causes, increased/decreased parameter Flashcards by Christine Hyldmo

causes of increased permeability of vessels due to non inflammatory causes

increased hydrostatic pressure of blood
- right sided heart fail
- liver hypertenion, fail, cirrhosis
- blockage of blood vessel
- renal fibrosis
decreased plasma colloid oncotic pressure
- decreaseof plasma albumin
impended lymphatic flow
hormonal effect
- aldosterone, ADH

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causes of increased permeability of vessels due to inflammatory causes

bacterial toxins
viral effects
parasitic toxin
inflammatory mediators

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causes of development of transudate

increased vessel permeability
increased hydrostatic pressure of blood
decrease of plasma colloid oncotic pressure
impended lymph flow
hormonal effects

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causes of development of exudate

increased permeabillity of vessels due to inflammatory cause
- bacterial, viral, parasitic, inflammatory mediator
increased migration of phagocytes
increased proliferation of mesothelial cells
increased production of inflammatory proteins

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major causes of septic exudates

trauma of cavity wall
proliferation and overgrowth of bacteria through walls of organs
- pneumonia, ileus, pancreatitis, pyometra
internal perforation of organs
- esophageal, gastric, small intestines, gall bladder, urine bladder
haematogenous or lymphatic spread of bacteria
- actinomyces, actinobacillus, nocardiosis

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major causes of non septic exudates

Virus - FIP
parasites: toxocara, dirofilaria immitis/repens
fungi: systemic mycosis on pleural wall
rupture of gall bladder: bile pigments seen in cells
urine bladder rupture
secondary inflammation process due to neoplasms or tissue necrosis
apperance of lymph: blockage of lymph vessels

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causes of development of modified transudates

long term stasis of fluid in cavities cause necrosis on neighbour tissue - secondary inflammation
in beginning of developing highly exudative process
if blood appear in cavity: trauma, rupture, coagulopathy, thrombocytopathy, bleeding neoplasms
neoplastic processes: carcinoma, adenocarcinoma, lymphoma,

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causes of neutrophil pleocytosis

bacterial meningitis
parasitic meningitis
granulomatosus meningioencephalitis
steroid responsive meningitis-arteritis

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cause of high eosinophil granulocyte count

eosinophilic meningioencephalitis

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causes of the proliferation of mixed cell population

viral encephalitis - distemper, lymphocyte count above 80%
GME: macrophages and neutrophils
fungal encephalitis: mononuclear, neutrophil, eosinophil
haed or spinal cord trauma: neutrophil
toxoplasmosis: lymphocytes

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causes of increased lactate concentration

bacterial meningitis
subarachnoid bleeding
ischemic attacks

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local and general consequences of ileus

local

intestinal spasm onto irritant
intestinal content not able to go aborally
- putrefaction
- water influx
intestine empty behind ileus
- walls stick together
vessels copressed at site of ileus
stagnant hypoxia
- behind block of venous flow
ischemic hypoxia
- after block of arterial flow
local anaerobic GL and lactic acidosis at site
- tissue necrosis
- bacteria out in abdomen
fluid accumulation infront of block
- water into abdomen

general

water filtrated through vessels into abdomen
- ascites, bacterial peritonitis
vomiting due to antiperistalsis
bacterial overgrowth
- gr- endotoxins into blood: endotoxaemia, shock
- gr + exotoxins: bacteraemia, sepsis, peritonitis
dehydration
hemmorhaghe in lumen - blood loss
stress, adrenalin effect
- intestinal atonia due to adrenalin
- no stimulus for emptying gall bladder
enlarged gall bladder
- no anti endotoxic effect
chronic cases: pancreatitis, liver damage
- due to intestinal hypoxia and bacteria
lactic acidosis
hypovolemia, shock
decreased renal function
mixed acidosis
hypokalaemia: muscle weakness, resp depresso
- hyperkapnia, hypoxaemia, resp acidosis

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haematological changes in acute pancreatitis

polycythaemia due to dehydration
degradation of red blood cells: memebrane damage due to enzymes
anemia: in chronic or severe cases
leukocyosis
neutophilia or penia, left shift
leukemoid reaction

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increased alphaamylase in what cases

acute ancreatitis
acute, subacute kidney failiure
FIP, other immune mediated diseases
lymphoma, myeloma
DM - macroamylasemia
ileus
gastric or intestinal perforation
parotitis
chronic enteritis

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increased lipase activity in case of

acute pancreatitis
acute, subacute kidney failiure
ileus
gastric or intestinal perforation
chronic enteritis

