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Pathophysiology 2 > Final > Flashcards

Final Flashcards

1
Q

Hypoglycaemia

A
  • induced (drugs) or spontaneous (hunting dog, decreased G Production or increased G consumption)
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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
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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)
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4
Q

hyperglycaemia

A
  • physiological = alimentary or postprandial
  • pathological = insulin deficiency or insulin resistance
  • consequences: oxidative stress, polyuria, if very high = blindness, diabetes ketaoacidosis
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5
Q

hyperosmolar coma

A
  • type 2 diabetes
  • complete failure of insulin effect
  • dehydration, hypovolemia, decrease glomerular filtration
  • absence of ketoacidosis
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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
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7
Q

complications of diabetes mellitus

A
  • acute = consequence of high hyper/hypoglycaemia

- chronic = blood vessel pathology or sorbitol pathway activaition (swelling, cellular dysfunction)

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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
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9
Q

equine paralytic myoglobinuria

A
  • sudden paralysis 15-20mins after exertion
  • restlessness, pain + stiff muscles
  • sporadic and chronic
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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
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11
Q

athersclerosis

A
  • chronic progressive disease of arteries with cholesterol and triglycerides in arterial walls
  • risk factors = hypercholesterolemia, hyperlipemia, hypertension
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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

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13
Q

what is ascites

A

fluid accumulation within abdominal cavity

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14
Q

causes of ascites

A

portal hypertension ->liver cirrhosis+ right side congestive heart failure
- hypoproteinaemia -> starvation

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15
Q

clinical signs of ascites

A
  • distension of lower abdomen, abdomen pain + discomfort

- lethargy, decrease appetite, subcutaneous edema

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16
Q

cirrhosis

A
  • end stage liver disease accompanied with diffuse fibrosis
  • stenosis/occlusion of hepatic veins
  • sinusoidal and portal hypertension
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17
Q

jaundice/icterus

A
  • yellowish pigmentation of skin + mucous memrbanes

- haemolytic (pre hepatic), hepatocellular (hepatic), cholestatic (obstructive, post hepatic)

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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
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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
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20
Q

hepatocellular jaundice

A
  • disorders of hepatocyte function -> impaired bilirubin metabolism -> decrease bilirubin conjugation and uptake and impaired excretion
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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
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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
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23
Q

obstructive icterus

A
  • impaired flow by extrahepatic ducts
  • intraluminal (gallstone, parasite)
  • extraluminal (tumour/inflammation)
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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
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25
Q

fatty liver

A
  • accumulation of triglycerides in cytosol of hepatocyte

- liver enlargement, yellow discolouration

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26
Q

mechanism of fatty liver development

A
  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
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27
Q

Von Willebrand disease

A
  • 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
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28
Q

DIC

A

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
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29
Q

DIC

A

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
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30
Q

ruminal acidosis

A
  • too much feed rich in easily digestible CH
  • too much acidic feed/ lack of fibre
    acute/chronic
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31
Q

acute acidosis

A
  • 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
Q

chronic acidosis

A
  • increase production of VFA = decrease of pH

- rumenitit,s luminal paraketosis, low-fat milk

33
Q

ruminal alkalosis

A
  • 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
Q

myocardial infarction

A
  • 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
Q

atrial fibrillation

A
  • 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
Q

mitral valve insufficiency

A
  • valves fails to close properly
  • regurgitation of blood into left atrium
  • hypertrophy and dilatation of left atrium and ventricular wall
37
Q

heart failure

A
  • 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
Q

sinus tachycardia

A
  • 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
Q

sinus bradycardia

A
  • 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
Q

arrhytmia

A 
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
Q

left heart failure

A
  • 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
Q

right heart failure

A
  • output of right ventricle less than input from systemic venous circulation
  • symptoms = cardiac edema, cardiac cirrhosis, ascites, hydrothorax
43
Q

diarrhoea

A

increase in volume of stool/frequency of defacations

  • loose stools
  • acute or chronic
  • osmotic, secretory
44
Q

osmotic diarrhoea

A

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
Q

secretory diarrhoea

A
  • 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
Q

stenosis

A

intestinal narrowing

  • primary = intestine damage, inflammation or tumour
  • secondary = abscess, adhesion around intestine + tumour from outside
47
Q

ileus

A

= 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
Q

asthma

A
  • 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
Q

lung emphysema

A
  • 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
Q

consequence of lung emphysema

A
  • 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
Q

atelectasis

A
  • aeration failure and lung collapse
  • alveolar collapsing disturbs lung circulation
  • necrosis, epithelial destruction
  • obstructive, compressive or postoperative
52
Q

lobar pneumonia

A
  • congestive stage = lowest blood oxiaenation
  • hepatisation stage (consolidation)
  • resolution stage
  • fever, hyperventialtion - dehydration
  • dyspnoea, tachypnoea, tachycardia, pleuritic pain, productive cough, consciousness disturbances
53
Q

bronocpneumnia

A
  • from bronchioles to alveoli
  • small foci of inflammation
  • hypostatic pneumonia
54
Q

lung edema

A
  • abnormal fluid accumulation in lungs
  • cariogenic lung edema
  • non-cariogenic lung edema (adult respiratory distress syndrome)
55
Q

cariogenic lung edema

A
  • hemodynamic
  • capillary pressure increase, congestive heart failure, pressure increases in left atrium and occlusive lung vein disease
56
Q

non-cariogenic lung edema

A
  • 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
Q

hormonal regulation of renal function

A
  1. renin-angiotensin-aldosterone system
  2. aldosterone
  3. antidiuretic hornone
  4. atrial natriuretic peptide
58
Q

renin

A
  • released from juxtaglomerular cells as a response to decreased blood pressure
  • converts angiotensinogen to angiotensin 1
  • AGT is converted to AGT II
59
Q

AGT II stimulates

A
  • vasoconstriction
  • Na Cl and water reabsorption in proximal tubule
  • K excretion in proximal tubule
  • secretion of aldosterone and ADH
60
Q

aldosterone

A
  • 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
Q

ADH

A
  • posterior pituitary gland

- Na and water reabsorption in distal tubule and collecting duct

62
Q

atrial natruiretic peptide

A
  • secreted from cardiac aura as response to increase BP
  • vasodilation - increased GFR
  • decrease Na and water reabsorption in distal tubule and collecting duct
63
Q

prerenal disorder of renal function

A

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
Q

stages of prerenal disorder

A 
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
Q

hepatorenal syndrome

A
  • liver cirrhosis, portal hypertension, ascite + edema, systemic hypovolemia and vasodilation
  • activation of sympaticus, renal vasoconstriction, uraemia and azotemia
66
Q

glomerulonephritis

A
  • 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
Q

mechanism of glomerulonephritis

A
  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
Q

nephritic syndrome

A

decrease GF, oliguria, azotaemia, mild proteinuria, water and sodium retention, hypertension, edema

69
Q

nephrotic syndrome

A

increased glomerular permeability, massive proteinuria, hypoalbuminemia, edema, decreased CO, decreased renal blood flow

70
Q

vascular renal disease

A

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
Q

tubulointerstitial renal disease

A
  • 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
Q

mechanism of tubulointerstitial renal disease

A 
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
Q

pyelonephritis

A
  • 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
Q

chronic renal failure

A
  • 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
Q

uremic syndorme

A 
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

Pathophysiology 2 (4 decks)

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