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ED fellowship- Medicine other > Hepatobilary > Flashcards

Hepatobilary Flashcards

1
Q

Discuss Hepatitis A

A

RNA enteroviral picornavirus
Spread via the faecal oral route or through contaminated water or food stuffs.
Not associated with chronic carrier state

Risk factors

1) person to person
- Transmission within households
- sexual transmission
- residential transmission
- day care
2) contact with contamintaed food or water
3) blood transudiosn
4) illicit drug use

The incidence of HAV has declined substantially since the implementation of the vaccination

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2
Q

Discuss clinical features of Hep a

A

Sefl limiting illness- rarely asscoaited with fulminant heaptic failure

Symptoms

  • nausea and vomiting
  • anorexia
  • fever
  • malaise and abdominal pain

Hep A associated with increase risk of preterm labour and gestational complcations

Diagnosis is with IGM

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3
Q

Discuss Hep B

A

Hep B is contained in a 42nm sturcture call the Dane particle. Within this enveloped virion are the viral DNA, DNA polymerase hepatitis B surface angtien and core antigen
Hepatits Be antigen is an immunologically distinct antigen not incorporated into virions instead it is secreted from cells into the serum of infected patients

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4
Q

Discuss diagnosis of Hep B

A

For screening of asymptomatic persons

  • HBsAG
  • hepatitis B surface antiody

Test for IgG HBc in

  • patients with HIV
  • those with hep C infection who are to undergo treatment with direct acting antivirals
  • patients who require immunosupressive therapy
  • blood and organ donors

Testing of anti HBc Allows one to differentiate immunity from HBV vaccination vs recovery from past HBV infection

HbsAG appears in serum 1-10 weeks after an acute exposure -prior to clinical symtpoms characteristic fro acute hepatitis - usually becomes undetetable in 4-6 months. persistance indicates chronic infection

ACUTE HEPATITS
-HBsAG +Ve and presence of IGM hepB core antibody

PAST INFECTION
-Charactersied by antiHBs and IgG anti HBc

IMMUNISATION
-AntiHBS only

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5
Q

Define chronic Hep B

A

Presence of HBsAG in serum longer than 6 months
HBV NDA level greater than 20000IU/ml
Persistent or intermittent elevation in ALT and AST

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6
Q

Discuss management of Hep B

A

Depends on clinical setting – appropriate measures should be taken to prevent infection in all exposed contacts and hep B vaccine should be administered to all household and sexual contacts

Acute treatment is mainly supportive - as a general rule patients with severe or protacted course or those with persistent symptoms or marked jaundice should be treated
-Entecavir or tenofovir are options for monotherapy

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7
Q

Discuss chronic hep C antiviral therapy

A

The goal of therapy in patients with chronic hepatitis c is to eradicate HCV RNA which is predicted by attainment of a sustained virologic response. SVR is associate with 97-100% change of being HCV RNA -ve during long term follow-up

All pateints with virologic evidence of chronic HCV infection should be considered for treatment. Direct acting antiviral therapy are the mainstay of treatment. -multiple regimes for hep c depedning on degree of cirrhosis

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8
Q

Discuss PEP

A

Effective pre and post exposure prophylaxis for HAV and HBV has been avaiable for more than 2 decades

Health care practitioners (HCP) exposured to blood or body fluid should have the wound and sites of contact washed with soap and water

SOURCE PATIENT
-HepBsAg and Hepc Virus RNA status of the source patient should be assessed.

HCP information

  • Dates of Hep B immunization
  • post immunization quantitive titre if known
  • previous testing for HBV and HCV
  • Tetanus Immunization Status
  • Current Medications
  • Current co-morbiditis

Exposure infomration

  • date and time of exposures
  • nature of the exoposure (non intact skin,mucosal, percutaneous, human bite)
  • type of fluid
  • body lcoations
  • For percutaneous injruies (depth of wound, solid vs hollow needle, shapr use in patient)

If HCP not immune and potential expsoure

  • Recieve HBIG and hep b vaccine followed by full course of vaccine
  • HBIG provides antiHBs and generally protects against infection with HBV for three to 6 months.
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9
Q

DIscuss alcoholic hepatitis

A

Accounts for just under 1% of world wide morality
Alcohol and its metabolites are toxic to most organ systems and are largely eliminated by metabolic degradation in the liver

Precise cause is not known is and is likley multifactorial

  • Co-existent malnutrition
  • accumulation of toxic metabolites
  • depletion of glutathione
  • abnormal metabolism of methionine
  • Excessive production of NADH

As alcohol related liver disease progresses beyond steatosis, –> fibrosis, cirrhosis and finally hepatocellular carcinoma may occur.

