Liver Flashcards
what are the 4 parts of the liver
4 lobes: right lobe, quadrate lobe, caudate lobe,and left lob.
liver is the primary __ reservoir in the body
liver is the primary blood reservoir in the body
what % of liver function is required for live
10—20% of function required for life
what are the sources of blood in the liver?
- 1a. Arterial blood, which provides the liver’s O2 supply and carries blood-borne metabolites for hepatic processing, is delivered by the hepatic artery.
- 1b. Venous blood draining the digestive tract is carried by the hepatic portal vein to the liver for processing and storage of newly absorbed nutrients.
- Blood leaves the liver via the hepatic vein.
what are kupffer cells?
macrophagic cells of liver
which direction does bile flow in, relative to blood im hepatocyte lobules
in the opposite direction
what is the primary liver’s mechanism for metabolizing drugs?
The liver’s primary mechanism for metabolizing drugs is via a specific group of cytochrome P-450 enzyme
which blood vessles drains into vena cava? what is the role of vena cava?
hepatic vein
vena cava carries blood around the body
liver role in protein metabolism?
- Liver is the site for both transamination and deamination of amino acids; liver repackages ammonia into urea through urea cycle which will go into kidney
- done by ALT and AST enzymes that stay in the liver
- Site for synthesis of proteins such as albumin and clotting-factors needed for blood coagulation
albumin and liver problems consequences
albumin is a colloid and has an important role in maintaining blood pressure
blood coagulation is important in healing-> someone with liver problems might have problems with healing
Liver function: Fat metabolism
- Liver receives triglycerides and redistributes via lipoproteins
- Cholesterol synthesis occurs in liver
- Site for fatty acid synthesis, ketone production, and fatty acid oxidation
Liver function: Vitamins/Minerals
- Primary site for vitamin and mineral storage, transport, and activation.
- All fat-soluble vitamins as well as zinc, iron, copper, and magnesium are stored in liver.
- Liver is involved in conversion of Vit D into active form -> Cholecalciferol is hydroxylated in the liver to 25-hydroxycholecalciferol
Liver function: Bile synthesis secretion
- Hepatocytes synthesize and secrete 600-1000ml bile/d
- Emulsifying agent
- Facilitates absorption of fatty acids, monoglycerides, cholesterol, and other lipids by forming micelles that are soluble in chyme.
- Without bile salts, a large percentage of ingested fats would be lost in feces.
what is the primary site for bile salt reabsorption? what happens if this site is damaged?
ileum
damage/inflammation of the ileum-> loss of bile salts so they don’t get recycled-> diarrhea
Liver function: Bile and heme metabolism
- When RBC degrade, Hgb released and broken down to heme and globin.
- Heme is converted to biliverdin and transformed into unconjugated bilirubin.
- Within the liver, bilirubin is conjugated and excreted in bile.
What is the biochemical marker of liver functioning
Bilirubin is a biochemical marker of liver functioning
Do we always make bile from scratch?
no
- Secreted bile salts consist of 95% old, recycled bile salts and 5% newly synthesized bile salts.
- 95% of bile salts are reabsorbed by the small intestine.
- Reabsorbed bile salts are recycled by enterohepatic circulation.
how does live impact bile salt recycling
liver helps in bile salt recycling
liver problems-> no recycling
gallbladder can oversecreat, but only up ti a point
Liver function in Carbohydrate metabolism
Glycogenesis, gluconeogenesis, oxidation via T C A cycle, glycogenosis, glycolysis
Liver function in Lipid metabolism
Lipogenesis, lipolysis, saturation/desaturation, ketogenesis, esterification of fatty acids, fatty acid oxidation, uptake/formation/breakdown of phosphotides, synthesis/ degradation/ esterification/ excretion of cholesterol, formation of lipoproteins
Liver function in protein metabolism
Synthesis of serum proteins, prothrombin, globin of hemoglobin, apoferritin, nucleoproteins, and serum mucoprotein; degradation of some proteins to peptides and amino acids; synthesis of urea
Liver function in enzyme metabolism
Synthesis of alkaline phosphatase, monoamine oxidases (MAO’s), acetylcholine esterase, oxidases, cholesterol esterase, dehydrogenases, beta glucuronidase, aspartate transaminase (AST), and alanine transaminase (ALT)*
Liver function in storage?
