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Week 2 Flashcards

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1
Q

What is pathology?

A

the study of disease

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2
Q

What is disease?

A

abnormality of cell / tissue structure and/or function

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3
Q

What is meant by general pathology?

A

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

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4
Q

What is meant by systemic pathology?

A

general processes occurring in each system

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5
Q

WHat are the levels of magnification?

A

gross
light microscopy
electron microscopu
molecular cell biology

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6
Q

What are the broad tissue types?

A 
epithelial
connective tissue
haematology-lymphoid
neuro-glial
melanocytic
germ cell
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7
Q

What types of environmental changes (stresses) are there?

A

external and internal

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8
Q

Give examples of external stresses

A

physical factors
chemical factors
infection
nutrition

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9
Q

Give examples of internal stresses

A

more or less functional demand
hormones/metabolic
immune response etc

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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
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11
Q

What are examples of categories of disease?

A

developmental
inflammatory
neoplastic
degenerative

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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
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13
Q

Give examples of physical agents that cause disease

A

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

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14
Q

What is hypoxia?

A

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

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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

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16
Q

describe reversible cell damage

A

changes due to stress in environment

return to normal once stimulus removed

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17
Q

Describe irreversible cell damage

A

permanent

cell death, usually necrosis follows

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18
Q

Describe the pathogenesis of cell injury

A

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

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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

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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

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21
Q

What is meant by necrosis?

A

unprogrammed cell death

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22
Q

What is infarction?

A

necrosis caused by loss of blood supply

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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

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24
Q

WHat can happen to the nucleus in necrosis?

