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BDS 1 BAMS > microbiology and pathology > Flashcards

microbiology and pathology Flashcards

1
Q

give an example of ectopia

A

normal tissue forming in the wrong place, merkels diverticulum - epithelium at small intestine

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2
Q

give an example of atrophy

A

break down of tissue, if not being used or in disease, osteoporosis - decreased bone density

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3
Q

what is hypertrophy and describe a disease in which this is a factor

A

increase size of cells - muscle cells have reduced mitotic ability so increase in size instead of dividing. heart failure, increased load on heart so muscle bulk increases - ventricular hypertrophy

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4
Q

what is hyperplasia and what can cause it

A

increase number of cells, tissue becomes much thicker , can be caused by medications - gingival hyperplasia by epilepsy medication.

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5
Q

what is metaplasia and give an example of this

A

change of one differentiated tissue to another, change in epithelial type - barrett’s oesophagus, in response to GORD, change from stratified squamous to simple columnar

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6
Q

what is the difference between metaplasia and dysplasi

A

metaplasia is controlled change, dysplasia is uncontrolled, cells dividing all through the tissue, not just at bottom - could become malignant

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7
Q

describe 3 differences between benign and malignant tumours

A

benign tumours are encapsulated, keeping their growth localised. malignant tumours have no capsule, can invade other tissues (metastases). benign tumours have fewer mitotic bodies so have a slower growth rate, malignant tumours have several mitotic bodies so grow much faster. benign tumour cells all look relatively normal and are all similar from same tissue of origin. malignant tumour cells are difficult to see where they come from, all very different and pleumorphic

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8
Q

name the 3 types of carcinogens

A

chemical - tobacco, alcohol
physical - ionising radiation, UV light
viral - HPV

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9
Q

how can carcinogens result in tumour formation

A

initiation - mutating gene of cell giving it neoplasmic potential, another factor then required to cause division and formation of tumour (promotion), then progression, as division continues, malignancy is developed

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10
Q

what is the role of proto-oncogenes

A

produce proteins involved in cell division, growth factors, growth factor receptors, signal transducer

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11
Q

how can proto-oncogenes play a role in cancer

A

one genetic mutation in this gene causes the production of oncogenes which produce oncoproteins - this stimulate cell proliferation, which if uncontrolled can result in tumour formation

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12
Q

what are tumour suppressor genes

A

genes which control cell division, prevents uncontrolled growth

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13
Q

how can tumour suppressor genes play a role in cancer

A

two mutations to this gene results in cells dividing and proliferating in an uncontrolled manner

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14
Q

what is P53 and how is this involved in tumour formation?

A

as cells undergo mitosis, they have check points to check for defective DNA, if this is detected, the P53 can send the cell for DNA repair. If this is not possible, P53 sends the cell into apoptosis, this prevents any mutation being passed down cell lineage. In cancer, this protein is not produced, so mutated genes are passed to all cells, forming more tumour cells

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15
Q

what are the 6 main hallmarks of cancer

A

self-sufficient growth signals, insensitive to anti-growth signals, limitless replicative potential, production and maintenance of angiogenesis, evade apoptosis and metasises and invade other tissues

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16
Q

what is the difference in spread between epithelial cancers and connective tissue cancers

A

epithelial spread via lymph nodes and then blood vessels, connective tissue (sarcomas) spread via blood vessels first

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17
Q

what is tumour grading?

A

looking at a tumour down a microscope, at the histological appearance of the tumour cells - high grade cells are very different to cells of origin (pleomorphic) and many mitotic bodies

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18
Q

what is tumour staging?

A

determining the extent of spread of the tumour, if it is localised or metastised

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19
Q

what staging mechanism is used for oral cancers?

A

TNM - tumour size, lymph node involvement and metastasis

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20
Q

what are the 3 E’s in cancer immunology and what do they mean?

