Final again ?

Question 1

Ascites

Answer 1

Def: Accumulation of fluid within the abdominal cavity

Cause: portal hypertension and hypoproteinaemia

Affects: dogs and rarely in pigs

Signs: distension of lower abdomen, abdominal discomfort, lethargy, decreased appetite

Question 2

cirrhosis

Answer 2

Def: end stage liver accompanied with diffuse fibrosis and loss of regular structure, can cause ascites
1. Sinusoidal hypertension
- drainage doesn’tt happen so get backflow and increased pressure = ascites
- increased lymph formation = ascites
- transudate is high in proteins so there’s osmosis and leakage = ascites
2. Leads to hypoalbuminemia
- decreased blood osmotic pressure, means plasma leaks into interstitium and cavity = ascites
3. Causes plasma leakage from blood vessels
- causes noadrenaline release and vasoconstriction, RAAS is activated, ADH is excreted = eddema and ascites
4. Decreased liver blood flow
Complications: hepatorenal syndrome, hepatic encephalopathy and hepatic hydrothorax

Question 3

hepatorenal syndrome

Answer 3

Def: precursor of kidney failure.
1. gets portal hypertension, so veins tries to dilate BV by releasing NO from endothelial cells
2. splanchic vasodilation -> decreased total peripheral resistance
3. increased CO to compensate for decreased peripheral resistance
4. hypovolemia -> decreased renal perfusion -> RAAS activation
5. increased total peripheral resistance
- leads to ascites
signs: decreased GFR, oliguria, uremia and increased serum creatinine

Question 4

hepatic encephalopathy

Answer 4

Decline in brain function that occurs as a result of severe liver disease.
PSS = abnormal connections of lood supply between portal veins and systemic circulation -> bypass (neurotoxins increase in circulation -> HE)
1. NH3 goes to liver
2. enters urea circle, which is impaired, therefore
3. increased ammmonia in blood, which can cross BBB (enter brain)
4. interfers with alpha-ketoglutarate -> glutamate -> glutamine
5. decreased ATP, cerebral edema, oxidative stress, depression, stupor/coma and tremor

Question 5

hepatic hydrothorax (pleural effusion)

Answer 5

Def: excessive accumulation of transudate in the pleural cavity.
1. increased vascular permeability -> fluid and proteins leak into pleural space - increased fluid formation
2. increased venous pressure, L/R heart failure = pleural effusion, if won’t travel back to heart efficiently
3. decreased plasma oncotic pressure (low amounts of protein in blood), fluid isn’t kept in vessels so leaks into intravellular space
4. decreased pleural pressure from atelectasis
symptoms: cough, shortness of breath (restricted lung expansion)
- lymphatics drain pleural fluid, but if there’s obstruction it wont empy or increased pressure = increased pressure in lymphatics

Question 6

fatty liver disease

Answer 6

Def: accumulation of triglycerides in the cytosol of hepatocytes
Mechanism:
1. Increased lipid influx to the liver from feed by chylomicrons
a. Increased FA within hepatocytes, increased esterification, increased VLDL formation and triglyceride deposition in hepatocytes
2. Increased lipid influx to the liver from adipose tissue
a. Due to energy deficit, increased lipid mobilisation, increased FA oxidation, increased FA esterification and insufficient VLDL formation due to apolipoprotein deficit, triglycerides deposited
3. Increased fatty acid and triglyceride synthesis from CHO
a. Increase in FA and triglyceride synthesis, when increased carb content (due to high insulin concentration), increased FA esterification, triglyceride deposition
4. Decreased VLDL formation and excretion
4 grades: (1) healthy liver and reversible, (2) fatty infiltration, (3) fatty degeneration and irreversible, (4) cirrhosis
Causes: energy deficit in ruminants (late pregnancy, early lactation), hormonal disorders (diabetes, hypothyroidism, hyperadrenocorticism), idiopathic fatty liver syndrome

Question 7

biotransformation

Answer 7

• Conversion of endogenous or exogenous compounds into soluble compounds that are easily excreted
• Endotoxins = products of metabolism
• Exotoxins = drugs, poisons from feed, products of microorganisms
• Occurs in ER involving cytochrome P450 and UDP
Detoxification: conversion to nontoxic metabolites
Bioactivation: increased toxicity after biotransformation CCL4 causes oxidative damage to hepatocytes, halothane causes hepatitis
Mechanism:
• Stage 1: no synthesis and goal is to increase the polarity of the compound via oxidation, reduction or hydrolysis
• Stage 2: synthesis of new compounds to increase polarity via conjugation, methylation and acetylation
Disorders: causes decreased inactivation and excretion of endogenous metabolites, so they accumulate = liver cirrhosis

Question 8

physiological mechanism of bilirubin

Answer 8

Physiological mechanism of bilirubin
1. Prehepatic stage: spleen
a. RBC enter spleen, phagocytosed by macrophages
b. Globin is broken down into AA, which is reused for other protein synthesis
c. Heme broken to biliverdin by hemoxidase
d. Biliverdin broken down to bilirubin by biliverdin reductase
e. Macrophage releases bilirubin, bilirubin binds to albumin and goes to portal circulation as unconjugated bilirubin
2. Hepatic stage: liver
a. Bilirubin and albumin separate within sinusoid and bilirubin enters the hepatocyte
b. Bilirubin reaches ER where it’s broken to glucuronic acid = conjugated bilirubin
c. Conjugated bilirubin, exits hepatocyte by passing through biliary system into S.I
3. Post-hepatic stage: intestines and kidney
a. Conjugated bilirubin transforms to urobilinogen and then stercobilinogen
b. Stercobilinogen is excreted via faeces and is brown
c. Urobilinogen goes through enterohepatic circulation

Question 9

haemolytic jaundice

Answer 9

Cause: (1) babesia canis, directly invade and infected RBC causing lysis, (2) other microorganisms, (3) immune mediated haemolytic anaemia
Mechanism:
1. increased haemolysis -> increasedbilirubin production in spleen
2. increased unconjugated bilirubin into liver
3. Liver to intestine is increased conjugated bilirubin  converted to stercobilin
4. increased absorption of urobilinogen
5. increased urobilin in urine

Question 10

hepatocellular jaundice

Answer 10

Cause: decreased bilirubin uptake by hepatocytes, decreased bilirubin conjugation and impaired bilirubin excretion
• Infectious hepatitis, toxic hepatitis, hepatic lipidosis, liver fibrosis and cirrhosis
Mechanism:
1. decreased bilirubin uptake by hepatocytes and conjugation
2. Impaired bilirubin excretion into bile canaliculi
3. Urobilinogen decreased, stercobilin decreased and results in pale faeces
4. increased urobilin, dark urine and increased bilirubin

Question 11

obstructive jaundice

Answer 11

Cause: impaired bile flow by extrahepatic ducts (biliary obstruction). Intraluminal obstruction (gallstones, parasites, inflammation), extraluminal obstruction (tumours)
Mechanism:
1. Conjugated bilirubin stays in liver and returns to systemic circulation
2. Urobilinogen and stercobilin decreased = pale, fatty stool
3. Conjugated bilirubin increased in blood, in kidney decreased in urobilin and increased bilirubin = greenish urine

Question 12

hypoventilation

Answer 12

Alveolar spaces aren’t filled with an adequate amount -> hypercapnia (increased CO2, hypoxemia and hypoxia)
Compensatory mechanism:
1. Reflex tachypnoea and increased depth of breathing
2. Decreased affinity of Hb to oxygen
3. Stimulation of vasomotor centre leading to tachycardia and hypertension
4. Increased erythropoietin

Question 13

hyperventilation

Answer 13

Causes compensatory metabolic acidosis, hypoxemia and hypoxia. There is stimulation of the respiratory centre during hyperthermia, encephalitis and meningitis

Question 14

asthma

Answer 14

Def: periodic episodes of severe and reversible bronchial obstruction in hypersensitive or hyperresponsive airways
Acute seizure: bronchoconstriction, inflammation, swelling and mucus secretion in the lumen
Cause: hypoxia, hypoxemia (vasoconstriction of lung blood vessels leading to right heart overload)
Signs: cough, severe dyspnoea, mucus expectoration, tachycardia, respiratory acidosis
Extrinsic: more common in young animals, partial or total obstruction of airways and severe hypoxia
Intrinsic: more common in adults, non-specific stimuli target on hyperresponsive mucosa
Status asthmaticus: severe asthma seizure, not responding to therapy

Question 15

chronic obstructive bronchitis

Answer 15

Causes: hypersecretion, diffuse obstruction and chronic productive cough
Caused: by inflammation as a result of prolonged inhalation of various irritants
• Mucosal gland hypertrophy and hyperplasia, fibrosis and induration of bronchial wall
1. hyper secretion stops sufficient gas exchange
2. mucus blocks up alveoli and airways so oxygen has thicker membrane to pass through to get to blood
3. if not enough oxygen, pulmonary arteriole will constrict so blood backs up, so goes to other alveoli
4. hypertrophy of heart -> cor pulonale -> right heart failure
Signs: progressive productive cough, sputum, weight loss, tachypnoea and cyanosis

Question 16

lung emphysema

Answer 16

Def: destruction of alveolar walls and septa, with big and permanently enlarged alveolar spaces
Mechanistic theory:
• Bronchiolitis causes histamine release and swelling leading to luminal obstruction
• Laboured inspiration and expiration occur
• Alveolar walls and capillary networks distend
• Causes capillary atrophy and redirection of circulation in healthy regions in the lung
• Increased pressure in pulmonary artery leads to right heart hypertrophy (cor pulmonale)
• Polycytemia as a compensatory mechanism occurs
• No longer works due to increased blood viscosity and a weak heart
Biochemical- enzymatic theory:
• Alpha 1 antitrypsin in an atnielastase deficiency
• Elastin function lost, so alveoli cannot retract
Consequence: decreased areas of gas exchange, loss of capillary network, loss of elastic fibre, loss of elastic fibres, pneumothorax, lung hypertension

Question 17

restrictive: respiratory system disease

Answer 17

Def: decreased lung movement and the decrease of total lung capacity (decreased elasticity of lung tissue or within the thorax)
Pleural disease:
• Pleuritis: can be wet, cause pain and atelectasis
• Hydrothorax = increased hydrostatic pressure or decreased oncotic pressure
• Pneumothorax = closed, open or ventile (can result in cardiac shock)

Question 18

atelectasis

Answer 18

Def: aeration failure and lung collapse
• Alveolar collapse disturbs lung circulation and can lead to necrosis, epithelial destruction and fibrosis of the lungs
Types:
• Obstructive = foreign body, inflammation, parasites
• Compressive = pneumothorax, hydrothorax
• Post-operative

Question 19

neonatal respiratory distress syndrome

Answer 19

Occurs: in premature piglets and puppies
Caused: insufficient amount of surfactant
During exhalation, the residual volume is exhaled and lungs collapse

