lec 2 liver pdf - حسن سالم

Lec 2

كورس ثاني

الدكتور حسن سالم الجميلي

باطنيه

Acute liver failure:

progressive deterioration in liver function and mental changes
progressing from confusion to coma in absence of evidence of
preexisting liver disease.

Lec 2

كورس ثاني

الدكتور حسن سالم الجميلي

باطنيه

. Clinical assessment

1-Cerebral disturbance

(hepatic encephalopathy and/or cerebral

oedema) is the cardinal manifestation of acute

liver failure. Cerebral oedema may occur due to increased intracranial
pressure

-unequal or abnormally reacting pupils, fixed pupils

- hypertensive episodes bradycardia, hyperventilation, profuse
sweating, local or general myoclonus, focal fits or decerebrate
posturing.

-Papilloedema occurs rarely and is a late sign.

nausea and vomiting. Right hypochondrial discomfort

. The patient may be

jaundiced

- death may occur in fulminant cases of acute liver failure before
jaundice develops.

Fetor hepaticus

can be present.

-The

liver

is usually of normal size but later becomes smaller.

- Hepatomegaly is unusual and, in the presence of a sudden onset of
ascites, suggests venous outflow obstruction as the cause (Budd–
Chiari syndrome.

Splenomegaly is uncommon

and never prominent.

Ascites and oedema

are late due to fluid therapy.

West haven classification of H.Encephalopathy

Lec 2

كورس ثاني

الدكتور حسن سالم الجميلي

باطنيه

invex:

PT, bilirubin, Plasma aminotransferase.

Plasma albumin remains normal unless the course is

prolonged. Percutaneous liver biopsy is contraindicated

because of the severe coagulopathy, but biopsy can be

undertaken using the transjugular route if appropriate.

Management

1-high-dependency or intensive care unit

2-Conservative treatment ..GW, mannitol,bowelsterlization by
metronidazole and neomycin.

3- N-acetylcysteine therapy may improve outcome, particularly in
patients with acute liver failure

due to paracetamol poisoning.

4-earlytransfer to a specialized transplant unit . Survival following
liver transplantation for acute liver failure

is improving, and 1-year survival rates of about 60%

can be expected.

Adverse prognostic criteria in acute liver failure:

-Indication for transplant in paracetamol poisoning

Lec 2

كورس ثاني

الدكتور حسن سالم الجميلي

باطنيه

Hepatic encephalopathy

neuropsychiatric syndrome caused by liver disease. As it progresses,
confusion is followed by coma. The

degree of encephalopathy can be graded from 1 to 4,

Examination --a flapping tremor (

asterixis)

inability to perform simple mental arithmetic tasks or

to draw objects such as a star (

constructional apraxia

;

and, as the condition progresses,

hyper-reflexia

and

bilateral extensor plantar responses

When an episode develops acutely, a precipitating factor may be found :

• Drugs (especially sedatives antidepressants)

• Dehydration (including diuretics paracentesis)

• Infection

•Hypokalaemia

• Constipation

• TIPS

•↑Protein load (including GI bleeding)

Lec 2

كورس ثاني

الدكتور حسن سالم الجميلي

باطنيه

Pathophysiology

disturbance of brain function by neurotoxins that are normally
metabolised by the liver. mainly nitrogenous substances produced in
the gut,

Ammonia

has traditionally been considered an important

factor.

Other:

γ-aminobutyric acid

(GABA) as a mediator

octopamine,

amino acids, mercaptans and fatty acids

that can act as

neurotransmitters.

Investigations

1-clinical

2-(

EEG

)shows diffuse slowing of the normal alpha waves with

eventual development of delta waves.

3-The arterial ammonia is ↑

Rx;

1-precipitatingfactors

2-suppress the production of neurotoxins by bacteria in the bowel.

Rifaximin

(400 mg 3 times daily) is a well tolerated,

non-absorbed antibiotic that acts by reducing

the bacterial content of the bowel and has been shown

to be effective..