A

Elimination - immune system is removing cancer cells
Equilibrium - immune system and cancer cells are balanced but immune system coping and controlling
Escape - due to immunosuppression or another disease, the cancer cells can escape the immune system and spread to other areas

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21
Q

describe the process of the gram stain

A

stain cells with crystal violet, then iodine. then treat cells with alcohol - if gram negative, this will wash away the iodine stain, if gram positive the stain will remain. then counter stain with safrinin, this will stain colourless gram negative cells pink.

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22
Q

why do certain bacteria retain the gram stain

A

gram positive cells have a lipid bilayer and an outer cell wall of peptidoglycan, between these layers is the periplasmic space. it is in here that the gram stain is retained, as alcohol cannot penetrate through the cell wall to get to here so it is not washed away

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23
Q

describe the structure of gram negative bacteria

A

has a lipid bilayer, peptidoglycan wall and periplasmic space between. but it also has an outer most lipopolysaccharide layer. there is then another periplasmic space between the LPS and peptidoglycan, this is where the iodine is trapped. however, as cells are treated with alcohol, this can penetrate through the LPS and wash away the stain, making it gram negative

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24
Q

what medication can be given for gram positive infections

A

penicilin - breaks down cross-link bonds in peptidoglycan wall

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25
Q

what is the difference between an endotoxin and exotoxin

A

exotoxin - peptides produced within the bacteria, normally gram positive, much more potent and lethal. endotoxin - embedded in LPS in gram negative bacteria, large amount required to be lethal

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26
Q

give an example of a gram positive cocci bacteria

A

in bunches like grapes - stauphlococcus aureus, in chains - streptococcus mutans

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27
Q

give an example of a gram positive bacilli bacteria

A

closstridium difficile

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28
Q

give an example of a gram negative cocci

A

n. meningitis

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29
Q

give an example of a gram negative bacilli

A

prevotallus intermedium

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30
Q

what people are more at risk for fungal infections

A

immunocompromised

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31
Q

what are the 3 types of fungi

A

candida, asperilligus, cryptococcus

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32
Q

how do candida get into the blood stream

A

have hypha that extend from spore, these hypha can get between cells, releasing enzymes to break down the attachments

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33
Q

how are fungal infections treated

A

main aim of treatment is to attack the cell membrane - ergostril, nystatin breaks this down so the cytoplasm leaks out, fluconazol prevents the production of the membrane

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34
Q

describe the structure of a fungi membrane and cell wall

A

wall - beta glucans and chitin, membrane - ergostril

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35
Q

describe structure of a virus

A

nuclei acids, protein coat, some have a lipid envelope, have HA and NA on outside - HA for entrance to a cell, NA for leaving a cell

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36
Q

what effects can a virus have on a cell

A

death, transformation (HPV changes epithelial cell to tumour cell) or latent infection - stays in cell, embeds its DNA into cellular DNA so it is always being replicated, when a person is stressed or immunocompromised, this breaks out of cell

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37
Q

name the steps in the chain of infection

A

infectious agent, reservoir, portal of exit, mode of transmission, portal of entry, susceptible host

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38
Q

what is a differential diagnosis

A

the diagnosis after a medical history and examination, determining what diseases could be linked to the symptoms and signs, but special tests required to determine which one

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39
Q

what are the 2 cell lineages for defence cells

A

myeloid and lymphoid

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40
Q

what defence cells contain granulocytes and what are these

A

granulocytes - vesicles of destructive enzymes and anti-microbial peptides. neutrophils, basophil, eosophil, mast cells

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41
Q

what is the role of the dendritic cell in immunity

A

dendritic cell is in the blood, has long processes which can extend into tissues when detect an infection. their main role is antigen presenting - runs from the site of infection to lymphoid tissue to present antigens to B and T cells

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42
Q

describe antigen presentation

A

dendritic cells internalise and degrade antigen into linear peptides. these are then attached to MHC proteins - either I or II. T cells then bind to these proteins - CD4 to MHC II, CD8 to MHC I

