Liver Flashcards Preview

Clinical Nutrition 1 > Liver > Flashcards

Flashcards in Liver Deck (41):

What is a splenomegaly?

enlargement of the spleen due to an increased resistance to blood flow in the liver, causing higher pressure in the portal venous system.


What is acanthosis nigricans?

A velvety discoloration of body creases and folds


What tissues are associated with AST (SGOT) liver enzymes?

Liver, skeletal muscle, cardiac muscle and kidney


What tissues are associated with ALT (SGPT) liver enzymes?

Only the liver = high levels mean liver cell injury


What enzymes are used to detect liver bile duct damage?

Cholestatic enzymes! They indicate disease to biliary system.


What are examples of cholestatic enzymes used to detect liver bile duct damage?

Alkaline phosphatase: enzyme from bile ducts, placenta and bone turnover = don’t use this value to evaluate bile duct condition in kids (high bone turnover) or pregnant women

Gamma-glutamyl transferase: only high if liver damage (better detection in all kinds of patients). GGT can be high after having a lomft to drink due to alcohol-induced liver inflammation → very sensitive enzyme


What are the different clin presentations of liver damage/disease?

First-time elevations = may be acute injury such as hepatitis A or alcohol-induced liver enzymes

Acute hepatitis = A or E, which is the inflammation of hepatocytes

Chronic hepatitis = B or C

Cholestasis = blockage of bile ducts (large and small)

Cirrhosis = liver inflammation, not always due to alcohol, fat accumulation or chronic hepatitis

Jaundice = accumulation of bilirubin causing yellowing of eyes


What might be the cause of bruising and deteriorating eyesight associated with the liver?

Both vitamin A and K are fat soluble vitamins, which respectively play a role in vision and bruising. The digestion of fat requires bile from the gallbladder, so if these vitamins aren’t properly absorbed, there might be a problem with the bile duct (blockage), causing low secretion of bile. This is usually characterized with elevated ALT (due to blockage, will have liver cell damage) and really high ALP levels (due to the blockage of bile ducts).


What is the difference between bilirubin and direct-bilirubin?

High levels of bilirubin are usually due to a high rate of RBC breakdown (breakdown of heme). Direct-bilirubin levels that are elevated indicate that the liver is having problems secreting the conjugated (direct) bilirubin, which could cause liver problems if accumulated in high amounts in the liver.


What is INR and what does it indicate?

INR (or International Normalized Ratio) is an indicator of how much your blood will clot. The higher the number, the thinner the blood, so the more time it will take for the blood to clot. Vitamin K is used to make blood clotting factors in the liver.


What is severe acute hepatitis?

It is when liver functions aren’t working properly, such as making blood clotting factors and having an elevated INR, this causes the patient to die quickly.


What are the clinical features of acute hepatitis?

→ can improve on its own

- Symptoms: fatigue, anorexia, nausea, jaundice

- ALT elevation: >10-fold

- Prognosis: usually self-limited

- Treatment: supportive


What are the clinical features of chronic hepatitis?

→ some have symptoms, some never will

Symptoms: variable

- ALT elevation: 1.5-10-fold

- Prognosis: variable, at risk for progression

- Treatment: at underlying cause


What are the different diseases that are cases of acute hepatitis and what are the clues/tests?

Hepatitis A: exposure history (clinical clues), IgM anti-HAV (diagnosis test)

Hepatitis B: risk factors (clinical clues), HBsAg, IgM anti-HBc (diagnosis test)

Drug-induced: compatible agent and timing (clinical clues), improvement after d/c agent (diagnosis tests). I.e. Tylenol at low doses is safest thing, but if overdose, can kill liver right away.

Alcoholic hepatitis: History of alcohol excess, ALT > 2, AST < 400 (clinical clues), biopsy (bx), improvement with abstinence (diagnosis tests). AST is higher than ALT (due to a vitamin B deficiency bc of malnourishment)

Ischemic hepatitis: history of hypotension (clinical clues), rapid improvement of ALT (diagnosis tests). → Lack of blood flow to the liver


What are the different diseases that are cases of chronic hepatitis and what are the clues/tests?

