cells to systems 2 Flashcards

(83 cards)

1
Q

what is blood regarded as and what does it contain

A

connective tissue containing plasma (55%), RBC (45%) and white blood cells and platelets - very small amount

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2
Q

components of plasma and percentages

A
  • 90-92% water.
  • 6-7% proteins
    ○ Albumin – colloid osmotic pressure
    ○ Globulin – enzymes, antibodies
    ○ Fibrinogen – polymerizes into fibrin during coagulation or clot formation
  • 2-3%
    ○ Fats
    ○ Carbohydrates (glucose)
    ○ Electrolytes
  • Bicarbonate (buffering action), calcium, chloride, magnesium, phosphorus, potassium, sodium
    ○ Gases (O2, CO2)
    ○ Chemical messengers - cytokines and hormones
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3
Q

structure and composition of red blood cells function and life-span

A
water 60% and haemoglobin 40% 
biconcave disk (max SA)
no nucleus or organelles in mammals 
stains eosinophilic 
corry O2, CO2 H+ (buffering) 
life-span 80d cat 100-120 d and humans 150 horses, cattle, sheep
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4
Q

what is the name for immature red blood cells what percentage of RBC, how long until mature and where mature

A

reticulocytes
1% of RBC, develop and mature in red bone marrow
circulate for a day before maturing

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5
Q

structure of haemoglobin, what contain and where does O2 bind

A

2 alpha and 2 beta chanis
contain haem - porphyrin ring containing Fe2+
O2 binds to Fe by occupying the sixth coordination position
4N bonds 1 globin bone 1 O2 bond per haem unit
each haemoglobin has 4 haem units and can bind H+ for buffering

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6
Q

CO2 how get into blood, how transported in blood and how move out of RBC
and how does CO2 cross RBC plasma membrane

A

diffuses across endothelial cells into blood - most transported by RBC as bicarbonate ions due to high levels of carbonic anhydrases or combined with haemoglobin
Cl-HCO3 exchanger channel transports bicarbonate out of RBC promoting formation of more bicarbonate within RBC
debate on how
1) Classical membrane diffusion
2) Diffusion through pores – “gas channels”
1. Aquaporin (AQP1)
2. Rhesus pore

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7
Q

platelets what is the other word for them, structure and composition, life span

A

thrombocytes
- Small, ovoid bodies
thrombocytes
- Cytoplasmic pieces ‘budded off’ from megakaryocyte
- ~ 2 μm diameter, disc shaped
• Lifespan 8-10 days (sequestered in the spleen - can mobilize quickly)
Dense granules
-ADP, serotonin (a vasoconstrictor), calcium
• Alpha granules
- Thrombospondin, fibrinogen

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8
Q

function of platelets and how exert effects

A

blood clotting
aggregation - platelet adherence - associated with endothelial cells injury; formation of platelet plug
○ Coagulation - fibrin formation, initiated at larger sites of injury; formation of a clot (thrombus)
○ Injury triggers two events
1. The activation and deposition of platelets at a wound site
2. Activation of coagulation pathway
- Prothrombin converted to thrombin
- Thrombin causes fibrinogen to polymerize into fibrin
- These lead to the formation of a fibrin seal on the deposited platelets which plugs the leak

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9
Q

haemopoietic

and what are haemopoetic stem cells

A

production of new RBC

multipotent - can form any blood cell line, they are present throughout life

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10
Q

what is needed to differentiate into red blood cells what produced by, where and what does it do

A

erythropoietin
produced by fibroblast-like cells in cortex and outer medulla of kidney
- Shortens cell cycle time
- Increased rate of maturation
- Increased rate of release from bone marrow
• Increased presence of circulating reticulocytes when erythropoietin is active
- Indicative of recent increase in erythropoiesis

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11
Q

what is the role of haemopoiesis

A

To maintain homeostasis:
- Short lifespan of mature blood cells requires continual replacement throughout life
• Enable a rapid response to life-threatening conditions :
- Blood loss - RBC numbers are tightly regulated
- Infection - WBC numbers increase to fight infection
• Remove and replace dangerous cell types:
- Neutrophils and eosinophils - Once activated they are damaging to surrounding tissues

