liver and gall blader Flashcards
gall blader
right upper quadrant with the liver, ependice
what the difference in pain in gall bladder vs. gall stone
s
gall stones
Stones composed of chemicals from Bile Three major types: Cholesterol Pigment Mixed 500K people have surgery each year in USA 20% of People > 65 have stones
gall stones
know the risk factors!!!!!! the f words
75% are Cholesterol Stones Found in GB Often solitary Usually round Risk factors: Fat Female Forty Fertile Flatulent 20 - 25 % are Pigment Stones May have other components as well (Mixed): Calcium Bilirubin + Cholesterol or Calcium Salts Multiple, Faceted 10 – 50 % Radio-opaque Risk factors: Hemolysis Infections
nature of the pain
gall stones: mechanical obstrucion- peristaltic
in inflammation: aching pain- stays
clinical features of liver disease
Most Asymptomatic
Cholecystitis
RUQ Pain
Fatty Food Intolerance
Obstruction
Colic
Jaundice
two types:
obstruction, perfuration
know
structure-function liver
Secretory
Bile
Conjugating
Bilirubin, drugs, toxins (detoxifying)
Metabolic
Fat, protein, carbohydrate
Liver damage interferes with these functions and is reflected in blood chemistry
usually has non specific symptoms
JAUNDICE
Yellow discoloration of mucosa, skin etc due to bilirubin pigment deposition
Total serum bilirubin > 35-51 umol/L
normal is less than 5
usually means liver desease but if not there doesnt mean they dont have it
Pre-hepatic
Excess bilirubin production e.g. Hemolysis
Hepatic
Liver disease due to viruses, drugs, alcohol, Cirrhosis
Post-hepatic
Obstruction to bile flow: gall stones, cancer pancreas
Aching right upper quadrant pain: Stretching of the liver capsule General feeling of being unwell General reduction in liver function Loss of appetite Reduction in liver functions
Clinical features of liver disease
acute!!!!!!!!!!!!!
Acute
Systemic features of illness - fever, malaise
Jaundice
Right upper quadrant pain
Itching in cholestatic injury
(bile goes into blood (bile salt) and get deposited in the skin
Symptoms of liver failure (bleeding, coma)
Clinical features of liver disease
chronic
Chronic Asymptomatic Vague complaints of being unwell Chronic persistent elevation of liver enzymes when lab. tests are done Symptoms of liver failure
very difficult to diagnose compared to acute
What is the purpose of further workup?
Determine Acute vs. chronic < or > 6 months Determine Hepatocellular vs. Cholestatic Damage to liver cells vs. obstruction to bile flow Find Causes Predict and manage Outcomes
What to do next?
questions and investigation
Further questions and physical examination
History
Duration ( > 6 months)
Drugs, alcohol, sex, transfusion, foreign travel, others.
Physical
Jaundice, complications, others
Investigations CLINICAL CHEMISTRY BILIRUBIN, ENZYMES, ALBUMIN, ETC. IMMUNOLOGICAL TESTING ANTIBODIES LIVER BIOPSY E.g. core biopsy Risks: Bleeding, Biliary peritonitis IMAGING
Hepatocellular vs. Cholestatic injury
Liver cell damage (reversible to irreversible; the latter from single cells to large areas) Intracellular enzymes (transaminases!!!!!!!!!!!!) leak out (level in blood will rise)
Bile flow obstruction
Bilirubin (Jaundice), bile salts (Itching) accumulate and an enzyme alkaline phosphatase!!!!!!! is released from biliary channels
first test: look for these two enzym : alc- bile flow problem,
his investigation
Bilirubin – High Transaminases- high Alkaline phosphatase – normal Albumin – normal PT (INR) – high Dependent upon factor VII (coagulation factor) What we know so far: Acute hepatocellular injury
Next step
Identify the underlying cause
3 main causes
viruses, alcohol, drugs
Identifying underlying cause; SEX, DRUGS & ALCOHOLAdditional findings from history and physical & investigations
Alcohol No history of alcohol abuse No physical findings of alcoholism GGT(gamma glutamyl transpeptidase) – not elevated Drugs / Toxins No history of exposure Ischemia No history or physical findings suggestive of ischemia
Viruses Serology (antigens and antibodies) Negative for HAV HBV HBsAg + Anti HBcAg + anti-HBeAg + Negative for HCV
OUTCOMES OF LIVER INJURY- acute
Acute
Complete recovery (about 90%)
Chronic liver disease
Death from liver failure
Most important predictor of outocme is Prothrombin time (INR)
OUTCOMES OF LIVER INJURY- chronic
Chronic
may Recovery (complete or with reduced function)- but not very common
Cirrhosis
Liver cancer
Death from liver failure
Most important predictor of outcome is the underlying cause
HEPATITIS - Acute and Chronic
Viruses
Hepatotropic viruses: A, B, C, D, E
Others: Herpes, HIV, CMV
Alcohol
Drugs
Others
Chronic hepatitis may be caused by autoimmune and metabolic conditions
VIRAL HEPATITIS: CLINICAL EFFECTS