A

nuclear fading
shrinkage
fragmentation

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25
What is coagulative necrosis?
firm, tissue outline retained. Haemorrhagic - blockage of venous drainage Gangrenous - larger area
26
What is colliquitive necrosis?
tissue becomes liquid and its structure is lost e.g. infective abscess, cerebral infarct
27
WHat is caseous necrosis?
combination of coagulative and colliquitive, appearing cheese-like: classical for granulomatous inflammation - especially TB
28
What is fatty necrosis?
Due to action of lipase on fatty tissue
29
In what normal situations does apoptosis occur?
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
30
Describe the morphology of apoptosis
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
31
Describe amyloid
organisation of soluble protein fibrils into specific abnormal, insoluble aggregates resembles fibrosis without prior inflammation can be stained by congo red
32
How can amyloid occur?
excessive production / accumulation of a normal protein or | production/accumulation of an abnormal protein and tendency to misfiled
33
describe AL amyloid
immunoglobulin light chain | produced by B-ce neoplasms e.g. multiple myeloma
34
Describe AA amyloid
serum amyloid associated protein (normal AP protein_ produced in liver produced in prolonged chronic inflammation e.e.g RA
35
What are the 2 types of calcification?
dystrophic and metastatic
36
Describe dystrophic calcification
deposition in abnormal tissue with normal serum calcium
37
Describe metastatic calcification
deposition in normal, living tissue with raised serum calcium often in connective tissue of blood vessels can compromise tissue function
38
What is inflammation?
a physiological response to tissue injury vascular and cellular components can be acute or chronic terminates in resolution, repair or continues
39
What are some causes of inflammation?
infection tissue necrosis(burn, radiation, injury, trauma) foreign material immune reactions
40
What are the 5 cardinal signs?
``` redness heat swelling pain loss of function ```
41
What vascular changes occur in inflammation?
vasodilation increased vascular permeability vascular congestion/stasis Endothelial activation
42
Describe vasodilation in inflammation
transient vasoconstriction then vasodilation starts in arterioles increased blood flow due to histamine, NO on vascular smooth muscle
43
Describe increased vascular permeability
``` 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 ```
44
What are the steps that WBCs migrate to the site of inflammation?
``` margination rolling adhesion migration (diapedesis) CHemotaxis ```
45
Describe margination
white cells more peripheral due to stasis
46
Describe rolling
``` white cells stick and detach from wall mediated by selecting upregulated by IL!, and TNF histamine, thrombin, PAF, Binds L-selectin on leukocytes ```
47
Describe adhesion
mediated by interns stimulated by IL1 and TNF chemokines also facilitate binding reorganisation of cytoskeleton
48
Describe diapedesis
chemokines act on leukocytes to stimulate migration across the endothelium
49
Describe chemotaxis
``` travel along a chemical gradient bacterial products cytokines IL8 complement leukotriene (from arachidonic acid) ```
50
What are involved in the activation of leukocytes and recognition of microbes?
toll like receptors g-protein coupled receptors onPMNs and macrophages Receptors for opsonins on surface of leukocytes receptors for cytokines on surface of leukocytes
51
Describe the roll of toll-like recptors
receptors for microbial products on the surface of leukocytes stimulate microbe killing and cytokine production
52
Describe G protein coupled receptors on PMNs and macrophages
Recognise products of short bacterial peptides, complement, prostaglandinds induce migration of cells and production of respiratory burst
53
Describe the roll of receptors for opsonins on surface of leukocytes
coating a particle target for ingestion | coating includes antibodies and complement
54
Describe phagocytosis
opsonisation engulfment using pseudopodia formation of phagosomes fusion with lysosomes containing enzymes to form phagolysososmes material destroyed and removed from cell by pinocytosis
55
Describe termination of the acute response
``` removal of stimulus neutrophils have short half life variation in cytokine stimuli neural impulses macrophages are activated to perform different functions ```
56
Give examples of cellular derived mediators of inflammation
vasoactive amines (histamine and serotonin) arachidonic acid metabolites nitric oxide cytokines
57
Give examples of plasma protein derived mediators of inflammation
complement | coagulation and kinin systems
58
What is the role of histamine?
from mast cells, basophils and platelets | vasodilation, increased vascular permeability, endothelial activation
59
What is the role of serotonin?
from platelets vasodilation increased vascular permeabiltiy
60
What is the role of prostaglandin?
from mast cells and leukocytes | vasodilation, pain, fever
61
What is the role of leukotriene?
from mast cells, leukocytes | increased vascular permeability, chemotaxis, leukocyte adhesion and activation
62
What is the role of platelet activating factor
from leukocytes, mast cells. | vasodilation, increased vascular permeability, leukocyte adhesion, degranulation, oxidative burst
63
What is exudate?
extra-cellular fluid with a high protein and cellular content
64
What types of exudate are there?
``` serous fibrinous suppurative haemorrhage mebranous pseudomembranous necrotising ```
65
Describe the action of neutrophil polymorphs
``` opsonisation phagocytosis intra-cellular killing of microorganisms oxygen dependent / independent release lysosomal products, propagating the response ```
66
Describe the actions of mast cells
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
What are the beneficial effects of acute inflammation?
dilution of toxins by oedema fluid increased entry of antibodies and drug transport fibrin traps micro-organisms stimulation of immune response
68
What are the detrimental effects of acute inflammation?
digestion of normal tissues swelling (epiglottis) inappropriate response
69
What are the 4 key clinical features on systemic inflammatory response?
increased RR Increased HR high or low temp low or raise WCC
70
Describe resolution of acute inflammation
``` 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
Describe healing by fibrosis
after substantial tissue damage tissue incapable of regeneration abundant fibrin exudate
72
Describe progression to chronic inflammation
persistent stimulus | tissue destruction leading to ongoing inflammation n
73
When is inflammation defined as chronic?
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
What are the factors which are imporant in whether inflammation becomes chronic?
``` site affected type of wound presence of infection and the type of organism involved presence of indigestible material treatment given background disease ```
75
What types of cells are involved in chronic inflammation?
macrophages plasma cells lymphocytes
76
what are the activated macrophage products involved in tissue destruction?
