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Pathophysiology > Final > Flashcards

Final Flashcards

1
Q

Neurotransmitters

A

Chemical substances that are synthesised at ends of neurons and serve to transfer nerve impulses from 1 neutron to another or from neutron to target cells.

  1. acetylcholine
  2. monoamines
  3. Amino acids
  4. neuropeptides
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2
Q

disorders in nerve impulse transmission at synapse

A

presynaptics
- decrease in AcH release and damage of lower motor nerves, chypotony and hyporeflexy.
- cranial nerves can be affectd
Post synaptic
- impossibility of Acc to achieve its function on receptors
- myasthenia gravis
Enzymatic
- absence of Acc and overstimulation of autonomic n.s
- disturbances in skeletal muscle function

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3
Q

myasthenia gravis

A
  • severe muscular weakness neuromuscualar and autoimmune disease
  • production of antibodies against Acc receptors -> rapid onset of fatigue and muscular weakness
  • no pain, disorders of consciouness
  • falling eyelid on 1 or both eyes
  • heavier gait, difficulty breathing
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4
Q

acetylcholine esterase inhibitors

A

organophosphorus compounds to treat myasthenia gravis

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5
Q

control circulation in brain

A
  • decreased blood flow (18-50%) of normal - reversible, such as acidosis, neuronal edema etc
  • decreased BF (below 18%) = irreversible, cell death. Oxygen consumed turns to anaerobic glycolysis
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6
Q

phases of circulation control in brain

A
  1. metabolic changes - increase oxygen consumption, increase in metabolic activity and increase blood flwo
  2. auto regulation of bp
  3. balance of gases in blood - arterial pCO2, vasodilation
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7
Q

oxygen deficiency in brain - complete energy breakdown

A
  • lack of oxygen = change in glucose metbaolism
  • glucose is used anaerobically and decrease in pH or acidosis
  • stored atp and glucose is used and when depleted ion channels stop workig
  • transmembrane gradient is disrupted and increase in free radicals
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8
Q

effect of specific structure of CNS on the edema

A
  • has BBB, little extracellular space and poorly developed lymphatic drainiange
  • poor drainage of XS fluid = edema
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9
Q

cerebral edeam

A
  1. cellular edema = no damage in BBB, result of metabolic change in ischemia
  2. vasogenic edema = damage in BBB, leaking of proteins into extracellular space
  3. interstitial edema = disturbances in drainage of CSF after inflammation of meninges
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10
Q

epilslepy

A
  • disorder of Cos function in which synchronised activation of large number of cerebral neurones occur
    1. idiopathic (genetic, innate)
    2. symptomatic (acquired or secondary) due to lesions on brain
    3. cryptogen (unidentified lesions on brain)
    stages
    1. prodromal = few hrs/days before seizure. change in behaviour and character (hiding, drooling and vomiting)
    2. aura = prior to sezireu, several seconds. turning head to one side, throwing head back
    3. ictus = 30-90s. tone of muscle increases, loss of consciousness
    4. postictus = recovering from.ictus. s/m/day. sleeping or lying down
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11
Q

tonic and colonic contractiosn

A 
tonic = prolonged muscle contractions that occur generalised in epileptic seizure
colonic = rhythmic, short-term muscle contractions with pauses in which muscle relaxation occurs
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12
Q

alkalosis, tetanie

A

during alkalosis, H+ is released from proteins and calcium is bound, causing hypocalcaemia and tetany because muscle is more irritated and sodium enters = muscle contracts

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13
Q

causes of N.S function disorders

A
  • lack of oxygen/disroders of blood circulation in brain
  • deficiencies in vitamins and minerals
  • autoimmune disease
  • trauma, anoxia, bleeding. infection, heart failure
    1. structural changes
    2. compression changes
    3. metabolic changes
    4. nutritional deficits
    5. endogenous intoxication
    6. endocrine disroders
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14
Q

chemical substances included in chemical bulletins

A 
NS = hormone and neurotransmittesrs
Endocrine = hormones
Inflammation = biomediators
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15
Q

consciouseness - disorders

A

cause = infection, degenerative, metabolic, vascular and trauam

  • somnolence = alive, drowsy, inert and responds slowl
  • stupur = looks like it’s sleeping, activated by strong stimuli
  • coma = unconscious doesn’t react
  • disorientation and confusion = inadequate response to environmental changes
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16
Q

latrotoxin

A

venom of black widow causes increase release of Acc and all reserves are depleted. no longer released. severe cramp and laxity and pain in joints