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amylase and creatinin changes of pancreatitis

urine amylase increase
urine creatinin increase
plasma amylase increase
plasma creatinin dont change (may increase)

amylase and creatinin changes in kidney failiure

urine amylase decrease
urine creatinin decrease
plasma amylase increase
plasma creatinine increase

causes of increased Br 1 level in serum

excess production of Br 1 due to increased RBC destruction
- acute hemolysis
- absorption of hemoglobin after large hemmorhage, haematoma - resorption icterus
- transfusion of stored blood
decreased uptake of Br1 from blood by liver cells
- impaired hepatic function
- acute hemolysis
decreased rate of conjugation of Br1 by liver cell
- impaired hepatic function

causes of increased Br 2 in serum

a few days after severe acute iv hemolysis
decreased excretion from liver cells
- impaired liver function
obstruction of bile canniculi within liver
- inflammation causing swelling
- fibrosis
- impaired hepatic function
rupture of biliary vessels, duct or gall bladder

causes of increased BSP retention

primary liver fail
- cirrhosis
- tumor
- lipidosis
- lipid mobilisation syndrome
decreased hepatic perfusion
- right sided heart fail
- portosystemic shunt
- arteriole-venous fistula in liver
- block of portal vessels
other
- decreased UDP-glucuronyl transferase activity in liver cells

causes of increased bile acid level in blood

liver injury, hepatic cell damage
- increased outflow to blood of bile acids from liver cells
bile duct obstruction or bile endothelial cel damage
- decreased secretion of bile acids to bile
- increased outflow to plasma
decreased liver function, low uptake
biliary stasis
portosystemic shunt

causes of decreased bile acid level in blood

decreased absorption from intestines
- intestinal wall damage
- surgical removal of ileum
- lymphangiectasia
severe liver cirrhosis
- decreased synthesis

causes for blood urea concentration increase

prerenal

GI:
- increased protein intake
- increased bacterial production / dysbacteriosis
- rumen alkalosis / poor energy status
- internal bleeding
protein catabolism
- starvation
- haemolysis
- hyperthyroidism
- fever
- (SIBO)
perfusion
- strangulation of A. Renalis
- heart fail
- dehydration
- low BP
- shock

renal

embolism inside kidney
CKD - fibrosis
hypoplasia
polycystic kidney disease
amyloidosis
kidney tumor
glomerular nephritis
NSAIDs

postrenal

obstruction of kidney pelvis, urether, urethra, bladder
rupture

causes of blood urea decrease

impaired liver function: decreased urea synth, increased NH3 level
Haemodilution / hyperhydration
decreased protein intake: starve, anorexia

increased blood creatinine

_prerenal_ * muscle * rhabdomyolysis * rhabdomyosarcoma * trauma * myositis * necrosis * GI: increased protein intake * perfusion: * A. Renalis strangle * heart fail * dehydration, low BP, shock _renal_ * embolism inside kidney * CKD - fibrosis * hypoplasia * polycystic kidney disease * amyloidosis * kidney tumor * glomerular nephritis * NSAIDs _postrenal_ * rupture of kidney, urether, bladder, urethra * (obstruction do not cause!!)

causes of decreased urine pH

* metabolic and respiratory acidosis: increased h excretion * vomiting: Na+ reabsorbed wih HCO3, less hco3 in urine * hypokalaemia: increased h excretion (na/k) * acidic drugs * distalis renalis tubularis acidosis: low hco3 excretion * abomasal displacement * toxicosis with acidifying agents

what changes if there is liver damage

* decreased osmotic pressure * increased ESR * increased PT * hormonal imbalance * increased enzymes in blood * coagulation disorders * decreased TIBC - decreased transferrin synthesis

causes of increased ammonia in the blood

* impaired liver function * decreased urea production * cirrosis * neoplasm * portosystemic shunt * lipidosis * ruminal alkalosis - ammonia toxicosis * protein overload * intake of rotten feed * hypomotility * intestinal overgrowth of ammonia producing bacteria * congenital enzymopathy

causes of increased AST

causes of ALT increase

* liver * cirrosis * chronic active hepatitis * cholangiohepatitis * virus hepatitis * lipidosis * bile duct obstruction * tumor, neoplasm * GCC, NSAIDs * other * pancreatitis * septicaemia * neoplasm * cu storage disease * haemolysis

GLDH increase

* liver: svere damage that break mitochondria * cirrosis * cholangiohepatitis * chronic ative hepatitis * liver tumor * lipidosis * bile duct obstruction

ALKP increase

* bone originated * young dogs, newborn, preggo * bone tumors: osteosarcoma * osteomyelitis * bone fractures, healing of fractures * paraneoplastic: lymphoid, lung, hepatic tumours * liver originated * cholestasis, intra/extra hepatic bile obstruction * bile acids * acute hepatic necrosis * liver cirrhosis * cholangitis * hepatic lipidosis * drugs: barbiturates, salicylates * increased SIAP: hyperadrenocorticism, chronic stress

GGT increase

liver originated * cholestasis, intra/extra hepatic bile obstruction * bile acids * acute hepatic necrosis * liver cirrhosis * cholangitis * hepatic lipidosis * drugs: barbiturates, ethanol

causes of increased urine pH

* feeding carnivores: transient increase * slight metabolic alkalosis, compensated by kidneys * UTI caused by urease producing bacteria * break down urea to ammonia * metabolic and respiratory alkalosis: decreased H+ excretion * proximal renal tubular acidosis: HCO3 excretion * alkalizing substances, overload of bicarbonate or lactate infusion * long storage time, urea decompose to ammonia * cats stress