Final end Flashcards
1
Q
Hepatorenal syndrome
A
- liver cirrhosis, portal hypertension, ascites + edema
- activation of sympaticus, renal vasoconstriction, uraemia and azotemia
2
Q
Nephritic syndrome
A
- immune complexes, lodge in capillaries
- elicit immune response to capilliaries
- increase WBC
- inflammed nad breakdown allowing RBC + WBC to leak through
- protein loss (mild)
- decrease GF
- water and sodium retention
3
Q
Nephrotic syndrome
A
- increase glomerular permeability
- podocytes aren’t working/lost
- protein leaks out (albumin decreased)
- frothy urine
- edema
- increased lipids
- decreased CO
4
Q
causes of prerenal disorder
A
- decreased renal perfusion
- venous pathology
- decreased arterial BP
- increased intrabadominal pressure
5
Q
stages of prerenal disorder
A
- compensatory = maintain normal kidney function. Afferent = dilation, effe = constrict, increase GFR, Na, H2O reabsorption. Increase blood vol + BP, secretion of prostaglandins and NO
- prerenal kidney failure
- decreased GFR as no more dilation and constriction
- strong sympathetic and RAAS activation
- prerenal uremia and azotemia
6
Q
frothy bloat
A
- small gas bubbles produced during fermentation in rumen are separated above ruminal content
- abnormal fermentation
= sudden production of large amount of gas
= gas trapped
= stable foam is formed, eructation canont occur
= rapid expansion - animal + plant influences formation of foam
- salivary mucine is antifoaming but production is decreased
- most common = grazing legume
- less common in dairy cattle
- no separation of gas, foam formed, no eructation, increased pressure in rumen.
= increased rumen motility
= increased pressure + stretching of wall
= hypotonia of rumen
= atony of rumen
death occurs due to suffocation
7
Q
bloat
A
- frothy bloat (primary)
= abnormal fermentation of luminal content - free-gas bloat (Secondary)
= mechanical disturbances
8
Q
hypertrophic cardiomyopathy
A
- inherited disorder
- left ventricular concentric hypertrophy and interventricular septal thickness
- inner diameter of left chamber is reduced - atrial dilatation of increased pulmonary pressure
- stagnation of blood in L. atria predisposes to formation of thrombus
- myocyte degenerative changes and interstitial fibrosis - decreased ventricular dilatation and contractions
9
Q
aortic regurgitation
A
- semi-lunar valve fails to close properly
- left ventricular eccentric hypertrophy -> compensation -> diastolic murmur
- relative insufficiency of mitral valve
- dilation of the left atrium
- pulmonary edema
- hypertrophy and dilation of right ventricle
10
Q
respiratory sinus arrhythmia
A
- change of rate of spontaneous depolarisation in SA node related to respiration
- helps to stabilise CO, allowing the HR increase during inspiration when left ventricular SV decrease
11
Q
supra ventricular arrhythmia
A
atrial extrasystole, supraventricular tachycardia, atrial flutter and atrial fibrillation
12
Q
atrial flutter
A
abnormal herat rhythm occurs when atrial pump rapidly, supra ventricular tachycardia
13
Q
sinus block
A
- disturbances in which impulses are generated in sinus node, cannot be conducted by atrial muscle
- 1 degree - delayed conduction from SA - atrial muslce
- 2 degree - inability to conduct some SA node
- 3 degree- none are conducted
14
Q
AV block
A
- partial/complete interruption of transmission (A->V)
- 1st - delay of conduction, prolonged P-Q interval
- 2nd - some aren’t conducted (Mobitz 1+ 2(
- 3rd inability to conduct
15
Q
cystic fibrosis
A
- genetic disease with abnormally thick mucus production in mucus glands
- lungs and pancreas mostly affected
- airway obstruction, athelectases and infection
- cor pulmonale and resp distress syndrome
16
Q
lung hypertension
A
- lung disease with vasoconstrictive/structural changes in BV
- left heart failure, 2ary to pressure increase in lung veins
- congenital heart malformation
- hypoxia and cor pulmonale
17
Q
chronic obstructive bronchitis
A
- hyper secretion, diffuse obstruction, chronic productive cough due to inflammation, mucosal gland hypertrophy and hypreplasia
18
Q
pleural disease
A
- pleuritis = wet/humid
dyspnea and pain = athetectases - hydrothorax = increased hydrostatic/ decreased oncotic pressure (liver and kidney disease)
- pneumothorax = closed/open/ventile
19
Q
bronchopneumonia
A
from bronchioles to alveoli
- small foci of inflammation
20
Q
neonatal resp distress syndrome
A
- premature partus, piglets and puppies
- insufficient amounts of lung surfactant