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17
Q

most common A.B disorder and casue

A
  • metabolic acidosis
  • decreased HCO3- and pH
    1. increased metabolic production of acid (lactic and ketone)
    2. bicarbonate loss
    3. decreased H+ excretion and HCO3- reabsorption (kidney damage)
    4. toxic compounds
    signs = nausea, vomiting, hypoxia…
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18
Q

respiratory acidosis

A
  • increased pCO2 and H2CO3, decreased pH
  • decreased ventilation - lung disease and depression of medullary respiratory centre
  • compensation of metabolic acidosis
  • signs = decreased respiratory rate, hypoxemia and hypoxia
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19
Q

metabolic alkalosis

A
  • increased HCO3- and pH
  • increased acid loss - vomiting of gastric content, base gain (rare)
  • signs = due to hypokalaemia (weakness, myalgia, muscle spasm)
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20
Q

alkalosis and causes of respiratory alkalosis

A
  • causes accumulation of bases/loss of acids
  • resp alaklosis occurs due to increased ventilation or decreases pCOP2 and increased pH
  • pain, fear, stress, hypoxia
  • signs = rare, tachypnoea
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21
Q

treatment of acidosis and alkalosis

A 
Acidosis = orally sodium bicarbonate into blood and increase HCO3- in blood/ IV sodium lactate/sodium gluconate
Alkalosis = ammonium chloride orally
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22
Q

endocrine system

A
  • consists of cells, tissues and organs that secrete hormone as primary or secondary fucntion
  • provides mechanism for commutation between cells and organs
  • process of secretion of biologicaly active substance into the body
  • regulates growth and development, reproduction, bhomeostasis and metabolism
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23
Q

hormones and types of chemical signalling

A
  • chemical messengers are compounds that serve to transmit a message. they’re endocrine, paracrine, autocrine, hormones, neuroendocrine hormones and neurotransmitters and cytokines
  • hormones coordinate activity of different cells of multicellular orgnaism
  • endogenous substance, high specificity and binding affinity to receptor or target cells
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24
Q

negative and positive connection of hormonal action

A 
negative = precise control of endocrine secretions,. controlled component of negative feedback loop can be ion conc, metabolic or hormone conc
positive = self-perpetuating events that can be out of control and don't require continuous adjustment
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25
Q

complete and partial endocrinopathy

A 
complete = all hormones secreted by a particular gland are affected
partial = only certain cells in gland responsible for particular hormone are affected
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26
Q

mechanism of endocrinopathy

A
  • occur when secretion of certain hormone from gland is excessive or too little
  • if they occur in secretion of hormone from glandd = glandular endocrinopahty
  • if outside gland = extra glandular
  • if inside gland itself = primary
  • if regulatory mechanism = secondary
  • most occur due to disorder in = hormone secretion/transmision
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27
Q

ectopic secretion of hormones

A
  • hormones produced ectopically by tumours re those which arise from signal or two genes
  • maybe due to synthesis of other hormones r3quires a large number go genes not ordinary expressed by tumour
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28
Q

effects of GH on protein metabolism and where it’s syntehsised

A
  • polypeptide that’s synthesised in adenohypophysis
  • effects = long-lasting anabolic effects for stimulating growth
  • GH increases transfer of AA to liver and protein synthesis
  • prevents protein catabolism
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29
Q

acromegaly and where it occurs

A
  • syndrome of excessive growth of bone and soft tissue and insulin resistance resulting from excessive secretion of GH
  • cats caused by acidophilic pituitary adenoma, secreting XS amount of GH
  • dogs = endogenous progesterone and exogenous progsstins
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30
Q

