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Pathophysiology > Final end > Flashcards

Final end Flashcards

1
Q

Hepatorenal syndrome

A
  • liver cirrhosis, portal hypertension, ascites + edema

- activation of sympaticus, renal vasoconstriction, uraemia and azotemia

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2
Q

Nephritic syndrome

A
  • immune complexes, lodge in capillaries
  • elicit immune response to capilliaries
  • increase WBC
  • inflammed nad breakdown allowing RBC + WBC to leak through
  • protein loss (mild)
  • decrease GF
  • water and sodium retention
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3
Q

Nephrotic syndrome

A
  • increase glomerular permeability
  • podocytes aren’t working/lost
  • protein leaks out (albumin decreased)
  • frothy urine
  • edema
  • increased lipids
  • decreased CO
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4
Q

causes of prerenal disorder

A
  • decreased renal perfusion
  • venous pathology
  • decreased arterial BP
  • increased intrabadominal pressure
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5
Q

stages of prerenal disorder

A
  1. compensatory = maintain normal kidney function. Afferent = dilation, effe = constrict, increase GFR, Na, H2O reabsorption. Increase blood vol + BP, secretion of prostaglandins and NO
  2. prerenal kidney failure
    - decreased GFR as no more dilation and constriction
    - strong sympathetic and RAAS activation
    - prerenal uremia and azotemia
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6
Q

frothy bloat

A
  • small gas bubbles produced during fermentation in rumen are separated above ruminal content
  • abnormal fermentation
    = sudden production of large amount of gas
    = gas trapped
    = stable foam is formed, eructation canont occur
    = rapid expansion
  • animal + plant influences formation of foam
  • salivary mucine is antifoaming but production is decreased
  • most common = grazing legume
  • less common in dairy cattle
  • no separation of gas, foam formed, no eructation, increased pressure in rumen.
    = increased rumen motility
    = increased pressure + stretching of wall
    = hypotonia of rumen
    = atony of rumen
    death occurs due to suffocation
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7
Q

bloat

A
  • frothy bloat (primary)
    = abnormal fermentation of luminal content
  • free-gas bloat (Secondary)
    = mechanical disturbances
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8
Q

hypertrophic cardiomyopathy

A
  • inherited disorder
  • left ventricular concentric hypertrophy and interventricular septal thickness
  • inner diameter of left chamber is reduced - atrial dilatation of increased pulmonary pressure
  • stagnation of blood in L. atria predisposes to formation of thrombus
  • myocyte degenerative changes and interstitial fibrosis - decreased ventricular dilatation and contractions
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9
Q

aortic regurgitation

A
  • semi-lunar valve fails to close properly
  • left ventricular eccentric hypertrophy -> compensation -> diastolic murmur
  • relative insufficiency of mitral valve
  • dilation of the left atrium
  • pulmonary edema
  • hypertrophy and dilation of right ventricle
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10
Q

respiratory sinus arrhythmia

A
  • change of rate of spontaneous depolarisation in SA node related to respiration
  • helps to stabilise CO, allowing the HR increase during inspiration when left ventricular SV decrease
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11
Q

supra ventricular arrhythmia

A

atrial extrasystole, supraventricular tachycardia, atrial flutter and atrial fibrillation

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12
Q

atrial flutter

A

abnormal herat rhythm occurs when atrial pump rapidly, supra ventricular tachycardia

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13
Q

sinus block

A
  • disturbances in which impulses are generated in sinus node, cannot be conducted by atrial muscle
  • 1 degree - delayed conduction from SA - atrial muslce
  • 2 degree - inability to conduct some SA node
  • 3 degree- none are conducted
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14
Q

