Final Flashcards
1
Q
Hypoglycaemia
A
- induced (drugs) or spontaneous (hunting dog, decreased G Production or increased G consumption)
2
Q
New born piglet hypoglycaemia
A
- 1st 2 days of life
- predisposition = undeveloped gluconeogenetic enzyme
- conditions: sow dependent, piglet dependent and environment
- hypoglycaemia due to increased G consumption =organic hyperinsulinemia, cachexia and neoplasms
3
Q
dairy cow ketosis
A
- disturbed carb and lipid metabolism
- type 1: starving, skinny cow syndrome
- type 2: spontaneous, fat cow syndroe
- type 3: alimentary, XS amount of butyric acid
- predisposition = physiologically lower blood glucose
- incidence = NEB period- clinically = cerebral hypoenergosis, intoxication with ketones (neurologic) and inappetence, weight loss (digestive)
4
Q
hyperglycaemia
A
- physiological = alimentary or postprandial
- pathological = insulin deficiency or insulin resistance
- consequences: oxidative stress, polyuria, if very high = blindness, diabetes ketaoacidosis
5
Q
hyperosmolar coma
A
- type 2 diabetes
- complete failure of insulin effect
- dehydration, hypovolemia, decrease glomerular filtration
- absence of ketoacidosis
6
Q
diabetes mellitus
A
- metabolic disease with hyperglycaemia -> absence/insufficient inuslin
- type 1/2
- insulin dependent; dogs, hyperglycaemia with hypoinsulinemia, genetic, pancreatitis, distrubed amylin transport, treated with oral hypoglycaemia drugs
7
Q
complications of diabetes mellitus
A
- acute = consequence of high hyper/hypoglycaemia
- chronic = blood vessel pathology or sorbitol pathway activaition (swelling, cellular dysfunction)
8
Q
hormones in hyperglycaemia
A
- increase insulin antagonist conc:
= STH: decrease number of insulin receptors
= glucagon:enhances glycogenolysis + gluconeogenesis
= glucocorticoids: decrease postreceptoral effects
= catecholamines: enhance gluconeogenolysis
= progestins: enhance gluconeogenesis
9
Q
equine paralytic myoglobinuria
A
- sudden paralysis 15-20mins after exertion
- restlessness, pain + stiff muscles
- sporadic and chronic
10
Q
undernutirion
A
- primary or secondary = decrease intake, increase loss, increase demands (2)
- acute/chronic - cachexia activation of gluconeogenesis, lipid
- mobilisation, decrease glomerular filtration, intestinal villi atrophy. Mainly protein deficiency: insulin slows down protein catabolism
11
Q
athersclerosis
A
- chronic progressive disease of arteries with cholesterol and triglycerides in arterial walls
- risk factors = hypercholesterolemia, hyperlipemia, hypertension
12
Q
rhabdomyolysis
A
sporadic
= excessive physical acrivitywith concurrent viral infections
= electrolyte disbalance + endocrinological
chronic
= polysaccharide storage nmyopathies
pathogenesis
= disturbed reactions between energy intake and consumption in msucles
- mechanisal stressin muscle cells
13
Q
what is ascites
A
fluid accumulation within abdominal cavity
14
Q
causes of ascites
A
portal hypertension ->liver cirrhosis+ right side congestive heart failure
- hypoproteinaemia -> starvation
15
Q
clinical signs of ascites
A
- distension of lower abdomen, abdomen pain + discomfort
- lethargy, decrease appetite, subcutaneous edema
16
Q
cirrhosis
A
- end stage liver disease accompanied with diffuse fibrosis
- stenosis/occlusion of hepatic veins
- sinusoidal and portal hypertension
17
Q
jaundice/icterus
A
- yellowish pigmentation of skin + mucous memrbanes
- haemolytic (pre hepatic), hepatocellular (hepatic), cholestatic (obstructive, post hepatic)
18
Q
causes of haemolytic icterus
A
- excess RBC destruction -> increase bilirubin foramtion
1. obligate intracellular paraistes: babesia -> destroys RBC
2. other microorganisms: bacteria + virus
3. immune mediated haemolytic anaemia (IMHA) - autoimmune haemolytic naemia
- neonatal isoerhtyrolysis in foals
19
Q
mechanism of haemolytic jaundice
A
- increase haemolysis ->increase production of bilirubin in spleen
- increase unconjugated bilirubin into the liver
- liver to intestine is increased conjugated bilirubin, converted to: increased stercobilin, increase absorption of urobilinogen and increase urobilin in urine
20
Q
hepatocellular jaundice
A
- disorders of hepatocyte function -> impaired bilirubin metabolism -> decrease bilirubin conjugation and uptake and impaired excretion
21
Q
causes of hepatocellular jaundice
A
- infectious hepatitis: leptospirosis, salmonellosis
- toxic hepatitis = inhalation anaeshtetic
- hepatic lipidosis = fat infiltration of hepatocytes
- liver fibrosis and cirrhosis
22
Q
mechanism of hepatocellular jaundice
A
- decrease bilirubin uptake by hepatocyte andconjugation
- impaired bilirubin excretion into bile canaliculi
- urobilinogen decerease, stercobilin decrease and results in pale faeces
- increased urobilin, dark urine and increase bilirubin
23
Q
obstructive icterus
A
- impaired flow by extrahepatic ducts
- intraluminal (gallstone, parasite)
- extraluminal (tumour/inflammation)
24
Q
mechanism of obstructive icterus
A
- conjugated bilirubin stays in liver + returns to systemic circulation, urobilinogen + stercogilin decreased = pale/fatty stool
- conjugated bilirubin increase in blood, in kidney decrease in urobilin and increase in biliruibin - greenish urine
25
fatty liver
- accumulation of triglycerides in cytosol of hepatocyte
| - liver enlargement, yellow discolouration
26
mechanism of fatty liver development
1. increased influx to liver from feed by chylomicrons:
- increase feed lipid content, increased FA esterification in hepatocytes, increase VLDL formation
2. increase lipid influx to liver from adipose tissue
- energy deficit, increaselipidmetbaolism,increased FAoxidation and in hepatocyte and esterification
- insufficiency VLDL formation
- TG deposition in hepatocytes
3. increased fa and TG syntehesis from carbs
- increased feed carb content
- exceed blood glucose, increase FA esterification
27
Von Willebrand disease
- inherited deficiency/abnormality of the factor
- disorders of primary haemostats
- spontaneous mucosal bleeding
- slow wound healing
- stored in platelet granules and endothelial cells
Role in primary haemostats
- platelet binding to sub endothelial collagen
- platelet aggregation and plug stabilisation
- bind FVIII and protect from degradation
vWD deficiency
- platelet plug formation
classification
type 1, 2 and 3
28
DIC
complex haemostats disorders
- excessive activation of haemostats with subsequent generation of excess thrombin and multiple clot formation caused by underlying disease
- sepsis, neoplasm, metastatic tumours
29
DIC
complex haemostats disorders
- excessive activation of haemostats with subsequent generation of excess thrombin and multiple clot formation caused by underlying disease
- sepsis, neoplasm, metastatic tumours
30
ruminal acidosis
- too much feed rich in easily digestible CH
- too much acidic feed/ lack of fibre
acute/chronic
31
acute acidosis
- loss of appetite -> reduced foo d intake
- bicarbonate and phosphate buffer of saliva
- VFA + H+_ = better absorption of VFA
- ruminates, dehydration and general weakness
- rich in CH = more VFA = increase endotoxins (ruminintis-> intoxication), metabolic acidosis and osmotic diarrhoea
32
chronic acidosis
- increase production of VFA = decrease of pH
| - rumenitit,s luminal paraketosis, low-fat milk
33
ruminal alkalosis
- excessive prodcuction of ammonia in rumen
- unbalanced meal, improper application of urea and taking larger amounts of rotten food
clinical signs
- severe intoxication after 10 mins after meal rich in urea - polyuria, disorder of rumen motility
34
myocardial infarction
- irreversible necrosis of heart muscle secondary to prolonged ischemia
results in:
- changes of intra+extracellular hemostasis of ions
- accumulation of anaerobic metabolic end products
- reduced production of energy ATP
- activation of local autonomic reflexes
- increase release of neurotransmitters
consequences
- pain, cariogenic shock and ventricular fibrillation
35
atrial fibrillation
- arrhythmia caused by irregular production of impulses in multiple foci in the aura independently and these foci are producing impulses during systole and diastole
36
mitral valve insufficiency
- valves fails to close properly
- regurgitation of blood into left atrium
- hypertrophy and dilatation of left atrium and ventricular wall
37
heart failure
- heart can't pump enough blood to meet body needs.
left heart failure and right heart failure
compensatory mechanism
- frank Starling mechanism
- concentric/eccentric hypertrophy
- neuro-humoral compensations
38
sinus tachycardia
- increase rate of pacing in SA node.