Question 20

lobar pneumonia

Answer 20

Localised on one or more lobuli, in affected areas no healthy tissue exists
Congestive stage: vascular congestion of alveolar walls and exudate accumulation in alveoli
• Lowest blood oxygenation
Hepatisation stage (consolidation): N, RBC and fibrin accumulation forming firm mass in lobuli
• Red: due to hyperaemia
• Grey: due to leukocytes and fibrin accumulation
• Yellow: tissue becomes softer and wet
Resolution stage: macrophages dissolve exudate and can be coughed out or resorbed through lymphatics
Symptoms: fever, hyperventilation, dehydration, dyspnoea tachypnoea and productive cough

Question 21

bronchopneumonia

Answer 21

• is characterised by small foci of inflammation which can merge
• Usually on ventral parts and caused by bacteria
• Spreads from bronchioles to alveoli
• Exudate in alveoli prevents oxygen diffusion, bronchioloi are filled with mucus and alveoli with exudate
• Alveolar walls become thick
• Hypostatic pneumonia
cause: influenza, measles, Tb

Question 22

aspiration pneumonia

Answer 22

Def: entrance of foreign bodies or fluids in trachea and lungs, causing obstruction, inflammation and swelling
• Airways are obstructed and lungs cannot move correctly, which compromises gas exchange
• Leads to possibility of infection and pulmonary abscesses
• Can progress to non-cardiogenic lung edema
signs: dysnea, fever, cough, abnormal lung sound
therapy: antibiotics

Question 23

cystic fibrosis

Answer 23

Def: genetic disease which causes abnormally thick mucus production in the mucous glands
• Lungs and pancreas mostly affected
• More prone to infection
Causes: airway obstruction, atelectasis and infection, cor pulmonale and respiratory distress

Question 24

cariogenic lung edema

Answer 24

1. exertion causes increased SNS so increase in HR and vasoconstriction
2. causes increased BP
3. increased after load
4. decreased ejection fraction
5. increased ESV
6. decreased CO
   - blood congests in LA (pressure increased), will continue to rest of system until no where to go (pul vein)-> pul cap -> pressure increases fluid shifts out into surrounding tissue, building up alveolo
   - managed by diuretics and vein dilators

Question 25

non-cariogenic lung edema

Answer 25

1. neutrophil activate and release protease, cytokines and ROS
2. causes increased alvoelar capillary permeability
3. type 1 + 2 pneumocyte die
4. decreases surfactant, leading to atelectasis
   Signs: cough, dyspnoea, restlessness, rapid + shallow breathing, tachycardia, stridor, foamy sputum
   occurs after: latent period, following actue lung injury/systemic cnditions; shock, MODs/pancreatitis

Question 26

lung hypertension

Answer 26

• Caused by lung diseases with vasoconstriction or structural changes in the blood vessels
cause: idiopathic, L/R shunts and portal hypertension
1. vasoconstriction + thickening of arterial walls
2. increased resistance to blood flow
3. right heart enlargement
4. cor pulmonale
5. cardiogeni shock
left heart failure causes secondary lung hypertension as it increases pressure in veins of lungs

Question 27

hormonal regulation of renal function

Answer 27

Renin-angiotensin-aldosterone system (RAAS)
- Renin is released from juxtaglomerular cells as response to decreased BP
- Renin converts angiotensinogen into angiotensin I -> angiotensin II
- Angiotensin II stimulates vasoconstriction

Aldosterone
- Released from adrenal cortex
- Stimulates the Na/K ATPase in the distal tubule and collecting duct leading to Na+ and Cl-

ADH
- Produced and released from posterior pituitary gland
- Water and sodium reabsorption in distal tubule and collecting ducts

ANP:
- Secreted from cardiac atria in response to increased BP, which is caused by an increase in extravascular fluid
•causes vasodilation of the afferent arteriole
•decreases salt and water reabsorption in the distal tubule and collecting duct
•decreases renin, aldosterone and ADH secretion

Question 28

pre-renal disorder

Answer 28

Caused: decreased renal blood flow due to systemic circulatory disorders
- reduced arterial blood pressure (severe hypovolemia, shock, heart failure)
- venous pathology (thrombosis, increased venous pressure)
- increased intraabdominal pressure (liver cirrhosis with ascites)
All decrease the renal perfusion, which leads to: deceased GFR, renal ischemia, decreased energy metabolism..

First stage: compensatory phase
•maintain the normal kidney function (GFR, tubular functions)
•afferent arteriole dilatation and efferent arteriole constriction in order to increase the GFR
•there’s increased water and sodium reabsorption
•sympathetic nervous system causes systemic and renal vasoconstriction leading to increased volume and BP

Second stage: prerenal kidney failure
•no more possibility of afferent arteriole dilation and efferent arteriole constriction
•decrease in GFR
•strong sympathetic and RAAS activation -> renal vasoconstriction, additional decrease in GFR ->oliguria
•also leads to failure of the liver (hepatorenal syndrome)
oliver cirrhosis, portal hypertension, ascites, edema, uraemia and azotaemia…

Question 29

glomerulonephritis

Answer 29

Def: inflammation of the glomeruli
causes: accumulation of microorganisms within glomeruli, antibody binding to basement membrane and deposition of antigen-antibody complexes within glomeruli
1. deposition of immune complexes, causes infiltration by immun e cells and platelets
2. release of cytokines, serotonin, histamine, protease leads to damage of GF barrier = increased permeability and proteinuria
3. damage cells for platelet binding, activation of coagulatio and fibrin deposition
4. fibrin decerased cap lumen + GFR
5. fibiroin enters bowman’s space, nodule press on cap -> decreased GFR

Question 30

nephritic syndrome

Answer 30

•Immune complexes in glomerulus
•Decreased GFR, oliguria, azotaemia , mild proteinuria, hypertension due to decreased GFR -> edema
- tubular compensatory mechanism: increase Na and water reabsorption -> hypovolemia -> hypertension -> nephritic edema

Question 31

nephrotic syndrome

Answer 31

•Increased glomerular permeability, massive proteinuria -> edema
•Loss of antithrombin III -> thrombin
•Decreased cardiac output
•Decreased renal blood flow

Question 32

renal artery stenosis

Answer 32

•Occur due to progressive development throughout life, or in older animals due to atherosclerosis
•decreased renal perfusion
•Renal artery stenosis can be compensated for by the autoregulation of GFR, but eventually kidneys will be exposed to chronic ischemia which decreases GFR
•Then RAAS activation, ADH and sympatheticus -> vasoconstriction -> renovascular hypertension -> fibrosis of tubules and glomeruli -> chronic renal failure

Question 33

thromboembolic renal disease

Answer 33

•Occur due to thrombi in arterial or venous blood stream
•Renal artery thrombus comes from the heart -> cause partial or total obstruction
•Partial obstruction -> reduced GFR and tubular reabsorption
•Total obstruction -> infarction of the parenchyma -> irreversible necrosis
•Renal vein thrombus comes from increased tendency to clot

Question 34

tubulointerstitial renal disease

Answer 34

Def: impaired structure and function of tubules and the surrounding interstitium, 3 main diseases: TI nephritis, pyelonephritis and ATN
Primary cause: toxins, drugs, ischemia and infection
Secondary cause: glomerulonephritis, vascular renal disease and urinary tract obstruction
Mechanism:
Early stage (1): normal glomerular function
• Tubular function is damaged  mild/moderate proteinuria
• Reduced reabsorption of albumins and smaller proteins  polyuria
• Reduced reabsorption of sodium with reduced secretion of H+  metabolic acidosis
Late stage (2): secondary glomerular injury
• Damaged tubular cells end obstructing the tubular lumen, leading to secondary glomerular damage
• Increases proteinuria, free tubular cells, urine casts and haematuria and leukocytes in the urine

Question 35

pyelonephritis

Answer 35

Def: inflammation of renal pelvis associated with ureter infection
Cause: ascending infection from the urinary tract via contaminated urine reflux into the renal pelvis
- Pathogens: E.coli, klebsiella, staph and strep
Acute: occurs rapidly with systemic signs of infection, pain and stranguria with pollakiuria. Urine changes include leukocyte, bacteria and urine casts

Chronic: severe disease with the destruction of renal parenchyma due to reduced tubular function. Kidneys cannot concentrate urine, reabsorb sodium or excrete H+ sufficiently anymore

Question 36

acute tubular necrosis

Answer 36

Def: degenerative disease of renal tubules w/o inflammation with acute degeneration and necrosis of tubular epithelium
Cause: nephrotoxins (antibiotics, analgesics, anaesthetics, heavy metals) and ischemia
1. RAAS activation and vasoconstriction leading to decrease in GFR and oliguria
2.Due to extensive tubular cell damage, cells end up obstructing tubular lumen -> increase in intratubular pressure, decreasing GFR -> oliguria
3. Increase in intratubular pressure causes tubular back leak -> interstitial edema
4. Tubular cell damage also leads to decrease sodium reabsorption -> further RAAS activation and vasoconstriction, decreasing GFR even further

Question 37

acute renal failure

Answer 37

Def: sudden loss of kidney functions
1. reduced Na+ reabsorption and K+ secretion
2. Reduced H+ excretion=metabolic acidosis
3. Decreased calcitriol= hypocalcaemia
4. =reduced GFR = hyperphosphatemia, oliguria, anuria and azotaemia
Prerenal: systemic circulatory disorders, low renal perfusion, ischemia
Renal: acute glomerulonephritis, acute tubulointerstitial nephritis, nephrotoxic injury leading to ATN
Postrenal: urinary tract obstruction

Question 38

chronic renal failure

Answer 38

Def: progressive and irreversible nephron damage and loss of kidney function
Consequence: any type of renal disease: glomerular, tubular, interstitial or vascular
Stage 1:
- Reduced GFR, Other functions are preserved

Stage 2:
•Further decrease of GFR, Reduced excretion leading to azotaemia, Reduced urine concentration
•Anaemia due to reduced erythropoietin
•Hypertriglyceridemia due to reduced lipoprotein lipase activity

Stage 3:
•Severe anaemia + arterial hypertension
•Disorders of cardiovascular, digestive and nervous system

Stage 4:
•Significantly reduced GFR to <5%
•Terminal uraemia leading to uremic syndrome

1. decreased GFR = increased Na and H20 reabsorption -> increased BP + peripheral edema
2. decreased GFR = increased K+ retention -> hyperkalemia -> muscle weakness
   3.metabolic acidosis -> diminished capacity to excrete H+ + generate HCO3 -> acidosis -> bone decalcifiation
3. mineral balance and osteohystrophy

Question 39

uremic syndrome

Answer 39

Def: clinical syndrome in 4th stage of chronic renal failure. Characterised by increased concentration of uremic toxins in the blood including urea, creatinine, guanidine, uric acid
Disorders of uremic syndrome: Carb metabolism (hyperglycaemia), acid-base imbalance (reduced H+ excretion), anaemia and hypocalcaemia (decreased production of erythropoietin and calcitriol), gastrointestinal disorders (stomatitis), heart and respiratory disorders, atherosclerosis, skin disorders and disorders of CNS

Question 40

basics of CHO metabolism

Answer 40

• In monogastric animals the final product is monosaccharides, which are absorbed into the blood
• In ruminants, glucose is an intermediate products, further digested into acetic acid, propionic acid and butyric acid (VFA)
• Acetic acid = main source for lipid synthesis
• Butyric acid = substrate for ketogenesis
• Propionic acid = glucoplastic and is a substrate for gluconeogenesis
• Glucose deficiency is usually in period of negative energy balance, after parturition and in early lactation period

Question 41

insulin, glucagon, catecholamine, GH, glucocorticoids, thyroid hormone

Answer 41

Insulin
• decreases blood glucose levels, enhances the entrance of glucose in cells, glucose phosphorylation, glycogen synthesis, lipogenesis and protein synthesis in muscles
Glucagon
• increases blood glucose levels. Increases glycogenolysis, gluconeogenesis and lipolysis
Catecholamines (adrenaline and noradrenaline)
• Increases blood glucose levels. Enhance glycogenolysis in the liver and muscles, as well as lipolysis and glucagon secretion. Adrenaline also stimulates adrenocorticotropic hormone secretion
Growth hormone
• Increases blood glucose. GH directly damages beta cells and insulin production. Also, inhibits glucose entrance and oxidation in cells
Glucocorticoids
• Increase blood glucose by enhancing gluconeogenesis. Decreases glucose consumption in all tissues except the brain. Increases glycogenolysis
Thyroid hormone
• Stimulate glycogenolysis, stimulates intestinal glucose absorption

Question 42

hypoglycaemia

Answer 42

Def: decrease in blood glucose concentration
•Cells cannot receive energy and ROS production is increased -> further damage of cells
•Stimulates the glucoreceptors, activates the adrenal medulla and releases: adrenaline, which increases glycogenolysis in the liver

Induced hypoglycaemia
•Induced with hypoglycaemic drugs
•Xylitol causing severe hypoglycaemia in dogs can cause hypoglycaemic shock and death
•Postabsorptional reactive hypoglycaemia occurs after abundant CHO intake, when insulin is released in high conc but too late, so BG drop beneath physiological range

Spontaneous hypoglycaemia
•Deficiency of contraregulative hormones
•Caused by endocrinological disturbances like hypoadrenocorticism and hypopituitarism
•Causes a decrease in concentration of insulin antagonists
•In hypoadrenocorticism, decreased cortisol levels induce decreased gluconeogenesis and increased sensitivity of target cells on insulin  hypoglycaemia
•Also occurs when there’s a deficiency of enzymes participating in gluconeogenesis or glycogenolysis

Question 43

hunters dog hypoglycaemia

Answer 43

•Occurs in dog that are hyperactive
•Don’t eat before hunting, active during hunting -> drop in BG levels
•Symptoms: disorientation, weakness, tremors, coma, death and collapse
•Disturbance is treated by glucose, or rub gums with honey or fruit juice

Question 44

hypoglycaemia of new-born piglets

Answer 44

•Occurs in first days of life
•Symptoms: apathy, weakness, convulsions, coma and death
•Predisposed because gluconeogenetic enzymes aren’t developed in 1st days after birth
•In order for it to develop, food must be present in the digestive system
•If they receive food during the 1st 10 days of life, piglets can starve up until 3 weeks without developing hypoglycaemia
•Depends on: sow, piglet and environment
•All conditions (mastitis, metritis, stress) can be indirectly responsible for hypoglycaemia in piglets
•Piglets which are born weak and cannot gain access to the sow are also in danger, along with anaemic and infected piglets
•High bedding which prevents piglets to move toward the sow

Question 45

gravidity toxemia in sheep

Answer 45

•Occurs at end of gravidity, particularly in sheep carrying two or more foetuses
•Occurs when parturition is close, since glucose is needed for fetal growth
•Ovine placenta can extract glucose from blood even when its concentration is low
•Ovine foetuses have relatively low blood glucose, the transplacental gradient of glucose – helps transport of glucose from mother to foetus
•Decreased food intake predisposes the disease
1. increased energy demand
2. starvation, glucose decrease = hypogly
3. XS fat metabolism, products KB= ketonemia
4. deue to high stress + hypo = high cholesterol
5. hypoglycaemia encephalopathy -> nervous signs
6. renal dysfunction

Signs: apathy and weakness, followed by neurological symptoms
Treatment: glucose and corticosteroid application or oral application of glucose precursor

Question 46

dairy cow ketosis (types)

Answer 46

• Disturbance in carb and fat metabolism. In affected animals there’s a decrease in BG levels and increase KB concentration in blood, urine and milk
• Biggest need for glucose occurs at the end of gravidity and beginning of lactation
• Glucose is needed for fetal growth and milk production
• Dairy cows can be ketotic without hypoglycaemia usually when sub clinic ketosis exists
Characterised by: anorexia, depression, ketonemia, ketolactia, ketonuria, hypoglycaemia and decreased milk production
Type 1 ketosis - Starvation or skinny cow disease
• Insufficient amount of calories needed for lactation, can be primary or secondary
• Primary = animal has normal appetite but doesn’t receive sufficient amount of food
• Secondary = along with diseases accompanied with appetite loss, most frequent two months after calving
Type 2 ketosis – spontaneous or fat cow disease
• Develops at peak of production, in healthy and well-fed animals
• Affected animals can spontaneously heal, but production is decreased and susceptibility remains
• Repeated ketosis leads to liver damage
• Obese cows tend to develop this type, since they have decreased appetite in the critical period, causing NEB due to decreased food intake
Type 3 ketosis – alimentary ketosis
• Feeding on rancid silage, abundant with butyric acid, due to clostridial bacteria contamination
• Ruminal epithelial has high capacity of activating butyric acid to acetoacetic and beta-hydroxybutyric acid
• High conc of butyric acid on ruminal epithelia absorb in bloodstream and ketosis develops as the consequence of toxicity of beta-hydroxybutyric acid

Question 47

pathogenesis of dairy cow ketosis

Answer 47

•Hypoglycaemia  glycogenolysis and gluconeogenesis  lipolysis  NEFA go to liver and undergo beta oxidation to ketone, sometimes stored
Net product of B oxidation = acetic acid  activated to acetyl CoA Krebs
•Oxaloacetate to end of Krebs – gluconeogenic so when decreased, 2x acetyl CoA fuse  acetoacetyl CoA  HMG-CoA  acetoacetate formed  reduced to B-hydroxybutyrate
•Ketones enter brain and muscle  energy
•Acidosis, coma and death

Question 48

hyperglycaemia

Answer 48

: increase in glucose concentration In the blood
• Can be physiological (after a meal of easily digestible CHOs, also known as postprandial) or alimentary
• After ingestion of CHO rich food, glucose is absorbed through the intestinal epithelia and transported to the liver. If extraction of glucose from the liver is incomplete, glucose enters the bloodstream and hyperglycaemia occurs
• Pathological hyperglycaemia can be consequence of insulin deficiency or insulin resistance
• Can be induced by some drugs
o Ketamine – increases adrenaline secretion
o Xylazine and detomidine – inhibits insulin secretion
o Progestines increase BG through promotion of gluconeogenesis and stimulation of GH release

Question 49

hyperosmolar coma

Answer 49

Def: Life threatening complication of severe hyperglycaemia, occurring in type II diabetics
•Insulin action is completely lost due to the cessation of production of insulin or complete insulin resistance
- Seen in older patients with acute gastrointestinal diseases with vomiting and diarrhoea, along with polyuria causing dehydration
oDehydration -> hypovolemia and decreased glomerular filtration
oDecreased glomerular filtration and excretion of glucose in urine -> accumulation of glucose in the blood
•Neurological symptoms appear as the consequence of dehydration of the brain cells due to hypertonicity of extracellular fluid
Treated: Liquid and insulin application

Question 50

diabetes type 1

Answer 50

• Insulin dependent
• Dogs (older)
• Characteristics: hypoinsulinemia and hyperglycaemia
• Genetics: immune mediated destruction of pancreatic islets after lymphocytic inflammation and lymphocyte infiltration
• Net effect Is insufficiency of beta cells with consequence of hypoinsulinemia, disturbed glucose uptake into cells, increase glycogenolysis and gluconeogenesis and hyperglycaemia with glycosuria
TYPE 2
- beg = hyperglycemia and hyperinsulinemia, beta cells basiclly get tired. obesity is leading cuase + males, treated with hypoglycaemic drugs

Question 51

acute complication of diabetes

Answer 51

• severe hyperglycaemia and severe hypoglycaemia
• type 1 have glycosuria, increased fat catabolism, severe ketogenesis which can lead to diabetic ketoacidosis, coma and death
• diabetes type II, stress, infection or corticosteroid application can induce severe hyperglycaemia, dehydration and hyperosmolarity which can progress to hyperosmolar coma, usually in older patients.

Question 52

obesity

Answer 52

• increased food intake, decreased energy consumption
• fat tissue in young animals is hard/impoos to lose since fat cells only undergo atrophy
• can occurs when satiety centre is disturbed
• expression of GLUT4 in obese cats is lowe than normal
• fat tissue is endocrinologically active + secrete adipokines + proinflam cytokines
• levels of adiponectin is decreased in obese and diabetic cats
• adiponectin increased insulin senstivity
• leptin is higher and leptin action is decreased
• leptins also involved in insulin senstivity
• insulin resistance as a consequence of obestiy is reversibel -> progress to diabetes

Question 53

diabetic ketoacidosis

Answer 53

life threatening complication when there’s accumulation of KB in blood, causes metabolic acidosis
- clinically presented with PUPD, diarrhoea and anorexia
- increased fat mobilsation due to lack of lipoprotective effects of insulin causes increaed beta oxidation of FA and decreased synthesis
- conc of AcCoA increased and ketogenesis occurs
- peripheral tissues of diabetic animals have lower capacity of ketone utilisation

Question 54

lipid metabolism

Answer 54

• triglycerides, phospholipid, sphingolipid, sterole + FA
• car+omni = SI, under pancreatic lipase, degrades triglycerides -> monoglycerides + FA
• phospholipids + degraded in SI -> phosphoglycerides + FA -> reasorbed + reesterified in intestinal mucosa
• ruminants in rumen
• HDL is produced in liver
• lipoproteins = triglycerides, cholesterol esters, proteins, phospholipids and apoproteins

Question 55

causes of fat malabsorption

Answer 55

• Can be deficiency of biliary acid salts, insufficiency of exocrine pancreas and disturbances in fat transportation
• Deficiency of biliary acid salts occurs during obstruction of bile ducts with stones, parasites, tumours, during catarrhal enteritis when Odie’s orifice is closed and bile cannot be transported to duodenum
• Can be a consequence of decreased bile synthesis during liver disease
• Bile acid salt deficiency decreases fat emulsification, lipase action and absorption, therefore undigested fat is present in faeces (steatorrhea)
• Decreased lipase secretion or its deficiency in degenerative and necrotic processes in pancreas or due to obstruction of duct

Question 56

hyerlipoproteinemia

Answer 56

•In monogastric: occurs after intestinal absorption of monoglycerides and FA produced by digestion of triglycerides from food with consequent increase of chylomicron concentration
•Peaks 2-6 hours after meal in dogs

Primary:
• Rare genetic diseases characterised by disturbances in lipid metabolism and increased plasma lipoprotein concentration

Secondary:
•Are symptoms of other diseases, such as acute pancreatitis, liver diseases, DM, hypothyroidosis and hyperadrenocorticism in dogs
•Acute pancreatitis: hypercholesterolemia isn’t clear.
- Hyperlipoproteinemia induced by other disorders can predispose the animal to pancreatitis,
- Hypercholesterolemia is frequent found in cholestasis along with hypertriglyceridemia.