AV block

A
  • partial/complete interruption of transmission (A->V)
  • 1st - delay of conduction, prolonged P-Q interval
  • 2nd - some aren’t conducted (Mobitz 1+ 2(
  • 3rd inability to conduct
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15
Q

cystic fibrosis

A
  • genetic disease with abnormally thick mucus production in mucus glands
  • lungs and pancreas mostly affected
  • airway obstruction, athelectases and infection
  • cor pulmonale and resp distress syndrome
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16
Q

lung hypertension

A
  • lung disease with vasoconstrictive/structural changes in BV
  • left heart failure, 2ary to pressure increase in lung veins
  • congenital heart malformation
  • hypoxia and cor pulmonale
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17
Q

chronic obstructive bronchitis

A
  • hyper secretion, diffuse obstruction, chronic productive cough due to inflammation, mucosal gland hypertrophy and hypreplasia
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18
Q

pleural disease

A
  • pleuritis = wet/humid
    dyspnea and pain = athetectases
  • hydrothorax = increased hydrostatic/ decreased oncotic pressure (liver and kidney disease)
  • pneumothorax = closed/open/ventile
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19
Q

bronchopneumonia

A

from bronchioles to alveoli

- small foci of inflammation

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20
Q

neonatal resp distress syndrome

A
  • premature partus, piglets and puppies
  • insufficient amounts of lung surfactant
  • during exhalation, residual vol is exhaled and lungs collapse
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21
Q

brisket disease in cattle

A
  • severe hypoxic response with vasoconstriction

- tachycardia, jugular veins dilatation, subcutaneous edema in neck

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22
Q

lung edema

A 
- abnormal fluid accumulation in lungs
cardiogenic lung edema
- capillary pressure increase, congestive heart failure, increased pressure
noncardiogenic 
- angio-mural edema
- capillary damage, ROS production
- alveolar pneumocytes type 2 damage
- penetration of plasma and erythrocytes
clinical signs 
- cough, dyspnoea, restlessness, tachycardia, foamy sputum
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23
Q

atelectasis

A
  • aeration failure and lung collapse
  • alveolar collapsing disturbs lung circulation
  • necrosis, epithelial destruction
    1. obstructive, 2 compressive, 3 postoperative
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24
Q

lung pneumonia

A

congestive, hépatisation and resolution stage

- fever, hyperventilation, dyspnoea and tachypneoa

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25
Q

lung emphysema

A
  • destruction of alveolar walls and septa
  • alveolar and interstitial
    mechanical theory
  • bronchiolitis, laboured breathing, cor pulmonale, alveolar walls and capillary network distension
    biochemical theory
  • alpha1 antitrypsin, elastine function is lost
    consequence
  • decreased area of gas exchange
  • loss of network and elastic fibres
  • increased residual vol
  • lung hypertension
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26
Q

iron deficiency anaemia in pigleta

A
  • sow = low permeability of transplacental barrier - milk contains small amount of iron
  • piglets = born with very low Fe stores, rapid growth + needs
  • environment = pigs raised in confinement without access to soil
    pathophysiology = tissue hypoxia, hypothermia, GI inflammation, insufficient Fe supply
    clinical signs = decreased appetite, inadequate efficiency of food utilisation, stunts growth, anaemia, pulmonary edema
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27
Q

hypersecretion

A
  • increased gastric juice secretion
  • increased conc of gastrin = acute and chronic gastrin, decrease gastrin catabolism, hypertrophy of tumour G cells
  • increased cos of corticosteroid -= acute and chronic stress
  • increased conc of histamine = mastocytoma
  • consequence = peptic ulceration, inactivation of pancreatic enzymes, deposition of bile salts, diarrhoea and steatorrhea
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28
Q

further biotransofmraiton in the liver

A

toxins (non polar) -> intermediate -> end product (more polar)

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29
Q

ammonia detoxification

A
  • waste product of AA metabol and pther N2 compounds
  • formed by AA deamination and urea degradation
  • place of origin: intestine, liver and kidney
  • SI => protein digestion -> ammonia
  • LI => bacteria degradation -> ammonia
    goes to portal circulation -> urea cycles -> urea
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30
Q

disorders of ammonia detoxification

A
  • decreased liver function -> decrease ammonia detoxification
  • liver cirrhosis -> NH3 bypass liver -> toxic action of the brain -> hepatic en ephalopathy
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31
Q

hepatic encephalopathy

A
  • liver failure, means decreased utilisation of ammonia and portosystemic shunting leads to accumulation of ammonia in systemic circulation, readily crossing BBB
  • depression, lethargy, ataxia, stupor, coma
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32
Q

causes of sideropenic anaemia

A
  • decreased intake (newborn)
  • decreased absorption ( insufficient secretion of HCl)
  • blood loss
  • increased demand
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33
Q