Hepatitis C: risk factors (clinical clues), anti-HCV, HCV RNA (diagnosis tests)

Hepatitis B: risk factors (clinical clues), HBsAg (diagnosis tests)

NASH or NAFL: obesity, DM, hyperlipidemia (clinical clues), US, liver biopsy (diagnosis test)

Hemochromatosis: arthritis, DM, family history (clinical clues), iron studies, gene test (diagnosis test)

Alcoholic liver disease: History of alcohol excess (clinical clues), biopsy, improvement with abstinence (diagnosis tests)

Autoimmune hepatitis: ALT 200-500, female, other autoimmune disease (clinical clues), ANA, ASMA (diagnosis tests)


Why is itchiness related to cholestatic?

Because bile acids will deposit in skin and make it itchy.


What is palmar erythema?

Red hands due to hyperestrogenemia


What is spider angiomata?

Spider-like texture on skin due to excess estrogen again


What are abnormal liver tests for cholestasis?

- Patients have modest elevation of alkaline phosphatase

- Symptoms often include fatigue and pruritus (severe itching of skin) at the end

- Prognosis: at risk for progression

Important to differentiate intrahepatic versus extrahepatic (usually obstructive) causes
→ if small duct problem, can’t be fixed or surgically repaired


True or false: NASH can only lead to hepatitis.

False. NASH can cause both cholestasis and hepatitis


What is the protocol to detect liver damage?

First measure the ALP levels → if they are elevated, could mean liver problem, high bone turnover or presence of a placenta, so measure GGT levels
→ if abnormal levels, then proceed with a liver ultrasound, if normal, pursue a nonhepatic cause
→ after the liver ultrasound, notice if the problem is either a dilated duct, a liver mass, or normal.
If it is a liver mass → ERCP (endoscopic retrograde cholangiopancreatography), if it is a liver mass → further imaging required, tumor markers as well as biopsy. If normal, pursue intrahepatic causes, antimitochondrial antibody, careful drug history and consider biopsy.


How do you diagnose conjugated hyperbilirubinemia?

Bilirubin is < or equal to 15 mg/dL (250 umol/L) in pure obstruction

Bilirubin > 20 mg/dL (350 umol/L) implies a nonobstructive (or mixed) cause

Bilirubin will be > 80% unconjugated and less than 5 mg/dL in hemolysis (85 umol/L)

Pain, fever, and/or palpable gallbladder imply obstruction

US (ultrasonogram) or CT may not detect dilated ducts in an acute obstruction


What is cirrhosis?

End stage of any chronic liver disease. It is characterized histologically by regenerative nodules surrounded by fibrous tissues (= lumpy liver). There are two clinical stages = compensated is when it is working fine, decompensated is when not working (can kill).


What is the development of chronic liver disease?

Chronic liver disease --> Compensated cirrhosis (where complications develop: variceal hemorrhage (spewing out blood bc of GI damage), ascites (fluid leaks out of liver in belly), encephalopathy (slurring, build up of ammonia in brain), and jaundice) → decompensated cirrhosis → death
→ decompensated cirrhosis shortens survival


What are the complications of cirrhosis?

Cirrhosis can firstly lead to portal hypertension, which causes variceal hemorrhage, ascites and encephalopathy. Ascites also lead to spontaneous bacterial peritonitis as well as hepatorenal syndrome. The second thing cirrhosis can induce is liver insufficiency, which is linked to encephalopathy as well as jaundice.
Portal hypertension can also lead to splanchnic and systemic vasodilation, lowering the effective arterial blood volume, which causes the activation of neurohumoral systems (RAAS), leading to sodium and water retention, expanding plasma volume, causing a hyperdanim circulation. This is cyclic and causes constant elevation of BP. The way to intervene is to fix the sodium intake of patients with hyperdynamic circulation.


Why is nutrition in cirrhosis hard to assess?

