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
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
26
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
27
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
28
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 ```
29
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
30
transaminase
liver cell damage
31
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
32
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
33
Portal Hypertension
``` Ascites Splenomegaly Enlarged porta-systemic shunts Esophageal varices Hemorrhoids Caput!!!! medusae Splenic vein thrombosis Contributes to hepatic encephalopathy ```
34
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
35
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.
36
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,