aplastic anaemia

A
  • pancytopenia = anaemia + leukocytopenia + thrombocytopneia
  • autoimmune destruction of hematopoeitic stem cell
  • causes = mostly idiopathic, infection, drug therapy, toxins ingestion, genetic disorders
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34
Q

sideropenic anaemia

A
  • when iron becomes limiting for erythropoeisis
  • in absence of iron, Hb cannot be product in suff quantities
  • microcytic hypochromic anaemia
    regenerative
  • sufficient iron absorption + blood loss in upper GI tract
    nonregenerative
  • concurrent: nutritional iron deficiency + suppress regeneration
    iron deficient RBC
  • shrinkage, membrane blebbing = features of apoptosis
  • keratocytes, acathyocytes, schisocyte
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35
Q

haemolytic anaemia

A
  • intravascular = destruction of RBC within blood vessles

- extravascular - phagocytosis of RBCs

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36
Q

hereditary stomatocytosis

A
  • alaskan malamute, inherited autosomal recessive trait
  • increased osmotic fragility of erythrocytes and shortened lifespan
  • membrane cytoskeletal defect
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37
Q

pyruvate kinase deficiency

A
  • insufficient ATP production
  • highly regenerative anaemia
  • erythrocyte 1/2 life is shortened
  • haemolytic anaemia
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38
Q

immune mediated haemolytic anaemia

A
  1. primary idiopathic IMHA -> mistakingly recognises RBC as foreign and produces autoantibodies against
  2. secondary -> immune system produces antibodies against erythrocytes by virus, bacteria..
  3. alloimmune hemolytic anaemia
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39
Q

neonatal isoerythrolysis in kittens

A
  • type B queen, mate to A or AB toms
  • kittens bearting type A antigen
  • signs within 24-36hrs
  • weakness, tachycardia, ear and tail tip necrosis
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40
Q

DIC

A
  • multiple clot formation

cause: sepsis, neoplasm, metastatic tumour

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41
Q

anaemia in chronic disease

A
  • normocytic normochromic anaemia
  • most common non-regenerative
  • mediated by inflammatory cytokines
  • decreased RBC lifespan and decreased RBC prodcution
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42
Q

thrombocytopenia

A
  1. decreased bone marrow production (drugs, infectious agents, necrosis, aplasia)
  2. increased platelet consumption (extensive acute bleeding + DIC)
  3. increased platelet destruction (immune mediated destruction)
    inherited and acquired
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43
Q

von willebrand disease

A
  • inherited deficiency
  • disorders of primary haemostasis
  • spontaneous mucosal bleeding
  • slow wound healing
  • vWD def = decreased platelet pug formation
  • type 1 = deficiency in amount of vWD
  • type 2 = relative decreased more severe
  • type 3= most severe, complete absence
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44
Q

fragmentation hemolytic anaemia

A
  • secodndary to vascular disease of DIC
  • mehcnaicla trauma
  • keratocytes, shcistocytes and cathocytes
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45
Q

anaemia due to infectious agents

A
  • extravascular hemolysis
  • decreased erythropoiesis
  • babesia, myocplasma
  • breakdown cell membrane
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46
Q

oxidant - induced haemolytic anamia

A
  • onions (dogs, cats), barassica species (rum), nitrate containing pnlants (rum)
  • minerals - sink (dogs), copper (sheep, dogs)
  • chemicals - skunk muscle (dogs>cats)
  • drugs - acetaminophen (cats,), Vit K (dogs)
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47
Q

anaemia of chronic kidney disease

A
  • non-regenerative anaemia
  • not presen t in all animals with kidney chronic
  • decreased erythropoietin production
  • increased hepcidin
  • decreased rBC lifespan
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48
Q

disorders of biotransofmration I liver

A
  • decreased inactivation and excretion of endogenous metabolites
  • accumulation Imn body -L toxic reaction
  • liver cirrhosis - toxins, bypass the liver
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49
Q

biotransformation in liver

A
  • conversion of endogenyous/ exogenous compounds
  • deotoxification = conversion to ineffective metbaolites
  • bioactiation = increased toxicity, CCL4 => CCL3
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50
Q