Some patients with cirrhosis will also have sarcopenia, which is having a huge belly full of fluid, which doesn’t give a distorted image of the patient’s health in some cases. Being sarcopenic increases overall mortality and nutritional supplements at night will increase muscle mass (help counter muscle wasting).


What effect does being obese have on NASH patients’ blood pressure?

Being obese with NASH increases both systolic and diastolic blood pressure. Diastolic dysfunction is how stiff your heart is, how hard it is for your heart to relax.


What is NASH?

Non-alcoholic steatohepatitis is a disease that histologically mimics alcoholic hepatitis and that also may progress to cirrhosis. It is the #1 most common disease in the developed world. There is an increase in hepatocyte death in addition to steatosis. The liver injury triggers a repair response that sometimes leads to cirrhosis.


Can fatty liver (steatosis) predict hepatitis or other liver damage?

No, because many people can have fatty liver and not get sick from it. Some other cases will progress to hepatitis more quickly than others.


What is the clinical syndrome (definition) for NASH?

Obesity, diabetes, hypertension and hyperlipidemia (specifically triglycerides!!!). No alcohol consumption (20g vs 40g), and the absence of other causes of liver disease.


Who is at risk of NASH?

Overweight/obesity, asian populations (need to consider BMI shift, so overweight more easily), underweight or anorexic patients (increased liver fat with low intake).


What are ballooning hepatocytes?

When fat infiltrates hepatocytes, which makes them explode after a while.


Why is low albumin alarming in liver disease and how can it be noticed?

Albumin is made in the liver, so if levels are low, there is most probably and issue with the liver. A symptom of hypoalbuminemia is Terry’s nails, which is when the white part at the bottom of nails goes much higher than normal nails.


What is the prevalence of NASH?

It has an overall prevalence of 20%, with 3% in non-obese, 19% in obese and 50% in morbid obese.


What are the major risk factors for advanced liver disease?

Older age (>45)
Obesity (BMI > 30)
Long-standing diabetes (> 15 yrs)
Triglycerides > 5.65 (2.8?) mmol/L → assured fatty liver > 5.65, > 2.8 could get it
ALT > 2 x ULN and/or AST > normal


What does a fibroscan measure?

It measures stiffness of the liver and the fat content without having to use an invasive technique such as liver biopsies.


How can liver disease be treated?

Even though diet is the treatment most commonly proven to help in clinical trials, other options were shown to also have a positive effect in certain studies such as statin/fibrate against hyperlipidemia, antihypertensives, drugs for obesity and pentoxifylline.


What are the weight loss/exercise recommendations for liver disease?

A 5-10% weight loss was shown to help in treating obesity through diet and exercise in order to help with liver disease. It was also shown that intensity of PA might be more important than duration, which significantly reduced or of having NASH. For weight loss, Orlistat was used to get to the target weight loss of 9-10% to notice improvement in histology.


Which new therapy is tested to be able to treat NASH through storing glycogen instead of fat?

GLP-1 agonists are used to stimulate insulin secretion from the pancreas, which would stimulate glycogen storage over fat storage in the liver.
FXR agonists reduce portal hypertension and lowers lipids by working through a nuclear receptor to reduce cholesterol synthesis.


Why may rapid weight loss be dangerous for the liver (bariatric surgery for example)?

Jejunoileal bypass in particular has been shown to cause a drastic weight loss in its patients, which causes the liver to overproduce fat, leading to increased steatosis, cirrhosis,liver failure and gallstones. If weight loss if gradual, works fine.


What are the different therapies for NASH?

In diabetics = aggressive glucose control using TZDs

In non-diabetics = vitamin E 800 IU, safety?

In hypertension = aggressive Rx; consider ARB or ACE-I
In hyperlipidemia = aggressive Rx; consider fibrates or statins

Diet and exercise with intial target of 10% weight loss = modify diet composition.

Vigorous exercise is encouraged where safe

Modest alcohol consumption may be protective for NAFLD patients

When appropriate, consider surgical options such as bariatric or transplant