- production of impulse is faster but regular
- causes= increase body temp, hyperthyroidism, anaemia/pregnancy, physical excercise/stress
it increases cardiac output
39
sinus bradycardia
- slow production of impulses by SA node
presence in other conditions can indicate pathology of heart
- decreased irritability of sinus node
- hypothermia
- hypo function of thyroid gland
- increased intracranial pressure, jaundice
40
arrhytmia
```
respiratory sinus arrhytmia
- change of the rate of spontaneous depolarisation in the SA node related to respiration
supra ventricular arrhythmia
- atrial extrasystole,
supra ventricular tachycardia
atrial flutter
atrial fibrillation
```
41
left heart failure
- output of left ventricle is less than total volume of blood received through pulmonary circulation -> becomes congested and BP falls
- symptoms = edema, cough, tachypnoea, syncope, weakness
42
right heart failure
- output of right ventricle less than input from systemic venous circulation
- symptoms = cardiac edema, cardiac cirrhosis, ascites, hydrothorax
43
diarrhoea
increase in volume of stool/frequency of defacations
- loose stools
- acute or chronic
- osmotic, secretory
44
osmotic diarrhoea
cause = intake of substances that are difficult to absorb and malabsorption due to pancreatic insufficiency
pathogenesis
- accumulation of large number of osmotic active ,molecules
- transition of fluid from BV into lumen of intesitine
- accelerate motility
45
secretory diarrhoea
- occurs when secretion of water into lumen exceeds absorption
causes = enterophathogenic micro-organisms, increase hydrostatic pressure, drugs
pathogenesis = bacteria with enterotoxins damage membrane so uncontrolled secretion of water
46
stenosis
intestinal narrowing
- primary = intestine damage, inflammation or tumour
- secondary = abscess, adhesion around intestine + tumour from outside
47
ileus
= intestinal obstruction
functional
- spastic = intestinal muscle spasms
- paralytic = paralysis of musculature
mechanical
- compressive = closing from outside, tumour, abscess, enlarged organs
- obstructive = closing from inside
- strangulation = torso intestine, invagination, volvulus
- consequence = retention of content, intestinal distension, spastic pain, bacterial growth
48
asthma
- periodic episodes of severe and reversible bronchial obstruction in hypersensitive or hyper responsive airways
acute seizure
= bronchoconstriciton, inflammation, swelling and mucus secretion in lumen...
= eosinophil accumulation - leukotriens
= hyperinflation of lungs = difficult exhalation
-= complete obstruction - atelectasis
= hypoxia and hypoxemia
clinical signs
-= cough, severe dyspnoea, mucus expectation, tachycardia, respiratory acidosis, cyanosis
49
lung emphysema
- destruction of alveolar walls and sea with big, permanently alveolar spaces
- alveolar and interstitial
- chronic obstructive disease in horses
mechanistic theory
= bronchiolitis
= laboured inspiration and expiration
= capillary network distension
= increase pressure in pulmonary artery
biochemical enzymatic theory
= a-1 antitrypsin, protection of granulocytic elastase and elastic function is lost alveolar cannot retract
50
consequence of lung emphysema
- decrease area for gas exchange
- loss of capillary network
- loss of elastic fibres
- decreased small bronchial support
- increased residual volume in lungs
- bullae - pneumothorax, infections
- lung hypertension and cor pulmonale
51
atelectasis
- aeration failure and lung collapse
- alveolar collapsing disturbs lung circulation
- necrosis, epithelial destruction
- obstructive, compressive or postoperative
52
lobar pneumonia
- congestive stage = lowest blood oxiaenation
- hepatisation stage (consolidation)
- resolution stage
- fever, hyperventialtion - dehydration
- dyspnoea, tachypnoea, tachycardia, pleuritic pain, productive cough, consciousness disturbances
53
bronocpneumnia
- from bronchioles to alveoli
- small foci of inflammation
- hypostatic pneumonia
54
lung edema
- abnormal fluid accumulation in lungs
- cariogenic lung edema
- non-cariogenic lung edema (adult respiratory distress syndrome)
55
cariogenic lung edema
- hemodynamic
- capillary pressure increase, congestive heart failure, pressure increases in left atrium and occlusive lung vein disease
56
non-cariogenic lung edema
- angio mural edema
- after lamentation period following acute lung injury or systemic condition
- capillaries damage, neutrophils aggregation, ROS production, proteases release in tissues
- alveolar pneumocytes type 2 damage - atelectasis
- penetration of plasma and erythrocytes in interstitial space and alveoli
- clinical signs
= cough, dysopnoea, restlessness, rapid and shallow breathing