mechanism of biotransformation

A

stage 1 = non synthesis = oxidant, reduced and hydrolysis

stage 2 = synthesis = coagulation, methy and acetyl

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51
Q

aetiopathogenesis of shock

A
  • hypvolemiac = loss of circulation gblood
  • cariogenic = disease of myocardium
  • distributive = inaqedquate blood vessel adatpion
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52
Q

disorders of haemostasis

A
  • acquired disroders -> due to underlying disease (old animals)
  • inherited (young) (dog) - von willebrand and haemopilhilia
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53
Q

pure red cell aplasia

A
  • absence of identifiable erythroid precurorsors
  • only erythroid line is affected
  • severe non-regenerative normocytic normoochromic
  • primary/secondary
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54
Q

cariogenic shocks

A

disease of myocardium ,myocardial infarction and pulmonary embolism

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55
Q

distributive shock

A
  • inadequate BV adaption to vol
  • increased minute vol, decreased arterial and increased venular pressure
  • due to decreased tone of Smooth muscle vol of blood in veins increased
  • neurogenic, septic, anaphylactic
56
Q

hypobolemic shock

A
  • internal and external bleeding

- loss of plasma and loss of body fluids

57
Q

asphyxia

A
  • gas exchange disturbance
  • accumulation of CO2 in blood: cramps, cyanosis, bradycardia, smooth muscle paralysis
  • breathing centres, paralysis and death
58
Q

vomiting

A
  • reflexive foreceuful expansion of part or all of content
  • pigs, dogs and cat vomit easily and herbivores rearely vomit
  • horses don’t vomit, udeerdeveliped and non sensitive vomiting centre, powerful cardia sphincter, diagonal entrance of esophagus
  • direct and indirect stimulation of vomit centre
59
Q

equine gastric ulcer syndrome

A
  • causes - travel, training, limited grazing

signs = weight loss poor hair coat, change in attitidue

60
Q

gastric ulcer

A

necrosis ingastric musocsa
1. mucosal barrier injury
2. back diffusion of luminal acid and into mucosa
3. degranulation of mast cells, releasing histamine
4. increased secretion of pepsin + HCl
5. mucosal erosion, damage of BV
6. ulcer
causes = drugs, helicobacter pylori, stress, neoplasia, systemic iseases
signs = anaemia, weakness, weight loss, vomithy

61
Q

hyposecretion

A
  • decreased gastric juice secretion
  • chronic atrophic gastritis and diffuse atrophy of mucosa
  • consequence = decreased HCl secretion, predisposing factor for infection of helicobacter spp
62
Q

phase 1 of gastric dilatation

A
  • accumulation of gas in the stomach, stomach doesn’t empty properly
  • light discomfort
  • dog is restless, salivation is increased, trying to von and stomach is bloated
63
Q

gastritis (inflame of gastric mucosa)

A
  • irritants in food, food allergies, drugs, potions, viral bacteria and parasite
  • acute = protective mucosal layer is altered, mucosal reddening, edema, superficial surface erosion leads to: increased`motility, stomach pain and vomiting
  • chronic = progressive thinning and degeneration of mucosa. Leads to: chronic superficial gastritis, chronic atrophy gastritis
64
Q

hormonal regulation of renal function

A
  1. renin-angiotensin-aldosterone system
  2. aldosterone
  3. adh
  4. atrial natruetic peptide
65
Q

renin

A

released from juxtaglomerular cells, AGT1-> II

- stimulates vasconstriction

66
Q

aldosterone

A

stimulates Na/K atpase.

Na,Cl and water reabsorption and K secretion. increased blood K conc

67
Q

luminal alkalosis

A

excessive production of ammonia in rumen. Unbalanced meal, improper application of urea
clinical signs = severe intoxication after 10 mins after meal rich in urea

68
Q

ADH

A

na and water reabsorption in distal tubule and collecting duct

69
Q

atrial natruiretic peptide

A

decrease Na and water reabsorption in distal and collecting duct
secreted by cardiac atria
vasondilation -> increased GFR

