Medical Abdomen Flashcards
Chronic liver disease
On examination
Inspect: general, hands, face, trunk, ankles
Abdo: inspect/palpate
sig negatives!
Peripheral Inspection
-
General
- Jaundice
- Ascites
- Cachexia
- Tattoos and track marks
- Pigmentation
-
Hands
- Clubbing (esp. in PBC)
- Leukonychia
- Terry’s nails (white proximally, red distally)
- Palmer erythema
- Dupuytren’s contracture
-
Face
- Pallor: ACD
- Xanthelasma: PBC
- Keiser-Fleischer rings
- Parotid enlargement (esp. c¯ EtOH)
-
Trunk
- Spider naevi
- Gynaecomastia
- Loss of 2O sexual hair
-
Ankles
- Peripheral oedema
Abdomen
-
Inspection
- Distension ± Para- / umbilical hernia
- Dilated veins
- Drain scars
-
Palpation
- ± hepatomegaly
- ± splenomegaly
- Shifting dullness
Significant Negatives
- Evidence of decompensation
- Jaundice
- Encephalopathy: asterixis, confusion
- Foetor hepaticus: ammonia and ketones
- Hypoalbuminaemia: oedema and ascites
- Coagulopathy: bruising
- Evidence of SBP: esp. if ascites
- Cause: xanthelasma, pigmentation, KF rings, tattoos
Definition of Chronic liver disease
Progressive destruction of the liver parenchyma over a period greater than 6 months leading to fibrosis and cirrhosis

CLD
Differentials
(common/rare)
- Common
- EtOH
- Viral
- NASH
- Rarer
- Genetic: HH
- AI: AH
- Drugs: methotrexate
History Qs in CLD case
(cases)
- EtOH
- Sexual Hx, IVDU, transfusions
- FH
- Other AI disease: e.g. DM, thyroid
- DH
Investigations in CLD case
Initial work up
(and 2 ‘other’)
Initial Workup
- Urine: dip ± MC+S (? UTI)
- Bloods: FBC, U+E, LFTs, INR, glucose
- LIVER SCREEN!
- Ascitic tap: chemistry, cytology, MC+S, SAAG
- PMN >250mm3 indicates SBP
- US + PV duplex
- Liver size and texture
- Focal lesions
- Ascites
- Portal vein flow
- Other:
- liver biopsy
- MRCP: PSC
CLD
Liver screen
(7-think ‘cause’)
- EtOH: MCV, GGT, AST:ALT >2
- Viral: Hep B and C serology
- NASH: lipids
- AutoAbs: SMA, AMA, pANCA, ANA
- Ig: ↑IgG – AIH, ↑IgM – PBC
- Genetic: caeruloplasmin, Ferritin, α1-AT
- Ca: AFP, Ca 19-9
Treatment of CLD
General/specific (to cause)
General
- MDT: GP, hepatologist, dietician, palliative care, family
- EtOH abstinence
- Good nutrition
- Cholestyramine for pruritus
- Screening: liver screen
- HCC: US + AFP
- Varices: OGD (propranolol+banding, acute UGI bleed: terlipressin)
Specific
- HCV: protease (-) + ribavarin
- PBC: ursodeoxycholic acid
- Wilson’s: penicillamine
- HH: venesection, desferrioxamine
Complications of CLD
(7)
- Varices: β-B, banding
- Ascites: fluid and salt restrict, spiro, fruse, tap, daily wt
- Coagulopathy: Vit K, FFP, platelets
- Encephalopathy: avoid sedatives, lactulose, rifaximin
-
Sepsis / SBP: tazocin or cefotaxime
- Avoid gent: nephrotoxicity
- Hypoglycaemia: dextrose
- Hepatorenal syndrome: IV albumin + terlipressin
Causes of CLD
(common-3/other-5)
Common
- Chronic EtOH
- Chronic HCV (and HBV)
- NAFLD / NASH
Other
- Congenital: HH, Wilson’s, α1ATD, CF
- AI: AH, PBC, PSC
- Drugs: Methotrexate, amiodarone, isoniazid
- Neoplasm: HCC, mets
- Vasc: Budd-Chiari, RHF, constrict. pericarditis
4 important complications of CLD
- Liver failure / decompensation
- SBP
- Portal HTN: SAVE (splenomegaly/ascites/varices/encephalopathy)
- HCC
Child-Pugh Grading of cirrhosis
Evaluates prognosis in Cirrhosis
Graded A-C using severity of 5 factors
- Albumin
- Bilirubin
- Clotting
- Distension: ascites
- Encephalopathy
A.5-6 = [0] 1 yr Mortality
B.7-9 = [20] 1 yr Mortality
C.10-15 = [50] 1 yr Mortality
CLD Decompensation precipitants
(HEPATICS)
- Haemorrhage: e.g. varices
- Electrolytes: ↓K, ↓Na
- Poisons: diuretics, sedatives, anaesthetics
- Alcohol
- Tumour: HCC
- Infection: SBP, pneumonia, UTI, HDV
- Constipation (commonest cause)
- Sugar (glucose) ↓: e.g. low calorie diet
General Management of CLD decompensation
(5)
- HDU or ITU
- Rx any precipitant
- Good nutrition: e.g. via NGT c¯ high carbs
- Thiamine supplements
- Prophylactic PPIs vs. stress ulcers
Important monitoring in CLD decompensation
(3)
- Fluids: urinary and central venous catheters
- Bloods: daily FBC, U+E, LFT, INR
- Glucose: 1-4hrly + 10% dextrose IV 1L/12h
Management of (6) Complications of decompensated CLD
- Ascites: daily wt, fluid and Na restrict, diuretics, tap
- Coagulopathy: Vit K, FFP, platelets
- Encephalopathy: avoid sedatives, lactulose, rifaximin
- Sepsis / SBP: tazocin or cefotaxime
- Hypoglycaemia: dextrose
- Hepatorenal syndrome: IV albumin + terlipressin
PAthophysiology of encephalopathy (CLD)
↓ hepatic metabolic function -> Diversion of toxins from liver directly into systemic system. -> Ammonia accumulates and pass to brain where
astrocytes clear it causing glutamate → glutamine -> ↑ glutamine → osmotic imbalance → cerebral oedema
Presentation of encephalopathy
(5)
- Asterixis, Ataxia
- Confusion
- Dysarthria
- Constructional apraxia
- Seizures
Single key invesigation in encephalopathy (CLD)
Plasma NH4 (raised!)
Teatement of encephalopathy
- Nurse in well lit, calm environment
- Correct any precipitants
- Avoid sedatives
- Lactulose
- ↓ nitrogen-forming bowel bacteria
- 2-4 soft stools/d
- Rifaximin PO: kill intestinal microflora
Hepatorenal syndrome
pathophysiology
(and classification)
Renal failure in pts. c¯ advanced CLF
Pathophysiology: “Underfill theory”
Cirrhosis → splanchnic arterial vasodilatation → effective
circulatory volume → RAS activation → renal arterial
vasoconstriction. Persistent underfilling of renal circulation → failure
- *Type 1:** rapidly progressive deterioration (survival <2wks)
- *Type 2**: steady deterioration (survival ~6mo)
Treatment of hepatorenal syndrome
- IV albumin + terlipressin
- Haemodialysis as supportive Rx
- Liver Tx is Rx of choice
SBP
Presenation
Pt. c¯ ascites and peritonitic abdomen
Complicated by hepatorenal syn. in 30%
SBP: Common organisms
Common organisms: E. coli, Klebsiella, Streps
SBP: 1 key investigation
ascites PMN >250mm3 + MC+S


