?

A

genetic mutations, chromosomal aberrations, teratogens and environmental factors

114
Q

Describe the possible consequences of ventricular spatial defect

A

uncorrected VSD can increase pulmonary resistance leading to reversal of the left to right shunt and corresponding cyanosis

115
Q

What are some of the symptoms of spina bifida?

A 
muscle weakness or paralysis
bowel and bladder problems
seizures
orthopaedic problems 
hydrocephalus
116
Q

What is a hamartoma?

A

malformation that may resemble a neoplasm that results from faulty growth in an organ

117
Q

What is meant by diverticulum?

A

circumsised pouch caused by herniation of lining mucosa of an organ through defect in muscular coat

118
Q

What are the potential effects of diverticular disease?

A

inflammation, bleeding, perforation, fistulation

119
Q

Where does Meckel’s diverticulum usually occur?

A

the terminal ileum

120
Q

What are some causes of atrophy?

A 
loss of innervation
diminished blood supply
inadequate nutrition
decreased workload
loss of endocrine stimulation
 ageing
121
Q

What is metaplasia?

A

reversible change from one fully differentiated cell type to another

122
Q

What is a neoplasm?

A

an abnormal tissue mass the growth of which is excessive and uncoordinated to adjacent normal tissue

123
Q

What is a benign neoplasm?

A

it grows without invading adjacent tissue or spreading to distant sites
usually well-circumscribed due to the lack of invasion of surrounding tissues

124
Q

What is a malignant neoplasm?

A

a neoplasm that invades the surrounding normal tissue
can spread to distant sites
usually is not well circumscribed

125
Q

What is the prefix for fat in tumour naming?

A

lipo

126
Q

What is the prefix for skeletal muscle in tumour naming?

A

rhabdo

127
Q

What is the prefix for smooth muscle in tumour naming?

A

leio

128
Q

What is the bone in tumour naming?

A

osteo

129
Q

What is the prefix for cartilage in tumour naming?

A

chondro

130
Q

What is the prefix for glands in tumour naming?

A

adeno

131
Q

What is the prefix for meninges in tumour naming?

A

menigio

132
Q

What is the prefix for vascular in tumour naming?

A

angio

133
Q

What is the ABCD in malignant melanoma?

A

asymmetry
border - irregular, faded
colour - even?
diameter - more than 1cm

134
Q

How are tumours staged?

A

TNM
size, local invasion
nodes - how many?
metastasis - distant?

135
Q

What is dysplasia?

A

disordered growth in which cells fail to differentiate fully, but are contained by the basement membrane
cell nuclei become hyper chromatic
nuclear membranes become irregular
nuclear to cytoplasmic ratio increases
dysplasia may regress, persist or progress

136
Q

What is carcinoma in situ?

A

full-thickness epithelial dysplasia extending from the basement membrane to the surface of the epithelium

137
Q

How can tumours metastasise?

A

lymphatic
haematogenous
transcoelemic spread

Phase 3 (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions