extra extra extra

Question 1

definition of ascites

Answer 1

accumulation of fluid within abdominal cavity

Question 2

cause of ascites

Answer 2

portal hypertension and hypoproteinemia

Question 3

who does ascites affect

Answer 3

rarely in pigs most in dogs

Question 4

signs of ascites

Answer 4

lower distended abdomen
abomdinal pain
lethary
decreased appetites

Question 5

mechanism of ascites

Answer 5

all pressure within the capillaries are sometimes imbalanced, this imbalance causes edema

Question 6

definition of cirrhossi

Answer 6

end stage liver failure accompanied with diffuse fibrosis and loss of regular structure

Question 7

mechanism of cirrhosis

Answer 7

1. Sinusoidal hypertension
   * Causes increased fluid leakage into Space of Disse with increased lymph formation
   * Makes it difficult for lymph to drain, so there’s overflow into peritoneal cavity = ascites
   * Transudate has high protein content and due to osmosis there’s fluid leakage = ascites
   * Also leads to portal hypertension causes increased capillary pressure in abdominal area and plasma leakage into peritoneal cavity = ascites
2. Leads to hypoalbuminemia
   * Decreased albumin synthesis in liver, protein leakage from sinusoids = hypoalbuminemia
   * Decreasing blood osmotic pressure, plasma leaks into interstitium and abdominal cavity = ascites
3. Causes plasma leakage from blood vessels
   * Causes noradrenaline release, causing vasoconstriction and increasing blood volume
   * RAAS is activated and ADH is excreted all causing edema and ascites
4. Decreased liver blood flow
   * Portosystemic circulation is unable to metabolise noxious compounds
   * Peripheral vasodilation occurs causing edema and ascites

Question 8

complications of cirrhosis

Answer 8

hepatorenal syndrome
HE
hepatic hydrothorax

Question 9

definition of hepatorenal syndrome

Answer 9

precursor of kidney failure

Question 10

mechanism of hepatorenal syndrome

Answer 10

Renal vasoconstriction due to peripheral vasodilation and intravascular volume depletion, causes decreased GFR, oliguria and uraemia

Question 11

define HE

Answer 11

Decline in brain function that occurs as a result of severe liver disease. Liver cannot remove toxins from the blood, leading to build-up of toxins in blood stream, causing brain damage

Question 12

mechanism of HE

Answer 12

• Toxins (NH3) bypass liver and have toxic action on the brain
• Ammonia is a waste product of AA metabolism and urea is formed by AA deamination and urea degradation
• S.I digest protein, deaminates AA and produces ammonia, bacteria in large intestine degrade urea producing ammonia. Through portal circulation, ammonia enters urea cycle and is bio transformed into urea and kidney excretes. Can also be converted to glutamine in the liver

Question 13

signs of HE

Answer 13

depression, tremor, stupor/coma

Question 14

hepatic hydrothorax/pleural effusion definition

Answer 14

excessive accumulation of transudate in pleural cavity

Question 15

mechanism of Hepatic hydrothorax

Answer 15

ascitic fluid effuses through diaphragmatic defects

Question 16

signs of hepatic hydrothorax

Answer 16

animal can cough, dyspnoea, hypoxia or respiratory failure

Question 17

what can hepatic hydrothorax result in?

Answer 17

hypoalbuminemia
portal hypertension
peripheral dilation
ascites and edema

Question 18

fatty liver disease def

Answer 18

accumulation of triglycerides in the cytosol of the hepatocytes

Question 19

mechanism of fatty liver

Answer 19

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

Question 20

4 grades of fatty liver

Answer 20

1 - healthy liver and reversible
2 fatty infiltration
3 fatty degeneration and irreversible
4 cirrhosis

Question 21

causes of fatty liver

Answer 21

energy deficit in ruminants (late pregnancy, early lactation), hormonal disorders (diabetes, hypothyroidism, hyperadrenocorticism), idiopathic fatty liver syndrome

Question 22

biotransformation definition

Answer 22

conversion of endogenous and exogenous compounds into soluble compounds that are easily excreted

Question 23

endotoxins

Answer 23

products of metabolism

Question 24

exotoxins

Answer 24

drugs, potions from feed, products of microorganisms

Question 25

where does biotransformation occur?

Answer 25

in ER involving cytochrome P450 and UDP

Question 26

detoxification

Answer 26

conversion to nontoxic metabolites

Question 27

bioactivation

Answer 27

increased toxicity after biotransformation CCL4 causes oxidative damage to hepatocytes, halothane causes hepatitis

Question 28

mechanism of biotransformation

Answer 28

stage 1
- no synthesis, increase polarity slightly by oxidation, reduction or hydrolysis

stage 2
- synthesis of new compounds to increase polarity via conjugation, methylation and acetylation

Question 29

disorder of biotransformation

Answer 29

causes decreased inactivation and excretion of endogenous metabolites, so they accumulate = liver cirrhosis

Question 30

definition of jaundice

Answer 30

yellow pigmentation of skin and MM, clinical signs for hyperbilirubinemia

Question 31

physiological mechanism of bilirubin

Answer 31

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 32

cause of haemolytic jaundice

Answer 32

babesia canis - directly invade and infected RBC causing lysis
other microorganisms
immune mediated haemolytic anamiea

Question 33

mechanism of haemolytic jaundice

Answer 33

1. increased haemolysis > increased bilirubin 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 34

hepatocellular jaundice cause

Answer 34

decreased bilirubin uptake by hepatocytes, decreased bilirubin conjugation and impaired bilirubin excretion

• Infectious hepatitis, toxic hepatitis, hepatic lipidosis, liver fibrosis and cirrhosis

Question 35

mechanism of hepatocellular jaundice

Answer 35

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 increasedbilirubin

Question 36

obstructive jaundice cause

Answer 36

impaired bile flow by extrahepatic ducts (biliary obstruction). Intraluminal obstruction (gallstones, parasites, inflammation), extraluminal obstruction (tumours)

Question 37

mechanism of obstructive jaundice

Answer 37

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 38

definition of hypoventilation

Answer 38

• Alveolar spaces aren’t filled with an adequate amount of fresh air so oxygenation of the blood in the lung capillaries is disturbed  hypercapnia (increased CO2, hypoxemia and hypoxia)

Question 39

compensatory mechanism of hypoventilation

Answer 39

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 40

hyperventilation

Answer 40

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

Question 41

definition of asthma

Answer 41

periodic episodes of severe and reversible bronchial obstruction in hypersensitive or hyperresponsive airways

Question 42

cause of asthma

Answer 42

hypoxia (decrease of air flow with increased need for air), hypoxemia (vasoconstriction of lung blood vessels leading to right heart overload)

Question 43

seize and signs of asthma

Answer 43

acute seizure: bronchoconstriciton, inflammation, swelling and mucus secretion in the lumen

signs: cough, severe dyspnoea, mucus expectoration, tachycardia, respiratory acidosis

Question 44

extrinsic/intrinsic asthma

Answer 44

extrinsic = more common in young animals, partial/total obstruction of airways and severe hyoxia

intrinsic = more common in adults, non-specific stimuli target on hyper responsive mucosa

Question 45

status asthmaticus

Answer 45

severe asthma seizure, not responding to therapy

Question 46

chronic obstructive bronchitis cause

Answer 46

hypersecretion, diffuse obstruction and chronic productive cough

Question 47

chronic obstructive bronchitis caused

Answer 47

by inflammation as a result of prolonged inhalation of various irritant

mucosal gland hypertrophy and hyperplasia
fibrosis and induration of bronchial wall

Question 48

signs of chronic obstructive bronchitis

Answer 48

progressive productive cough, sputum, weight loss, tachypnoea and cyanosis

Question 49

lung emphysema definiton

Answer 49

destruction of alveolar walls and septa with big and permanently enlarged alveolar spaced

Question 50

theory of lung emphysema

Answer 50

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

Question 51

consequence of lung emphysema

Answer 51

decreased areas of gas exchange
loss of capillary networ
loss of elastic fibre
pneumothorax, lung hypertension

Question 52

restrictive respiratory system disease defintion

Answer 52

decreased lung movement and decrease of total lung capacity

Question 53

pleural disease

Answer 53

pleuritis: wet, cause pain and atelectasis

hydrothorax= increased hydrostatic pressure / decreased oncotic pressure

pneumothorax = closed, open or ventile (can result in cardiac shock)

Question 54

atelectasis definition

Answer 54

aeration failure and lung collapse
- alveolar collapse disturbs lung circulation and can lead to necrosis, epithelial destruction and fibrosis of the lungs

Question 55

types of atelectasis

Answer 55

obstructive = foreign body, inflammation, paraistes
compressive = pneumothorax, hydrothoax
post-op

Question 56

neonatal respiratory distress syndrome

Answer 56

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

Question 57

lobar pneumonia

Answer 57

localised on one or more lobule, in affected areas, no healthy tissue exists

Question 58

stages of lobar pneumonia

Answer 58

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

Question 59

symptoms of lobar pneumonia

Answer 59

fever, hyperventilation, dehydration, dyspnoea tachypnoea and productive cough

Question 60

symptoms of lobar pneumonia

Answer 60

fever, hyperventilation, dehydration, dyspnoea tachypnoea and productive cough

Question 61

bronchopneumonia

Answer 61

• 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

Question 62

aspiration pneumonia

Answer 62

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

Question 63

cystic fibrosis definition

Answer 63

genetic disease which causes abnormally thick mucus production in the mucus glands

Question 64

cystic fibrosis others (what’s more affected and causes)

Answer 64

• Lungs and pancreas mostly affected
• More prone to infection
  Causes: airway obstruction, atelectasis and infection, cor pulmonale and respiratory distress

Question 65

cardiogenic lung edema

Answer 65

• Is haemodynamic
• Capillary pressure increases causing congestive heart failure and pressure increase in left atrium, occluding lung veins
• The fluid that accumulates in interstitial spaces, is low in proteins and decrease oncotic pressure in interstitium
• Pulmonary volumes and air circulation are decreased and respiratory work increased
• Managed by diuretics and vein dilators

Question 66

non cardiogenic lung edeam

Answer 66

• Is an Angio-mural edema
• Occurs after the latent period, following acute lung injury or systemic conditions: shock, MOD or pancreatitis
• Capillaries are damaged, which causes neutrophil aggregation and ROS production
• Proteases are released in the lung tissue leads to inflammation
• Damage to alveolar pneumocytes type II causes decreased surfactant production, leading to atelectasis, allows for penetration of plasma and erythrocytes into interstitial space and alveoli

Question 67

signs of non-cariogenic lung edema

Answer 67

cough, dyspnoea, restlessness, rapid and shallow breathing, tachycardia, stridor, foamy sputum

Question 68

lung hypertension

Answer 68

• Caused by lung diseases with vasoconstriction or structural changes in the blood vessels
• Left heart failure causes secondary lung hypertension as it increases pressure in the veins of the lungs
• Can also be a result of congenital heart malformations
• Hypoxia occurs due to pulmonary artery vasoconstriction
• Cor pulmonale is hypertrophy and dilation of the heart, as well as right heart failure. Causing acute cardiogenic shock or can be chronic with polycytemia and increased blood viscosity

Question 69

hormonal regulation of renal function

Answer 69

RAAS
aldosterone
ADH
ANP

Question 70

RAAS

Answer 70

• Renin is released from juxtaglomerular cells as response to decreased BP
• Renin converts angiotensinogen into angiotensin I
• Angiotensin I then converted to angiotensin II
• Angiotensin II stimulates vasoconstriction

Question 71

aldosterone

Answer 71

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

Question 72

ADH

Answer 72

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

Question 73

ANP

Answer 73

• 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 74

cause of pre renal disorders

Answer 74

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, disorders of tubular reabsorption and secretion and renal failure

Question 75

1st stage of pre renal disorder

Answer 75

COMPENSATORY PHASE
* maintain the normal kidney function (GFR, tubular functions)
* afferent arteriole dilatation and efferent arteriole constriction in order to increase the glomerular filtration pressure and readily increase the GFR
* there’s increased water and sodium reabsorption in response to angiotensin II, aldosterone and ADH
* sympathetic nervous system causes systemic and renal vasoconstriction leading to increased volume and BP

Question 76

2nd stage of pre renal dirosrder

Answer 76

• 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)
  o liver cirrhosis, portal hypertension, ascites, edema, uraemia and azotaemia…

Question 77

definition of glomerulonephritis

Answer 77

inflammation of the glomeruli

Question 78

cause of glomerulonephritis

Answer 78

accumulation of microorganisms within glomeruli, antibody binding to basement membrane and deposition of antigen-antibody complexes within the glomeruli
* upon immune complex deposition, inflammation develops. Immune complexes are deposited into the subendothelial, subepithelial or mesangial part of the basement membrane, causing leukocyte infiltration and mesangial cell proliferation causing inflammation

Question 79

mechanism of glomerulonephritis

Answer 79

• deposition of immune complexes in the glomeruli, causes infiltration by immune cells and platelets
• then release of cytokines, serotonin, histamine, proteases leading to inflammation and damage of glomerular filtration barrier  increased permeability and proteinuria
• damage cells for platelet binding, activation of coagulation and fibrin deposition
• fibrin decreases capillary lumen and the GFR
• fibrin enters the bowman’s space and makes nodules that press on capillaries  decreasing GFR

Question 80

decreased GFR from glomerulonephritis

Answer 80

• decreased area of glomerular filtration barrier
• decreased glomerular blood flow and filtration pressure
• oliguria
• tubular compensatory mechanism: increased Na+ and water reabsorption  hypovolemia  hypertension  nephritic edema

Question 81

increased glomerular membrane permeability. - glomerulonepritis

Answer 81

• proteinuria causes hypoalbuminemia and decreased osmotic pressure:
  o edema, decreased blood volume, decreased CO  heart failure, decreased renal blood flow  kidney failure  nephrotic syndrome
• haematuria, lipiduria, pyuria

Question 82

nephritic syndrome

Answer 82

• Immune complexes in glomerulus
• Decreased glomerular filtration, oliguria, azotaemia , mild proteinuria, hypertension due to decreased GFR  edema

Question 83

nephrotic syndrome

Answer 83

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

Question 84

renal artery stenosis

Answer 84

• Occur due to progressive development throughout life, or in older animals due to atherosclerosis
• Stenosis is the narrowing of a vessel, so when the renal artery is narrowed, there’s 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 85

thromboembolic renal disease

Answer 85

• 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 86

definition of TI renal disease

Answer 86

impaired structure and function of tubules and the surrounding interstitium, 3 main diseases: TI nephritis, pyelonephritis and ATN

Question 87

cause of TI renal disease

Answer 87

Primary cause: toxins, drugs, ischemia and infection
Secondary cause: glomerulonephritis, vascular renal disease and urinary tract obstruction

Question 88

mechanism of TI renal disease

Answer 88

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 89

TI nephritis def

Answer 89

inflammatory process of renal tubules and intersititum

Question 90

TI nephritis infectious/non infectious

Answer 90

Infectious: viral or bacterial septicaemia, where pathogens localise in the capillaries of the interstitium leading to inflammation. There’s subsequent degeneration of tubular cells and leakage into the interstitium  interstitial edema
* Results in tubular function damage due to the edema
Non-infectious: caused by drugs and toxins that directly cause degeneration and necrosis of tubular cells. Allows for fluid to leak into the interstitium  interstitial edema

Question 91

def pyelonephritis

Answer 91

Def: inflammation of renal pelvis associated with ureter infection

Question 92

cause of pyeloneprhtisi

Answer 92

ascending infection from the urinary tract via contaminated urine reflux into the renal pelvis
* Expansion of infection to tubules and interstitium  tubulointerstitial nephritis
* Pathogens: E.coli, klebsiella, staph and strep

Question 93

acute/chronic pyelonephritis

Answer 93

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 94

def ATN

Answer 94

Def: degenerative disease of renal tubules without inflammation with acute degeneration and necrosis of tubular epithelium
* Most common cause of acute renal failure

Question 95

cause of ATN

Answer 95

nephroxotins (atb, analgesics, anaesthetics, heavy metals)
ischema

Question 96

mechanism of ATN

Answer 96

• RAAS activation and vasoconstriction leading to decrease in GFR and oliguria
• because of damage, there’s tubular obstruction, increase in tubular pressure, decreasing gGFR > oliguria
• Increase in intratubular pressure causes tubular back leak  interstitial edema
• Tubular cell damage also leads to decrease sodium reabsorption  further RAAS activation and vasoconstriction, decreasing GFR even further

Question 97

acute renal failure def

Answer 97

sudden loss of kidney functions

Question 98

acute renal failure

Answer 98

• First, there’s a reduced Na+ reabsorption and K+ secretion
• Causes: hyponatremia and hyperkalaemia in the body
• Reduced H+ excretion, leading to metabolic acidosis
• Decreased calcitriol leads to hypocalcaemia
• Leads to reduced GFR, causing 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 99

chronic renal failure def

Answer 99

progressive and irreversible nephron damage and loss of kidney function

Question 100

stages of chronic renal filuare

Answer 100

Stage 1:
* Reduced GFR to 30%
* Other functions are preserved
Stage 2:
* Further decrease of GFR to 15%
* Reduced excretion leading to azotaemia
* Reduced urine concentration
* Anaemia due to reduced erythropoietin
* Hypertriglyceridemia due to reduced lipoprotein lipase activity
Stage 3:
* Severe anaemia
* Severe arterial hypertension
* Disorders of cardiovascular, digestive and nervous system
Stage 4:
* Significantly reduced GFR to <5%
* Terminal uraemia leading to uremic syndrome

Question 101

ureic syndrome def

Answer 101

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

Question 102

disorders of ureic syndrome

Answer 102

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 103

insulin

Answer 103

• decreases blood glucose levels, enhances the entrance of glucose in cells, glucose phosphorylation, glycogen synthesis, lipogenesis and protein synthesis in muscles

Question 104

glucagon

Answer 104

• increases blood glucose levels. Increases glycogenolysis, gluconeogenesis and lipolysis

Question 105

catecholamine

Answer 105

• Increases blood glucose levels. Enhance glycogenolysis in the liver and muscles, as well as lipolysis and glucagon secretion. Adrenaline also stimulates adrenocorticotropic hormone secretion

Question 106

GH

Answer 106

• Increases blood glucose. GH directly damages beta cells and insulin production. Also, inhibits glucose entrance and oxidation in cells

Question 107

glucocorticoids

Answer 107

• Increase blood glucose by enhancing gluconeogenesis. Decreases glucose consumption in all tissues except the brain. Increases glycogenolysis

Question 108

thyroid hormone

Answer 108

• Stimulate glycogenolysis, stimulates intestinal glucose absorption

Question 109

acetic acid

Answer 109

main source for lipid syntehsis

Question 110

butyric acid

Answer 110

substrate for ketogenesis

Question 111

propionic acid

Answer 111

glucoplastic and substrate for gluconeogensis

Question 112

def of hypoglycaemia

Answer 112

decrease in blood glucose concentration

• Cells cannot receive energy and ROS production is increased  further damage of cells
• Stimulates the glucoreceptors in the hypothalamus and through neural endings, activates the adrenal medulla and releases: adrenaline, which increases glycogenolysis in the liver. When glycogen stores are spent, precursors of liver glucose synthesis become glycerol from fatty tissue, lactate and pyruvate as well as AA in muscles

Question 113

induce hypoglycaemia

Answer 113

• Induced with hypoglycaemic drugs
• Xylitol (in chewing gum) 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
• Leucine

Question 114

spontaneous hypoglycaemia

Answer 114

• 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 115

hunter dog hypoglycaemia

Answer 115

• 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 116

hypoglycaemia of new born pigletms

Answer 116

• Occurs in first days of life (up till day 3)
• 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 117

gravidity toxemia in sheep (mechanism, signs, treatment)