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43
Q

what is the role of natural killer cells

A

respond to cells infected with virus or tumour, tries to kill these whilst waiting for adaptive immunity to kick in

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44
Q

what is koch’s postulates

A

the theory that one bacteria or organism causes one disease. can be proved by taking a sample of those with the disease and growing in culture, showing the organism is present, then putting this organism in an animal model, showing the disease will form, then removing this again and culturing to show its present

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45
Q

how can bacteria attach to surfaces

A

pilli - projections of the outer wall, allow for adhesion, or are capsulated - capsule is thick and sticky

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46
Q

give an example of an infection in which pilli are required

A

UTI - need to stick on to mucosal membrane so they are not washed away by urine

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47
Q

how are capsulated bacteria more dangerous

A

the capsule allows them to hide from the immune system, they are not phagocytosed or attacked therefore they replicate in large numbers and can then be fatal

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48
Q

what are non-professional immune cells

A

epithelial cells and fibroblasts

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49
Q

what are the 3 divisions of innate immunity

A

physical barrier, cellular mechanisms, plasma factors

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50
Q

how do antimicrobial peptides work

A

they are cationic, so are attracted to negatively charged membranes - bacteria. this brings them close to bacteria, then they have a water loving and lipid loving part. the lipid loving part tries to get through bacterial membrane as the water loving part stays outside, creates a pore through which the cell cytoplasm of bacteria leaks through and the cell is lysed

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51
Q

what proteins in saliva have antimicrobial peptides

A

cystatin, lactoferrin, lysosome

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52
Q

how can secretory IgA provide immune defence

A

it is found on mucosal membranes, binds to flagella of bacteria, prevents it moving, stops bacteria from adhering to surfaces and binds to antigens

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53
Q

give an example of a pattern recognition receptor

A

toll-like receptor

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54
Q

what binds to pattern recognition receptors

A

microbial associated molecular patterns - cell wall or membrane or nucelic acids specific

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55
Q

what is the result of activation of pattern recognition receptors

A

activates phagocytosis, alters gene transcription to produce chemokines and cytokines

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56
Q

what is the role of chemokines in innate immunity

A

sets up a chemokine concentration gradient to recruit immune cells to the site of infection

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57
Q

how can leukocytes be recruited in from the bloodstream

A

cytokines activate the endothelial cells to produce selectins - these can bind to carbohydrates in the leukocytes. slows the movement of leukocytes so they are not travelling as fast - neutrophil rolling. integrins are then activated which stop the neutrophils from moving so they can then be pulled through the gap junctions in endothelial cells by CD31

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58
Q

how do neutrophils attack foreign cells

A

has neutrophil extracellular traps, these hold the bacteria close to the neutrophil, it then degranulates releasing antimicrobial peptides to kill the infection

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59
Q

explain phagocytosis

A

the phagocyte engulfs the bacteria so it is in a vesicle in the cell - phagosome, this then fuses with a lysosome to form a phagolysosome, this then breaks the infection down to residual bodies and waste

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60
Q

how does phagocytosis differ to antigen presentation

A

antigen presentation also engulfs the cell and then fused with a lysosome - phagolysosome but instead of waste being produced, it is broken down to smaller peptides these are then paired with MHC proteins

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61
Q

what co-receptor is required for activation of CD4 or CD8

A

CD3, anchors TCR and antigen

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62
Q

describe the basic structure of the TCR

A

two chains, one alpha, one beta, each with a constant region and a variable region

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63
Q

how many gene segments make up the variable region in the alpha chain of the TCR

A

2, joining segment and variable segment

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64
Q

how many gene segments make up the variable region in the beta chain of the TCR

A

3, joining, diversity and variable segment

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65
Q

how is diversity of the TCR generated

A

due to gene re-arrangment, many possible combinations of genes which results in different proteins structures

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66
Q

how is it decided if a t cell will be a helper cell or cytotoxic in thymic education