- during exhalation, residual vol is exhaled and lungs collapse
21
Q
brisket disease in cattle
A
- severe hypoxic response with vasoconstriction
- tachycardia, jugular veins dilatation, subcutaneous edema in neck
22
Q
lung edema
A
- abnormal fluid accumulation in lungs cardiogenic lung edema - capillary pressure increase, congestive heart failure, increased pressure noncardiogenic - angio-mural edema - capillary damage, ROS production - alveolar pneumocytes type 2 damage - penetration of plasma and erythrocytes clinical signs - cough, dyspnoea, restlessness, tachycardia, foamy sputum
23
Q
atelectasis
A
- aeration failure and lung collapse
- alveolar collapsing disturbs lung circulation
- necrosis, epithelial destruction
1. obstructive, 2 compressive, 3 postoperative
24
Q
lung pneumonia
A
congestive, hépatisation and resolution stage
- fever, hyperventilation, dyspnoea and tachypneoa
25
Q
lung emphysema
A
- destruction of alveolar walls and septa
- alveolar and interstitial
mechanical theory - bronchiolitis, laboured breathing, cor pulmonale, alveolar walls and capillary network distension
biochemical theory - alpha1 antitrypsin, elastine function is lost
consequence - decreased area of gas exchange
- loss of network and elastic fibres
- increased residual vol
- lung hypertension
26
Q
iron deficiency anaemia in pigleta
A
- sow = low permeability of transplacental barrier - milk contains small amount of iron
- piglets = born with very low Fe stores, rapid growth + needs
- environment = pigs raised in confinement without access to soil
pathophysiology = tissue hypoxia, hypothermia, GI inflammation, insufficient Fe supply
clinical signs = decreased appetite, inadequate efficiency of food utilisation, stunts growth, anaemia, pulmonary edema
27
Q
hypersecretion
A
- increased gastric juice secretion
- increased conc of gastrin = acute and chronic gastrin, decrease gastrin catabolism, hypertrophy of tumour G cells
- increased cos of corticosteroid -= acute and chronic stress
- increased conc of histamine = mastocytoma
- consequence = peptic ulceration, inactivation of pancreatic enzymes, deposition of bile salts, diarrhoea and steatorrhea
28
Q
further biotransofmraiton in the liver
A
toxins (non polar) -> intermediate -> end product (more polar)
29
Q
ammonia detoxification
A
- waste product of AA metabol and pther N2 compounds
- formed by AA deamination and urea degradation
- place of origin: intestine, liver and kidney
- SI => protein digestion -> ammonia
- LI => bacteria degradation -> ammonia
goes to portal circulation -> urea cycles -> urea
30
Q
disorders of ammonia detoxification
A
- decreased liver function -> decrease ammonia detoxification
- liver cirrhosis -> NH3 bypass liver -> toxic action of the brain -> hepatic en ephalopathy
31
Q
hepatic encephalopathy
A
- liver failure, means decreased utilisation of ammonia and portosystemic shunting leads to accumulation of ammonia in systemic circulation, readily crossing BBB
- depression, lethargy, ataxia, stupor, coma
32
Q
causes of sideropenic anaemia
A
- decreased intake (newborn)
- decreased absorption ( insufficient secretion of HCl)
- blood loss
- increased demand
33
Q
aplastic anaemia
A
- pancytopenia = anaemia + leukocytopenia + thrombocytopneia
- autoimmune destruction of hematopoeitic stem cell
- causes = mostly idiopathic, infection, drug therapy, toxins ingestion, genetic disorders
34
Q
sideropenic anaemia
A
- when iron becomes limiting for erythropoeisis
- in absence of iron, Hb cannot be product in suff quantities
- microcytic hypochromic anaemia
regenerative - sufficient iron absorption + blood loss in upper GI tract
nonregenerative - concurrent: nutritional iron deficiency + suppress regeneration
iron deficient RBC - shrinkage, membrane blebbing = features of apoptosis
- keratocytes, acathyocytes, schisocyte
35
Q
haemolytic anaemia
A
- intravascular = destruction of RBC within blood vessles
- extravascular - phagocytosis of RBCs
36
Q
hereditary stomatocytosis
A
- alaskan malamute, inherited autosomal recessive trait
- increased osmotic fragility of erythrocytes and shortened lifespan
- membrane cytoskeletal defect
37
Q
pyruvate kinase deficiency
A
- insufficient ATP production
- highly regenerative anaemia
- erythrocyte 1/2 life is shortened
- haemolytic anaemia
38
Q
immune mediated haemolytic anaemia
A
- primary idiopathic IMHA -> mistakingly recognises RBC as foreign and produces autoantibodies against
- secondary -> immune system produces antibodies against erythrocytes by virus, bacteria..