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12
Q

where does haemopoiesis occur

A
Embryo:
	- yolk sac, liver & spleen
• Foetus:
- liver, spleen & bone marrow
• After birth
- bone marrow
• Juvenile: long bones & flat bones (pelvic bones & vertebrae)
• Adult: flat bones - pelvis & ends of long bones
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13
Q

regulation of Haemopoiesis

A
involves differentiation of HSC 
in bone marrow interact with:
- Stromal fibroblasts
- Osteoblasts
- Endothelial cells
- Extra-cellular matrix
receptors on HSC bind to 
- Stromal adhesion molecules
- Membrane bound stromal growth factors
- Soluble growth factors
- Extra-cellular matrix
which all control gene expression and directs development
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14
Q

list steps in what occurs after large blood loss

A

1) Fall in circulating RBC mass
2) Tissue hypoxia - lack of oxygen
3) Stimulates EPO production by renal peritubular cells
4) EPO occupies specific receptor sites on progenitor cell membranes
5) Resulting in
- shortened cell cycle time
- Increased rate of maturation
- Increased rate of release of RBC from bone marrow
6) Increased red cell mass and increased delivery of O2 to tissues, removing stimulus for EPO synthesis and erythropoiesis returns to normal

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15
Q

where is adaptive immunity found

A

vertebrates only

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16
Q

functions of mast cells and basophils, eosinophils

A

mast cells and basophils - release factors which increase blood flow and vascular permeability
eosinophils - secrete factors which kill protozoa and worms

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17
Q

name a type of protein involved in innate immunity, where found and its function

A

Acute phase proteins (C-reactive protein, mannan binding protein) - found in the liver - activate complement and opsonise pathogens

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18
Q

two broad types of leukocytes and sub types within

A

1) Granulocytes
1. Neutrophils
2. Eosinophils
3. Basophils
2) Agranulocytes
1. Lymphocytes
2. Monocytes

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19
Q

percentage of leukocytes in the blood for sheep

A
Neutrophils - 30%
Eosinophils - 5% 
Basophils 0.5%
Lymphocytes 62% 
Monocytes 2.5%
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20
Q

list the 3 killing mechanisms of neutrophils

A

1) Phagocytosis
2) Degranulation - primary azurophilic and secondary specific granules
3) NETs - neutrophil extracellular traps - entrap the pathogen with molecules secreted from the neutrophil

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21
Q

functions of basophil function

A
  • Major role in allergic and inflammatory reactions
  • Surface receptors for IgE
  • Limited phagocytic and bactericidal activity
  • Predominant source of IL-4 and IL-13 in allergic disease
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22
Q

mast cell functions within the gastrointestinal tract, airways and blood vessels

A

Gastrointestinal tract - important for parasites and worms
Airways - decreased diameter - prevent more pathogens from entering and increased mucus secretion - entrap the microbes
Blood vessels - as mast cells degranulate increase permeability of the blood - if get systemic infection can cause anaphylactic shock as too much leakage through blood vessels throughout body causing a decrease in blood volume and pressure

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23
Q

eosinophil function

A

Major role in controlling parasitic infestation
Possible roles against bacterial and viral
infections
tissue remodeling

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24
Q

examples of mediators produced by mast cells and basophils and eosinophils

A

histamine - increase vascular permeability
prostaglandin - vasodilation
cytokines - IL-3,4,5 - mast cell proliferation - inflammation
eosinophils
peroxidase, hydrolases - degrades helminithic and protozoan cell walls
leukotrienes - increase vascular permeability