70
Q

acute renal failure

A
  • sudden loss of kidney function
  • decrease Na reabsorbed, H excretion, decreased calciferol, decreased GFR
  • oliguria and azotemia
  • cause :
    prerenal = systemic circulatory disorder
    renal = acute glomeruloneprhtiis
    poystrenal = urinary tract obstruction
71
Q

uremic syndrome

A
  • terminal stage of chronic renal failure
  • disorders in carb metabolism (hyperglycaemia)
  • acid base imbalance (metabolic acidosis)
  • anaemia
  • atherosclerosis
  • gastro disorders
  • uremic coma
72
Q

chronic renal failure

A
  • progressive and irreversible kidney damage
    1. decrease GFR, other functions preserved
    2. further decrease, decreased excretion-azotemia, decreased urnie conc
    3. severe anaemia and arterial hypertension = disorders of CV, digestive a d NS
    4. decrease GFR and uremic syndrome
73
Q

causes of hepatocellular jaundice

A
  • infectious hepatitis
  • toxic hepatitis
  • hepatic lipidosis
  • liver fibrosis and cirrhosis
74
Q

mechanism of hepatocellular jaundice

A
  • decrease bilirubin uptake by hepatocytes and conjugation
  • impaired bilirubin excretion into bile cannuliculi
  • urobilinogen decreased, stercobilin, decrease and results in pale faeces
  • increase urobilin, dark urine and increase bilirubin
75
Q

obstructive jaundice

A
  • impaired Flow by extra hepatic ducts
    = intralumuinal (gallstones, parasitic)
    = extraluminal (tumour/inflammation)
76
Q

mechanism of obstructive jaundice

A
  • conjugated bilirubin stays in liver and returns to systemic circulation
  • urobiliniogen and stercobilin decrease = pale/fatty stool
  • conjugated bilirubin increase in blood, in kidney decrease in urobilim and increase in bilirubin - greenish urine
77
Q

causes of haemolytic icterus

A
  • excess RBC destruction -> increase bilirubin formation
    1. obligate intracellular parasite
    2. other microorganisms
    3. immune mediated haemolytic anaemia
78
Q

mechanism of haemolytic jaundice

A
  • increase haemolysis -> increase bilirubin production in psleen
  • increased unconjugated bilirubin into liver
  • liver to intestine is increased conjugated bilirubin converted to stercobilin
  • increased absorption of urobilinogen
  • increase urobilin in urine
79
Q

mechanism of fatty liver

A
  1. increase lipid influx to liver from feed by chylomicrons. Increase lipid content, increase FA esterification and increase VLDL formation.
  2. increased lipid influx to liver from adipose tissue.
    energy deficit, increase lipid metabolism, increased FA oxidation, insufficient VLDL formation
  3. increase FA + TG synthesis from carbs
    increased carb context
    exceeded blood glucose, increase FA esterification
80
Q

myocardial infarction

A
  • irreversible necrosis of heart muscle secondary to prolonged ischemia when a portion is deprived of oxygen due to blockage of coronary artery
  • result:
    = change of intra and extra cellular homeostasis
    = accumulation of anaerobic metabolism
    = reduced production of energy
    = increased production of ROS
    = activation of local autonomic reflexes
    = increase release of neurotransmitters
81
Q

symptoms of heart failure

A

right = congestion of peripheral tissues
- edema and ascites/liver congestion
- GI tract congestion
= anorexia, GI distress and weight loss

82
Q

consequences of myocardial infarction

A

metabolic consequences, mechanical, electro…

  • decreased contractiliy
  • cardiogenic shock
83
Q

mitral valve insufficiency

A
  • fails to close properly
  • regurgitation into L. atria
    = hypertrophy and dilation of L. atrium
    = hypertrophy and dilation of ventricular wall
84
Q

heart failure

A
  • when heart can’t pump enough blood
    = left = output of L Ventricle < total volume of blood received
    = right = output of R < input from systemic
85
Q

compensatory of heart failure

A
  1. frank starling mechanism
  2. concentric/eccentric hypertrophy
  3. neuro-humoral
86
Q

mitral stenosis

A
  • decrease in mitral valve area
  • impairment of blood Flow to left ventricle
  • left atrial hypertrophy -> compensation
    > increase pressure and vol in L. atrium and in pulmonary veins (pulmonary edema)
  • hypertrophy and dilation of right ventricles = systemic venous congestion -> edema
87
Q