Question 57

hypolipoproteinemia

Answer 57

• Occur due to decreased cholesterol production and hypoadrenocorticism
• Hypocholesterolemia during protein loss enteropathies includes decreased lipoprotein production due to catabolic state, if lymphangiectasis occur, loss of lipids produced by enterocytes occurs

Question 58

atherosclerosis

Answer 58

Def: chronic progressive arterial disease characterised with deposition of some lipid metabolism products in arterial walls and deformations of arterial walls
•Middle and old age, herbivorous and omnivorous
•Consequences: stroke and cerebrovascular insult, could less seriously cause ischemia or necrosis
Risk factors: Hypercholesterolemia, increased hydrostatic pressure and presence of glycolyzed proteins, increasing ROS production
1. damage increased permeability so LDL can enter tunica media
2. WBCs attach to adhesion molecules and squeeze through into media (diapedesis)
3. produce free radicals + oxidize LDL molecules which are good at activating WBC
4. monocytes engulf these oxidsed LDL
5. causes production of foam cells
6. foam cells then die, releasing contents
7. foam cells built up, forms a fatty streak which is thrombogenic
8. platelets release PDGF -> encourages smooth muscle growth, secretes collagen, proteoglycan + elastin = fibrotic cap
9. fibrous cap + fatty streak = plaque

Question 59

equine metabolic syndrome

Answer 59

•Obesity caused by excessive eating
•Along with insulin resistance, manifestation of laminitis
•Insulin resistance includes decreased activit of tyrosine kinase insulin receptor and decreased postreceptive phosphorylation
•In horses with insulin resistance significantly lower expression of GLUT4 at the surface of muscular and fat cells
Symptoms:
• Obesity, esp in the neck region
• Laminitis = inflammation of lamellar structures of the hoof, characterised by sudden lameness without visible mechanical cause and increased hoof temperature (condition is painful)
• Polyuria and lethargy

Question 60

laminitis

Answer 60

Cause: indigestion due to large amount of easily digestible carbohydrates consumptions, increased physical activity and stress
• Abundant amounts of easily digestible carbs results in increased fermentation of undigested carbs in caeca and accumulation of lactic acid
• Increased lactic acid concentration, endotoxins and exotoxins concentration leads to circulatory disturbances, particularly in legs and consequent laminitis
• Early stages in acute laminitis are ischemia of laminar arteriolas and venulas
• Arterial blood is shunted to venous return through numerous BV anastomoses in hoof and bypasses corium
• Laminitis during equine metabolic syndrome is a result of vascular dysfunction
o Primary insult is related to changes in BV function due to hyperinsulinemia, which decreases circulation in hoof
o Insulin can cause vasoconstriction through sympaticus stimulation and by activation of nitrogen activated protein-kinase pathway

Question 61

fat cow syndrome

Answer 61

• Peak of lactation period, diet for dairy cows has to meet the need for milk production
• If feeding continues in later lactation to dry period, conditions for excessive fat accumulation and obesity occur
• Obese dairy cows are more prone to pospartal metabolic diseases compared to non-obese
• Often accompanied with fatty liver
o Fatty liver decreases functional capacity of hepatocytes, gluconeogenesis and immune system
• Since period after calving and at beginning of lactation is the one when energy is most needed, NEB occurs
• Special digestion and metabolism of ruminants, physiologically lower glucose in blood concentration predispose ruminants to metabolic disturbances
• Under hormonal imbalance that develops in that period, with decreased insulin and increased contra insulin hormones fat tissue lipolysis occurs to balance NEB
• Released fatty acids are transported to liver, bound to albumin. When concentration of fatty acids released after lipolysis exceeds liver capacity to be metabolised, triglycerides are accumulated in liver cells and conditions for fatty liver development are presented
• Triglycerides accumulation in hepatocytes, particularly when is prominent, compromises functional capacity of liver, as consequence, bilirubin and bile acid levels in blood increase since bile transport in duodenum is compromised ,,,,
• During NEB, lipomobilisation can lead to fatty liver, increased ketogenesis and additionally decrease appetite and food intake

Question 62

protein deficiency

Answer 62

protein defiency due to decreased production
- decreasedi ntake of AA from diet/incomplete absotion in intestinal mucosa during some GI disease, starvation and CHO deficiency

due to decreased AA utilisation
- after absorption AA to liver.. swelling due to hypoalbuminemia

immobilisation
- muscles become atrophic + bones osteoporotic, due to metaboic loss of proteins, decreased synth and increased catabolism

due to increase loss of proteins
- lost during severe bleeding, indirect = increased by catabolism

consequence of protein loss
- loss of muscle mass and strenght
- albumins maintian oncotic pressure - edema
- decreased Ca -< hypocalcemia
- hypo increased ooxic effect on unconjugated bilirubin
- decreased erythocyte production and anameia, decreased immunoglobulin production therefore increase risk of infection

Question 63

equine paralytic myoglobinuria

Answer 63

• Acute disease manifested with sudden paralysis of striated muscles and in severe cases with myoglobinuria
• clinical signs are appearing after 15-30 minutes after exercise
• animals are straining whilst trying to urinate, don’t want to move and in severe cases = colic
• pain, distress, clenched muscles of the hindlimbs is also visible
• diagnosis is confirmed after lab tests on blood and urine: increased creatine kinase, AST, LH
• chronic = due to inherited dysfunction triggered by the environment
Pathogenesis:
• due to myofibril destruction, myoglobin enters the blood and myoglobinemia occurs
• since the renal threshold for myoglobin is low, myoglobinuria soon manifests
• clinical signs affects horses include lameness and stiff hindlegs, painful muscles when palpated and usually recumbent
• pectorals may also be impaired
• pathological changes vary from severe necrosis to signs of regeneration
Therapy:
• based on pain relief, correction of electrolytes and acid-base balance, prevention of renal damage caused by myoglobinuria and dehydration as well as NSAID
Sporadic paralytic myoglobinuria
• Overwhelming physical activity
• Electrolyte balance caused by inadequate diet or loss in sweat
• Selenium and Vit E deficiency
• Excessive CHO intake that are easily digestible
• Hormonal disbalance due to oestrus
• Lactic acidosis
• Environmental factors are important
Chronic paralytic myoglobinuria
• Caused by a glycogen storage disturbance (polysaccharide storage myopathy)

Question 64

undernourishment

Answer 64

• Condition in which the intake of essential nutrients is inadequate
• Can be primary (acute or chronic, depending on nutrient insufficiency) or secondary
During acute starvation,
• after sudden cessation of food intake or an inability to eat, survival depends on storage. Depends on quality and quantity of ingested food and if it persists it causes chronic starvation. First phase show irritability, followed by depression and stupor. Glycogen is the first energy source used, afterwards, lipid and protein catabolism follow, so body mass is reduced. Lipomobilisation and increased ketogenesis can result in metabolic acidosis
• Animal adapt to low energy intake by decreasing its basal metabolism through decreased secretion of thyroid hormones and other hormones
• Insulin secretion is decreased and glucose entrance in all the tissues except the brain is reduced.
• Free FA and AA levels in the sera increase
• Substrates are used in gluconeogenesis in the liver
• Secretion of glucocorticoids, glucagon and GH increases resulting in gluconeogenesis and decreased glucose utilisation in tissues
During chronic starvation or general undernourishment,
• primary or secondary to other disease, gluconeogenesis is activated and lipid catabolism is increased
• brain tissue utilises ketones in a larger extent
• if proteins are unavailable, especially albumins, hypoproteinaemia with consequent oncotic pressure decrease can occur resulting in edema and ascites
• decreased glomerular filtration contributes to water accumulation in the organism
• intestinal villi undergo atrophy, which can lead to additional protein loss, disturbances in digestion and absorption
• secretions of the pituitary gland, thyroid gland, pancreas and sexual organs is disturbed

Question 65

physiology of the rumen

Answer 65

• Microorganism in the rumen are anaerobes or facultative anaerobes. These are mostly bacteria, protozoa and fungi which degrade carbohydrates, proteins and fats into:
  oVFA, long chain FA, glycogen, small amount of glucose, vit B complex, vit K, ammonia and AA
  •By products of fermentation are gases
  • Main pathway of CHO degradation starts with starch or cellulose which is then converted to glucose, then pyruvic acid
  • Pyruvic acid may be converted to acetyl CoA when is then converted to acetic acid or butyric acid
  • Cellulolytic bacteria degrade cellulose to glucose
  • Starch may be converted to glucose may be used in protozoa and converted to glycogen or may be processed by amylolytic bacteria of the rumen into lactic acid. Lactic acid may then be converted to propionic acid, the major substrate for gluconeogenesis

Question 66

acute rumen acidosis

Answer 66

• Occurs when there’s feed rich in carbohydrates which increases the amyloltic bacteria population and increases the production of lactic acid
• Lactic acid build-up causes a drop in pH
• Compensatory mechanisms by the rumimant includes loss of appetite to reduce food intake, increase of saliva which has bicarbonate and phosphate as buffers, better absorption of VFAs and the proliferation of bacteria which converts lactate to VFAs
o Lactobacillus decarboxylate AA into biogenic amines, which cause intoxication and damage the CNS, liver, kidney and heart
o Lactic acid is absorbed into the blood and causes metabolic acidosis
o Lactic acid fermentation increases osmotic pressure, inhibits water absorption from the rumen into the blood, causes dehydration, haemoconcentration, intoxication and osmotic diarrhoea
o Lactic acid fermentation causes inhibited motility of feed leading to endotoxin build-up and intoxication
o Endotoxins increase the concentration of VFAs and lactates, further decrease the pH and cause high osmotic pressure leading to ruminitis
Clinical signs
• Loss of appetite and inhibited rumination
• Rumen hypomotility with retention of content
• Ruminitis = inflammation and ulceration of the mucous membranes of the rumen. Bacteria enter the blood, cause liver abscesses, changes in the lungs, heart, kidneys and joints
• Dehydration
• Metabolic acidosis and intoxication
• Loss of coordination, general weakness, shock and death