= stridor, productive cough and foamy sputum
57
hormonal regulation of renal function
1. renin-angiotensin-aldosterone system
2. aldosterone
3. antidiuretic hornone
4. atrial natriuretic peptide
58
renin
- released from juxtaglomerular cells as a response to decreased blood pressure
- converts angiotensinogen to angiotensin 1
- AGT is converted to AGT II
59
AGT II stimulates
- vasoconstriction
- Na Cl and water reabsorption in proximal tubule
- K excretion in proximal tubule
- secretion of aldosterone and ADH
60
aldosterone
- adrenal cortex
- stimulates Na/K ATPase in distal tubule and collecting duct
- Na, Cl and water reabsorption and K secretion
- increased blood K concentration stimulates ALD secretion
61
ADH
- posterior pituitary gland
| - Na and water reabsorption in distal tubule and collecting duct
62
atrial natruiretic peptide
- secreted from cardiac aura as response to increase BP
- vasodilation - increased GFR
- decrease Na and water reabsorption in distal tubule and collecting duct
63
prerenal disorder of renal function
cause
= decreased renal blood flow due to systemic circulatory disroders
= reduced arterial BP
= venous pathology + increased intraabdominal pressure
decreased renal perfusion
- decreased GFT, renal ischemia, renal failure
64
stages of prerenal disorder
```
1 stage. compensatory phase
= maintain normal kidney function
= afferent dilate + efferent constrict
= increased GFR
= increase Na and water reabsorption
= increased BP and volume
= local secretion of prostaglandins and NO
2. stage. prerenal kidney failure
= decrease GFR
renal vasoconstriction
```
65
hepatorenal syndrome
- liver cirrhosis, portal hypertension, ascite + edema, systemic hypovolemia and vasodilation
- activation of sympaticus, renal vasoconstriction, uraemia and azotemia
66
glomerulonephritis
- decreased area of glomerular filtration barrier
- damage and increased permeability of glomerular filtration berries
causes
1. accumulation of microorganisms within glomeruli
2. antibody binding to basement memrbane
3. deposition of antigen-antibody complex within glomeruli
67
mechanism of glomerulonephritis
1. immune complex deposition and inflammation development
2. damage of glomerular filtration barrier
3. releasing of cytokines
4. damage of filtration barrier
5. platelet binding
6. fibrin decreases capillary lumen and GFR
68
nephritic syndrome
decrease GF, oliguria, azotaemia, mild proteinuria, water and sodium retention, hypertension, edema
69
nephrotic syndrome
increased glomerular permeability, massive proteinuria, hypoalbuminemia, edema, decreased CO, decreased renal blood flow
70
vascular renal disease
obstruction or stenosis of renal BV
1. renal after stenosis
= thrombi from heart
= partial obstruction - reduced GFR and tubular reabsorption
= total = infarct of renal parenchyma + irreversible necrosis
2. thromboembolism of renal artery or vein
= increased blood clotting tendency
= slow ischemia development
= congestion of glomeruli and peritublar capilliares
71
tubulointerstitial renal disease
- impaired structure and function of tubules and surrounding interstitium. Tubulointerstitial nephritis, pyelonephritis, acute tubular necrosis
causes
= primary: toxins, drugs, ischemia, infection
= secondary: glomerulonephritis, vascular renal disease
72
mechanism of tubulointerstitial renal disease
```
early stage: normal glomerular function
- damaged tubular function
- mild/moderate proteinurina
- reduced Na reabsorption + H+ secretion
late stage: secondary glomerular injury
- damage tubular cells obstruct lumen
- secondary glomerular damage
- increased proteinuria
- free tubular cells
```
73
pyelonephritis
- inflammation of renal pelvis associated with ureter infection
- by spreading the infection from urinary tract(ascending)
- contaminated urine reflex into renal pelvis
- expansion of infection to tubules and intersititum
- pathogens
acute
= rapid onset, systemic sings of infection, difficult and frequent urination and urine changes
chronic
= severe disease with destruction of renal parenchyma. reduced tubular function
74
chronic renal failure
- progressive and irreversible nephron damage and loss of kidney function
1. stage = reduced GFR, other functions preserved
2. stage = further decrease of GFR, reduced excretion
3. stage = severe anaemia and arterial hypertension, disorders of CV, digestive + NS
4 stage = significanty reduced GFR
75
uremic syndorme
```
clinical syndrome in terminal stage of chronic renal failure. Increased conc of uremic toxin in blood
disorders in ureic syndrome
= disorders in carb metabolism
= acid-base imbalance
= anaemia and hypocalcaemia
= gastrointestinal disroders
= heart and respi disroders
= atherosclerosis
```