growth hormone deficiency

A
  • dwarf growth, lack of GH secretion particularly affects young
  • growth is lacking, abnormally short hair and later alopecia
  • uni/bilateral cryptocrchidism in males and oestrus absent in female
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31
Q

species specific with exchange of GH

A
  • dog = GH originates from pituitary and epithelial of hyperplasic mammary gland canal (autonomic secretion)
  • pulsating pituitary GH secretion changes during luteal phase of estrus cycle
  • progetterone inhibits GH secretion
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32
Q

ADH

A
  • antidiuretic hormone regulates water balance in body
  • increases reabsorption of water in distal tubules and collecting ducts by inserting aquaporins in luminal membrane
  • high level of ADH = construction = increase in BP
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33
Q

diabetes insipidus

A
  • characterised by polyuria and polydipsia causes either due to kcal of ADH secretion/ increased degradation
  • central DI = dilation of urine despite strong osmotic stimuli for ADH secretion, absence of kidney disease and increase in urine osmolarity
  • nephrogenic DI = insensitive kidney tubules to action of ADH
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34
Q

hypoparathyroidism

A
  • clinical signs include: ataxia, seizures and lens catarcats
  • chargctetisised by hypocalcaemia, normal or increased phosphate and normal magnesium
  • dogs due to lymphocytic infiltration, atrophy and fibrosis
  • decreased conc of intact parathyroid hormones confirms primary hypoparathyroidism
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35
Q

hyper function of parathyroid fland

A
  • primary = parathyroid chief cell neoplasia/hyperplasia
  • autonomous PTH secretion with hypercalcemia, hypophospathaemia…
  • secondary = increased Via D
  • clinical signs = vomiting, anorexia, polyuria
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36
Q

postpartum hypocalcaemia f cows

A
  • in high producing dairy cow, resulting in paresis
  • decrease serum Ca, P and Mg = normal, vit D increase
  • caused by demand for Ca for milk production
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37
Q

puerperal eclampsia of bitches

A
  • inability of Ca homeostasic mechanism to compensate for loss of Ca in milk
  • cause of lactation associated hypo cal in dog
  • mostly in small breeds 2-3weeks after whelping
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38
Q

pathophysiological mechanism for formation and pasture tetatnia in cattle

A
  • decrease in Ca + P because PTH doesn’t cause release of Ca2+ from bones/absorption from intestine or reabsorption from kdiney
  • lack of adequate receptor for PTH on target cells
  • to cure = parenteral prep containing Ca2+
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39
Q

hyperthyroidism (thyrotoxicosis)

A
  • disorder of thyroid gland, secreting excess hormone. due to neoplasia, hypersensitivity or thyroid receptor = primary
  • secondary due to increase secretion of TSH from adenohypophysis - grave’s disease. weight loss, hyperactivity, tachycardia animal is restless, swears of BMR increased. kidney damage, polydipsia and polyuria occur. Gasp and breath rapidly, vomit, increase volume of fat in faeces
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40
Q

hypothyroidism

A
  • primary cause = lymphocytic thyroiditis, idiopathic and congenital
  • secondary cause = pituitary malformation and neoplasia, congenital (define in TSH)
  • teritary = iatrogenic (iodine treatment), antithyroid drug, thyroidectomy
  • signs=decerased metabolic rate, reproductive disorders, skin and hair changes
  • lethargy, somnolence, ataxia, sinus bradycardia, diarrhoea, constipation, retardation in bone
41
Q

congenital hypothyroidism- retenism

A

disproportionate dwarfism, CNS and PSN abnormality and mental deficiency. stunted disproportionate growth. Skeleton = dystrophic, soft tissue = normal