Question 67

chronic rumen acidosis

Answer 67

• Occurs after increased production of VFAs in the rumen 2-3 hours after a meal rich in easily digestivle carbohydrates
• Decreases the pH and limits the absorption of VFAs and pH return to physiological limits
• Continuous administration of poorly balanced meals leads to permanent production of larger amounts of VFAs and the onset of clinical signs
Clinical signs
• Ruminitis = fibrous thickening of ruminal mucosa and loss of papilla
• Ruminal parakeratosis = papillae are enlarged and hardened, several can adhere together to form bundles, reducing the absorption of nutrients
• Low milk fat due to inhibition of fatty acid synthesis in the mammary gland
• Laminitis = histamines and endotoxin damage of endothelium of BV underneath the hoof wall leads to ischemia and necrosis of the lamina
• Demineralisation of bone = degradation of the bone in order to release bicarbonate ions

Question 68

luminal drinking

Answer 68

• Failure of the reticular groove reflex
• Oesophageal groove is a muscular structure at the lower end of the oesophagus leading from the cardio to reticulo-omasal orifice
• When closed, it forms a tube allowing milk to go directly into the abomasum
• Oesophageal groove reflex is an unconditioned reflex when the animal is eager for milk, water consumption doesn’t usually initiate groove closure
• It occurs when milk spills into the reticulorumen and is fermented to short chain FA and/or lactic acid. Causes a drop in the pH of ruminal contents to below 5. There’s then inflammation of the forestomach mucosa, systemic absorption of organic acids and metabolic acidosis
Chronic
• Causes parakeratosis of the ruminal mucosa, impairment of ruminal motility, chronic or recurrent tympany and atrophy of intestinal villi
Primary
• Causes of it is stress after prolonged transport, change in feeding or bucket feeding
• Stress causes inappetence, depression, poor growth, hair loss, recurrent tympany, ventral abdominal distension and passing of clay-like faeces
Secondary
• Secondary to other disorders like neonatal diarrhoea, anorexia, painful disease with cough, otitis and phlebitis
• Causes acute ruminal acidosis, teeth grinding, arching of the back, abdominal distension

Question 69

rumen alkalosis

Answer 69

• Excessive production of ammonia in the rumen
• Can be due to an unbalanced meal (rich in protein, poor in CHO), improper application of urea, taking larger amounts of food where E.coli and vulgaris outgrow normal flora of rumen and generate a large amount of ammonia
• Foods rich in proteins increases proteolytic activity in the rumen, increase ammonia concentration and increase pH above 7
• Ammonia is then absorbed into the blood and given to the liver for detoxification
• Ammonia is also used to create glutamic acid along with alpha-ketoglutarate from the citric acid cycle, which then converted to GABA
• An increase in GABA causes hypoenergosis of the brain, leading to excitation and spams
Clinical signs (10 mins after a meal rich in urea)
• Polyuria, disorder of rumen motility, strong abdominal movements, cyanosis, foam on the nose and mouth, hypersensitivity to sound, muscle tremors, heavy breathing and paralysis  death
Subclinical form:
• Decreased appetite, hypotony and atony of the rumen, recurrent bloat, decrease in milk production, diarrhoea, paresis and possible development of metabolic alkalosis

Question 70

frothy bloat

Answer 70

• Caused by abnormal fermentation of carbs and proteins
• There’s some sudden production of a large amount of gas, which is trapped in little bubbles within the rumen
• Stable foam layer is formed in the rumen so eructation cannot occur, there’s rapid expansion of the rumen and reticulum
• Soluble leaf proteins form monomolecular layers around the gas bubbles
• Salivary mucin is antifoaming, but production of saliva is reduced at this point
• Bloat producing pastures are more rapidly digested and may release a greater amount of small chloroplast particles that trap gas bubbles and prevent their coalesce
• Frothy bloat occurs most commonly in animals grazing legumes like alfalfa
• In feedlot cattle, less commonly in dairy cattle, frothy bloat occurs on high grain diets
• There’s no separation of gas and a foam layer is formed, so there’s no eructation and there’s increased pressure in the rumen, this increases rumen motility
• The increased pressure and stretching of the wall slows down the contraction of the rumen causing hypotonia and finally atony of the rumen
• Increased intraruminal pressure increases intraabdominal pressure, putting pressure on vena cava caudalis lumen, reducing blood flow back to the heart, decreasing minute volume and reduced perfusion to vital organs, like the lungs, leading to dyspnoea and hypoxia
• Increased intraruminal pressure causes the production of a large amount of CO2 in the rumen, leading to hypercapnia, and stimulates the respiration centre, causing dyspnoea and hypoxia
• Increased intraruminal pressure increases intrathoracic pressure, reducing breathing capacity and leading to dyspnoea and hypoxia
• Death from frothy bloat occurs due to suffocation

Question 71

free gas bloat

Answer 71

• Caused by some obstruction of eructation
• Eosophagel obstruction due to foreign body
• Stenosis or pressure from some enlargement outside of the oesophaus
• Damage of the vagus nerve and nerve pathwyas involvedin the eructation reflex
• Diaphragmatic hernia
• Tetanus
• Leisons of the reticular wall
• Ruminal atony that occurs in anaphylaxis and in grain overload, causing a decrease in rumen pH and possibly esophagitis and ruminitis that can interfere with eructation
Acute bloat is the complete inability to remove gases,
Chronic bloat is the partial inability to remove gases and the bloat develops progressively

Question 72

traumatic indigestion

Answer 72

• Forestomach motility depends on 1. Constant temperature, 2. Optimal H+ ion concentration, 3. Anaerobic conditions and 4. Continuous mixing of rumen content
Disturbance in forestomach motility:
• Most common = foreign body in the reticulum
• Adhesions: fixate reticulum to rumen or diaphragm
• Damage of vagus nerve: inflammation, mechanical damage, pressure
• Damage of reticuloruminal centre: histamine, barbiturates, anaesthetics, meningitis
• Decreased or increased pH: inhibited acetyl CoA esterase activity
• Stress: transport weaning, difficulty calving, where motility is blocked due ot the release of adrenaline and noradrenaline that inhibit contraction of forestomach smooth muscles

Question 73

traumatic reticuloperitonitis

Answer 73

• Perforation of the reticulum with a sharp foreign body like a wire or nail
• Ruminant swallows some metal object which falls directly into the reticulum or passes into the rumen and is carried into the reticulum by ruminal contractions
• Reticulo-omasal orifice is elevated, which tends to retain heavy objects in the reticulum
• Honeycomb-like reticular mucosa traps sharp objects
• Contractions of the reticulum causes the penetration of the wall by the foreign object
• There’s then leakage of ingesta and bacteria contaminates the peritoneal cavity leading to peritonitis and adhesions
• Can penetrate the diaphragm and enter the thoracic cavity and pericardial sac
• Liver or spleen may be pierced and infected resulting in abscessation or septicaemia
Clinical signs:
• Sudden onset of ruminoreticular atony and sharp fall in milk production
• Decreased faecal output
• Rectal temperature is often mildly increased
• Cow has arched bac, anxious and unwilling to move
• Forced sudden movements as well as defecating, urinating, lying down, getting up and stepping over barriers may be accompanied
In chronic cases:
• Feed intake and faecal output are reduced and milk production remains low
• Signs of cranial abdominal pain become less apparent and the rectal temperature returns to normal
• Some cattle develop vagal indigestion syndrome because of the adhesion that forms after foreign body perforation
Signs of pleuritis and pericarditis:
• Depression, tachycardia
• Pleuritis is manifested by fast, shallow, respiration, muffed lung sounds and pleuritic friction
• Traumatic pericarditis is most commonly characterised by muffled heart sounds
• Jugular vein distension and congestive heart failure with submandibular edema
• Penetration through the pericardium into the myocardium usually results in extensive haemorrhage into the pericardial sac or ventricular arrhythmia and sudden death

Question 74

regenerative anaemia

Answer 74

• Means that the bone marrow is responding to the lack of RBCs in the blood
• Can be seen as increased reticulocytes
• Polychromatophils are usually not seen in horses, cattle, sheep and goats, more in dogs and pigs
• Polychromatophils are never seen in horses
• Higher MCV
Causes:
• Haemolysis (extravascular or intravascular)
• Haemorrhage (external, due to lack of proteins or caused by internal factors)
Haemolytic regenerative anaemia causes:
• Immune mediated haemolytic anaemia
• Erythroparasites
• Other infectious agents
• Oxidation injury
• Fragmentation injury
• Histiocytic disorders
• Inherited RBC defects
• Metabolic conditions
Haemorrhagic regenerative anaemia causes:
• Trauma
• GI bleeding from neoplasia, NSAIDs, renal disease
• Urogenital bleeding
• Coagulopathies from liver disease, rodenticides toxicity
• Chronic external blood loss leads to poorly regenerative, or nonregenerative iron deficiency anaemia

Question 75

non-regenerative anaemia

Answer 75

Preregnerative anaemia (1)
• Takes 3-5 days for the reticulocytes to be released from the bone marrow into the circulation
• During this time, the anaemia will appear nonregenerative, even though it’s regenerative
Decreased production of bone marrow due to systemic disease (2)
• Inflammatory disease, nutritional deficiency, chronic kidney disease, metabolic/endocrine disease, anaemia’s associated with FIV and FeLV
Decreased production of bone marrow from primary bone marrow disease: (3)
• Pure RBC aplasia, aplastic anaemia due to retrovirus, myelodysplastic syndrome
Nonregen anaemia due to decreased production has several mechanisms:
• Insufficiency production or activity of erythropoietic substances due to chronic kidney disease
• Erythropoiesis suppression due to drugs, cytokines and tumours
• Nutritional deficiency, especially in Fe and Cu
• Defective Hb synthesis usually secondary to Fe deficiency
• Defective DNA synthesis
• Destruction of bone marrow haematopoietic cells
• Replacement of haemopoiesis due to neoplasia