Answer 117

• 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
• Hypoglycaemia leads to gluconeogenesis and lipolysis and acetyl CoA accumulation and KB synthesis
  Signs: apathy and weakness, followed by neurological symptoms
  Treatment: glucose and corticosteroid application or oral application of glucose precursor

Question 118

def dairy cow ketosis

Answer 118

• 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

Question 119

signs of dairy cow ketosis

Answer 119

anorexia, depression, ketonemia, ketolactia, ketonuria, hypoglycaemia and decreased milk production

Question 120

type 1 dairy cow ketosis

Answer 120

• 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

Question 121

type 2 dairy cow ketosis

Answer 121

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

Question 122

type 3 dairy cow ketosis

Answer 122

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 123

pathogenesis dairy cow ketosis

Answer 123

• 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 124

parenterally applied glucose for dairy cow ketosis

Answer 124

• relieve symptoms promptly, as well as oral application of glycerol and propionic acid
• GH application decreases ketosis in next lactation, since cows accumulate less fat tissue and more muscles
• In NEB more proteins than fat are mobilised as gluconeogenetic substrate
• Glucocorticoids can be used as they stimulate gluconeogenesis, glycogenolysis and utilisation of glucose in tissues
• Insulin can be used, since lipid mobilisation is decreased and glycolysis is increased

Question 125

define hyperglycemia

Answer 125

increase in glucose concentration
* 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 126

insulin deficiency

Answer 126

• Occurs when there’s damage to the beta cells of the islets of Langerhans in the pancreas
• Compromises the mechanisms of synthesis, storage and secretion of insulin
• Insulin deficiency occurs in type I diabetes

Question 127

insulin resistance

Answer 127

• Condition in which insulins effects are decreased due to decreased sensitivity or decreased response of insulin
• Decreased sensitivity to insulin is a condition where a higher conc of insulin is needed for max effect
• Resistance occurs when conc of insulin antagonists in the blood are increased, or when receptors for insulin in the target cells are damaged. Both cases, hyperglycaemia occurs

Question 128

consequences of hyperglycemia

Answer 128

• Oxidative damage of cells. Kidney threshold for glucose is surpassed, glycosuria occurs and its osmotic activity causes a loss of water  glycosuria is accompanied with polyuria
• Glucose is an excellent medium for microorganism growth, prolonged glycosuria is often accompanies with bacterial and fungi infections
• Ocular lens, erythrocytes, neurones, digestive system cells, renal cells and beta cells of the pancreas don’t need insulin for glucose transportation, so it enters those cells in an excessive amount and uncontrolled
  o Enhances sorbitol pathway in cells so that fructose and sorbitol are accumulated
  o Those substances have a high osmotic activity so water enters these cells, causing swelling, dysfunction and irreversible damage
• Prolonged hyperglycaemia results in insulin suppression and pancreatic amyloidosis due to the oxidation of amyloid
• Can cause blindness, diabetic ketoacidosis, neuropathies, dehydration, pancreatic amyloidosis, insulin resistance and UTI

Question 129

hyperosolar coma (def, mech, treatment)

Answer 129

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
o Seen in older patients with acute gastrointestinal diseases with vomiting and diarrhoea, along with polyuria causing dehydration
o Dehydration  hypovolemia and decreased glomerular filtration
o Decreased 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 130

def DM

Answer 130

metabolic disease characterised with hyperglycaemia as consequence of disturbed insulin secretion, disturbed biological action of insulin or a combination of both disturbances

Question 131

type 1 DM

Answer 131

• 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

Question 132

type 2 DM

Answer 132

• Beginning of the disease with hyperglycaemia and hyperinsulinemia
• Advanced stages, hypoinsulinemia occurs as a consequence of beta cell depletion, more common in cats
• Obesity is the leading cause, males are more prone too
• Treated with oral hypoglycaemic drugs to prevent complications caused by hyperglycaemia

Question 133

pathogenesis DM

Answer 133

• Deficiency or dysfunction of insulin in the development
• Persistent hyperglycaemia is main diagnostic criterium
• Healthy animals, homeostasis is maintained. In diabetic animals - hyperglycaemia
• Utilisation of glucose in peripheral tissues is decreased and production in the liver through gluconeogenesis is increased
• Glucose is absorbed from the GI tract or synthesised through gluconeogenesis or released through glycogenolysis and accumulates in the blood
• Utilisation of glucose in the tissues is decreased, therefore glucose remains in the blood
• Deficiency/dysfunction of insulin progresses, balance of glucose in the blood is taken to a higher level and finally exceeds the renal threshold
• Glycosuria begins, glucose has osmotic activity so polyuria develops
• Animal compensates by drinking more water or polydipsia
• Since glucose cannot enter cells and utilisation is decreased, there’s energy disbalance. Catabolism of lipids and proteins begins. Lipomobilisation occurs, depending on the insulin deficiency, since insulin stops the activity of lipoprotein lipase. Due to high lipoprotein concentration in the blood, plasma become turbid and levels of total triglycerides and cholesterol increases
• Protein catabolism begins and AA are used as gluconeogenic substrate which leads to muscular weakness and weight loss
• Since glucose cannot be transported into neurons sensitive to glucose in the hypothalamus due to lack of central insulin action on appetite regulation, although hyperglycaemic, animals are hungry and polyphagia develops