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10
Q

Discuss ix and management of alcoholic hepatitis

A

Moderate elevation of AST and ALT - compared to viral hepatitis a relative predominance of AST is expected
-raised bili, WBC and deranged coag

Consideration for treatment – remains mostly supportive

  • Alcohol abstinence and withdrawal
  • Hydration
  • Nutrition (thiamine and electrolyte disturbances such as hypophosphataemia and hypomagnesiumia)
  • monitoring for complications (chirrosis )
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11
Q

Discuss cirrhosis

A

Generic term for end stage chronic liver disease characterised by the destruction of hepatocytes and repalcement of normal heaptic architecture with fibrotic tissue and regenerative nodules.

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12
Q

List aetiologies of liver cirrhosis

A

Most common

  • Chronic viral hepatitis (B and C)
  • Alcoholic liver disease
  • Haemochromatosis
  • NASH

Less common

  • Autoimmune hepatitis
  • primary and secondary bilary cirrhosis
  • primary sclerosing cholangitis
  • medications (methotrexate, isoniaid)
  • wilsons
  • alpha 1 antitrypsin
  • coeliac
  • idiopathic portal fibrosis
  • infection
  • right heart failure
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13
Q

Discuss clinical features of cirrhosis

A

Symptoms

  • May be asymptomatic or report nonspecific symptoms such as anorexia, weight loss, weakness and fatigue.
  • Decompensated patients may present with jaundice, pruritis, signs of upper GI bleeding, abdominal distension or confusion

Signs

  • Decresed BP due to reduction in SVT
    1) skin
  • jaundice
  • spider angiomata

2) head and neck
- parotid gland enlargement
- feotr hepaticus

3) Chest
- gynaecomastia –> increased production of androsetnedione and increased conversion of estrone to estradiol.

4) abdo
- ascites - fluid wave, flank dullness to percussion, shifting dullness.
- hepatomegaly
- spelnomegaly
- caput medusae

5) extremity
-palmar erythema
-nail changes
0clubbing
-dupuytrens contracture

6) neuro
- asterixis (seen in uremia and severe heart failure also)

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14
Q

Discuss IX of cirrohsis

A

Transaminases are rarely more than minimally eleavted.
Bili might be raised but usually not until advanced disease is present
Alk phos out of proportion is suggestive of biliary cirrhosis
-Coags
-mild to modereate anaemia and thrombocytopenia
-Albumin

US is routinely used during the evaulation of cirrhosis. 91% sens and 94% spec

CT not commonly used specifically for cirrhosis similar information to that of Ultrasound with added drawback of radiation

MRI sensiitve and specific though not massively superior to US

Liver biopsy is the gold standard for diagnosis

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15
Q

List major complications of cirrhosis

A 
Variceal haemorrahge 
ascites
SPB 
hepatic encephaloapthy 
hepatocellular carcinoma 
hepatorenal syndrome 
hepatorpulmonary syndrome
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16
Q

Describe variceal haemorrhage and risk factors for the same

A

GIT emergency that is one of the major causes of death in patients with cirrhosis

Risk factors

  • seize of varices
  • appearance of varices
  • severity of liver disease
17
Q

Discuss management of variceal heamorrhage

A

-Two wide bore IV lines
-Treat hypotension with initial bolus of crystaloid than rotem guided resus - should be aiming for HB >70 as target unless risk of major adverse event from anaemia ( CAD or signifiacnt ongoing bleeding) than aim for >80
Overtransfusions can worsen bleeding - restrictive transfusion strategies are associated with better outomes
-urgent gastro consult
TXA not indicated for GIB (HALT-IT)

Give PPI IV80mg of pantoprazole
-evidence of active bleeding

If known or suspected oesophagogastric varicela bleeding or cirrhosis

1) -IV ceftriaxone 1g - reduces the risk of mortality, infection and rebleeing)
2) octreotide 50mcg IV bolus followed by 50mcg/hr
3) consider terlipressin a vasopressin analogue with an initial dose of 2mg IV Q4hourly down tirated to 1mg Q4hourly as bleeding is controlled - has been associated with hyponatraemia and should be monitored

Balloon tamponade may be performed as a temporizing measure for patients with uncontrollable haemorrhage due to varices (sengstaken-blakemore tube)

Variceal ligation and beta blockage (propanolol is an effective treatment to prevent rebleeding)
-If rebleeding occurs patients may need a transjugular intrahepatic portosystemic shunt (TIPS) - creats low resistance channel between the heaptic vein and the portal vein - prevents further bleeding

18
Q

Discuss risk stratification tool for GI Bleeding

A

Glasgow, Blatchford bleeding score
-Stratifies upper GI bleeding patients who are low risk and candidates for OPD management

HB
BUN
Initial BP 
Sex
HR >100
Melena
Recent syncope 
Hepatic disease histroy 
Cardiac failure present

ROCKALL score

  • Determines severity of GI bleeding prior to endoscopy - has score for post endoscopy for risk of rebleeding
  • Age
  • shock
  • comborbidities

ADD - diagnosis and major stigmato of recent heamorrhage on scope to score for post enddoscopy score for rebleeding risk

19
Q

Discuss ascites

A

Occurs as a consequence of portal hypertension impaired hepatic lymph flow, hypoalbumineamia and renal salt retention.

Removal of very large quantities of ascitc fluid can result in body fluid and electrolyte abnormaltiies intravescular volume depleetion and HD instability.

If removing large amounts of ascitic fluid colloid infusion is required to avoid adverse CVS, renal and neurohumeral responses

Typically patients are given 6-8 grams of albumin for every litre of fluid removed if over 5 litres is to be taken

20
Q

Discuss spontaneous bacterial peritonitis

A

Defined as an ascitic fluid infection wihtout an evident intrabadoinal surgically treatable source. An elevated ascitic fluid absolute PMN coung (>250) is adeqaute to make a presumptive diagnosis of SBP and start therapy

The pathophysiology of SBP is related to a combination of impaired phagocytic function in the liver and to portal systemic htn - which can cause bowel mucosal oedema, alterations in gut flora and transmural migration of enteric organisms.

E.coli and klebsiela are the most frequently identified organisms.

21
Q

DIscuss clinical features of bacterial peritoniits

A

Shoudl be considered in anyone with the following and advanced liver disease

  • fever
  • abdominal pain m
  • altered mental status
  • abdominal tenderness
  • diarrhoea
  • paralytic ileus
  • hypotension
  • hypothermia
22
Q

Discuss diagnosis of SBP

A 
Diagnosis is made on culture of ascitic fluid. 
>250PMN is consistent with SBP
Send fluids for 
-culture 
-cell count and differential 
-gram stain 
-albumin 
-protein 
-glucose 
-lactate dehydrogenase
-amylase

Need to differentiate SBP from secondary bacterail peritonitis
-Secondary has higher mortality and will have surgical options for treatment
the following ascitic fluid results suggest secondary (Runyon’s critera)
-TOtal protein >1 g/dl (10g/L)
-Glucose <2.8
LDH>upper limit for normal serum
In addition to above polymicrobials culture or bilirubin is suggestive of secondary

23
Q

Discuss management of SBP

A

Ceftriaxone 2g TDS

Renal failure develops in 30-40% if patients with SBP and is a major cause of deaht - this risk may eb decreased with an infusion of IV albumin (1.5g/kg within 6 hours of diagnosis)

High risk patient 
-Cirrhosis and GI bleeding 
-Recurrent SBP  
-Patients with cirrhosis and ascites if the ascitic fluid protein is <1.5g/dl along with either renal impairment (creat >106) or liver failure (child pugh >9 and a bili >3) 
THese should ahve prophylaxis for SBP 
-Bactrim once daily 800/160
-cipro 500mg dailey
24
Q

Discuss Child pugh score

A

Estimates cirrhosis severity –> not as good as Meld NA

Bilirubin

  • <34.2 umol/l
  • 34.2-51.3 umol/l
  • > 51 .3

Albumin

  • > 35 g/l
  • 28-35
  • <28

INR
<1.7
1.7-2.2
>2.2

Ascities
Absent
Slight
Moderate

Encephalopathy

  • nil
  • Grade 1-2
  • Grade 3-4

Grade A <7points ‘

  • life expectancy 15-20 years
  • Abdominal surgery periop mortality 10%

Grade B 7-9

  • indications of liver transplan
  • periop motrality 30%

Grade C >10

  • life expectancy 1-3 years
  • peri op mortality 82%
25
Q

Discuss melds sodium score

A

Stratifies severity of end stage liver disease for transplant planning

Dialysis twice in the past week 
Creatinine '
Bilirubin 
INR 
Sodium
26
Q

Discuss hepatic encephalopathy

A

Clinical state of altered cerebral function resulting from the diseased livers failuer to perform its noral metabolic function

AMmonia is normally absorbed and converted to urea by the liver. IN severe heaptic disease ammonia accumualtes and crosses the BB and combines sequentially with alpha-ketoglutarate and glutamate to form glutamine.

27
Q

Discuss clinical features of hepatic encephalopathy

A

Cognitive findings vary from subtle deficits that are not apparent wihtout sspecialised testing to more over finding with impairment in attention reaction time and working memory

Disturbance in diurnal sleep pattern aer common initial manifestations of hepatic encephaloapthy and typically precede other mental state changes. As hepatic encphaloapthy progresses patients may develop mood changes disoreintation inappropriate behaviour somnolence confusions and unconsciousness.

Neuromuscular impairment in patient with overt heaptic encphealoapthy include bradykinesia, asterixis, slurred speech, ataxia and nystagmus

28
Q

Discuss grading of hepatic encephalopathy

A

Minimal - abnormal results on psychometric or neurophysiological testing wihtout clinical manifestations

Grade 1- changes in behaviour, mild confusion, slurred speech, disorded sleep

Grade 2- lethargy moderate confusion

Grade 3- marked confusion (stupor), incoherent speech, sleeping but arousable

Grade 4 - coma unresponsive to pain

29
Q

Discuss IX of hepatic encephalopathy

A

Ammonia level
LFTs
Coags

alpha fetoprotein

Psychometric testing

  • Number connection test (Reitan test)
  • Psychometric hepatic encephalopathy score
30
Q

Discuss aetiology/precipitant of heaptic encephalopathy

A
  • GIT bleeding
  • Electrolyte abnormalities including hypokalemia and alkalosis
  • Venous thrombosis
  • Ileus and constipation
  • Sedative medications
  • Dehydration and hypovolaemia
  • AKI or CKD
  • INfection
31
Q

Discuss management of hepatic encephalopathy

A

ABCD
Supprotive measures and correction of precipitants

Lower blood ammonia

  • Lactulose 30-45ml 2-4 times a day - titrated to achieve two to three soft stools per day - reduces absorption via somotic carthartic effect and altering the colonic pH
  • If above not effective rifaxim 400mg TDS

Nutrition

  • 30-35 kcal/kg and max 1-1.5g vegetable protein/kg
  • Branch chain amino acid infusions/supplements
32
Q

Discuss hepatic abscesses

A

Fall into two broad categories pyogenic and amoebic

Usually asscoiated with biiary tract obstruction or chloangitis

Organisms are both anerobic and aerobic
- e.coli, klebsiella, pseudomonas and enterococcus, anaerobic strptococci and various bacteroides

Clincal presentation is characterised by onset of high fever, chills, RUQ pain, nausea and vomiting. Acute presentation are the norm

Treat with triples if bacterial

Ameobic abcess are most commonly caused by entamoeba histolytica - treat with metronidizole 750mg PO or iV TDS for 7-10 days
-most serious complications is rupture into adjacent anatomical structures. Involvement of the lung occurs in 20-35% of cases of extrahepatic disease ogten manifesting as massive pleural effusion

33
Q

Describe Budd Chiari syndrome

A

Causes by heaptic venou outflow obsturction located anywhere above the level of the heaptic venules.
Seen commonly in hypercoaguable state such as factor 5 protein s and c thrombophilia antithrombin 3 myeloprolifterative disorder and the OCP

Clinical presenation varies from fulminant heaptic failure in acute high grade obsturction to the insidious onset of jaundice to ascites in more subacute forms

Can be difficult to distinguish fulminant hepatic failure from budd chiari, and viral or tox causes. Important to do so as surgical option to decompress can lead to favourable outcome in budd chiari if done early enough (TIPS)

ED fellowship- Medicine other (15 decks)

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