A

the epithelial cells of the cortex of the thymus express either MHC I OR II, if the T cell binds to I it will become CD8, if it binds to II, it will become CD4

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67
Q

what is positive selection in thymic education

A

only t cells that bind to an MHC protein will develop further, those that do not will be sent for apopotosis

68
Q

what is negative selection in thymic education

A

if t cells bind to self-antigens, they are sent for apoptosis

69
Q

what is required for t cell activation

A

binding of TCR to antigen, binding of co-receptors on APC to T cell (CD28 - CD80), and release of cytokines from APC for the T cell to develop into a subtype effector cell

70
Q

what is the role of Th1 cells

A

activates macrophages and produce IgG

71
Q

what is the role of Th2 cells

A

activates B cells - normally IgE

72
Q

what is the role of Tfh cells

A

activates B cells and support humoral immunity

73
Q

what is the role of T17 cells

A

produce IL-17, supports innate immunity

74
Q

what is the role of treg cells

A

regulate t cells, reduces the immune response, apoptosis of T cells and inhibits dendritic maturation

75
Q

how are t memory cells generated

A

when effector T cells are produced, most are short lived but some remain - these are memory cells for a second infection

76
Q

how do CD8 cells generate cytotoxic

A

after binding, causes release of granules which contain granzymes, these can get through the membrane of the infection and then stimulate apoptosis pathways in the cell

77
Q

what is the general structure of the antibody and where does the antigen bind

A

two chains - one light and one heavy, antigen binds to the fab region - fc region is the constant region

78
Q

what segments make up the heavy chain of the antibody

A

one variable gene segment, one constant, followed by a hinge segment, after this follows 2 more constant segments

79
Q

what segments make up the light chain of the anitbody

A

just one variable and one constant

80
Q

how does the antibody generate diversity

A

different antibody for each antigen, due to a number of genes to choose from, several combinations of these genes are possible, so different structures able to be formed

81
Q

what are the main classes of antibody and what are their functions?

A

IgG - most numerous, small, exists in tissues, responsible for resistance, IgE - recruits mast cells and basophils, involved in parasitic infections and allergy, IgM - immature antibody, produced initially until IgG can be produced, IgD - main receptor on the B cell, IgA - secretory, found on mucous lining, important innate

82
Q

describe B cell maturation and development

A

mainly just gene rearrangment to produce a specific B cell receptor. at first, IgM expressed as BCR but as matured, replaced with IgD although the cell can still secrete IgM

83
Q

what is negative selection in B cell development

A

presents the B cells with self-antigens, if any B cells bind to them, they are removed and sent for apoptosis

84
Q

name 3 roles of antibodies

A

opsonisation for phagocytosis, natural killer cells and mast cell degranulation, neutralises bacterial toxins, activates complement

85
Q

what is the main goal of B cell activation

A

differentiation to plasma cells, which then generate a large number of the specific antibody

86
Q

what are the two ways in which B cells can be activated

A

within lymphoid tissue with T cells - thymus dependant

outwith the lymphoid tissue, not requiring T cells - thymus independant

87
Q

how do T cells activate B cells

A

B cells and T cells bind to same antigen, when T cell binds and is activated, the subtype effector cell is produced (Th2 or Tfh), B cell binds to this along with co-receptors (CD40). Cytokines are then released from the effector cell and these cause the B cells to differentiate into plasma cells which then produce antibodies

88
Q

what is avidity

A

class switching in thymus dependant activation, when plasma cells first produced, initially they produce IgM but then they produce IgG for a stronger response, these are also required for generation of memory cells

89
Q

How do B cells produce memory cells

A

when plasma cell produces IgG antibody, some of these remain once the infection passes, then at a second infection, the IgG cells can bind directly to the antigen for a much faster response - IgM stage is not required

90
Q

what is affinity

A

the strength of bond between antibody and antigen, this increases with more infections, affinity at the second infection will be stronger than the first, this will then leave memory cells with a stronger affinity