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25
monocytes what do they do
reach functional maturity after leaving bloodstream and become macrophages
26
functions of macrophages
➣ Antigen presenting cells (APC) – initiate immune response ➣ Highly phagocytic • Ingest and kill microbes - PAMPS • Clearance of RBC, WBC, apoptotic cells - DAMPS - damaged cells ➣ Produce cytokines – signalling and amplification of immune response ➣ Produce colony stimulating factors – haematopoiesis
27
dendritic cells function and where found
activate T cells found in small quantities in tissues that are in contact with external environment - skin and intestines
28
where are B cells derived in mammals, birds, and ruminants
bone marrow bursa of fabricuis ileal peyers patches
29
list different classes of antibodies what structure and function
1) IgM - µ - pentamer - best at fixing complement and the monomer severs as the B cell receptor 2) IgG - ƴ - monomer - highest percentage of total antibody in serum - neutralises toxins and opsonisation 3) IgA - α - dimer - has secretory component, can cross gut membrane, secreted into mucus, tears, saliva and colostrum 4) IgE - Ɛ - monomer - binds to mast cells and basophils - antibody of allergy and ant parasitic activity 5) IgD - δ - monomer - can be a B cell receptor
30
functions of natural killer cells
1) killing injured cells 2) killing infected cells 3) killing phagocytosed microbes
31
how do innate cells recognise pathogens
Pattern-recognition receptors (PRRs) - detect microbes by binding to pathogen-associated molecular patterns (PAMPs) ➣ PRRs expressed by cells of innate immune system - macrophages, dendritic cells, granulocytes, endothelial cells, mucosal epithelial cells ➣ Recognize unique microbial molecules (PAMPs) shared by groups of related microbes not found associated with mammalian cells. ➣ Results in activation of innate immunity ➣ Limited repertoire (recognize 103 molecular patterns)
32
list 4 PAMPs
1) flagella protein 2) capsule polysaccharides 3) unmethylated DNA 4) pilin protein from pili
33
what are the receptors that recognise PAMPs called and give example
Toll-like receptors | TLR3 - viral DS RNA
34
List and describe the 4 tissue responses to damage
1) acute inflammation - initial response, non-specific, eliminate dead tissue, protect against local infection 2) restitution (ideal outcome) - damaged area replaced by normal tissue with function 3) fibrous repair (scar tissue) - tissue architecture destroyed, original cell type cannot grow 4) chronic inflammation - tissue destruction persists, ongoing attempts to heal by fibrous repair, ongoing immune response
35
acute inflammation definition and what is the most common cell type
A rapid and short duration response to an injurious agent that delivers mediators of host defence to the site of injury neutrophil
36
list 3 causes of acute inflammation
1) most commonly mechanical trauma - splinter etc 2) biological causes (e.g. bacterial infections, allergies to foreign proteins) 3) Thermal or chemical injuries
37
What are the 5 cardinal signs of inflammation, there other name and what causes them
1) Redness (rubor) - vessel dilation and increased blood flow - skin 2) Swelling (tumor) - accumulation of exudate fluid 3) Heat (calor) - vessel dilation and increased blood flow 4) Pain (dolor) - chemical mediators and pressure on nerve endings 5) loss of function (functio laesa) - consequence of other 4 signs
38
what is the name for inflammatory mediators involved in acute inflammation and their functions
autocoids biological factors that act like local hormones - paracrine different biological actions including modulation of the activity of smooth muscles, glandular secretinon, sensory nerves (pain and itch) and other tissues - permeability of vascular and airway
39
List 3 autocoids
1) histamine 2) bradykinin 3) substance P
40
histamine what cells released from, function and stimuli that induces this realease
released from mast cells (mucosal surfaces) also basophils (blood), enterochromaffin cells in the stomach function - Acts through GPCR receptors Three responses: 1) Reddening- vasodilatation at initiating site 2) Wheal- increase in vascular permeability 3) Flare- spreading response through sensory fibres stimuli - Antigen via IgE antibodiesm - allergic response generally – Complement fragments (C3a/C5a) – Neuropeptides – Cytokines and chemokines – Bacterial components – Physical trauma - scratching
41
bradykinin what is it when generated and functions