Preicteric (before jaundice) phase Acute infection : Fever, anorexia, Nausea, Vomiting. Epigastric discomfort, muscle pain, rash Hepatic enlargement and tenderness Revolted by tobacco Icteric (during jaundice) phase Jaundice increases for 1-2 weeks, then decreases: Dark urine, pale stool Leukopenia followed by lymphocytosis Splenomegaly (mild)
VIRAL HEPATITIS B DNA virus- very bad to get
DNA virus (complete virion: Dane particle)
Core: DNA polymerase in a protein coat - HBcAg, associated with HBeAg)
Surface protein coat; HBsAg
Hepatitis B
Transmission: Blood and Sex 40-180 days incubation Relatively serious illness Diagnosis: Clinical features and determining antigen and antibody profile in the serum Recovery: 90% full recovery; 10% complications Liver failure, Chronic hepatitis, Cirrhosis, Carrier state, Cancer
VIRAL HEPATITIS A
RNA virus- best to get
Fecal-oral spread Sewage, contaminated food, shellfish Sporadic or endemic Children in underdeveloped countries tourists Short incubation period (15- 45 days) Mild illness, full recovery, No chronic or carrier state
VIRAL HEPATITIS C RNA virus
Spread: Blood, venereal Often asymptomatic 15-150 days incubation Clinical course similar to Hep B (less severe usually) Fluctuating liver chemistry Tendency to chronicity (cirrhosis)
the worst to get - can never get rid of
FATTY CHANGE (STEATOSIS)
Normally, liver takes up fats and incorporates these into lipoproteins for export.
Steatosis: Accumulation of fats (triglycerides) in liver (5kg instead of 1.2kg- can happen in 24hours- gets white)
Usually asymptomatic or vague discomfort of pain in the right upper abdominal quadrant
Fatty Change (Steatosis)
Fat can accumulate in cells as:
Macrovesicular (single large droplet)
Alcohol, Toxins -CCl4, Steroids, Drugs
Microvesicular (multiple small droplets)
if stop drinking can go back withiin 24 hours but if do it too often then the cells can burst- causes inflammation- acute can come and go in 24hours
His investigations
Test results Bilirubin – Mildly High Transaminases- high Alkaline phosphatase – normal Albumin – slightly low PT (INR) – mildly reduced What we know so far: Chronic hepatocellular injury
Next step Identify the underlying cause Given the history GGT high Liver biopsy
Alcoholic Liver Disease
Common cause of acute / chronic liver disease
Spectrum:
Fatty change
Hepatitis with Mallory hyaline
Fibrosis / Cirrhosis
Multifactorial
Diversion of metabolic resources
Direct hepatotoxicity
Stimulation of collagen synthesis
Similar changes outside of alcohol: Non-alcoholic steatohepatitis (NASH)
Obesity, rapid weight loss, diabetes, drugs
abnormal accuamulation of neutrofils, alcohol
transaminase
liver cell damage
CIRRHOSIS
Generalized hepatic fibrosis & regenerative nodules.
Not a specific disease (end-stage organ damage)
Relatively inefficient organ: relationship between vessels and cells is less than optimal
Causes are the same as those of chronic liver injury
Following liver cell necrosis, there is replacement fibrosis
Regenerative nodules form
Active cirrhosis: fibrosis + continuing inflammation
repeated apesodes of cell injury- bumps are liver cells trying to regenerate
chronic inflammation- scarring - hardening of the liver
fibrous tissues contract- smaller
bile cant go through ducts
structuraly abnormal and functionally abnormal
active cirrhosis- continuous damage and inflammation
CIRRHOSIS: COMPLICATIONS
PORTAL VENOUS OBSTRUCTION leading to PORTAL HYPERTENSION
HEPATIC FAILURE
LIVER CELL CARCINOMA (~ 10%)- due to all the regeneration
veins: hemorrhoids, varices (eosophagus)- rupture when eating
Portal Hypertension
Ascites Splenomegaly Enlarged porta-systemic shunts Esophageal varices Hemorrhoids Caput!!!! medusae Splenic vein thrombosis Contributes to hepatic encephalopathy
HEPATIC FAILURE
Two basic problems
Synthesis of clotting factors
Failure to eliminate endogenous waste products
Manifests as jaundice, encephalopathy and metabolic derangements
Two types: acute and chronic
Rapid onset- massive necrosis
Slow onset- cirrhosis
Diagnosis and Current status
Alcohol induced liver cirrhosis (Current age: 40)
Active with ongoing inflammation
Prognosis
In the absence of social supports unlikely to have full recovery.
Considerations:
Bio-psycho-social model of disease
Societal norms and existing laws…
Most likely cause for death will be one or a combination of the following:
Liver failure due to progressive cirrhosis
Fatal Head injury
Hepatocellular carcinoma
Death facilitated by the social environment he is in.
TUMORS OF THE LIVER
Benign tumors are rarely of clinical significance
Metastatic!! (where did it come from) carcinoma is the commonest liver tumor
ALSO, LIVER IS THE COMMONEST METASTATIC SITE
Primary malignant tumors: Hepatocellular carcinoma,