- alloimmune hemolytic anaemia
39
Q
neonatal isoerythrolysis in kittens
A
- type B queen, mate to A or AB toms
- kittens bearting type A antigen
- signs within 24-36hrs
- weakness, tachycardia, ear and tail tip necrosis
40
Q
DIC
A
- multiple clot formation
cause: sepsis, neoplasm, metastatic tumour
41
Q
anaemia in chronic disease
A
- normocytic normochromic anaemia
- most common non-regenerative
- mediated by inflammatory cytokines
- decreased RBC lifespan and decreased RBC prodcution
42
Q
thrombocytopenia
A
- decreased bone marrow production (drugs, infectious agents, necrosis, aplasia)
- increased platelet consumption (extensive acute bleeding + DIC)
- increased platelet destruction (immune mediated destruction)
inherited and acquired
43
Q
von willebrand disease
A
- inherited deficiency
- disorders of primary haemostasis
- spontaneous mucosal bleeding
- slow wound healing
- vWD def = decreased platelet pug formation
- type 1 = deficiency in amount of vWD
- type 2 = relative decreased more severe
- type 3= most severe, complete absence
44
Q
fragmentation hemolytic anaemia
A
- secodndary to vascular disease of DIC
- mehcnaicla trauma
- keratocytes, shcistocytes and cathocytes
45
Q
anaemia due to infectious agents
A
- extravascular hemolysis
- decreased erythropoiesis
- babesia, myocplasma
- breakdown cell membrane
46
Q
oxidant - induced haemolytic anamia
A
- onions (dogs, cats), barassica species (rum), nitrate containing pnlants (rum)
- minerals - sink (dogs), copper (sheep, dogs)
- chemicals - skunk muscle (dogs>cats)
- drugs - acetaminophen (cats,), Vit K (dogs)
47
Q
anaemia of chronic kidney disease
A
- non-regenerative anaemia
- not presen t in all animals with kidney chronic
- decreased erythropoietin production
- increased hepcidin
- decreased rBC lifespan
48
Q
disorders of biotransofmration I liver
A
- decreased inactivation and excretion of endogenous metabolites
- accumulation Imn body -L toxic reaction
- liver cirrhosis - toxins, bypass the liver
49
Q
biotransformation in liver
A
- conversion of endogenyous/ exogenous compounds
- deotoxification = conversion to ineffective metbaolites
- bioactiation = increased toxicity, CCL4 => CCL3
50
Q
mechanism of biotransformation
A
stage 1 = non synthesis = oxidant, reduced and hydrolysis
stage 2 = synthesis = coagulation, methy and acetyl
51
Q
aetiopathogenesis of shock
A
- hypvolemiac = loss of circulation gblood
- cariogenic = disease of myocardium
- distributive = inaqedquate blood vessel adatpion
52
Q
disorders of haemostasis
A
- acquired disroders -> due to underlying disease (old animals)
- inherited (young) (dog) - von willebrand and haemopilhilia
53
Q
pure red cell aplasia
A
- absence of identifiable erythroid precurorsors
- only erythroid line is affected
- severe non-regenerative normocytic normoochromic
- primary/secondary
54
Q
cariogenic shocks
A
disease of myocardium ,myocardial infarction and pulmonary embolism