disturbances of impulse production

A
  1. nomotopic disturbances of impulse production - sinus: tachycardia, bradycardia, arrest and extrasystole
  2. heterotypic disturbacnes
    - active/passive hetertrophy
88
Q

sinus bradycardia

A
  • slow produciton
  • reduced irritability, hypothermia, hypothyroidism
  • increased intracrhail pressure
  • increased vagal tone - hyperpolarisation
89
Q

atrial fibrillation

A
  • arrhythmia caused by irregular production of impulses in multiple foci in atria independently
  • foci producing impulses during systole and diastole
90
Q

heart block

A

disorder in heart rhythm caused by obstruction in electrical conduction system
1. 1st degree = delayed conduction
2. 2nd degree = partial/incomple
3. 3rd degree = total
SA, interatrial, AV, interventricular block

91
Q

malabsorption

A

decreased ability to digest +/or absorb nutrients from food

  • inflammation, disease of CV/ lymphatic
  • increased HCl secretion
  • pancreatic enzyme deficiency, inadequate bile secretion
  • idiotpathic
92
Q

enteritis

A

infection, intoxication, trauma, ischemia, neplasm

93
Q

intestinal motility disorders

A 
hypermotility
- rough, rotten, mouldy food, toxic substances
hypo motility 
- concentrated food
intestinal spasm 
= inappropriate diet
intestinal atony
= complete loss of motility, distension of instesinte
94
Q

traumatic reticuloperitonitis

A
  • perforation of reticulum with sharp foreign body
  • falls into reticulum
  • honeycomb traps sharp objects
  • contractions cause perforation of the wall
  • leakage containates peritoneal caivyt
  • can also pierce other organs
  • clinical signs: fecal output decreased, arched back
  • chronic cases: signs of abdominal pain, less apparent
95
Q

inflammatory bowel disease

A
  • unknown etiology
  • no sex predisposition - breed predisposition
  • GALT, genetic, biochem, ischemic disorders
  • signs = chronic vomit + diarrhoea, edema, ascites, anorexia, polyphagia
  • differential diagnosis = pancreatitis, tumour, parasites, kidney and liver failure
  • biochemical/hematological analysis
96
Q

GDC in dogs and horse

A
  • sudden excessive expansion of stomacch due to impaired digestion in the stomach
  • breed, genetic lean body condition, stress, aggressive/fearful behaviour, activity acute mmeal
  • rotation 90-360, serious consequence of cardio, renal and GI
97
Q

mechanism of GDV

A
  1. increased quantity of gas and presure
  2. mucus ischemia (or lead to gastric tachyarrhythmia)
  3. edema, haemorrhage, infarct, ulcers
98
Q

phase 2 of GDV

A

decreased blood flow in stomachh, gastri mucosa damaged
very restless, whining and panting
legs apart, lowered head, stomach is bloated

99
Q

phase 3 of GDV

A

Necrosis of stomach, spleen and others

- white mucous membranes

100
Q

Ruminal acidosis

A
  • too much feed rich in easily digestible carb. too much acidic feed/lack of fibre
    acute acidosis
  • loss of appetite -> reduced food tintake
  • bicarbonate and phosphate buffer of saliva
  • VFA and H = better absorption of VFA
  • ruminitis, dehydration, general weakness
    chronic acidosis
  • increased production of VFA = decrease of pH
  • ruminants, luminal paraketosis
101
Q

ileus

A

= intestinal obstruction
1. functional
spastic (Pb/insecticide poisoning)and paralysis (sympathetic system dominates)
2. mechanical
compression = closed from outside (tumour/abscess)
obstructive = closing from inside
strangulation = torso intestine, invagination…
consequence = retention of content, intestinal distension, bacterial growth