Question 76

haemolytic anaemia

Answer 76

• Intrinsic anaemia: hereditary Stomatocytes, pyruvate kinase deficiency
• Extrinsic anaemia: primary autoimmune haemolytic anaemia, secondary immune mediated, alloimmune (neonatal erythrolysis) fragmented haemolytic anaemia, infection
• Destruction or removal of RBC from the bloodstream. Can be intravascular or extravascular
• Can cause haemolytic icterus
Extravascular
• Phagocytosis of RBCs with the destruction inside macrophages
• Occurs within the bone marrow, spleen or liver
• Hb cannot escape into the circulation and common symptom is splenomegaly
o Antibody coated or irregular RBC, phagocytosis by macrophage, degradation In lysosome, intracellular haemoglobin, biliverdin leaves macrophage to hepatocytes and bilirubin biliary clearance
Intravascular
• There’s destruction of RBCs within the blood vessels leading to haemoglobinemia, haemoglobinuria and decreased haptoglobin
• 1. RBC in circulation
• 2. Direct lysis by stress, toxins or compliment activation
• 3. Intravascular free Hb
• 4. Bounds to haptoglobin for hepatic clearance
• 5. If too much Hb for haptoglobin, renal excretion leading to haemoglobinuria

Question 77

neonatal isoerythrolysis

Answer 77

• If parents have different blood types and the neonate inherits the blood group of the sitre
• The colostrum then will contain antibodies against the baby’s RBC and it occurs in horse, cat, dogs, cattle and pigs
• In foals born to mares of different blood type to the stallion, the mare is sensitised to the stallion\s blood group most often through previos preganncies or at delivery causing retroplcental bleeding, where the foal’s blood comes into contact with the mare’s circulation during the last weeks of pregnancy
• In kittens type B queens mate with type A or AB toms, so the kittens have anti A antibodies causing haemolysis after ingestion of colostrum causing fading kitten syndrome
• Noticeable sign is ear and tail tip necrosis, most signs occur within 24-36 hours after birth, after the suckling of colostrum
• Neonates are weak, have pale mucous membranes, tachycardia, tachypnoea, haemoglobinuria and hemoglobinemia

Question 78

oxidant - induced haemolytic anaemia

Answer 78

• Onions (dogs, cat), brassica species (rum), nitrate containing plants (rum)
• Minerals = zinc (dogs), copper (sheep, dog)
• Chemical = skunk musk
• Drug = acetaminophen (cats), Vit K (dogs)

Question 79

sideropenic anaemia

Answer 79

• Occurs when iron is too limited for erythropoiesis
• Occurs in the absence of iron, so Hb cannot be produced in sufficient quantities
• Causes microcytic hypochromic anaemia
• Immature RBCs in the bone marrow stop dividing once a critical concentration of Hb is reached within the cell, so iron deficiency ends up causing more divisions of the progenitor RBCs resulting in smaller mature RBCS
• RBCs are shrunken and have membrane blebbing, which are features of apoptosis. Increased mechanical fragility is seen as keratocytes, acanthocytes and schistocytes
Regenerative
• When there’s sufficiency iron absorbed or there’s blood loss in the upper GI tract, since some iron and blood can be absorbed by the intestines
Non-regenerative
• With concurrent nutritional iron deficiency and other diseases that suppresses regeneration of RBCs
Causes:
• Decreased intake of iron (in new-born animals, like puppies and piglets)
• Decreased absorption of iron (insufficient HCl secretion and IBD)
• Blood loss
• Increased demand of iron

Question 80

iron defieicny anaemia in piglets

Answer 80

Sows
• Have a low permeability of the transplacental barrier
• Milk contains small amount of iron
Piglets
• Born with very low iron stores, sufficient for only 4 days
Environment
• Pigs raised in confinement without access to soil or faeces containing iron will lead to iron def
Pathophysiology
• Rapid expansion of plasma volume due to colostrum
• Insufficient iron supply = microcytic hypochromic anaemia
• Tissue hypoxia
• Underdeveloped glucostatic regulation (hypoglycaemia)
• Fe is a coenzyme of gluconeogenic enzymes
• Hypothermia
• GI inflammation or parasites interfere with absorption
Clinical signs:
• Decreased appetite, inadequate efficiency of food utilisation, stunted growth, tremors, anaemia, pulmonary edema, dilation of the hart and drop in blood pressure and death

Question 81

anaemia of chronic disease

Answer 81

• Inflammatory diseases can cause mild to moderate normocytic normochromic anaemia that’s usually nonregenerative
• TNF alpha, IFN gamma, IL1 and IL6 are mediators of this anaemia
• Mechanism: 1. Decreased RBC lifespan and 2. Decreased RBC production
• Toxins, inflammatory cytokines, compliments and free radicals induce direct RBC damage by binding to the surface of the RBX leading to extravascular haemolysis
• Decreased RBC production occurs due to the suppression of erythropoiesis by inflammatory cytokines
• Iron homeostasis becomes disturbed as there’s decreased absorption of iron and iron sequestration within macrophages
• Hepcidin causes a decrease in iron concentration
• Cytokines also inhibit the release or production of erythropoietin from the kidneys
• Hyperglobinemia, hypoalbuminemia decreased iron, increased APP
• Causes nonregenerative anaemia with echinocytes
• As kidneys go through some disease, there’s decreased erythropoietin production. Meanwhile, inflammatory cytokines cause the increased activation of hepcidin which further suppresses erythropoiesis by using up Fe stores. Toxins from uraemia during chronic kidney disease as well as cytokines also directly suppresses erythropoiesis
• Uremic toxins promote extravascular haemolysis, so RBCs are dying earlier on

Question 82

aplastic anaemia

Answer 82

• Characterised by pancytopenia, leukocytopenia and thrombocytopenia
• Most common mechanism of aplastic anaemia is autoimmune destruction of the hematopoietic stem cell
• Causes are mostly idiopathic but can become induced by infection, drug therapy, toxin ingestion, genetic disorders, radiation or immune mediated

Question 83

pure red cell aplasia

Answer 83

• Total absence of identifiable erythroid precursors in marrow
• Only the erythroid line is affected
• Causes severe nonregenerative normocytic normochromic anaemia

Question 84

thrombocytopenai

Answer 84

1. Decrease bone marrow production = diseases, infections, drugs
2. Increased platelet consumption = extensive bleeding, DIC
3. Increased platelet destruction = immune mediated
   Pseudo-thrombocytopenia
   • Platelet clumping in vitro (cats – venipuncture)

Question 85

von willebrand disease

Answer 85

• Inherited disease
• Disorders of primary haemostasis
• Spontaneous mucosal bleeding
• Slow wound healing
• vWF def = decreased platelet plug formation
• class;
o type 1 = deficiency in amount of vWF
o type 2 = more severe
o type 3 = complete absence and most severe

Question 86

sinus tachycardia

Answer 86

• Increased rate of the SA node pace
• Production of impulses is faster, but regular
• Increases CO
• Extreme heart rates can reduce SV and CO, SV becomes reduced because of decrease ventricular filling time
• Excessive shortening of certain phases of cardiac revolution decreases cardiac output, causes ischemia of the heart and causes heart failure
Causes:
• Increased body temperature (increases metabolic speed and oxygen consumption)
• Physical exercise or stress (increases concentration of catecholamines in the blood)
• Hyperthyroidism
• Anaemia and pregnancy

Question 87

sinus bradycardia

Answer 87

• Slow production of impulses by SA node
Can indicate a pathology of the heart of pathology of the system that controls its rate:
• Reduced irritability of the sinus node (beta blockers and the cold)
• Hypothermia
• Hypofunction of the thyroid gland
• Increased intracranial pressure
• Jaundice

Question 88

respiratory sinus arrhytmia

Answer 88

• Change of the rate of spontaneous depolarisation in the SA node related to respiration
• Increased respiratory volume during inspiration causes inhibition of vagal neurones and sympathetic system becomes dominant during inspiration
• Reflux influences from slowly adapting stretch receptors in the lungs – during inspiration they inhibit activity of the cardioinhibitory centre and it leads to the dominance of cardioexcitatory centre
• Helps to stabilise CO by allowing the heart rate to increase during inspiration when the left ventricular SV decreases
Brainbridge’s reflex
• Distension of the right atrium by increased venous return in inspiration leads to the acceleration of the heart rate by local and reflex mechanisms
• Negative pressure in the chest during inspiration leads to the augmentation of the venous return from lower parts of the body

Question 89

sinus arrest

Answer 89

• Medical condition where the SA node of the heart transiently ceases to generate electrical impulses
• Since the heart contains multiple pacemakers, the interruption of the cardiac cycle generally lasts only a few seconds before another part of the heart with lower automacy begins pacing and restores the heart action
• Manifestation of the sinus arrest on an ECG is a brief period of irregular length with no electrical activity before either the SA node resumes normal pacing or another pacemaker begins pacing
• If no other pacemaker begins pacing during an episode of sinus arrest, it becomes a cardiac arrest
Common causes:
• Strong activation of the vagus nerve or increased sensitivity of the SA node to acetylcholine
• Damage of the SA node by disease: ischemia, inflammation, degenerative changes and toxic influences

Question 90

passive heterophy

Answer 90

• When sinus node fails in its role as a pacemaker, latent pacemakers can drive the heart and an escape beat is arising from an ectopic focus in the atria, the AV junction or in the ventricles
• Ectopic impulse in this instance is always late appearing only after the next anticipated sinus beat fails to materialise
• If sinus node failure is only brief, the ectopic focus may generate only a single escape beat
• If the sinus node failure is prolonged, the ectopic focus produces a rhythm of escape beats to assume full pacing function
• This escape mechanism offers protection against total cardiac standstill in the event of sinus node failure
• Reduced heart rate: slower firing rate of latent pacemakers
• Preuatomatic pause: ECG will show passive heterotopic activity from latent pacemaker with a delay

Question 91

active heteropy

Answer 91

• Impulses depolarising heart muscles are produced outside of the SA node and they are produced faster than is the normal rate of the SA node
• Consequences of lack of ATP and membrane dysfunction lead to the reduction of the resting membrane potential. Types of arrhythmia caused by active heterotrophy depends on the site of origin: supraventricular vs ventricular
Causes and mechanism:
• Reduction of the resting membrane potential
• Change of automaticity
• Change of refractory phase

Question 92

supra ventricular arrhythmia

Answer 92

• Atrial extrasystole or premature atrial depolarisation
• Supraventricular tachycardia
• Atrial flutter
• Atrial fibrillation
• Production of extra beats in the atria or AV junction zone. They differ only by the number of produced impulses. Isolated impulses lead to premature atrial depolarisation while permanent pacing will lead to supraventricular tachycardia. They can be produced by one ectopic focus of beats or more than one ectopic foci. More than one ectopic focus may indicate that the damage of the atria and AV zone is more serious

