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SLE323-Advanced biomed science > cellular changes of disease > Flashcards

cellular changes of disease Flashcards

1
Q

neutrophils and exp?

A

granulocytes, phagocytosis (eating and spitting) most abundant leukocytes in blood, first to respond

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2
Q

lymphocytes and exp?

A

mediated cellular and humoral immunity, B cells differentiate into plasma cells which secretes immunoglobulins.

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3
Q

monocytes and exp?

A

transfers to macrophages which is used in the process of phagocytosis.

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4
Q

eosinophil and exp?

A

moderates allergic reaction and important for parasitic infection.

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5
Q

basophil and exp?

A

facilitates allergic reaction through the release of histamine and serotonin.

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6
Q

3 reasons why we loss against infectious bacteria?

A

1) microorganisms multiply very fast and evolve quickly
2) humans take time to reproduce meaning they take time to evolve from this disease.
3) the microorganisms have a upper hand.

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7
Q

whats happening in that video? (hint- neutrophil and bacteria)

A

the neutrophil is engulfing the foreign bacteria and the round cells are lymphocytes.

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8
Q

function of the immune system?

A

prevent infection and ERADICATE infections

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9
Q

what happens in the first 6-12hrs of infection?

A

its the innate response (skin/epithelal cells (inc pathogens and microbes), phagoctyes NK cells and complement),

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10
Q

a drug that induces adaptive immunity?

A

Vaccines and monoclonal antibodies

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11
Q

what happens days after the infection?

A

the adaptive response occurs which activates the B lymphocytes -> antibodies, and T lymphocytes -> Effector T cells

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12
Q

how is out immune system regulated? found?

A

hemopoietic stem cell, bone marrow

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13
Q

MHSC

A

multipurpose hematopietic stem cell (hemocytoblast, self - renewal (cell division independently and don’t change their state

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14
Q

what is differentiation into mature myeloid site?

A

(innate immunity)

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15
Q

what is differentiation of mature lymphode cells?

A

(aquired immunity) - T cells, B cell

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16
Q

everyday how much rbc is produced?

A

we produce 10^12 rbc , wbc and platelets.

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17
Q

what mediates inflammation?

A

hemopoietic cells

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18
Q

triggers of inflammation?

A

PACDEI
Pathogens
Abrasion (cut)
Chemical irritation
Distortion of cells
Extreme temp
Ischeamia (O2 drops in cells), water comes in and ATP produce drops and to much calcium released) or hypoxia

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19
Q

symptoms of inflammation?

A

RPHS
Red due to hyperemia (^ blood flow)
Pain due to bradykinin (fluid pressure on nerves)
Heat due to hyperemia
Swelling due to ^ capiliary permiability and filtration.

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20
Q

what causes blood vessels to dilate and low bp?

A

the peptide bradykinin

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21
Q

first 6-12hrs of infection during phagocytes?

A

BIPLD
1. bacteria attach to membrane of cell
2. indigested to cell forming (phagosomes) (bacteria ball inside)
3. phagosomes join with lysosomes
4. lysosome enzyme inside phagosomes digest bacteria
5. digested product removed out of cell

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22
Q

How many microbial cells (bacterial) ?

23
Q

microbes that reside in an on the body are called?