102
Q

constipation

A
  • faeces stretch rectum + stimulate stretch receptors, which transmit signals to spinal cord
  • spinal reflexes stimulate contraction of rectum
  • also relaxes internal anal sphincter
  • impulses from Brain keep external anal sphincter conrractd
  • cause: lack of fibrous cellulose substances -> scars, traumas, neuromuscular disorder
  • consequence: colic, vomiting and intoxication
103
Q

intestinal bloat

A
  • increase production of gas/inability to eliminate gas
  • primary bloat = horse, easily digest diet, enterosaspsms
  • 2ndary bloat = ileus, inability of elimination, overgrowth of bacteria
104
Q

disorders of pancreatic juice secretion

A 
- pancreatitis 
acute = activation of digestive enzymes in pancreatic tissues. Ros-lipid peroxidation in membranes -> trypsin, elastase and lipase
- pancreatic insufficiency 
= undigested protein, fat and starch
= stearorrhoea
= loss of body mass
105
Q

piglet hypoglycaemia

A
  • 1st days of life, characterised with hypoglycaemia
  • apathy, weakness, convulsion and death
  • predisposed = gluconeogenetic enzymes aren’t developed
  • depends where the piglets can suck
    1. depends on sow
    2. depends on piglets
    3. on environent
  • high bedding prevents piglets moving to sow
106
Q

hunter’s dogs hypoglycaemia

A

dogs don’t eat before hunting, decrease BG levels

107
Q

diarrhoea

A
  • increase volume of stool/frequency of defecation. acute/chronic
    osmotic diarrhoea
    = cause = intake of susbtances that are difficult to absorb and Malabsorb due to pancreatic insufficiency
    = pathogenesis accumulation of large number of osmotic active molecules, transition of fluid from BV to lumen and accelerated motility
    secretory diarrhoea
    = occurs when secretion of water into lumen exceeds absorption
  • cause= enterohepatic microorgan, increase hydro pressure and drugs
    = hormones secreted by certain type of tumours and some metals
  • prolonged opening of Cl ions
108
Q

active heterophy

A
  • extrasystole, tachycardia, flutter and fibrillation
  • impulses depolarising heart muscle are produced outside of SA node and faster than normal
  • reduction of resting membrane potentiak
  • types: supra ventricular or ventricular
109
Q

asthma

A
  • periodic episodes of severe and reversible bronchial obstruction
  • extrinsic/intrinsic seizures
  • bronchoconstriction, infla, swelling and mucus secretion-
  • difficult exhalation and athelectasis
  • hypoxia and hypoexmia
110
Q

free gas bloat

A
  • eosph obstruction due to foreign body
  • stenosis/pressure from enlargement outside esophag
  • damage of N.vagus
  • diaphragmatic hernia
  • tetanus
  • lesions of reticular wall
  • acute bloat = complete inability to remove gas
  • chronic bloat = partial inability to remove gas and bloat develops progressively
111
Q

acute gastric dilation in horses

A
  • overeating fermentable feedstuf
  • lactobacillus -> large production of acidic compounds and gas
  • spams of cardiac sphincter
  • lactate and bacterial toxins -> spasmodic pain (colic)
  • swelling and trembling
  • rupture of stomach -> content leaks into abdominal cavity
  • rupture of diaphragm -> stomach enters thoracic cavity
  • distension, pain, haemocon, dehydration and alkalosis
112
Q

ascites

A
  • fluid accumulation within abdomen cavity
  • causes = portal hypertension/hypoproteinaemia
  • clinical signs = distension of lower abdomen, abdomen pain and discomfort, lethargy, decreased appetite, subcutaneous edema
113
Q

sinus tachycardia

A
  • increased rate of pacing in SA node
  • causes = increase body temp, physical exercise/stress, hyperthyroidism, anaemia and pregnancy
  • increased CO
  • extreme HR I tachycar can decrease Stroke vol and CO
114
Q

gravity toxaemia in sheep

A
  • occurs at end of gravidity
  • occurs when term of parturition is close
  • ovine foetuses have relatively low glucose
  • decrease food intake
  • clinical signs = apathy and weakness
  • mild cases are treated with glucose and corticosteroids
115
Q

hyperglycaemia

A
  • increase glucose conc in blood, postprandial/alimentary

- can be consequence of deficiency/resistance

116
Q

glucocorticoids

A

increase glycogenolysis, gluconeogenesis, decease glucose consumption in cells and increase effect on BCG