91
Q

describe thymus independant activation of B cells

A

something released from microbe that the B cell can bind to - LPS from gram negative bacteria binds to BCR - this then activates the B cell, producing plasma cells and releasing antibodies - but only IgM produced with no memory cells left

92
Q

what is meant by tolerance

A

when b and t cells do not respond to normal cells, when an immune response is not desired - e.g. self-antigens

93
Q

what is central tolerance

A

tolerance that is made in either the thymus or the bone marrow. for T cells this is the positive and negative selection they undergo in thymic education. For b cells, this is the negative selection in b cell maturation

94
Q

what is peripheral tolerance

A

tolerance that is made out with the bone marrow or thymus, in lymph nodes. For t cells, when they are activated they require 3 steps. without one of these, anergy occurs and cell sent for apoptosis, even if antigen binds to TCR. For B cells, most of these need to bind to T cells for activation, unlikely a B and T cell will bind to same self-antigen

95
Q

give an example of breach of tolerance

A

sjorgen’s syndrome, autoimmune against salivary ducts

96
Q

what 3 processes are involved in acute inflammation

A

vascular dilation, vascular permeability and neutrophil migration

97
Q

what is the vascular response to acute inflammation

A

increased vascular dilation and calibre - more capillaries recruited to increase flow to the area. also increase the permeability to become leaky

98
Q

how is inflammatory exudate formed

A

when the capillaries increase permeability, immune cells can enter the area along with fluid and salts from the blood vessel

99
Q

what is inflammatory exudate composed of

A

immune cells, fluid and salts, glucose, complement protein, fibrin

100
Q

name 2 chemical mediators of acute inflammation

A

histamine and prostaglandins

101
Q

how is histamine released

A

through degranulation of mast cells and basophils in response to complement

102
Q

what is the role of histamine

A

vascular dilation and permeability, neurotransmitter for itch

103
Q

what is the role of prostaglandins

A

regulate cytokines and chemokines, vascular dilation, tissue remodelling, activates pain pathway

104
Q

how can prostaglandins be inhibited

A

NSAID like ibruprofen will ihibit COX-II to prevent production of prostaglandins

105
Q

what activates the fibrin, coagulation and kinin system

A

hageman factor (factor XII)

106
Q

describe the activation of bradykinin

A

hageman factor converts prekalikrien to kalikrien, this then activates kininogen to bradykinin

107
Q

what is the role of bradykinin

A

activates complement, causes vascular permability, increases cytokines and chemokines for inflammation, activates pain pathway

108
Q

how is the fibrinolytic pathway activated

A

plasminogen converted to plasmin which converts fibrin to soluble fibrin particles

109
Q

what is the role of the fibrinolytic pathway

A

to reduce blood clots when they are no longer required to prevent clotting to death, also plasmin activates the complement pathway

110
Q

what is suppuration

A

formation of an abscess

111
Q

what is an abscess

A

a collection of dead neutrophils and bacteria, encompasses in pyogenic membrane - prevents it from travelling to anywhere

112
Q

what is required for resolution of acute inflammation

A

limited tissue damage, rapid elimination of causative agent and a tissue that is able to regenerate

113
Q

how does chronic inflammation differ from acute

A

less neutrophils, more macrophages and lymphocytes, productive producing more new fibres rather than exudative

114
Q

what are the types of chronic inflammation

A

non-specific, specific and granulomatous

115
Q

when does non-specific chronic inflammation occur

A

when acute inflammation has failed to resolve, get bouts of inflammation followed by resolution, changing between tissue damage and tissue formation

116
Q

what is specific chronic inflammation

A

when a specific causative agent causes the chronic inflammation

117
Q

what are granulomas and how are they formed

A

when macrophage presents antigen and activates T cell, Th1 cell causes macrophage to form epitheliod macrophages, these then fuse together to form giant cells - forms a wall against the infective agent