Question 134

acute complications of DM

Answer 134

• 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 135

chronic complications

Answer 135

• connected to vascular damage, present as micro or macrovascular damage
• diabetes enhances large BV atherosclerosis which then causes coronary diseases, stroke and extremity diseases which are a consequence of poor circulation

diabetic retinopathy
diabetic neuropathy
diabetic nephropathy

Question 136

diabetic retinopathy

Answer 136

o small BV in back of the eye release proteins and blood into the retina, along with microaneurysms and neovascularisation
o spontaneous bleeding from young BV can lead to scar formation on the retina and retinal ablation
o cataracts and glaucoma

Question 137

diabetic nephropathy

Answer 137

o in the beginning, small renal BV walls become more permeable, therefore proteins and urine leakage begins
o later stage, filtration is decreased and lost
o toxins accumulate in blood which leads to azotaemia and patients need dialysis
o can be controlled through BP control

Question 138

diabetic neuropathy

Answer 138

o consequence of decreased circulation and ischemic damage of the nerves as well as sorbitol pathway activation and swelling of neurones
o symptoms include insensitivity, burning sensation or pain in the feet or legs

Question 139

obesity

Answer 139

• Body mass of an organism exceed the ideal by 20% it’s a consequence of increased food intake and decreased energy consumption, particularly early age, while GH is secreted
• Fat tissue formed in young animals is hard or impossible to lose since fat cells can only undergo atrophy
• If fat tissue is accumulated after the growth is accomplished, it’s easier to lose it
• It can occur when satiety centre is disturbed (Prader Wili’s syndrome)
• Expression of insulin sensitive GLUT4 in muscles and fat cells of obese cats is significantly lower compared to cats with normal body weight
• In liver and muscle cells of obese cats, there’s lower expression of insulin signalling genes
• Fat tissue is endocrinologically active and secretes numerous bio mediators
  o Secretes: adipokines (leptin, resistin, adiponectin) and proinflammatory cytokines (TNFa, interleukins 1,6,9)
• Levels of adiponectin produced only in fat tissues is decreased in obese and diabetic cats  insulin resistance and chronic inflammatory processes in the organism
• Adiponectin increases insulin sensitivity in cells and has anti-inflammatory effects
• Leptin levels are higher than in healthy cats and leptin action is decreased
• Leptin is also involved in insulin sensitivity
• Insulin resistance as a consequence of obesity is reversible  progress to diabetes

Question 140

diabetic ketoacidosis def and treatment

Answer 140

: life threatening complication of diabetes when there’s an accumulation of KB in blood, causes metabolic acidosis and disturbances in electrolyte concentration

treatment: liquid electrolytes and insulin application

Question 141

pathogenesis of DKA

Answer 141

• Clinically presented with PUPD, vomiting, diarrhoea, anorexia, dehydration, ketonuria and later stages with lethargy, weakness, epileptic seizures and coma
• Increased FA mobilisation due to the lack of liporotective effects of insulin causes increased beta oxidation of FA in the liver and decreased synthesis
• The conc of AcCoA increases and ketogenesis with abundant synthesis of acetoacetic acid, beta hydroxybutyric acid and acetone begin
• Peripheral tissues of diabetic animals have a lower capacity of ketone utilisation
• Acetoacetic acid and beta hydroxybutyrate are acidic anions and their increase leads to the decrease of other anions like bicarbonates, sodium and chloride ions in the blood
• Decreased levels of bicarbonates in the blood stimulate the respiratory centre and cause hyperventilation with deep and laboured breathing in order to correct the metabolic acidosis
• When respiratory compensation fails, acidosis develops
• Renal threshold for ketones is low and they are lost in urine, along with water and bicarbonates
• Acidic ketones are buffered with ammonia ions from glutamine in the renal tubules and so large amounts of ketones are lost along with sodium and potassium
• Water and electrolyte lost due to polyuria can cause hypovolemic shock. Increased plasmatic osmolarity due to hyperglycaemia in renal failure can cause transition of water from the cells to the blood and intracellular dehydration of cerebral neurones and hyperosmolar coma

Question 142

causes of fat malabsorption

Answer 142

• 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 143

hyperlipoproteinemia (primary rare), secondary

Answer 143

• Are symptoms of other diseases, such as acute pancreatitis, liver diseases, DM, hypothyroidosis and hyperadrenocorticism in dogs
• Acute pancreatitis: hypercholesterolemia or hypertriglyceridemia occur but mechanisms isn’t clear. Hyperlipoproteinemia induced by other disorders can predispose the animal to pancreatitis, can be due to obstructive cholestasis. Decreased intravascular lipolysis or processing of plasmatic lipoproteins leads to increased concentration of VLDL or chylomicrones
• Hypercholesterolemia is frequent found in cholestasis along with hypertriglyceridemia. It’s considered to be due to increased cholesterol production in liver, decreased secretion in bile and disturbed intake of LDL In hepatocytes

Question 144

hypolipoprotenami

Answer 144

• 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 145

definition of atherosclerosis (who affects and consequences)