42
Q

goitre

A
  • any enlargement of thyroid gland that isn’t result from neoplasia/inflammation can occur due to disturbances in biosynthesis of T3and T4 hormone, reduced secretion into blood - increased conc of TSH in blood
  • increased hyperplasia of thyroid gland
  • iodine deficiency/antithyroid substances are taken
  • clinically = growth retard, decreased resistance and death (in young), bacterial infection of GI in older
43
Q

diabetes melitus

A
  • absolute/relative insulin deficiency due to deficit insulin secretion by beta cells
  • type 1 (IDDM) - genetic susceptibility and immunologic destruction of beta cells - insulin deficiency (autoantibodies)
  • type 2 (NIDDM) = insulin resistance or dysfunction beta cells
44
Q

chorronic complication of diabetes in dogs and cats

A

blindess, anterior uveitis resulting from cataract formation, peripheral neuropathy of hind limbs, causing weakness, inability to jump, chronic pancreatitis…

45
Q

glucotxocity

A
  • beta cell failure induced by chronically elevated glucose levels through decrease insulin secretion and insulin gene expression
  • chronic increased of plasma glucose impairs insulin action and secretion
46
Q

lipotoxicity

A
  • chronic elevation of plasma FA, affects insulin secretion and cation
  • chronic exposure of beta cells to FA elicit accumulation fo malonyl-CoA and long chain Fatty-acyl-CoA, increased FA oxidation and esterification
47
Q

amylin

A
  • secrete by b-langerhans in non-insulin dependent diabetes
  • increased secretion of amylin, it accumulated in pancreas in form of IAPP
  • cytotoxic effects. on B- langer and destroys decreasing prod action of insulin and therefore type I
  • acts as neuroendocrine hormoens
    0 suppresses glucagon and increases feeling of satiety
48
Q

diabetic ketoacidosis

A
  • KB, acetoacetate and beta-hydroxybutyrate are formed
  • originate from oxidation of non esterified in liver when used as energy
  • insulin conc is decreased, ketone excretes in urine, glucose, Na, K and magneiusm increases, water and electrolyte loss
  • azotaemia and decreased fluid volume and perfusion
49
Q

hyperadrenocoritcism (cushings)

A
  • collection of signs and symptoms due to prolonged exposure to cortisol
  • endogenous cause (overproduction of cortisol, pituitary/adrenal tumour or ectopic ACTH syndrome)
  • exogenous (glucocorticoids)
50
Q

hanging/pendulating abdomen

A
  • occurs in cushings/ secondary hyperadrenocorticism
  • cortisol promotes transfer of FA that accumulate in liver and abdomen
  • hepatomegaly and fatty liver occur, weakening abdomen muscles, due to catabolic aciton of cortisol
51
Q

hypoadrenocorticism in African creature, dog and cat

A

African skunk = casuedby excessive secretion of sex hormones from reticular zone of adrenal gland.
- dogs = pituitary dependent disorder characterised by excess ACTH production

52
Q

conn syndomre

A
  • primary hyperaldosteronism. increased renal absorption of Na+ and water. increased excretion of K and H
  • hypokalaemia, metabolic alkalosis, increased volume of extracellular fluid = stiff gait, weakness, lethargy
53
Q

Addisons disease (primary)

A
  • deficient production and secretion of glucocorticoids and/or mineralocorticoids by adrenal cortex
  • destruction of cortex causes the deficiency (primary)
  • secondary = impaired glucocortical secertion
  • causes = idiopathic adrenocorticcal atrophy, drug-induced and bilateral adrenalectomy
  • decreased aldosterone = decreased absorption of Na and water, failing to excrete K leading to either hyponatremia/hyperkalaemia
  • lack of cortisol leads to decrease tolerance to stress, loss of appetite, vomiting, diarrhoea, abdominal pain and lethargy
54
Q