118
Q

what is oro-facial granulomatous

A

when granulomas are found on the soft tissues in the mouth, may exist along with crohn’s disease - known as oral crohn’s

119
Q

what are the subsets of macrophages

A

M1 - inflammatory, causes inflammation

M2 - anti-inflammatory, growth factors for tissue production

120
Q

how can chronic inflammation cause destructive damage

A

inflammatory macrophages activated at one area whilst anti-inflammatory cells in the adjacent, causes tissue production at one area but this is dysregulated, more destructive than productive

121
Q

What contributes to the destruction of gingiva in periodontal disease

A

MMP’s, lack of TIMP’s and NOS and ROS

122
Q

how does the function of MMP’s differ in health and disease

A

in health - MMP’s remodel ECM to allow cells to flow through the tissue or for angiogenesis. These are regulated by TIMP’s.
In disease - cytokines and plasmin upregulate MMP’s so they remove more ECM, they also inhibit the production of TIMP’s so the removal of ECM is unregulated

123
Q

in health, how is osteoblastogenesis and osteoclasogenesis balanced

A

osteoclasts are activated by RANKL binding to RANK, this is then turned off and osteoblasts activated by osteoprotogerin

124
Q

in periodontal disease, what contributes to the alveolar bone loss

A

macrophages activate RANKL which stimulates osteoclasts for bone resorption. Due to high levels of RANKL, OPG is down-regulated, therefore nothing controlling osteoclasts or activating osteoblasts

125
Q

what is the difference between regeneration and repair

A

regeneration occurs when the tissue damage is minimal and the inflammation is resolved, allowing cells of the same function to be produced. Repair involves wound healing and scar tissue formation, function is not regenerated

126
Q

what are the different cell types of proliferative capacity

A

labile, stable and pernament

127
Q

name the steps involved in wound healing

A

haemostasis, inflammation, proliferation and remodelling

128
Q

what is involved at the haemostasis step of wound healing

A

vasoconstriction, platelet aggregation and coagulation to prevent blood loss

129
Q

what occurs at the inflammation stage of wound healing

A

vasodilation, influx of immune cells removing an infection or debris. causes wheal and flare

130
Q

what occurs at the proliferation stage of wound healing

A

granulation tissue formation. vascular permeability and angiogenesis to allow nutrients to enter site of infection. then get fibroblasts entering and laying down collagen to form the wound

131
Q

what occurs at the remodelling stage of wound healing

A

the collagen fibres are rearranged to improve the strength of the tissue, as it reaches the epithelial level, epithelial cells are laid down and the wound contracts to close by myofibroblasts.

132
Q

what controls angiogenesis in wound healing

A

growth factors released from cytokines, VEGF is main one

133
Q

what stages are involved in fracture healing

A

inflammation, soft callus, hard callus and remodelling

134
Q

what occurs at the initial stage of fracture healing

A

inflammation, influx of immune cells to remove any infection, vascular dilation and permeability

135
Q

how is the soft callus formed in fracture healing

A

due to influx of chondrocytes and fibroblasts, results in formation of fibrocartilage

136
Q

how is the hard callus formed in fracture healing

A

once soft callus laid down, mineralisation of this occurs to produce woven bone, not in any structure

137
Q

what occurs at the remodelling stage of fracture healing

A

over time, the hard callus is changed into cortical bone in lamellae arrangement, but this takes time

138
Q

what is fibrosis

A

extensive deposition of collagen fibres, scar tissue laid down but dysregulated due to ongoing inflammation

139
Q

what causes fibrosis

A

M2 cells releasing anti-inflammatory cells and growth factors to deposit collagen fibres, despite the ongoing inflammation. results in more destruction rather than productive

140
Q

what is a hypersensitivity reaction

A

an exaggerated reaction to an antigen

141
Q

describe sensitisation in type 1 hypersensitivity reaction

A

antigen binds to t cell - t cell produces Th1 effector cell, this binds to B cell, b cell produces plasma cells which produce IgE antibodies - these antibodies then bind to mast cells and basophils at the Fc region