Storage of glycogen, fats, fatty acids, and fat-soluble vitamins
Describe stages of liver damage
- Healthy liver
- Fatty liver: can happen in PN
- Liver fibrosis: functional cells start beiign replaced with scar tissue. 10-20% of functional cells
- Cirrhosis: irreversible, we can also manage symptoms
Biochemical test to assess liver function and what it reflects
Bilirubin, Alanine aminotransferase (ALT) Aspartate aminotransferase (AST) Gamma-glutamyl transferase (GGT) Alkaline phosphatase (ALP) Prothrombin time
Normal levels for bilirubin test and what does it show?
DIrect: 2–9 μmol/L; total: 3–17 μmol/L
Reflets ability of liver to conjugate and excrete bilirubin
Normal levels for ALT test and what does it show?
Alanine aminotransferase (ALT) 17–63 IU/L Most sensitive to detect hepatocellular injury (esp. secondary to infectious hepatitis)
Normal levels for AST test and what does it show?
Aspartate aminotransferase (AST)
15–37 IU/L
Less specific enzyme to detect hepatic disease
Normal levels for GGT test and what does it show?
Gamma-glutamyl transferase (GGT)
5.0–55.0 IU/L (F)
15.0–85.0 IU/L (M)
Elevation indicative of hepatocellular injury secondary to alcohol abuse
Normal levels for ALP test and what does it show?
Alkaline phosphatase (ALP)
50–136 IU/L
Increased activity occurs in hepatic disease, but non-specific.
Normal levels for prothrombin time test and what does it show?
Prothrombin time
10–14 s
# of seconds for blood to clot; prolonged with hepatic disease
what are the common causes of cirrhosis?
Chronic HCV (hepatitis C virus) & Alcoholism
what are the 2 types of cirrhosis
- Compensated Cirrhosis: Cirrhosis without ascites (accumulation of fluid in peritoneal cavity) or encephalopathy.
- Decompensated Cirrhosis: Cirrhosis with ascites and/or encephalopathy (partially caused by accumulation of ammonia in the brain).
muscle status in cirrhosis patients? Why?
often muscle wasting is present
Decreased carbohydrate use and storage capacity, plus an increase in fat and protein
catabolism, which leads to a chronic catabolic state…depleting muscle reserves!
cirrhosis and glucose levels
Without adequate glycogen synthesis, cannot respond quickly to drop in BG → hypoglycemia
cirrhosis and blood pressure
Normal blood flow cannot occur within the liver if scar tissue is present → portal hypertension and esophageal varices
cirrhosis and oncotic pressure
Inadequate synthesis of serum proteins (e.g., albumin). Albumin maintains oncotic pressure. Reduced concentration of albumin in blood lowers oncotic pressure→ascites (fluid accumulates in peritoneal cavity)
cirrhosis and water retention due to water shifting
Blood volume drops (because fluid has shifted to “third spaces”), and stimulates kidneys to retain sodium and water → worsened ascites
cirrhosis and mental problems
Liver cannot metabolize products that are toxic to brain (e.g., ammonia)→ hepatic encephalopathy (HE)
Describe portal hypertension
Increased BP in hepatic portal vein which carries blood from digestive tract to the liver
Liver damage may result in blockage that leads to an increased blood pressure -> blood builds up and results in collateral circulation and enlarged veins e.g. esophageal varices that can lead to bleeding oesophagus-> risk of haemorrhage
signs of portal hypertension
- ascites caused by fluid leaking into abdominal cavity under high blood pressure
- gastrointestinal bleeding from varices (extremely dilated veins)
- encephalopathy (reduced mental capacity and consciousness)
CIRRHOSIS: Nutrition goals
reduce development of/ alleviate major complications such as encephalopathy and reduce development of/ alleviate manifestations of portal hypertension, such as ascites.
is malnutrition common in cirrhosis patients?
yes
60% of patients
what are common mineral and vitmain deficiencies in cirrhosis?
• Vitamin and mineral deficiencies commonly include: Thiamin, folate, vitamin A, D, zinc and selenium
Nutritional treatment in cirrhosis?
Tx involves maximizing oral intake (early satiety d/t ascites), avoiding hypoglycemia, correcting micronutrient deficiencies, and controlling physiological side effects of ascites with sodium and fluid restrictions.
How can we reduce encephalopathy?
