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Pathology 205 > liver and gall blader > Flashcards

liver and gall blader Flashcards

1
Q

gall blader

A

right upper quadrant with the liver, ependice

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2
Q

what the difference in pain in gall bladder vs. gall stone

A

s

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3
Q

gall stones

A 
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
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4
Q

gall stones

know the risk factors!!!!!! the f words

A 
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
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5
Q

nature of the pain

A

gall stones: mechanical obstrucion- peristaltic

in inflammation: aching pain- stays

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6
Q

clinical features of liver disease

A

Most Asymptomatic

Cholecystitis
RUQ Pain
Fatty Food Intolerance

Obstruction
Colic
Jaundice

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7
Q

two types:

obstruction, perfuration

A

know

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8
Q

structure-function liver

A

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

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9
Q

JAUNDICE

A

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
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10
Q

Clinical features of liver disease

acute!!!!!!!!!!!!!

A

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)

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11
Q

Clinical features of liver disease

chronic

A 
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

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12
Q

What is the purpose of further workup?

A 
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
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13
Q

What to do next?

questions and investigation

A

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
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14
Q

Hepatocellular vs. Cholestatic injury

A 
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,

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15
Q

his investigation

A 
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

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16
Q

3 main causes

A

viruses, alcohol, drugs

17
Q

Identifying underlying cause; SEX, DRUGS & ALCOHOLAdditional findings from history and physical & investigations

A 
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
18
Q

OUTCOMES OF LIVER INJURY- acute

A

Acute

Complete recovery (about 90%)
Chronic liver disease
Death from liver failure

Most important predictor of outocme is Prothrombin time (INR)

19
Q

OUTCOMES OF LIVER INJURY- chronic

A

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

20
Q

HEPATITIS - Acute and Chronic

A

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

21
Q

VIRAL HEPATITIS: CLINICAL EFFECTS

A 
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)
22
Q

VIRAL HEPATITIS B DNA virus- very bad to get

A

DNA virus (complete virion: Dane particle)
Core: DNA polymerase in a protein coat - HBcAg, associated with HBeAg)
Surface protein coat; HBsAg

23
Q

Hepatitis B

A 
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
24
Q

VIRAL HEPATITIS A

RNA virus- best to get

A 
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
25
Q

VIRAL HEPATITIS C RNA virus

A 
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

26
Q

FATTY CHANGE (STEATOSIS)

A

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

27
Q

Fatty Change (Steatosis)

A

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

28
Q

His investigations

A 
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
29
Q

Alcoholic Liver Disease

A

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

30
Q

transaminase

A

liver cell damage

31
Q

CIRRHOSIS

A

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

32
Q

CIRRHOSIS: COMPLICATIONS

A

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

33
Q

Portal Hypertension

A 
Ascites
Splenomegaly
Enlarged porta-systemic shunts
Esophageal varices
Hemorrhoids
Caput!!!! medusae
Splenic vein thrombosis
Contributes to hepatic encephalopathy
34
Q

HEPATIC FAILURE

A

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

35
Q

Diagnosis and Current status

A

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.

36
Q

TUMORS OF THE LIVER

A

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,

Pathology 205 (23 decks)

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