142
Q

what happens in a type 1 hypersensitivity reaction at the second exposure

A

antigen binds to the IgE antibody on the mast cells and basophils, this then causes degranulation of these cells - results in release of histamine, vascular dilation, can cause mucous secretions

143
Q

what is localised degranulation in type 1 reaction called

A

atrophy, normally has a genetic component

144
Q

how can a type 1 reaction be fatal

A

widespread degranulation, results in vascular dilation and oedema, laryngeal oedema and bronchial constriction

145
Q

what is a hapten

A

a small allergen that has to bind to a carrier protein to exert its effect, penicillin is a hapten

146
Q

how can a type 1 reaction be treated

A

anti-histamine - blocks release of histamine, reducing the symptoms, hydrocortisone cream inhibits histamine, epinephrine through an EpiPen - reverses effects of anaphylatic shock

147
Q

give an example of a type 2 hypersensitivity reaction

A

in blood transfusion, if wrong blood type delivered, antibodies in patients blood will attack the antigens on the donor blood - result in haemolysis

148
Q

how do type 3 hypersensitivity reactions occur

A

antibody-antigen complexes that are intermediate in size, not phagocytosed, in blood vessel causes complement release and attracts neutrophils, results in inflammation of the blood vessel - vasculitis, arthur reaction

149
Q

what is serum sickness

A

when the type 3 reaction is not localised, more widespread, can cause a rash and fever, can result from penicillin

150
Q

what are type 4 reactions also known as and why

A

delayed hypersensitivity due to recruitment of T cells as this requires more time

151
Q

give an example of a type 4 reaction

A

contact dermatitis - release of macrophages

152
Q

what determines if cell injury is reversible or not

A

the tissue that is damaged - its ability to generate repair, how susceptible it is and how it can adapt
the extent of damage - once past a certain point, repair unable regardless of factors

153
Q

what can cause cell injury

A

hypoxia, ischaemia, chemical damage, ionising radiation, infections, nutritional imbalance

154
Q

what are 2 mechanisms of cell injury that is reversible

A

cloudy swelling and fatty change

155
Q

how does cloudy swelling occur

A

lack of oxygen results in lack of ATP so carriers across membrane altered, allows Na to enter cell, water follows this causing a swelling of the cell

156
Q

how does fatty change occur

A

triglycerides build up in cells, causing an increase in lipid vacuoles, occurs in liver after alcohol

157
Q

what is blebbing

A

when parts of the cell break away from the membrane, as this becomes uncontrollable, cell passes point of no return

158
Q

what occurs in necrosis

A

blebbing uncontrollable, cytoplasm leaks out of cell, get an immune reaction to this, increase inflammation and phagocytosis of the cell

159
Q

define necrosis

A

cell death in response to tissue damage

160
Q

how can you tell a cell is necrotic

A

the nucleus becomes black, then smaller fragments then it disappears

161
Q

what is the effect of necrosis

A

functional effect is dependant on the area, always get inflammation which then results in scar production

162
Q

what are the types of necrosis and give examples of each

A

coagulative - structure remains but becomes fibrotic, myocardial infarction, liquefactive - cells are lysed producing a puss, bacterial infections, caseous - mass lysis of tissue, normally granulomas are broken down - TB

163
Q

when is apoptosis required

A

if DNA damage detected in cells, cells infected with viruses, to immune cells when immune reaction no longer required, epithelial cells when dead

164
Q

what are some differences between apoptosis and necrosis

A

inflammation with necrosis, not with apoptosis, apoptosis requires ATP, cells shrink with apoptosis, enlarge with necrosis, cell membrane intact and nucleus contained with apoptosis

165
Q

what is amyloidosis

A

deposition of amyloid protein by abnormal plasma cells, blocks tissue and organ, can cause organ failure, result of chronic inflammation or multiple myeloma

BDS 1 BAMS (13 decks)

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