Question 93

atrial flutter

Answer 93

FLUTTER
Disturbance of the electrical activity of the heart caused by ectopic focus with even higher activity than is typical for common tachycardia
• Depolarisation spreads across the muscle, which is not optimally repolarised after previous depolarisation, which is why the ECG shows specific type of the P waves with a saw tooth shape
• If AV zone loses its filtering ability, all the impulses will go to the ventricles with serious reduction of the CO due to extremely short, diastolic phase and may lead to heart failure and even cardiogenic shock
FIBRILLATION
• Arrythmia caused by irregular production of impulses in multiple foci in the atria independently and these foci are producing impulses during systole and diastole
• Irregular contraction of the ventricle
• Ventricular filling is limited with passive inflow of blood leading to a decrease in CO as well as a drop in BP

Question 94

ventricular flutter and fibrillation

Answer 94

Flutter
• Caused by high rate of one ectopic focus in the ventricles
• Activation of ventricles with such a high rate doesn’t allow an effective contraction nor relaxation of the muscle and also limits diastolic filling
• CO is reduced to nearly 0, there’s considerable hypoperfusion in the systemic circulation
Fibrillation
• Fatal arrhythmia caused by the uncoordinated activity of multiple foci of extra activity of the ventricles
• Result is chaotic activation of small fields of musculature around the foci, ventricle fails to produce any effective contraction and pressure – zero CO = circulation stops

Question 95

mechanisms leading to impaired conduction

Answer 95

• Decrease in resting membrane potential towards zero
• Presence of inflammatory infiltrate
• Accumulation of amyloid
• Excessive fibrosis in the heart
• Hypertrophy and dilation
• Change of ion channel function

Question 96

heart block

Answer 96

• 1. First degree block: delayed conduction
• 2. Second degree block: partial or incomplete conduction
• 3. Third degree block: absent conduction
• SA, Interatrial, AV and interventricular

Question 97

sinus block

Answer 97

• Disturbance in which the impulses are generated in the sinus node, but for some reason they cannot be conducted to atrial muscle
1st degree
• Delayed conduction from SA node to atrial muscle
• No haemodynamic effect
• ECG may show sinus rhythm or sinus bradycardia
2nd degree
• Inability to conduct some of the SA node generated impulses to the atria
• There’s occasional lack of conduction which is seen as a lack of the P QRS and T on the ECG
• Haemodynamic impact depends on how many times the impulses are not conducts
3rd degree
• None of the electrical impulses are conducted to the atria
• There’s activation of the secondary pacemaker in the AV zone with junctional rhythm
• Clinical manifestation can be cardiogenic syncope, a transient loss of consciousness caused by reduced cerebral blood flow with a tendency to spontaneously recover mainly after secondary rhythm

Question 98

atrioventricular bloc

Answer 98

• AV block is the partial or incomplete interruption of the impulse transmission from the atria to ventricle
1st degree
• Delay of atrioventricular conduction
• This is seen as a prolonged P-Q interval
2nd degree
• Some impulses that reach the AV zone are not conducted to the ventricle
• Some of the P wave are not followed by QRS complexes
Mobitz type 1
• Progressive slowing of the conduction in the AV zone from beat to beat until the conduction of impulse fails
• This repeats periodically in cycles
• There’s progressive prolongation of the PQ intervals, until there’s no QRS complex following the P wave
Mobitz type 2:
• Presence of prolonged PQ intervals, all equal but some of the P waves aren’t followed by QRS complex
• There’s a high risk that this block can become a complete AV block
3rd degree:
• Completely inability of the AV zone to conduct impulses
• Impulses are normally produced in the SA node, but cannot be conducted to the ventricles
• Complete AV block, if not followed by activation of alternative pacemaker, will lead to asystole and stokes Adam syndrome
• The ventricular rhythm usually begins after several seconds and this interval is = Preuatomatic pause
• Atria are depolarised by the impulse from the SA node in a normal pacing process, but ventricles are depolarised from the ventricular conductive system
• There’s no relationship between atrial and ventricular depolarisation = atrioventricular dissociation

Question 99

ventricular stenosis and insufficiency

Answer 99

Valvular stenosis
• Occurs when the tissue forming the valve leaflets become stiffer, narrowing the valve opening and reducing the amount of blood that can flow through it
• Can cause obstruction of blood flow and as a result the chamber behind the effected valve must build up more pressure to overcome resistance (leads to valvular insufficiency)
Valvular insufficiency/ regurgitation
• Occurs when the leaflets don’t close completely letting blood leak backwards across the valve
• Backward flow is referred to as regurgitant flow
• Causes blood flow to flow retrograde, the heart chamber which received the additional retrograde flow is then forced to pump the added regurgitant volume together with the volume being received

Question 100

mitral stenosis

Answer 100

• Decreased mitral valve area
• Impairment of blood flow to the left ventricle
• Left atrial hypertrophy as compensation
• Increased pressure and volume in the left atrium
• Increased pressure in the pulmonary veins and capillary bed leading to pulmonary edema
• Hypertrophy and dilation of the right ventricle
• Relative insufficiency of the tricuspid valve
• Regurgitation of blood into the right atrium
• Systemic venous congestion leading to edema

Question 101

mitral valve insufficiency

Answer 101

• Mitral valve fails to close properly
• Regurgitation of blood into the left atrium
• Hypertrophy and dilation of the left atrium and ventricular wall for compensation
• Increase of blood in left atrium
• Elevation of pulmonary capillary pressure leading to pulmonary edema
• Hypertrophy and dilation of the right ventricle for compensation
• Relative insufficiency of the tricuspid and mitral valve
• Decompensation of the left and right side of the heart
• Congestive heart failure and edema

Question 102

aortic valve insufficiency

Answer 102

• Semilunar valves fail to close properly
• Blood flows in reverse direction during ventricular diastole
• Left ventricular eccentric hypertrophy for compensation
• Diastolic murmur
• Relative insufficiency of mitral valve
• Dilation of the left atrium
• Elevation of pulmonary capillary pressure leading to pulmonary edema
• Hypertrophy and dilation of the right ventricle
• Relative insufficiency of the tricuspid valve causing edema

STENOSIS

Question 103

hypertrophic cardiomyipathy

Answer 103

• Most common of the cat
• There’s higher incidence in males, especially of the Persian breed
• Believed to be an inherited disorder in most cases
• Dogs, it’s less frequent but also more in males, like in the GSD
• Left ventricular concentric hypertrophy and interventricular septal thickness. Inner diameter of the left chamber is reduced, with impaired diastolic filling and higher than normal blood volume in the left atrium causing atrial dilation and increased pulmonary pressure
• Stagnation of blood in the left atrium predisposes the formation of thrombus of the caudal abdominal aorta, causing paresis of the hind leg

Question 104

dilated cardiomyopathy

Answer 104

• Most common cause of congestive heart failure in boxers, Dobermans, pinshcers, danes…
• More often in middle ages males than females, even in cats
• Causes reduced contractility and impaired systolic function with consequent ventricular congestion and atrial and ventricular dilation
• Hearts ability to pump blood is diminished because the left ventricle is large and weak
• Various degrees and forms of myocardial degeneration occur

Question 105

restrictive cardiomyopathy

Answer 105

• Rarely occurs, but happens in male cats
• There’s two main endocardial lesions that disrupt ventricular filling:
o Severe focal or diffuse endocardial fibrosis causing adhesion of the papillary muscles’, thickening and shortening of the mitral leaflets and fusion of the chordae tendinea
o Occasionally there’s adhesion of the entire endocardium and significantly diminished ventricular cavity
• Endocardium is extremely thickened by the presence of hyaline and fibrous and granulation tissue
• In myocardium, there’s frequently detected hypertrophy of the muscle cells and interstitial fibroplasia with disorganisation of the cardiac muscle cells

Question 106

L heart failure

Answer 106

• Occurs when the output of the LV is less than the total volume of blood received from the right side of the heart from pulmonary circulation
• As a result the pulmonary circuit becomes congested with blood that cannot be moved forward, and systemic blood pressure falls
Symptoms:
• Edema of the lungs and pleural effusion due to elevated hydrostatic pressure in the blood vessels of the lungs
• Cough due to pressure of the enlarged left atrium to the left bronchus leading to the stimulation of cough receptors and lung edema
• Tachypnoea and dyspnoea: reduced elasticity and reduction of ventilated parts of parenchyma leading to decreased oxygen saturation
• Syncope: loss of consciousness caused by lack of blood or oxygen to the brain
• General weakness and exercise intolerance because of reduced perfusion and tissue oxygenation and reductio of muscle mass
• Compensatory tachycardia
• Pallor or cyanosis
• Drop In blood pressure

Question 107

right heart failure

Answer 107

• Occurs when output of RV is less than the input from the systemic venous circuit
• Result, the systemic circuit becomes congested with blood and output of blood to the lungs decreases
Symptoms:
• Generalised edema due to increased venous hydrostatic pressure  cardiac edema
• Passive hepatic congestion resulting in atrophy, degeneration, necrosis and fibrosis of polygonal liver cells  cardiac cirrhosis
• Ascites due to elevated pressure in the portal vein and increased permeability of the capillary endothelium
• Hydrothorax due to increased venous hydrostatic pressure along with increased capillary endothelial permeability
• Dilation of the jugular vein

Question 108

compensatory mechanisms

Answer 108

• Several natural compensatory mechanism are called into action during heart failure in an effort to counteract the effect of falling CO on perfusion to vital organs:
• Frank starling
• Concentric and eccentric hypertrophy
• Neurohumoral compensation
o Activation of adrenergic receptors increase contractility and HR with centralisation of the bloodstream
o RAAS activation with increased secretion of ADH causes salt and water retention and blood flow to juxtamedullary nephrons
Limitations of the Frank Starling mechanism:
• Represents the relationship between the SV and end diastolic volume
• States that the SV of the heart increases in response to an increase in the volume of blood in the ventricles before contraction, end diastolic volume
• End diastolic fibre length increases, ventricular muscle responds with dilation and increased force of contraction
• In failing heart, diastolic fibre length is continuously increased, causing heart to enlarge
• But when fibre reaches its critical length, contractility is reduced so CO decreases
Limitation of hypertrophy
• Increased oxygen demand increases the risk of development of ischemia
• Increase in volume of the myofibrils isn’t accompanied by an increase in the number of mitochondria
• the disparity between increased myocardium mass and coronary reserve causes relative coronary insufficiency  occurs in concentric hypertrophy
• there’s also reduced muscle wall compliance, there’s less mechanical efficiency, meaning increased oxygen consumption for the same amount of work during eccentric hypertrophy

Question 109

decompensation during heart failure

Answer 109

hypotension causes baroreceptor stimulation and stimulation of the sympathetic increases the rate of contraction and vasoconstriction of the arterioles,= preserve the circulation to the brain and heart. this increases cardiac workload by increasing the afterload leading to increased oxygen consumption and arrhythmia

• ADH causes water reabsorption in the distal tubules and vasoconstriction. Angiotensin stimulates smooth muscle growth hyperplasia, hypertrophy and apoptosis of the cells leading to progression of heart dysfunction