• Prevent/correct malnutrition.
• Protect/Preserve muscle mass!
-providing sufficient protein is important to preserve muscle mass. Damaged liver will delegate its role of converting ammonia into urine to muscles
How can we reduce ascites?
we have both water and Na retention (Hypervolemic hyponatremia)
• Restrict Na to 2g/d
• Restrict fluids ONLY if neurologic symptoms or serum Na <125 mmol/L (some reference <120)
• The mainstay of therapy of hyponatremia in patients with cirrhosis is fluid restriction (1-1.5 L/d) to a level sufficient to induce a negative water balance.
Hypertonic IV is indicated only in symptomatic patients with profound hyponatremia (< 110 mmol/L), or within hours of liver transplantation.
What is the pathophysiology of Hypervolemic hyponatremia
• Observed secondary to advanced cirrhosis and portal hypertension.
• Water AND sodium retention, but water retention relatively greater than
Na retention (therefore serum Na appears low).
do we use hypertonic IV in cirrhosis patients?
Hypertonic IV is indicated only in symptomatic patients with profound hyponatremia (< 110 mmol/L), or within hours of liver transplantation.
Your patient with ascites and hyponatremia needs enteral, what formula is likely to meet the patient’s needs? A. 1kcal/ml B. 2kcal/ml C. 1.5 kcal/ml D. 1.2 kcal/ml
B. 2kcal/ml
Patient with cirrhosis, ascites and hyponatremia patient needs a PEG
True or False?
False
PEG will puncture the abdomen and start infusing formula into the stomach-> not gonna work as the abdomen is full of fluid
can we administer feed via a tube with varices?
if there is oesophageal varices, we can still feed the patient with the tube, but we want small tube- smallest French size that is compatible with the formula used
if there is bleeding-> stop the feed, wait for 48h until bleeding stops-> start again
what are esophageal varices
Esophageal varices are enlarged veins in the esophagus. They’re often due to obstructed blood flow through the portal vein, which carries blood from the intestine, pancreas and spleen to the liver.
varices is not a counter-indication for EN, but bleeding is
Your patient has been on a 1.5L fluid restriction for 48 hours, but hyponatremia persists. What might you do?
2020-10-21
A. Check I/O
B. Provide patient with education to adhere to fluid restriction
C. Check to see if patient is eating out/family bringing food in
D. Check to see fluid restricted diet is ordered
E. Consider reduction to 1L/d.
F. All of the above.
F. All of the above.
water restriction is the last thing to consider
Details of an Anthropometric assessment in cirrhosis patients
• Weight….often inaccurate!
- ASPEN dry weight calculation, subtract:
- 3-5kg for mild ascites
- 7-9kg for moderate ascites
- 14-15kg for severe ascites
• IBW preferred over dry weight (ESPEN).
Details of an food assessment in cirrhosis patients
- Meal patterns (to see how often they eat to control hypoglycemia)
- Adequacy of intake
- Fluid and salt intake
- salt substitute use -i f yes, does it contain potassium (important in case pt takes potassium sparing diuretic)
Functional assessment in cirrhosis patients
• Aim for a measurement of muscle mass, such as mid-arm circumference and/or calf-circumference
• Aim for measurement of muscle function, such as handgrip (HG)
• Compare to population norms and compute a z-score: E.g., mean HG score for 80-year-old female is 20kg (SD 4.3)
• Calculate z-score: pt score – mean SD
= 13kg-20kg/4.3 = -1.6
Common meds in cirrhosis patients
• Tx: HE, lactulose: Don’t be alarmed by ++ diarrhea!
- stimulates ammonia release from body tissues via diarrhea
• Tx: Ascites, diuretics to correct fluid balance
- Furosemide = K+ wasting-> High K diet
• Spironolactone = K+ sparing
- Avoid excessive K intake, K supplements,
salt substitutes (contain potassium chlroide)
Physical exam in cirrhosis pts
- Subjective assessment of fat and muscle stores (e.g., temporalis muscle)
- Ascites (can measure abdomen) -> measuring tape around belly
- Micronutrient deficiencies
- Nutrition-impact symptoms
manual treatments of cirrhosis
- Paracentesis: draining fluid from abdomen’ also results in protein loss
- TIPS (shunt): in case pt has oesophageal varices and portal hypertension- > reroutes their blood
