Liver Diseases Flashcards

1
Q

Exam of the Liver

A

It is located deep in the diaphragmatic dome, asymmetrically

Phys exam is impossible

Ancillary:

  • US and US guided biopsy
  • Nuclear scintigraphy
  • Biopsy
    • Clincopatho exams- specific and non-specific indicators of liver disease
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2
Q

Some notes about US

A

It is limited because the liver is covered by the lungs

Must compare the echogenicity of the spleen and liver

At the 7th ICS on the left- the left liver lobe and spleen are overlapping, this is a good site for biopsy

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3
Q

Clinicopatho exams: specific indicators of liver disease

A

SDH (not stable in the blood)

GGT

Bile acids

Arginase

GLDH

Direct bilirubin

Ammonia

Bromosulphthalein half-life

Branched chain aa to aromatic aa ratio

Urine bilirubin

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4
Q

Clinicopatho exams: Non-specific indicators of liver disease

A

Total and indirect bilirubin

LDH-3

AST

(ALT) conc is v low in Eq

ALP

Decr in blood urea nitrogen

Globulins

decr Albumin

decr Glucose

PTT, APTT (as these are produced in the liver)

Triglyceride

Incr or decr WBC’s

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5
Q

Urine Bilirubin

A

The total doesn’t give you info about the fractions!

Direct=conjugated, indirect=unconjugated

Incr direct is more reliable, but both should be measured

Incr indirect: anorexia, haemolysis, intestical obstruction

  • Prehepatic icterus: incr indirect (direct may incr slightly)
  • Hepatic: Liver disease/damage!! Both increase, esp indirect, direct is less than 25% of the total
  • Posthepatic: cholestasis: direct incr, more than 30% of total

Normal amount does NOT rule out liver disease

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6
Q

Significance of GLDH and Bile acids

A

Are elevated with hepatopathies!!!

Indicate gross liver function

**because total bile acids are a FUNCTIONAL parameter- they indicate gross liver function- the other enzymes may only indicatr liver damage

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7
Q

Clinical signs of hepatic insufficiency

A

Because of large capacity: Greater than 80% of mass must be affected before clinical signs!! similar to kidneys in this case

Good regenerative properties

Disease may be present without insufficiency

Diseases are not necessarily manifesting

  • Depression
  • Anorexia
  • Colic
  • HEPATIC ENCEPHALOPATHY
  • Weight loss
  • Icterus
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8
Q

Less common signs of hepatic insufficiency

A

photosensitization: primary liver, secondary skin! Dermal acc of phylloerythrin (this should be removed by a healthy liver)

Dx

Bleeding

Ascites

Dependent edema

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9
Q

Rare signs of hepatic insufficiency

A

Steatorrhea

Tenesmus

Generalized seborrhoea

Pruritis

Endotoxic shock: decr clearance of toxins from portal circ

Polydypsia

Pigmenturia- from Br or Hgb

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10
Q

Hepatoencephalopathy

A

If neuro symptoms- always run normal bloods to rule it out! kidney failure can also display neuro signs when urea adn creatinine are not excreted

Depression

Yawning

Ataxia, paresis

Circling

Forward walking

Dementia/confusion

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11
Q

Treatment of liver disease

A

Diet!! low protein- give more branched chain aa’s because the aromatic aa’s are already high. Also decr oil and fat

IV fluids and electrolytes: cover acid-base requirements

IV glucose

IV brached chain aa’s

Vitamins, mineral oil

Oral neomycin (not usually given systemically) to decrease NH3 prod in gut so that less is being abs!

Sedatives

Protection from sunlight- photosens!!

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12
Q

Theiler’s disease

A

Serum associated hepatitis

Horse usually had serum product a few weeks before signs

Common cause of acute, diffuse hepatic necrosis in adults

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13
Q

Clinical signs of Theiler’s disease

A

Adults

Peracute/acute onset of signs of hepatic failure

Usually develop hepatoencephalopathy very quickly

Anorexia

Fever

Icterus

Colic

Dependent edema

Haem diathesis

Photoderm

Sudden death

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14
Q

Lab results of Theiler’s disease

A

Incr direct and indirect bilirubin

Incr GGT, AST and SDH

Incr bile acids

Glucose: incr, decr or stays the same

Decr BUN

Prolonged clotting

Albumin normal

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15
Q

Diagnosis of Theiler’s disease

A

History (serum/plasma few wks prev)

Abrupt onset of the clinical signs

Liver biopsy: necrosis, hepoptosis and haem!

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16
Q

Theiler’s disease: treatment and prognosis

A

Supportive

Sedation- mania

Usually stabilise withing 2 wks and then the liver regenerates

Euth if mania persists after initial sedation and glucose

17
Q

Tyzzer’s Disease

A

Clostr. Piliforme

1-6 wks foals

Acute depression

Loss of suckling reflex

Fever, tachycard, tachypnoea

Icterus

Recumbency

Seizures

Coma

Progresses to death v quicly

18
Q

Main causes of icterus in foals

A

Sepsis

Neonatal isoerytholysis

Tyzzer’s- clinical signs on day 2/3

Lepto

19
Q

Theiler’s disease: diagnosis and treatment

A

Difficult diagnosis: age, icterus, conc of liver parameters.

Only definite by necroscopy

Treatment: supportive, penicillins, TTC’s (usually ineffective)

20
Q

Pyrrolizidine alkaloid toxicosis

A

Plants!! Senecio, Crotalaria RAGWORT

Ingestion of them for up to 4 mnths

Usually source is contam feed

21
Q

Pyrrolizidine alkaloid toxicosis: Clinical signs

A

Depression

Weight loss

Icterus

Photoderm

Hepatoencephalopathy

22
Q

Pyrrolizidine alkaloid toxicosis: treatment

A

Remove contam feed

Supportive

Poor prognosis

23
Q

Cholangiohepatitis

A

Bact coming from intestines, enter the bile ducts

Mainly adults

Foals with gastroduodenal ulcer disease: reflux of duodenal contents into the bile ducts

24
Q

Cholangiohepatitis: clinical signs

A

Non-specific:

Fever

Icterus

Colic

Incr hepatic enzymes

Leucocytosis and neutrophilia

25
Q

Cholangiohepatitis: diagnosis

A

US!!

Dilated bile ducts- doppler necessary to differentiate from the vessels

Liver biopsy: should take 3 samples: preserve one in formalin and one in physio saline. Conduct culture- will show bact so you can then give appropriate AB’s

26
Q

Cholangiohepatitis: treatment

A

Trimethoprim/ sulphonamides

Enrofloxacin

Supportive therapy

27
Q

Cholelithiasis

A

Stone formation in the biliary ducts

Bact inf usually

Colic, fever, icterus

Lab: incr fibrinogen, GGT and ALKP

Diagnosis: US, biopsy and culture

28
Q

Cholelithiasis: treatment

A

Long-term broad spec AB’s

DMSO

Surgery

Shock wave therapy?

29
Q
A