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27 Cards in this Set

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MECHANISM: Jaundice
Failure of metabolism or excretion of bile
= Yellow colouration of tissues owing to bile paigments
MECHANISM: Bleeding
Failure of hepatic synthesis of clotting factors
= Easy bruising + Prolonged clotting time of blood (↑PTT)
MECHANISM: Oedema
Failure of hepatic synthesis of albumin
-> ↓ Oncotic pressure in plasma/blood vessels
-> Osmosis of fluid out of blood vessels
-> Extravascular swelling of water
MECHANISM: Ascites
Low serum albumin + portal hypertension
-> Osmosis of fluid out of blood vessels
-> Fluid in peritoneal cavity
MECHANISM: Gynaecomastia + Testicular atrophy
Failure of liver to detoxify endogenous oestrogens
= Enlarged male breasts + Testicular atrophy
MECHANISM: Hepatic Encephalopathy
Failure of liver to detoxify ammonia + excitatory amino acids (from protein breakdown)
= Altered consciousness, lack of coordination, may lead to coma
MECHANISM: Haematemesis and or Melaena
Portal hypertension
-> Bleeding from oesophageal varices or per rectum
= Vomiting blood and/or passing bloody stools
Lab evaulation of liver disease

Name serum measurements for:

Hepatocyte integrity
Cytosolic hepatocellular enzymes:
AST,
ALT,
LDH
Lab evaulation of liver disease

Name serum measurements for:

Biliary system
Bile substances:
Serum bilirubin (total, conj. and unconj.),
urine bilirubin,
serum bile acids

Plasma membrane enzymes (from damage to bile analiculus): Serum ALP,
GGT,
5’nucleotidase
Lab evaulation of liver disease

Name serum measurements for:

Hepatocyte function
Proteins secreted into blood: Serum albumin,
PT

Hepatocyte metabolism:
serum ammonia,
aminopyrine breath test,
galactose elimination (IV injection)
Name 5 most common patterns following hepatic injury
- Hepatocyte degeneration and intracellular accumulations (cell swelling; accumulation of fat/copper/iron)
- Hepatocyte necrosis and apoptosis
- Inflammation (steatohepatitis, infective)
- Regeneration
- Fibrosis
Describe Hepatic Failure
Most severe consequence of liver disease.
Result of
- Sudden + massive destruction (i.e. fulminant hepatic failure)
- More commonly: End-stage progression/chronic liver disease

Results when 80-90% of hepatic functional capacity is lost

Transplant gives best prognosis

Mortality w/o transplant = 80%
List and describe 3 causes of Hepatic Failure
1) Acute liver failure
Acute liver illness associated w/ encephalopathy within 6 months of initial diagnosis
- Fulminant when encephalopathy occurs within ~2 wks of jaundice
- Sub-fulminant if ~3 mths after jaundice
Cause: Massive necrosis
- Usually drug/toxin-related (e.g. paracetemol), or immune-mediated hepatocyte destruction (e.g. viral hapatitis)

2) Chronic liver disease
Most common cause
End-stage of relentless chronic hepatitis, ending in cirrosis

3) Hepatic destruction w/o overt necrosis
Viable but dysfunctional hepatocytes
(e.g. tatracycline toxicity or acute fatty liver of pregnancy)
CLINICAL FEATURES: Liver Failure
Same, regardless of cause

- Jaundice: Almost inevitably occurs
- Hypoalbuminemia: predisposition to peripheral edema
- Fetor hepaticus: Breath smells "musty" or "sweet & sour"
(Related to
- GIT bacteria -> Formation of mercaptans
- Shunting of splanchnic blood from portal -> systemic circulation)
- Palmar erythema
(Impaired oestrogen metabolism -> Local vasodilation)
- Spider angiomas
(Hyperestrogenamia -> Central, pulsating, dilated arteriole; small vessels radiate from it)
- Gynecomastia, hypogonadism
(Hyperestrogenamia)
Life-threatenting complications of Hepatic Failure
Very high risk of cencephalopathy + multi-organ failure

Respiratory failure (w/ pneumonia & sepsis)

Renal failure (major killer)

Coagulopathy
(Impaired hepatic synthesis of clotting factors)
-> Can lead to MASSIVE GIT bleeding (death usu. occurs in weeks -> months)
Define Hepatic Encephalopathy
Spectrum of distrubances in consciousness, ranging from
- subtle behavioural abnormalities,
- to marked confusion and stupor
- to deep coma/death
Associated signs of Hepatic Encephalopathy
Rigidity
Hyper-reflexia
Asterixis (i.e. Hepatic flap)
MECHANISM: Hepatic Encephalopathy
CNS/neuromuscular dysfunction thought to be related to:

Ammonia build-up
-> Impaired neuronal function + promotes brain oedema
(Reversible)
Dx: Hepatic Encephalopathy
Number connection tests,
line tracing tests,
serial dotting test,
digit symbol test,
digit symbol
test,
block design test
Life-threatening complications of hepatic failure:

Hepatorenal Syndrome

Definition
Renal failure in patients w/ severe chronic liver disease, with no known intrinsic causes of renal failure.
Incidence is 8%/yr in patients with cirrhosis and ascites.
Life-threatening complications of hepatic failure:

Hepatorenal Syndrome

Characteristics
Usually precipitated by:
Infection,
GIT hemorrhage,
or major surgery

Heralded by
drop in urine output,
rising BUN/creatinine,

Eventually develops into:
Na retention,
impaired free-water excretion,
↓ renal perfusion/glomerular
fltration.
Life-threatening complications of hepatic failure:

Hepatorenal Syndrome

Prognosis + Tx
Median survival =
2 weeks (rapid-onset)
to 6 months (insidious onset)

Tx = Transplant
Life-threatening complications of hepatic failure:

Hepatorenal Syndrome

Major diagnostic criteria
Hepatic failure,
portal HTN,
creatinine > 1.5mg/dL or GFR <40 mL/min,
no shock/ongoing bacterial infection/nephrotoxic agents or fuid losses,
no improvement after diuretic
withdrawal/IV saline,
proteinuria,
normal renal US
Life-threatening complications of hepatic failure:

Hepatorenal Syndrome

Proposed therapies
Liver transplant,
TIPS (Transjugular intrahepatic portosystemic shunt),
vasoconstrictors + albumin,
renal vasodilators,
renal replace-
ment therapy
Life-threatening complications of hepatic failure:

Hepatopulmonary syndrome

Definition
Clinical triad of
1. chronic liver disease,
2. hypoxemia (usually V/Q mismatch),
3. intra-pulmonary vascular dilatations (IVPD)
Life-threatening complications of hepatic failure:

Hepatopulmonary syndrome

Mechanism
Vasoactive substances, especially enhanced NO production.
Life-threatening complications of hepatic failure:

Hepatopulmonary syndrome

Clinical features
↓ arterial O2 saturation and ↑ dyspnoea on moving from supine to upright.

Oxygen therapy can help

Transplant is only curative treatment