Addison/adrenal crsis

A
  • disease reaches acute stage and has life threatening symptoms
  • found in state of collapse
  • weak pulse profound bradycardia, abdominal pain
  • rapidly progressive
55
Q

increased adrenaline and noradrenaline secretion

A
  • A = hypertension, tachycardia and arrhythmia
  • NA = sinus tachycardia and arrhythmia, increased BP, increased shortness of breath
  • animal loses weight, epistaxis
56
Q

regulate concentration of magnesium in blodo

A
  • PTH stimulates absorption of Mg from intestine, resorption from kidney and release from bone
  • aldosterone and thyroxine stimulate excretion in faeces and urinec
57
Q

congenital growth disroder

A

genetic defects, toxins/ infectons

  • irreversible
  • aplsia/hypoplasia
58
Q

acquired growth disrders

A

compensatory/protective changes in response to need for increase/decrease cell metabolism
- reversible after removal of causative agent
> atrophy, hypertrophy, hyperplasia, metaplasia and dysplasia

59
Q

neoplastic growth

A
  • excessive growth of abnormal cells that exceeds growth or normal tissue. is irregular and disorganised and doesn’t respond to control mechanism of cell growth
60
Q

biological behaviour of tumour

A 
benign= 1 place, slow, encapsulated, well differentiated, don't metastatsise
malignant = grow rapid, poor differentiation, metastasize
61
Q

aetiology of tumours

A
  • multiple genetic and epigenetic changes that occur over a long period of tiem
  • oncogenic/carcinogenic substance can cause tumours
  • physical, chemical or viral
62
Q

stages of oncogenesis

A
  1. initiation - chemical/physical carcinogens, irreversibly damage DNA and cause genetic mutations
  2. promotion -after action of stimulus, being to grow and proliferate forming a benign tumour
  3. progression - development of malignancy
63
Q

vascularisation of neoplasms

A
  • BV surrounding tissue penetrate and vascularise tumour and degree of growth and biological behaviour depends on vascularisation
  • avascular (1-2mm, dormant stage) vascular (beginning of angiogenesis and exponential growth)
  • tumour angiogenesis is excessive and persistent
64
Q

tumour spread

A
  1. transcoelomic - spread on visceral and parietal surfaces in abdominal and thoracic cavities
  2. lymphatic tumour cells spread through existing lymphatic pathways and 1st settle in nearest lymph node
  3. hematogenous - on veins, venues and capillaries
65
Q

invasion of tumour cells

A
  • 1st penetrate walls of BV
    1. mechanical pressure
    2. motility of tumour cells
    3. enzymatic destruction of tissue barriers
66
Q

metastasis

A
  • transfer of tumour cells from site to distant orgnas
    1. separation from primary tumours
    2. invasion of surrounding tissue
    3. entry into lymphatic/BV
    4. intravasation, extravasation and vascularisation
67
Q

effects of tumours in carriers

A
  • direct/indirect
  • direct = replaces healthy tissue, pressing on surround tnormal tissue + BV, rupture of hollow organs and tumour emboli
  • indirect = paraneoplastic effects
68
Q

oncogenic viruses

A
  • cause neoplasia - adneovirus, poxvirus, papopvrisu

- retrovirus vauses Marek’s diseass, feline leukaemia and bovine leukemia

69
Q

marek’s disease

A
  • highly contagious - chickens
  • alpha herpes virus
  • t-cell lymphoma, infiltration of lymphocytes
  • transmission by dust or dander, enters by inhalation
    0 causes: damage and enlargement of peripheral nerves, lymphoid tumour…
    blindness, and immunosuppression
70
Q

cat lekaaemia

A
  • retrovirus - immunosuppression and anaemia
  • transmitted by saliva, nasal discharge, faeces/milk
  • enters: cleaning, bites, mating
  • some can carry without symptoms
71
Q

bovine leukosis

A
  • delta retrovrisu
    -= persisten tlymphocytsosi lymphoma
  • transmission = blood
    enters = blood sampling, vaccination
72
Q

main source of formation of ROS

A

sources of ROS generation: endogenous or exogenous. Endogenous = metabolism, exogenous = environment, therapy and diagnostics

73
Q

state consequences of oxidative lipid damage

A

consequences are changes In membrane fluidity and permeability, changes in cell integrity and formation of lipid per oxidation products that are toxic to cell and chemotactic