117
Q

growth hormone

A

decrees glucose entrance in cells, increase blood glucose

118
Q

thyroid homrone

A

stimulates glycogenolysis, stimulates intestinal glucose absorption

119
Q

undernourishment

A
  • nutrients are inadequate
  • primary or secondary -> acute.chronic, depending on type of nutrient insufficiency
  • decrease BMR, decerase insulin, free FA and AA increase
  • secretion of corticoids, glucagon and GH increase
  • chronic starvation/general undernourishment
120
Q

equine paralytic myoglobinuria

A
  • acute disease with sudden paralysis of striated muscle with myoglobin
  • 15-30 mins after exercise
  • animals strain, don’t move, pain, distress, dehydation
  • pathologically = muscular necrosis
  • therapy = pain relief, prevention of renal damage
  • sporadic = overwhelmed, electrolyte disbalcne , SE and Vit E defieicny, hormonal disbalance
  • chronic = glycogen storage disturbances and disturbances in muscular contractility
121
Q

diabetic ketoacidossi

A
  • life threatening complication of diabetes
  • presented with polydypsia/polyruia, von, diarhoea
  • increase FA mobilisation, conch of AcCoA increase and ketogeneis begins
  • deep laboured breathing activated to correct acidossi
  • can cause hyperosmolar coma
  • accumulation of ketone bodies
122
Q

pathogenesis of diabetes

A
  • utilisation of glucose in peripheral tissue is decrease and production I liver through gluconeogenesis incresaes
  • utilisation is reduced, so it stays in blood
  • secretion of urine begins (glycosuria), polydyp and polyuria develop
  • lipid and protein catabolism occur
  • insulin stops activity of lipoprotein lipase
123
Q

leptin

A

suppresses food intake- made by fat cells

124
Q

atherosclerosis

A
  • chronic arterial disease with deposition of lipid metab
  • consequence = stroke and cerebrovascular insult, ischemic tremor
  • risk factors = hypercholesterolemia, increase hydrostatic pressure, increase ROS production
  • endothelial damage means it’s exposed to blood production of thromboxane increases, inhibition of thrombocyte aggregation is decreased
  • foamy cells are produced and accumulation is 1st reversible
  • apoptosis of foamy cells -> fibrotic cap is formed
  • atheroma = bulging and closing of vessel lumen
    = smaller = lipid and thin cap, prone to rupture
    = larger = rich in CT and less dangerous
125
Q

dibetes mellitus

A
  • characterised with hyperglycaemia - disturbed action of insulin
  • type 1 - most common in dogs -> hypoinsulinemia + hyperglycaemia, cause = genetically predisposed or destruction of pancreatic islets
  • type 2 = hyperglycaemia and hyperinsuluminemia then hypoglycaemia - most common in cats - obesity. treated with oral hypoglycaemia dugs
    other types can appear seoncayr to pancreatic disease and hyperadnreocortisicm
  • glucocorticoids and progestins for a long period of time
126
Q

hyperosmmolar coma

A
  • life threatening condition of hyperglycaemia
    insulin action is lost or resistant
  • actue gastro disease with vomiting and diarrhoea
127
Q

inslulin

A
  • release when blood glucose conc is high, therefore decreases glucose
  • stops catabolic processes: glycogenolysis, lipolysis and proteolysis, enhances entrance of glucose into cells
128
Q

glucagon

A

speeds up glycogenolysis and gluconeogenesis

- increases blood glucose

129
Q

catecholamines

A

increase glycogenolysis, lipolysis, glucagon secretion and increase blood glucose

130
Q

progestines

A

increase glucose level through gluconeogensis and stimulation of GH

131
Q

consequence of hyperglycaemia

A
  • oxidative damage of cells
  • bacterial and fungal infection of urianry system
  • enhances sorbitol pathway
  • proloneed -> insulin suppression
  • severe -> blindess, diabetic ketoacidosis
132
Q

hypoglycaemia

A

decrease of blood glucose
stimulates glucoreceptors in hypothalamus
presented with mild hypoglycaemia: sepsis and hypoadrenocorticism

133
Q

induced hypoglycaemia

A

hypoglycaemic drugs, xylitol, hyeprinsulinemia in dog

abundant carb intake when insulin released in high conc

134
Q

spontaneous hypoglycaemia

A

when deficiency of contrargulative hormones exist

  • hypoadrenocorticism and hypopituiatism
  • def of enzymes participating in gluconeogenesis and glycogenolysis
135
Q

dairy cow ketosis

A

disturbances in fat and carb metabolism
decrease in blood glucose and increase KB

rest on paper

Pathophysiology (3 decks)

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