Question 110

myocardial infarction

Answer 110

• irreversible necrosis of heart muscle secondary to prolonged ischemia which occurs when a portion of the heart is deprived of oxygen due to blockage of the coronary artery
• main pathological processes leading to the changes of electrical and mechanical functions is reduced oxygen deliver to myocardium and lack of oxygen leads to the complex metabolic and adaptation processes resulting in:
o changes of intra and extra cellular homeostasis of ions (K, Na, Ca, Mg)
o accumulation of anaerobic metabolic end products, mainly lactic acid
o reduced production of energy
o increased production of ROS
o activation of local autonomic reflexes
o increased release of neurotransmitters
Three zones of damage
• 1. Zone of infarction
o Area of necrosis, it’s irreversible but can be stopped from increasing in size
• 2. Zone of injury
o Still some recovery possible, access to blood and possibility to be viable
• 3. Zone of ischemia
o Full recovery is possible
Consequences:
• Metabolic (anaerobic metabolism leads to lactic acid, hypoenergosis and pain)
• Mechanical (loss of contractile muscle mass, decreased contractility, cardiogenic shock)
• Electrophysiological (blocks, ectopic centres, bradyarrhythmia, tachyarrhythmia, ventricular fibrillation

Question 111

vomiting

Answer 111

• Reflexive, forceful expansion of content
• Pig, dog and cat = easily, herbivores = rarely
• Horses don’t vomit = underdeveloped and non-sensitive vom centre, powerful sphincter and diagonal oesophagus
• Direct stimulation = neoplasm, inflammation, hypoxia
• Indirect stimulation = pain, stress
• Consequence: tooth damage, stomach rupture, malnutrition, hypovolemia, dehydration

Question 112

GDV

Answer 112

• Sudden excessive expansion of stomach due to impaired digestion
• Breed, genetics, stress, activity after meal
• Rotation 90-360o
• Consequence = cardio, renal and GI problems
• Can result in endotoxemic shock
Mechanism:
• 1. Increased quantity of gas and pressure
• 2. Mucous ischemia (or lead to gastric tachyarrhythmia)
• 3. Edema, haemorrhage, infarct and ulcer
Phases
• 1. Accumulation of gas in stomach, light discomfort, restless, salivation increased, trying to vomit and stomach bloated
• 2. Decreased blood flow, mucosa damaged, development of hypovolemic shock, restless, whining, panting, legs apart, lowered head and dark red mucous
• 3. Necrosis of stomach, spleen etc. Endotoxic shock, heart failure, death, can’t get up, white/blue mm

Question 113

diarrohoea

Answer 113

• Increased volume/frequency of stool
Secretory
• Constant secretion of water and electrolytes into lumen
• Causes: hormones, drugs
• Electrolyte deficiency
• Doesn’t stop by fasting
• E.coli.. prolonged opening of chloride ions
• Secretion exceeds absorption
Osmotic
• Indigestion problem
• Nutrients reach lumen and act osmotically active substance  cause  osmotic gradient  influx of water into lumen
• Malabsorption due to pancreatic insufficiency

Question 114

hyper secretion of gastric juice

Answer 114

• Increased gastric juice secretion
• 1. Increased conc of gastrin = gastritis, decreased catabolism of gastrin/hypertrophy and tumour of G cells
• 2. Increased conc of corticosteroid = acute/chronic stress
• 3. Histamine = Mastocytoma
Consequence:
• Peptic ulceration, deposition of bile salts, diarrhoea, steatorrhea

Question 115

malabsorption

Answer 115

• Inability to digest and/absorb nutrients from food
• Causes; damage to intestine from infection, inflammation, trauma, surgery
• Increased HCl
• idiopathic

Question 116

hyposecretion of gastric juice

Answer 116

• Decreased secretion
• Chronic gastritis
• Diffuse atrophy of mucosa
Consequence
• Decreased HCl secretion, helicobacter and insuff food production

Question 117

intestinal motility disorder

Answer 117

Hypermotility = rough, rotten, mouldy, toxic substance, decreased food utility and absorption
Hypomotility = concentrate feed, constipation, increased water absorption
Intestinal spasm = inappropriate diet
Intestinal atony = complete loss, distension of intestine and final stage of ileus

Question 118

IBD

Answer 118

• Unknown aetiology
• No sex predisposition, but breed
• GALT, genetic, biochem, ischemic disorder
• Signs: chronic vomiting and diarrhoea, edema, ascites and anorexia
• Differential diagnosis = pancreatitis, tumour, parasitic, kidney and liver failure

Question 119

gastric ulcer

Answer 119

= necrosis of mucosa
1. Mucosal barrier injury
2. Back diffusion of luminal acid into mucosa
3. Degranulation of mast cells releasing histamine
4. Increased secretion of pepsin and HCl
5. Mucosal erosion and damage of BV
6. Ulcer
Cause: Drug, helicobacter, stress (ACTH + adrenaline), neoplasm
Signs: Anaemia, weakens, weight loss, vomiting

Question 120

gastritis

Answer 120

• Inflammation of gastric mucosa
• Irritant in food, allergies, drugs, poisons, virus
Acute
• Protective mucosal layer is altered, mucosal reddening, edema, superficial surface erosion
• Leads to: increased motility, pain and vomit
Chronic
• Progressive thinning of mucosa and degeneration
• Leads to superficial/atrophic gastritis

Question 121

ileus

Answer 121

• Intestinal obstruction
• 1. Function  spastic (Pb/insecitide poisoning), paralysis
• 2. Mechanical
o Obstructive = closing from side (foreign body)
o Compressive = closing from outside (tumour/abscess)
o Strangulation = torsio intestine, invag
Consequence:
• Retention of feed, overgrowth of bacteria, intestinal distension and hypovolemic shock

Question 122

disorders of pancreatic juice

Answer 122

Pancreatitis
• Acute = activation of digestive enzymes
• Trypsin = activation of other enzymes
• Elastase = degrades elastin
• Lipase = fatty necrosis
Pancreatic insufficiency
• Undigested protein, fat and starch
• Steatorrhea
• Loss of body mass

Question 123

constipation

Answer 123

• Faeces stretches rectum
• Stimulates stretch receptors, transmits signals to spinal cord
• Causes contractions and relaxing of internal anal sphincter and keeps open external sphincter
• Cause = lack of fibrous tissue, neoplasm, scars
• Consequence = colic, vomit, intoxication

Question 124

gastric dilation in horses

Answer 124

• Overeating fermentable feedstuff
• Lactobacillus  large production of acidic comp and gas
• Spasm of cardiac sphincter
• Lactate and bacterial toxin  colic
• Swelling and trembling
• Rupture of stomach and diaphragm
• Distension pain, haemoconc, dehydration and alkalosis  death

Question 125

DIC

Answer 125

• Multiple clot formation and diffuse bleeding
• Cause = sepsis, neoplasm, snake venom toxicities
• 2 pathways  intrinsic and extrinsic which both activate thrombin
•  fibrin  fibrinolysis
• Results in ischemia  organ dysfunction  haemorrhage and haemodynamic

Question 126

cardiogenic shock

Answer 126

• Occurs in conditions of sudden decline in cardiac work, producing insufficient arteriovenous pressure gradient
• Alterations in myocardium, cardiac valves, pericardium and big blood vessels
• Due to insufficient production of pressure arteriovenous gradient in cardiogenic shock adaptive mechanism are less efficient, accelerating towards MODs
• Type of shock is by sudden drop of minute volume and increased venal pressure
• Myocardial infarction, pulmonary embolism, trauma, heart tamponade can cause it

Question 127

distributive shock

Answer 127

• Irregular vascular adaption to the containing volume, causing arteriovenous pressure, gradient loss, despite normal cardiac function and maintained blood volume
• Neurogenic, septic and anaphylactic shock are included
• Sepsis – bacterial sepsis releases endotoxins, stimulating NO production
• Anaphylaxis – immunocomplex formation causes degranulation of mast cells and basophils, released vasoactive substances systematically decrease BV tone leading to loss of arteriovenal pressure gradient
• Neuropathogenic – consequence of vasomotor centre dysfunction during trauma, meningitis, intoxication or peripheral nerve disease, causes tone loss

Question 128

hypovolemic shock

Answer 128

• Sudden drop in circulating blood volume which exceeds 35% when venal pressure is below normal
• Caused by external or internal bleeding, loss of plasma or water and electrolytes from extracellular space
• External bleeding – trauma, peptic ulcer, etc
• Internal bleeding – haemothorax, hemoperitoneum, etc
• Plasma is lost during severe skin burns, peritonitis, ascites and hydrothorax
• Water and electrolytes are lost during dehydration due to diarrhoea, vomiting, polyuria, endocrine loss of sodium and due to increased water perspiration during severe skin burns

Question 129

pathophysiological course of shock

Answer 129

Compensated stage
• Homeostatic mechanism are activated promptly
• Increased sympathetic nervous system tone – circulation centralisation
• Catecholamines release: tachycardia, increased myocardial contractibility, BV tone and tachypnoea
Refractory stage
• If homeostatic mechanism fail to correct the AV pressure gradient, metabolic and tissue dysfunction will progress to refractory stage
• Prolonged peripheral hypoenergosis – individual cell necrosis
• Loss of cells, acid metabolites accumulation, hypoenergosis – activation of regulatory feedback mechanisms – MODs
• Changes in microcirculation
• Decompensation = hypokinetic stage (acid metabolite accumulation, decreased precapillary sphincter tone, increased vascular permeability, secondary hypovolemia), as energy metabolism worsens it leads to paralytic stage (blood volume in capillaries rise, causing decrease in effective blood volume

Question 130

outcomes of shock

Answer 130

• Restoration of sufficient AV pressure gradient without cellular loss
• Restitution of circulation with the loss of functional reserve of organs
• Restitution of circulation with permanent damage of organs systems
• Death during shock

Question 131

stages of shock

Answer 131

Early
• Mild hypoxic hypoenergosis
• Decreased or normal arterial systolic pressure
• Mildly increased diastolic pressure
• Moderate tachycardia and decreased pulse pressure
• Mild metabolic acidosis with respiratory compensation
• Oliguria or anuria
• Restlessness, slow reactions, pale and cold skin
Fully developed shock
• Severe hypoenergosis, necrosis of individual cells
• Microcirculatory dysfunction
• Severely decreased systolic
• Severe tachycardia
• ARDS, respiratory acidosis
• Oliguria, anuria
• Restlessness, stupor, pale, wet
Late stage
• Necrosis of numerous tissue cells
• Decreased functional load
• Microcirculatory paralytic dysfunction
• Severely decreased arterial pressure
• Consumptive coagulopathy
• Anuria
• Respiratory failure
• Skin is cold, sticky, greyish