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Health Studies > Hep Cirrhosis Roop/Reza > Flashcards

Hep Cirrhosis Roop/Reza Flashcards

1
Q

If fecal analysis shows that its positive for fat what does this mean?

A

Steatorrhea

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2
Q

Define malabsorption. On a basic level, what can cause this?

A

imperfect absorption of food material by the small intestine

causes
-destruction of epithelial cells (can’t absorb inside cell)
-digestion issues
-unable to move nutrients to the blood (transporter issue)

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3
Q

Describe the digestion of lipids

A

-Requires bile to emulsify (breakdown into smaller pieces) -> MAINLY pancreatic lipase (can also have lingual lipases)

-Need to be packaged into chylomicron goes into lacteals → takes lymph into vena cava > FAT BYPASSES THE LIVER

-Everything else → blood → liver

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4
Q

What happens during the emulsification by bile?

A

large fat droplets are broken down with bile into smaller ones

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5
Q

What happens during enzymatic digestion by pancreatic lipase?

A

triglycerides are broken down into fatty acids by pancreatic lipase (some free glycerol is also formed)

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6
Q

Absorption of products of fat digestion depends on…..

A

size

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7
Q

Short and medium-chain fatty acids and glycerol (small products) are absorbed into the….

A

blood via capillary

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8
Q

Long chain fatty acids and monoglycerides (large products) form into triglycerides and are transported in ____________ into lymph vessels

A

chylomicrons

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9
Q

What happens to bile acid production and secretion with cirrhosis of the liver?

A

fats are not emulsifying

bile acid production and secretion is decreased

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10
Q

Explain the presence of jaundice

A

accumulation of bilirubin

bile includes= salts, acid, bilirubin (gives a pigment, breakdown pigment of heme)

accumulation of bile in plasma = jaundice

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11
Q

Explain what happens to dietary fats in the small and large intestine. What is the cause of diarrhea?

A

goes from small to large intestine and absorbs water

fat in large intestine keeps water there bc of “osmotic load” -> this means that its keeping water in large intestine = DIARRHEA

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12
Q

Name the fat soluble vitamins. Why are they named this?

A

Vitamin A, D, E, and K

Named fat soluble vitamins because they dissolve in the fat

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13
Q

What happens to fat-soluble vitamins in a pt with liver cirrhosis?

A

The pt is not reabsorbing any fat soluble vitamins, so pt will have numerous vitamin deficiencies

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14
Q

What will deficiency of vitamin A lead to? What foods contain vitamin A?

A

night blindness

spinach, kale, broccoli, carrots, etc

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15
Q

Vitamin D deficiency will lead to what? What foods are high in vitamin D?

A

osteoporosis (lack of reabsorption of calcium)

salmon, tuna, beef liver, sardines

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16
Q

Vitamin E deficiency will lead to what? What foods are high in vitamin E?

A

muscle weakness, lack of muscle coordination, and nerves are compromised (vit. E protects the myelin sheath on nerves)

sunflower seeds/oil, almonds, peanut butter/peanuts

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17
Q

Vitamin K deficiency will lead to what? What foods are high in vitamin K?

A

blood clots (we need vitamin K to make clotting factors in the liver)

deficiency in vit. K causes bruising/bleeding

Spinach, Brussel sprouts, broccoli, asparagus

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18
Q

What are the 4 stages of liver damage?

A

1) healthy liver
2) fatty liver (deposits of fat lead to liver enlargement)
3) liver fibrosis (scar tissues forms)
4) cirrhosis (growth of connective tissue destroys liver cells)

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19
Q

Alcoholic liver disease occurs in 3 histologic stages. What are they called?

A

1) alcoholic fatty liver/steatosis
2) alcoholic hepatitis
3) alcoholic cirrhosis

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20
Q

Is alcoholic fatty liver/steatosis reversible? What are the risk factors? What are some S&S?

A

yes, its reversible

risk factors=
-obesity
-type 2 DM

hepatomegaly

Physical symptoms (fatigue, weight loss, etc.)
-feeling sick
-loss of appetite.
-yellowing of the eyes and skin (jaundice)
-swelling in the ankles and tummy.
-confusion or drowsiness

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21
Q

Is alcoholic hepatitis reversible? What are some S&S? What does histology look like?