``` toxic oxygen metabolites proteases neutrophil chemotactic factors coagulation factors arachidonic acid metabolites nitric oxide ```
77
What are the activated macrophage products involved in fibrosis?
``` growth factors (PDGF, FGF) fibrogenic cytokines (TGF beta) angiogenesis factors remodelling collagenases ```
78
What are the predominant cell types in granulomatous inflammation?
activated macrophages with a modified appearance (epithelia macrophages) and giant cells (formed from fused epitheloid macrophages) lymphocytes
79
What is caseous necrosis characteristic of?
tuberculosis
80
What are some causes of chronic granulomatous inflammation?
TB, leprsoy, toxoplasmosis foreign materal sarcoidosis, crown's disease response to tumour (e.g. hodgkin lymphoma)
81
Describe epithelia macrophages
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
What is formation of granulomas a manifestation of?
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
Describe atherosclerosis and inflammation
macrophage key role endothelial injury (sheer stress, smoking etc) recruitment of macrophages, become foam cells, lymphocytes release chemical mediators
84
Describe chronic granulomatous disease
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
What are the three phases of cutaneous wound healing?
inflammation proliferation maturation
86
How do wounds heal?
``` 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
Describe the inflammatory phase of fracture healing
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
Describe the repair phase of fracture healing
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
Describe the remodelling phase of fracture healing
occurs slowly over months and years returns bone to its original shape, structure and mechanical strength facilitated by mechanical stress
90
What are the local factors that influence wound healing?
``` type, size and location of wound movement of wound infection presence of foreign / necrotic material irradiation poor blood supply ```
91
What are the systemic factors that influence wound healing?
``` age nutrition (vitamin C, zinc) systemic disease (e.g. renal failure, diabetes) drugs (esp. steroids) smoking ```
92
What is carried out in the external examination in an autopsy?
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
What are the outcomes of MI that can cause death?
arrhythmia or acute left ventricular failure | cardiac rupture through weakened muscle
94
What is an embolism?
a mass of material that can move through the vascular system and is capable of blocking the lumen
95
What can an embolus be?
thrombus air fat amniotic fluid
96
What can cause a blood vessel to rupture?
high pressure congenital weakness weakened by disease eroded into
97
What are virchow's triad?
hypercoagulable state vascular wall injury circulatory stasis
98
describe arterial thrombi
"white thrombus" many platelets, small amounts of fibrin
99
Describe venous thrombi
"red thrombus" many fibrin with trapped red cells
100
What are the risk factors for DVT?
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
How is DVT diagnosed?
clinical decision rule blood tests - fibrin D-dimer image venous system of leg
102
How is VTE prevented?
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
What are the risk factors for arteriosclerotic cardiovascular disease?
``` smoking hypertension hyperlipidaemia diabetes obesity family history ```
104
What are the visible structures seen in a chest X-ray?
``` trachea hilum lungs diaphragm heart aortic knock;e ribs scapulae breasts stomach ```
105
What are important invisible / obscure structures in a chest X-ray?
``` sternum oesophagus spine fissures pleura aorta ```
106
in which lung is aspiration more common and why?
on the right - straight main bronchus
107
What can blunting of the costophrenic recess indicate?
collection of fluid, pleural thickening
108
What are emergency indications for CXRs?
``` acute respiratory symptoms chest pain septic screen acute abdomen post central line / chest drain insertion ```
109
What are indications for elective CXRs?
persistant/chronic respiratory symptoms pre-operative work up metastatic screen TB contacts
110
Describe imunohistochemistry
staining technique which yields brown staining of specific proteins
111
What are the applications of IHC?
tumour diagnosis and classification prediction of prognosis of treatment efficacy and diagnosis of effective disease
112
What is a developmental anomaly?
any congenital defect that occurs when normal growth and differentiation of the foetus is disturbed
113
What can cause developmental anomalies?
genetic mutations, chromosomal aberrations, teratogens and environmental factors
114
Describe the possible consequences of ventricular spatial defect
uncorrected VSD can increase pulmonary resistance leading to reversal of the left to right shunt and corresponding cyanosis
115
What are some of the symptoms of spina bifida?
``` muscle weakness or paralysis bowel and bladder problems seizures orthopaedic problems hydrocephalus ```
116
What is a hamartoma?
malformation that may resemble a neoplasm that results from faulty growth in an organ
117
What is meant by diverticulum?
circumsised pouch caused by herniation of lining mucosa of an organ through defect in muscular coat
118
What are the potential effects of diverticular disease?
inflammation, bleeding, perforation, fistulation
119
Where does Meckel's diverticulum usually occur?
the terminal ileum
120
What are some causes of atrophy?
``` loss of innervation diminished blood supply inadequate nutrition decreased workload loss of endocrine stimulation ageing ```
121
What is metaplasia?
reversible change from one fully differentiated cell type to another
122
What is a neoplasm?
an abnormal tissue mass the growth of which is excessive and uncoordinated to adjacent normal tissue
123
What is a benign neoplasm?
it grows without invading adjacent tissue or spreading to distant sites usually well-circumscribed due to the lack of invasion of surrounding tissues
124
What is a malignant neoplasm?
a neoplasm that invades the surrounding normal tissue can spread to distant sites usually is not well circumscribed
125
What is the prefix for fat in tumour naming?
lipo
126
What is the prefix for skeletal muscle in tumour naming?
rhabdo
127
What is the prefix for smooth muscle in tumour naming?
leio
128
What is the bone in tumour naming?
osteo
129
What is the prefix for cartilage in tumour naming?
chondro
130
What is the prefix for glands in tumour naming?
adeno
131
What is the prefix for meninges in tumour naming?
menigio
132
What is the prefix for vascular in tumour naming?
angio
133
What is the ABCD in malignant melanoma?
asymmetry border - irregular, faded colour - even? diameter - more than 1cm
134
How are tumours staged?
TNM size, local invasion nodes - how many? metastasis - distant?
135
What is dysplasia?
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
What is carcinoma in situ?
full-thickness epithelial dysplasia extending from the basement membrane to the surface of the epithelium
137
How can tumours metastasise?
lymphatic haematogenous transcoelemic spread

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