74
Q

oxidative stress

A

imbalance between formation of ROS and their removal by antioxidants. there’s increased oxidant production and reduced antioxidant protection

75
Q

oxidation damage to lipids

A

H2 separated by hydroxyl radical and lipid radical is formed. lipid radial is formed by Oxygen into lipid peroxyl radical which acts on adjacent FA chain, allowing oxidation to spread. leading to formation of lipid peroxide or decomposition into smaller molecules su has aldehydes or ketones

76
Q

definition of inflammation

A

protective response of vascularised tissue on initial stimulus/injury. this can be caused by microorganisms, mechanical trauma, radiation, heat. Causes cascade of vascular and cellular events in capillary beds.

77
Q

how to classify inflammation

A

according to duration: parachute, subacute, acute and chronic
according to strength: at mild, moderate and strong
considering lesions: focal, multifocal, locally extensive and diffuse
according to type of exudate: serous, fibrinous, suppurative, granulomatous, necrotising, hemorrhagic, eosinophilic

78
Q

list exogenic etiological factors of the inflammatory resposne

A

microorganisms, physical, chemical and nutritive

79
Q

endogenous etiological factors of inflammatory response

A

newly formed molecules or antigens from degenerated, dysplastic or neoplastic cells. oxidative stress and immune reactions

80
Q

inflames and what’s its role

A

inflammasomes are innate immune system receptors and sensors thet regulate the activation of caspase-1 and induce inflammation in response to infectious microbes and molecules derived from host proteins

81
Q

vascular events in acute ifnlammation

A
  1. vasodilation - increased blood vol in capillary beds. histamine, serotonin, NO< prostaglandins etc
  2. increased blood flow - increased hydrostatic pressure. fluid leakage into extravascular space (transudate)
  3. increased vascular permeability - leakage of plasma, proteins and cells into extravascular space (exudate)
    - increased blood viscosity and haemoconc
  4. stasis of blood flow
82
Q

mechanisms involved in formation of edema

A

edema in actue inflammation is due to vascular changes. vasodilation, increased blood flow, increased vascular permeability, stasis of blood flow

83
Q

dynamics of inflammation

A

is a chain reaction activated by chemical and neurogenic mediators.

  • causes vascular changes
  • inflammation cells are activated and moved towards periphery of blood stream (margination)
  • inflammation cells move along endothelium unitl they stop and are firmly attached to endothelium (adhesion)
  • after cells adhere they pass into intersititum (emigration)
84
Q

phases of cell inflammatory dynamics

A
  1. margination - inflammation cells go to endothelium
  2. adhesion - inflammation cells connect with endothelium
  3. emigration - inflammation cells exit BV into interstitium
  4. chemotaxis - inflame cells attracted to certina substances move to site of cause
  5. accumulation - large number of inflammation cells at site of causative agent
  6. phagocytosis - inflammation cells remove causative agent
85
Q

microbial mechanisms of phagocytosis

A

oxygen dependence - during phagocytosis, neutrophils begin to consume increased amounts of oxygen because of oxidative explosion
enzyme NADPH-oxidase reduces molecular oxygen via electron transfer from NADPH and generates superoxide ion and NADP…

86
Q

oxidative explosion of phagocytosis

A

stimulation of neutrophils during phagocytosis, large amounts of oxygen are consumed and the ROS required for phagocytosis is generated
neutrophils also produce NO
most are produced by NADPH oxidase and superoxide anions are formed

87
Q

indicate mechanisms by which lysosome enzymes can cause tissue damage

A

lysosomal suicide = phagocytosis of bacterium, bacteria overcomes phagolysosome and bursts. so enzymes are ruptured, exit cytoplasm and damage intracellular skeleton and organelles.

regurgitation - phagocytic vacuole is formed around bacterium. premature fusion of lysosomes into phagolysosomes and enzymes are released from it before its completely closed

frustrated phagocytosis = phagocyte encounters foreign substance that’s too large to phagocytose, cannot form phagosomes, so lyosomsal enzyme are released on stimulus and damage to surrounding tissue occurs