Answer 145

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

Question 146

risk factor of atherosclerosis

Answer 146

• Hypercholesterolemia, increased hydrostatic pressure and presence of glycolyzed proteins, increasing ROS production

Question 147

pathogenesis of atherosclerosis

Answer 147

• Response to endothelial damage
• Occurs when elevated blood pressure
• Damaged endothelium allows LDL to enter, monocytes eat LDL and cholesterol, dies and forms foam cells
• Release cytokines  foam cells build up, forming fatty streak which is thrombogenic
• Platelets enter, release PDGF  encourage smooth muscle growth, secretes collagen, proteoglycan and elastin = fibrotic cap
• Fibrous cap + fatty streak = plaque

Question 148

equine metabolic syndrome

Answer 148

• Obesity caused by excessive eating and changes in lifestyles in horses
• Along with insulin resistance, manifestation of laminitis
• Insulin resistance means disturbances in insulin signalisation, including decreased activit of tyrosine kinase insulin receptor and decreased postreceptive phosphorylation with changes in metabolic and vascular insulin effects
• In horses with insulin resistance significantly lower expression of GLUT4 at the surface of muscular and fat cells is noted
• Compensated insulin resistance is a condition in which pancreas produces more insulin, in combination with decreased insulin clearins it leads to hyperinsulinemia
• Decompensated insulin resistance characterises pancreatic insufficiency, hypoinsulinemia and type II (rare in horses)

Question 149

equine metabolic syndrome symptoms

Answer 149

• Obesity, particularly 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 150

cause of laminits

Answer 150

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

Question 151

pathogenesis of laminitis

Answer 151

• 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 152

protein deficiency

Answer 152

due to”
- decreased production
- decreased AA utilisation
- immobilisation
- due to ancrease loss of proteins

Question 153

protein deficiency due to decreased production

Answer 153

• Can be due to a decreased intake of AA from the diet or incomplete absorption in the intestinal mucosa during some GI disease
• Dietary deficiency occurs in starvation, when are nutrients are deficient, or starvation with mainly protein deficits
• Due to CHO deficiency, insulin secretion is decreased and its anabolic effect on proteins is absent, therefore protein catabolism increases
• AA are used as substrates for gluconeogenesis or plasma protein production
• During general starvation, hypoproteinaemia will appear after a quarter of total muscle mass is lost
• If starvation is mainly due to protein deficiency, insulin is released preserving muscular mass from degradation
• Few AA for plasma protein synthesis is available and hypoproteinaemia will appear
• Young animals are particularly sensitive, during growth and development since the need for protein is huge

Question 154

protein deficiency due to decreased AA utilisation

Answer 154

• After absorption, AA are transported ot the liver
• Liver supplies the body with AA and plasma proteins
• During liver insufficiency, disturbances in AA and proteins metabolism impact the whole animal
• It’s particularly visible as swelling which is due to hypolbuminaemia and oncotic pressure decrease, and increased prone to bleeding due to decreased production of coagulation factors

Question 155

protein immobilisation

Answer 155

• During immobilisation, muscles become atrophic and bones osteoporotic due to metabolic loss of proteins as a consequence of decreased synthesis and increased catabolism

Question 156

increased loss of protein

Answer 156

• Proteins can be directly lost during severe bleeding, plasma loss, proteinuria, through the digestive system or effusions into body cavities
• Indirect loss happens during increased catabolism

Question 157

consequence of protein loss

Answer 157

• Due to metabolic adaption of the tissues, proteins are not equally lost from all tissues
• Loss of muscle mass and strength, bones become visible
• Albumins maintain oncotic pressure and extracellular fluid distribution, therefore during hypoalbuminemia, edema occurs
• Decreased calcium binding during hypoalbuminemia leads to hypocalcaemia but concentration of ionised calcium remains normal and tetany will not occur
• Hypoalbuminemia increases toxic effects on unconjugated bilirubin since there’s a lack of albumin transporter for unconjugated bilirubin transport
• During protein deficiency, globin synthesis and erythrocyte production is decreased and anaemia occurs, due to decreased immunoglobin production, there’s an increased risk of infections

Question 158

equine paralytic myoglobinuria

Answer 158

• 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

Question 159

pathogenesis of equine paralytic myoglobinuria

Answer 159

• 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

Question 160

therapy of eqine paralytic myoglobinuria

Answer 160

• based on pain relief, correction of electrolytes and acid-base balance, prevention of renal damage caused by myoglobinuria and dehydration as well as NSAID

Question 161

sporadic paralytic myoglobinuria

Answer 161

• 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

Question 162

chronic paralytic myoglobinuria

Answer 162

• Caused by a glycogen storage disturbance (polysaccharide storage myopathy)

Question 163

undernourishment

Answer 163

• Condition in which the intake of essential nutrients is inadequate
• Can be primary (acute or chronic, depending on nutrient insufficiency) or secondary

Question 164

during acute starvation

Answer 164

• Depends on quality and quantity of ingested food and if it persists it causes chronic starvation.