autocoid - local peptide mediator generated after plasma exudation during inflammation causes vasodilation, increased vascular permeability and stimulates sensory nerve endings to cause pain
42
substance P what is it where released and what causes
neuropeptide neurotransmitter released from peripheral terminals of sensory nerve fibres (skin) and leukocytes such as eosinophils causes local pain, itch, vasodilation
43
eicosanoids what are the types and what derived from
1) prostanoids - prostaglandin and thromboxanes 2) leukotrienes Arachidonic acid not stored by cells but produced on demand
44
action of eicosanoids
* Act through selective G protein-coupled receptors (GPCRs) each has own receptor * Smooth muscle: constriction (thromboxane as if cut yourself and activate platelets don’t want excess blood loss) or dilation (prostacyclin) * Blood platelets: aggregation (thromboxane A2 produced by platelets) * Leukocytes: chemoattractant (leukotriene B4) * Gastric acid secretion: inhibition * Kidney: increased renal blood flow and water/sodium excretion - homeostatic controls
45
roles of eicosanoids in inflammation
- Redness: vasodilation at site of inflammation - Swelling: wheal formation due to increase in vascular permeability - Pain - Fever
46
cytokines give some examples, what produced by
* Include chemokines, interferons, interleukins (6 and 10) , lymphokines, tumour necrosis factor * produced by broad range of cells, mainly immune cells like macrophages, B lymphocytes, T lymphocytes.
47
list the 3 major processes in acute inflammation
1) vasodilation 2) exudation 3) emigration of leukocytes
48
vasodilation what does it involve, what signs of inflammation involved and what molecules induce
•Arterioles, capillaries, post capillary venules increase in blood flow - calor and rubor - Arteriolar dilation/opening of capillaries (hyperemia/redness) •Histamine, NO, prostaglandin I2, bradykinin
49
exudation what occurs and mechanism
- Increased vascular permeability - Leakage of plasma proteins draws out water Mechanism Retraction of endothelial cells – gap formation 1) Endothelial cell contraction (fast, venules only) - Histamine, bradykinin, leukotrienes 2) Delayed, prolonged leakage - (endothelial degeneration) - formation of holes 3) Leukocyte-dependent endothelial injury - Reactive oxygen species, enzymes released from neutrophils
50
what are the two types of substances involved with increased vascular permeability
1) transudate - fluid, low protein, few cells 2) exudate - fluid and cells, high protein, may be infectious
51
what does exudate contain and function of these
•Fluid - Containing salts, high protein - Dilutes/buffers toxins in the tissues; also contains antibodies - Allows diffusion of inflammatory mediators - Circulation via lymph takes antigens to local lymph nodes •Fibrin - Formed from small soluble precursor plasma protein, fibrinogen - Polymerises via blood coagulation cascade - Meshwork of threads blocks migration of bacteria, prevents further swelling and aids migration of leukocytes •Neutrophils - front line •Macrophages - pro-inflammatory , a few lymphocytes
52
what are the 3 steps in emigration of leukocytes during acute inflammation
1) Endothelial cell activation ○ expression of adhesion mols on blood vessels ○ Stimulated by inflammatory mediators (cytokines), tissue damage 2) Margination ○ Mediators cause neutrophils to adhere to the endothelium ○ ICAM receptors cause firm adhesion to the blood vessels 3) Emigration (extravasation - coming out of blood vessels) ○ Neutrophils move through blood vessel walls into damaged tissue ○ Chemokine gradient - attract the neutrophils - highest concentration at the site of inflammation •Monocytes/macrophages emigrate later by similar mechanism
53
what is pain caused by
- Damage/injury to peripheral nerve endings - Effect of inflammatory mediators on nerve endings (nociceptors) - Pressure on nerve endings from tissue swelling
54
heightened pain sensitivity in inflammation why
- Hypersensitivity of nerve endings - Amplification of pain pathways in the spinal cord ○ Caused by mediators such as prostaglandin E2, IL-1β
55
itch what nerve fibres initiate and where, what may accompany and caused by
- Unmyelinated nerve fibers for itch and pain both originate in the skin - Itch may accompany local skin inflammation caused by - Effect of inflammatory mediators on nerve endings (puriceptors) ○ E.g. histamine, serotonin, prostaglandins - Substance P releases histamine from mast cells Scratching leads to self trauma and more inflammation - itch scratch cycle
56
fever how assist with healing process, what induced fever and the types and how it induced fever