88
Q

role of collagenase from neutrophils during an inflammatory reaction

A
  • collagenase allows neutrophils to pass through basement membrane
  • move through interstitum
  • breaking down collagen and allowing leukocytes to reach the pathogen.
  • also enables movement of CT cells through interstitial
89
Q

what are kinins dew hat is the role of them in inflammation respons

A

kinins are polypeptides that are formed by the cleavage of a quininogen protein by the action of the kallikrein protease. They are bio mediators of inflammation that increase blood vessel permeability and cause vasodilation or vasoconstriction depending on local conditions. They cause bronchoconstriction, increased permeability, edema and increase histamine release. They create pain. The most famous is bradykinin.

90
Q

what is PAF

A

Platelet-activating factor is a potent phospholipid activator and mediator of many leukocyte functions, platelet aggregation and degranulation, inflammation and anaphylaxis.

91
Q

what is TNF

A

Tumour necrosis factor is a cytokine- a small protein used by the immune system for cell signalling.

92
Q

explain anti-inflammatory effect of glucocorticoids

A
  • reduce inflam by inhibiting enzyme phospholipase A2 which acts by producing arachidonic acid.
  • reduces number and activity of leukocytes and permeability of BV
  • stabilise lysosomal membranes, suppress t lymphocytes and their division and suppress proinflam expression. Cytosol proteins, reduce fever, promote lymph atrophy. Tissues, reduce the number of circulating eosinophils and lymphocytes.
93
Q

describe acute phase response in local inflammation

A
  • caused by action of inflammatory mediators: IL-1, IL-6 and TNF-L, leading to change in CNS and liver
  • CRP, SAA protein and ceruloplasmin begin to be produced in the liver
94
Q

how fever causes

A

divided into aseptic, inflammatory, infectious, paraneoplasitc, resorptive, iatrogenic and dysregulatory

  • occurs as a response of organism to the presence of a certain infectious agent
  • release of various bio-mediators of inflammation
  • produce prostaglandins
  • also occur when there’s no inflammation reaction - exposed to various physical and chemical rfactors
  • 3 stages of fever
    1. stadium increment (sudden rise in temp, accompanied by shivering)
    2. stadium acme
    3. stadium decrement (meiomediatoris cease to it)
95
Q

positive proteins of acute pahse

A 
C reactive protein (CRP) - dogs, pigs
serum amyloid A (SAA) - horse, cat
Haptoglobin (Hp) ruminants
ceruloplasmin (Cp)
fibrinogen
96
Q

negative proteins of the acute phase

A

albumin and transferrin

97
Q

SIRS and MODS

A

SIRS = systemic inflammatory reaction syndrome
MODS= multiple organ dysfunction syndrome
SIRs occurs when there’s uncontrolled increased in circulatory inflammatory mediators or cytokines
3 stages: local injury/infection, hemeostasis disorder and developed SIR
- most often leads to MODS due to excessive permeability of BV and vasodilation, leading to hypovolemic shock and reduced perfusion of blood into tissues and organs.

98
Q

possible outcomes of inflammatory reactions

A

best possible outcome of inflammation is removal of causative agent and return o cells to their original state.

  • tissue damage was too great or it’s a tissue that doesn’t have ability to mitosis, there’s a process of repatriton or replacement
  • chronic inflamma, - due to impossibility of revmogin the causative agents damage tissue progresses and is replaced by CT, resultinggn in reduced functional capacity of the tissue.
99
Q

what conditions and in what way can affect the course of inflammatory reaction

A

In diabetes mellitus due to changes in metabolism, increased protein glycation leads to a decrease in the possibility of healing. Hyperadrenocorticism also slows down inflammatory processes due to the anti-inflammatory action of glucocorticoids. With a reduced concentration of protein, the production of inflammatory cells and bio mediators of inflammation is reduced, so the inflammatory reaction slows down. Haematological disorders, neutropenia and aplastic anaemia reduce the response.

Pathophysiology (3 decks)

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