Lactulose

(15–30 mL 3 times daily) is increased gradually until the

bowels are moving twice daily. It produces an osmotic laxative effect,
reduces the pH of the colonic content, thereby limiting colonic
ammonia absorption,. -

4-Chronic or refractory encephalopathy is one of the main

indications for liver transplantation.

Lec 2

كورس ثاني

الدكتور حسن سالم الجميلي

باطنيه

Viral hepatitis

Clinical features of acute infection

-prodromal illness --headache, myalgia, arthralgia, nausea and
anorexia usually precedes the development of jaundice by a few days
to 2 week.

-Vomiting ,diarrhoea ,abdominal discomfort is common.

-Dark urine and pale stools may precede jaundice.

Exam:. The

liver

is often tender but minimally enlarged. mild

splenomegaly and cervical LAP

Complications

• Acute liver failure

•Cholestatic hepatitis (hepatitis A)

• Aplastic anaemia

• Chronic liver disease and cirrhosis (hepatitis B and C)

• Relapsing hepatitis

Investigations

1-A hepatitic pattern of LFTs

,transaminases

between 200 and 2000 U/L in an acute infection (usually lower and
fluctuating in chronic infections)

bilirubin

reflects the degree of liver damage.

Lec 2

كورس ثاني

الدكتور حسن سالم الجميلي

باطنيه

ALP

rarely exceeds twice the upper limit of normal

Prolong indicates the severity of the hepatitis but rarely exceeds

25 seconds

WBC

=normal with a relative lymphocytosis.

Serological tests

confirm the aetiology of the infection.

Management

→

Most individuals do not need hospital care

→

sedatives and narcotics, which are metabolised in the

liver, should be avoided

→

No specific dietary modifications are needed

→Alcohol should be avoided during the acute illness.

→

Elective surgery should be avoided in cases

of acute viral hepatitis, as there is a risk of post-operative

liver failure.

→Liver transplantation is very rarely indicated for

acute viral hepatitis complicated by liver failure

Hepatitis A

hepatitis A virus

-picornavirus group of enteroviruses.

-highly infectious , spread by the faecal–oral route.

-asymptomatic, excrete the virus in faeces

for about 2–3 weeks before the onset then for a further 2 weeks.

-Infection is common in children

-common in areas of overcrowding and poor sanitation.

- In contrast to hepatitis B, achronic carrier state does not occur.

Investigations

▲

HAV is only present in the

blood

transiently during the incubation

period. Excretion in the

stools

occurs for only 7–14 days after the

onset of the clinical symptoms

▲

Anti-HAV IgM is diagnostic of an acute HAV infection.

▲

Titres of this antibody fall to low levels within about 3 months of

recovery

▲

Anti-HAV IgGis marker of previous HAV infection. Its presence

indicates immunity to HAV.

Lec 2

كورس ثاني

الدكتور حسن سالم الجميلي

باطنيه

MX:

▲

-prevented

by improving social conditions

, especially

overcrowding and poor sanitation

▲

inactivated virus vaccine

..immunization should be considered for

1- chronic hepatitis B or C infections.

infected

close contacts of HAV

those at particular risk, such as

2
patients, the elderly, those with other major disease &pregnant
women.

3- People travelling to endemic areas

▲

Immediate protection by

immune serum globulin

---

1- after exposure

2-outbreak of hepatitis, in a school or nursery those at risk prevents
secondary spread to families.

Three imp.notes:

no role

for antiviral drugs in the therapy of HAV infection

-Acute liver failure is rare in hepatitis A (0.1%) and chronic infection
does

not occur

In adults, a cholestatic phase with elevated ALP levels may

complicate infection

Hepatiti s E

RNA virus

-The clinical presentation and management of hepatitis

E are similar to that of hepatitis A.

- faecal–oral route;

-does

not usually

cause chronic liver disease, although some cases

have been described, usually in immunocompromised patients

epatitis A in that infection

Hepatitis E differs from h

during pregnancy is associated with the development of

acute liver failure, which has a high mortality

-IgM antibodies to HEV are positive.