- Increased mobility of leukocytes, phagocytosis - Increased proliferation of T cells •Pyrogens: substances that induce fever. - Endogenous: cytokines, such as interleukin 1 (α and β), IL-6, TNF-α - Exogenous: e.g. the bacterial toxin, lipopolysaccharide (endotoxin) Pyrogen causes a release of PGE2 - prostaglandin E2 •PGE2 acts on the hypothalamus (‘thermostat’) in the brain: - generates a systemic response back to the rest of the body, causing heat-creating effects to match a new temperature level.
57
pathological classifications of acute inflammation according to nature of exudate what are the 4
1) Serous - Least severe; mild inflammation - Only water and low MW solutes pass out of plasma 2) Catarrhal (Quatar how to say) - Exudate formed on mucosal surfaces so has excess mucus production - Mucus mixed with serous fluid plus cell debris, inflammatory cells 3) Fibrinous - More severe change in vascular permeability - Fibrinogen converted to fibrin - Grossly appears as yellow gel - very sticky substance - Occurs on serosal or mucosal surfaces 4) Suppurative - Purulent exudate (pus) - Large numbers of leukocytes mainly dead neutrophils - Severe tissue damage
58
what is an abscess what occurs eventually and treatment
- Localised collection of pus caused by suppurative inflammation - Response to pyogenic bacteria - Confined by wall of fibrous tissue eventually ○ Body trying to protect itself and stop the spread of the abscess however fighting against the enzymes released from the dead cells such as proteases that breaking down the connective tissue and spreading the abscess ○ Eventually get a wall preventing spread and increasing the pressure - Treatment - need to allow the puss to completely drain out in order for the skin to heal
59
what is a phlegmon example and empyema
Phlegmon - Spreading diffuse suppurative inflammation - Within loose connective tissue - Margins poorly defined - e.g. Cellulitis - common in horses Empyema - Accumulation of pus within a body cavity
60
resolution of inflammation
1) Apoptosis and removal of leukocytes 2) Macrophage switch from pro-inflammatory to phagocytic and anti-inflammatory 3) Stop signal - Resolvins, lipoxins, protectins Without proper resolution get chronic inflammation
61
endotoxaemia (sepsis) what is it caused by and the steps
- Caused by things such as colic 1) Lipopolysaccharide from bacteria binds to specific receptos on monocytes and WBC 2) Cause the release of pro-inflammatory mediated - cytokines - Activate leukocytes - Destructive factors such as oxygen free radicals and protein-degrading enzymes 3) Septic shock and multiple organ dysfunction resulting in death
62
chronic inflammation what are the causes
- Foreign bodies - if doesn't remove body continue to respond to it - Autoimmune disease - continuring stimulation body antigens - Persistent infection - mycobacterial infection - Hypersensitivity/Allergic disease - body continual exposed to antigens sensitive to
63
time frame for peracute, acute, subacute, chronic
Peracute (immediate) – minimal inflammation | Acute (
64
List the 3 features of chronic inflammation
1) changes in inflammatory cell population 2) inflammatory tissues damage 3) tissue repair
65
describe the changes in inflammatory cell population in chronic inflammation and what are subtypes of chronic inflammation in terms of cell populations
From neutrophils to T lymphocytes 1) Lymphocytic/Lymphoplasmacytic inflammation 2) Granulomatous inflammation 3) Eosinophilic inflammation 4) Often mixed, and may have neutrophil component - “Chronic-active” inflammation - if lots of neutrophils
66
lymphocytic inflammation what is it also called, what is the types of lymphocytes involved
``` •Also called non-suppurative inflammation •Mix of lymphocytes: - cytotoxic T cells - helper T cells (Th cells) - B cells •Plasma cells may be present - Lymphoplasmacytic inflammation - if large number of plasma cells •Perivascular distribution common •Sometimes form nodular aggregates - Lymphoid follicles ```
67
causes of lymphocytic inflammation
1) Auto-immune disease - Type 1 diabetes 2) Viral infections - Rabies - Viral hepatitis in humans 3) Hypersensitivity diseases - Inflammatory bowel disease 4) Idiopathic Lymphoplasmacytic stomatitis
68
what is macrophage dominanted inflammation called and what does it create and what may macrophage form into
granulomatous inflammation also called histiocytic inflammation form discrete or coalescing nodules in tissues cells may fuse to form Giant Cells
69
what are the subtypes of granulomatous inflammation and what disease results in this