A

microbiota

24
Q

microbiome is

A

the genes encoded by the microbiota

25
neutrophils
the most first to fix foreigners multiple nucleosite survive for few hours granulocyte
26
monocytes
less in blood differentiate into macrophages in the tissue one nucelosite macrophage surviver for longer periods of time in the tissue. agranulocyte
27
the inflammatory cells are producing
28
how do we repair after inflammation?
VCT Vascular phase (blood vessels) Cellular phase Tissue repair
29
foreign object breaks through the epitheial cell...
ohh no now vasodilation occurs in the blood vessel which has allowed the macrophages and the neutrophils to be released.
30
during Vascular phase of inflammation repair
DPBL Dilation of blood vessels Permeability of CAPILLARY increases (WBC stick to wall, substances are passing through the blood to damaged area, swelling) Blood flow increase - to remove damaged and toxic cells and redness Leukocytes produce immune cell activating mediators such as histamine, cytokines and more.
31
how do they know when foreign bacteria come in they activate...
pattern receptors on the surface of macrophages
32
substances involved in mediating inflammation (6)
HKPLPP Histamine released by mast cells Kinins- protein in blood cause infla, irritate nerve endings and affect bp (more low bp) Prostaglandins- lipid (fat) mediator (LM) released by damaged cells, prolong PAIN Leukotrienes- LM made by leukocytes/non blood cells, cause contractions in trachea (TOO much can cause asthma and allergic rhinitis. Polypeptide cytokines- GM-CSF and IL-6 releeased by neutrophils and macrophages to site of damage and PRIME activation of phagocytic ability of neutrophils and macrophages. Polypeptide chemokines- CXCL1 and CCL2 released to stimulate more immune cells to come fight.
33
what is pus?
it all the wbc that have invaded the site of infection meaning there is alot of dead phagocytes causing pus
34
how do WBC leave the blood vessel and what are they regulated by?
they leave through a process called DIASPEDSIS squeezing through the endothelial cells, they are regulated by chemokines (CXCL1 and CCL2)
35
chemokines and cytokines
it wouldn't activate neutrophils and you wouldn't get pus development.
36
cellular process of tissue repair include
necrosis due to injury or apoptosis cell proliferation (mitosis) remodelling of extracellular matrix angiogenesis (vascularisation)
37
what causes a cell die due to injury
necrosis
38
(cellular phase) you get cut what happens ..
1. bacteria (pathogens) enters under the skin 2. macrophages will recognise the invaded bacteria and engage them. 3. activates macrophages to release chemokines and cytokines. 4. chemkines and cytokine recrut of more White cells and the residence cells that are there (eg mast cells and more) 5. neutrophils will diapedesis out of the vessels. 6. neutrophils will engulf them phagosistos them then eliminate them through diapodesis. 7. the wbc will kill the bacteria stopping them from creating a systemic problem in the vascular system.
39
when mast cells come across bacteria...
histamine is released causing vasodilation and swelling of the vessel walls and increases permability of the walls allow wbc to be released.
40
chemokines and cytokines call what WBC
neutrophils
41
apoptosis and affect on tissue
SSANNIR suicide shrinks active needs ATP no acute inflam intact memebrane requires caspases it is there to remove unwanted cells eg. alzheimer disease is too much apoptosis of neurons.
42
necrosis and effect on tissues
ISINABN injury swells inactive no ATP active inflam broken membrane no caspase it is when cells die due to injury or disease e.g. avascular necrosis loss of blood supply to bone due to cell injury.
43
intrinsic cell apoptosis is
starts inside cell by MITOCHONDRIA and apoptotic signals activation for caspase 9 enzyme.
44
extrinsic cell apoptosis is
binding of death ligands to cell surface receptors apoptotic signals activate caspase 3/6/7 enzyme.
45
caspases
an enzyme that control cell death and inflammation
46
what is a regulator for tissue repair?
PGF polypeptide growth factors - they regulate by binding to the surface receptors, then activate the inside signals and cellular process for mitosis. eg EGF receptor (epiderma growth factor)
47
tissue repair includes the extracellular matrix which does ..
controls cell growth, structural support, regulates proteins and structural support.
48
what components helps with the rebuilding of the skin to be strong and elastic after injury?
the extracellular matrix components such as: CFLIP Collagen Fibronectin Laminin Integrins Proteoglycans
49
what do fibroblasts do?
they help with rebuilding of the tissue through connective tissue cells, producing growth factors and produce collagen and fibronectin.
50
stages of wound repair?
FCRPG 1. fibroblast migration 2. collagen producing epithelial cells 3. re-epitheialisation 4. producing granulation tissue 5. growth factors
51
angiogenesis - regulated?
growth of blood vessels from old blood vessels and it increases capiliary density. Regulated by factors VEGF and FGF
52
when does scar repair occur?
3 weeks after injury can continue for 6 months or longer
53
re-epthelialization
the re building of the epithial skin layer. - hemotosis (clotting) - inflammation (inflam cells) - proliferation (granulation tissue) - remodelling (scar)
54
how do scars develop?
Through the process of re-epithelilaisation. HIPR Hemostasis - clot and scab develops Inflammation- inflammatory cells (macrophages on site) Proliferation- granulation tissue develops (capilary grows and creates network where fibrogenic and Angiogenic start to deposit collagen Remodelling - collagen becomes dense and vascularity is reduced and new scar is formed.

SLE323-Advanced biomed science (7 decks)

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