First phase :irritability, depression and stupor. Glycogen is the first energy source used, then 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 BMR 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

Question 165

during chrinic starvation/general undernourishment

Answer 165

• 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 166

acute rumen acidosis

Answer 166

• 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
  = loss of appetite to reduce feed 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 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 Endotoxins increase the concentration of VFAs and lactates, further decrease the pH and cause high osmotic pressure leading to ruminitis

Question 167

clinical signs of acute rumen acidosis

Answer 167

• 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 168

chronic rumen acidosis

Answer 168

• 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

Question 169

clinical signs of chronic rumen acidosis

Answer 169

• 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 170

rumen alkalosis

Answer 170

• 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 171

frothy bloat

Answer 171

• 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 172

free gas bloat

Answer 172

• 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 173

traumatic reticuloperitoniitis

Answer 173

• 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

Question 174

clinical signs of traumatic reticuloperitonitis

Answer 174

• 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

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

Question 175

signs of pleuritis and pericarditis

Answer 175

• 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 176

regenerative anaemia def

Answer 176

• 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

Question 177

hemolytic regernative anaemia causes

Answer 177

• Immune mediated haemolytic anaemia
• Erythroparasites
• Other infectious agents
• Oxidation injury
• Fragmentation injury
• Histiocytic disorders
• Inherited RBC defects
• Metabolic conditions

Question 178

hemorrhagi regenerative anaemia causes

Answer 178

• 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 179

non regenerative anaemia

Answer 179

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 180

hemolytic anaemia def

Answer 180

• 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

Question 181

extravascular hemolytic anaemia

Answer 181

• 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

Question 182

intravascular hemolytic anaemia

Answer 182

• 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 183

neonatal isoertyhrolysis

Answer 183

• 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 184

oxidant - induced haemolytic aanemia

Answer 184

• 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 185

sideropeni anaemia

Answer 185

• 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

Question 186

causes of sideropneic aanemia

Answer 186

• 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 187

iron deficiency anameia in piglets

Answer 187

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 188

anaemia of chornic disease

Answer 188

• 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 189

aplastic anaemai

Answer 189

• 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 190

pure red cell aplasia

Answer 190

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

Question 191

thrombocytopenia

Answer 191

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 192

von willebran dsiease

Answer 192

• 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 193

sinus tachycardia (+ cause)

Answer 193

• 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 194

sinus bradycardia

Answer 194

• 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 195

respiratory sinus arrhythmia

Answer 195

• 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 196

sinus arrest

Answer 196

• 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 197

passive hetertophy

Answer 197

• 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 198

active heterotopy

Answer 198

• 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 199

supraventriuclar arrhythmia

Answer 199

• 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 200

atrial flutter

Answer 200

• 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

Question 201

trial fibrillation

Answer 201

• 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 202

ventricular flutter

Answer 202

• 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

Question 203

ventricular fibrillation

Answer 203

• 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 204

mechanism leading to imparied condutons

Answer 204

• 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 205

sinbus block

Answer 205

• 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 206

AV block

Answer 206

• 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 207

valvular stenossi

Answer 207

• 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)

Question 208

valvular insuffieicny

Answer 208

• 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 209

mitral stenosis

Answer 209

• 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 210

mitral insufficiency

Answer 210

• 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 211

aortic insufficiency

Answer 211

• 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

Question 212

aortic stenosis

Answer 212

• Obstruction of blood flow across the aortic valve
• Left ventricular pressure overload
• Left ventricular concentric hypertrophy leading to compensation
• Atrial contribution for compensation
• Systolic murmur
• Decompensation due to inadequate supply of the heart muscle with oxygen and nutrients leading to coronary insufficiency

Question 213

hypertrophic cardiomyopathy

Answer 213

• 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 214

DCM<

Answer 214

• 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 215

restrictive cardiomyopathy

Answer 215

• 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 216

L heart failure

Answer 216

• 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 217

R heart failure

Answer 217

• 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 218

myocardial infarction

Answer 218

• 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

Question 219

zones of damage in myocardial infarction

Answer 219

• 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

Question 220

consequence of myocardial infarction

Answer 220

• 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 221

vomiting

Answer 221

• 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 222

GDV

Answer 222

• 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 223

dirrahoea

Answer 223

• 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 224

hypersecretion of gastric juice

Answer 224

• 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 225

hyposecretion of gastric juice

Answer 225

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

Question 226

intestinal motility disorder

Answer 226

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 227

IBD

Answer 227

• 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 228

gastric ulcer

Answer 228

= 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 229

gastritis

Answer 229

• 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 230

lleus

Answer 230

• 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 231

pancreatitis

Answer 231

• Acute = activation of digestive enzymes
• Trypsin = activation of other enzymes
• Elastase = degrades elastin
• Lipase = fatty necrosis

Question 232

pancreatic insufficiency

Answer 232

• Undigested protein, fat and starch
• Steatorrhea
• Loss of body mass
• LACK OF ENZYMES

Question 233

constipation

Answer 233

• 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 234

gastric dilation In horses

Answer 234

• 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 235

DIC

Answer 235

• 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 236

cardiogenic shocks

Answer 236

• 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 237

distrivbutibe shock

Answer 237

• 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 238

hypvolemic shock

Answer 238

• 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