1) Pyogranuloma – central accumulation of neutrophils - puss 2) Caseating granuloma/necrogranuloma - “Cheesy” centre composed of dead tissue - Seen particularly with tuberculosis and some parasites Johne's disease - Granulomatous enteritis - cattle - Diarrhoea - loss of body condition - Whole tissue is thickened - gut
70
eosinophilic inflammation when occurs and what occurs
- Primarily parasitic or allergic disease | - Affected tissues often have green appearance (eosinophils are actually green!)
71
inflammatory tissue damage in chronic inflammation what does it result from
- Damage by the original insult - bacteria, viruses directly attack cells - Release of inflammatory mediators - free radicals, protease's, complement - Cellular phagocytosis or apoptosis - macrophages may phagocytose other cells - Tissue death due to circulatory compromise
72
Tissue repair healing process what are the two major pathways
1) regeneration - ideal situations - function and structure of tissue restored 2) fibrosis
73
Regeneration what is it, what does it depend on and cell types involved
- Replacement of damaged tissue with the original cell type Dependent on: - Viability of original cells - need cells to proliferate from - Type of tissue - how much mitotic activity available in that tissue - Preservation of connective tissue scaffold Cell types 1. Labile cells Undergo constant turnover and can regenerate completely from germinal cells - Epidermis of skin, intestinal epithelium, bone marrow 2. Stable cells Normally quiescent (non-dividing), but have the ability to regenerate if required - Hepatocytes, osteocytes, renal tubular epithelium. 3. Permanent cells - Considered terminally differentiated - Do not regenerate - Neurons, cardiac muscle
74
fibrosis what it is what occurs with it
- Replacement of damaged tissue by fibrous connective tissue (scar tissue) - Restores structure at expense of function - non-functional tissue - Occurs in competition with regeneration
75
what are the 3 phases of fibrosis
1) inflammatory phase 2) proliferative phase 3) mature phase and scar formation
76
inflammatory phase of fibrosis what are the two steps and describe
1) Clearance of damaged tissue debris - Neutrophils and macrophages 2) Replaced by fibrin coagulum - Dry scab on the wound - provides protective layer and scaffold for the next phase
77
proliferative phase of fibrosis what occurs and what are the two steps and describe
- Production of granulation tissue 1) Neovascularisation - new blood vessels growing into the area - Provides oxygen and nutrients for healing - New vessels develop under influence of growth factors (eg. VEGF, FGFs, Angiopoietins) and hypoxia 2) Fibroplasia - Production of collagen stroma - Migration of fibroblasts and deposition of immature type 3 collagen - early stage of stoma that places fibrin coagulum - Occurs under influence of growth factors (PDGF, FGFs, TGF-β)
78
mature phase and scar formation of fibrosis what occurs
•Reorganization of collagen and change in collagen type (Type 3 to Type 1) - Organized parallel with lines of tension - maintain maximal strength in tissue •Contraction of connective tissue - scar will shrink •Maturation and regression of vasculature - doesn't need much blood so regression of blood vessels - why scars look white
79
differences between secondary and primary intention healing
- More inflammation - More granulation tissue - More fibrosis/scarring - Prolonged healing
80
list some factors influencing healing and how
- Infection - sources of chronic inflammation that slows down healing - Foreign material - same as above - Nutrition - starving low protein levels so cannot use up much protein to heal up tissues - survey - vitamin C is needed - Movement/pressure - quite fragile so will break down - Vascular/Oxygen supply - Hormones - some inhibit healing - Concurrent disease - diabetes - non healing ulcers - Age - older cells don't divide as readily as younger
81
what is aberrant healing and the types
abnomral healing 1) Proud flesh - Excess of granulations tissue - expand as a mass - make hard to heal as epithelium cannot migrate over the surface 2) Keloids - Excess scar tissue
82
what are the 3 consequences of scar tissue and describe
1) strictures - can occur due to salmonellosis - ulcer of the colon undergoes fibrosis scar tissue formation and contract down so no longer defecate 2) adhesions - occurs if have fibrin coagulation 3) restricted movement
83
normal platelet count and which species has large variation from this
250million/ml | horse about 1/2 normal amount