A

yes, its reversible if pt stops drinking permanently

S&S:
-increase belly size (ascites)
-yellowing of the skin and whites of the eyes (jaundice)
-N/V
-fever and weakness
-hepatomegaly

Histology=
-ballooning/inflammation of neutrophils
-fatty changes/necrosis of liver cells
-enlargement of hepatocytes

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22
Q

Is alcoholic cirrhosis reversible? What are some S&S? What does histology look like?

A

no, its irreversible

S&S:
-Itchy skin
-GI bleeding
-Losing muscle tone (atrophy)
-Bruising easily
-Loss of appetite and weight loss
-Yellowing of the skin and eyes (jaundice)
-Fluid build-up and swelling of the legs (edema) and abdomen (ascites)
-Bleeding in your mouth (mouth bleeds) or vomiting blood.

liver failure and limited function, extreme jaundice

Histology- nodular and fibrotic

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23
Q

If there’s impaired ammonia detoxification in the liver what happens to the brain?

A

-ammonia and glutamine neurotoxicity
-alterations in cerebral blood flow
-neuroinflammation

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24
Q

If there’s impaired ammonia detoxification in the liver what happens to the intestines/stomach?

A

-slow fecal transit
-high bacterial load
-increased ammonia production
-ammonia undergoes the portosystemic shunt from intestines/stomach to the brain

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25
Q

Describe normal ammonia metabolism

A

-mucosal enzymes and colonic bacteria will undergo protein metabolism
-ammonia will be released and enter portal circulation
-ammonia will enter urea cycle and urea will come out

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26
Q

Describe hyperammonemia metabolism

A

-hepatic failure and ammonia accumulation
-ammonia will enter systemic circulation

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27
Q

Describe chronic liver disease metabolism

A

-hepatic failure and ammonia accumulation
-ammonia will enter systemic circulation
-ammonia will reach the neurons and will be abnormally functioning
-this increases neurotransmission, increases glycolysis, and decrease cytokines
-this will lead to hepatic encephalopathy

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28
Q

Describe new, acute hepatic encephalopathy metabolism

A

-hepatic failure and ammonia accumulation
-ammonia will enter systemic circulation
-ammonia and glutamate will undergo a reaction with glutamine synthetase
-this will increase glutamine and decrease lactate
-this will lead to brain edema and edematous neurons

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29
Q

What is a decompensated liver?

A

an acute deterioration in liver function in a patient with liver cirrhosis and is characterized by jaundice, ascites, hepatic encephalopathy, hepatorenal syndrome or variceal hemorrhage

30
Q

Why do we see esophageal varices (similar to varicose veins in the legs)?

A

Due to regurgitation (due to when normal blood flow to liver is blocked by a blood clot or scar tissue)

Liver is fibrotic so blood begins to go backward → will fill up the smaller veins

31
Q

Ascites is fluid in the peritoneum. Why does this occur?

A

-Oncotic pressure → lack of this bc no proteins in blood vessels (lack of albumin which is made by the liver)
-Not making proteins in the liver
-Fluid leaking out of blood vessels

32
Q

What kind of cancer are you subject to with liver cirrhosis?

A

Hepatocellular cancer

33
Q

Ammonia can cross BBB and lead to….

A

hepatic encephalopathy

34
Q

What are the 4 grades of hepatic encephalopathy?

A

Grade 1) altered sleep patterns, impaired handwriting and math abilities, decreased attention span
2) asterixis (hand tremor when wrist is extended), disoriented
3) hyperactive reflexes, extensor plantar response, stupor
4) coma

35
Q

What is another name for Babinski reflex?

A

extensor plantar response

36
Q

What are the 3 sources of free fatty acids that can be accumulated in the liver?

A

1) Non-esterified fatty acids (NEFAs)
2) de novo lipogenesis (DNL)
3) Diet

37
Q

Why is insulin resistance characterized by low insulin sensitivity and low glucose disposal in peripheral tissues can be a cause of non-alcoholic fatty liver disease?

A

Hormone sensitive lipase is inhibited by insulin but insulin promotes ACC (acetyl coa carboxylase), the rate-limiting enzyme in fatty acid synthesis, which is done in the liver.

Since we are not uptaking the glucose in the periphery, we still have to do something with the glucose so the liver turns it into fat.

Insulin also promotes capillary lipoprotein lipase

Continuously fat is being delivered to tissue but the fat tissue does not respond to insulin

38
Q

Why can alcoholics show signs of hypoglycemia?

A

Alcoholics will produce increased insulin secretions thus causing low blood sugar.

Additionally, glucose production is inhibited while excess alcohol is metabolized so that the body is not overwhelmed.

Hypoglycemia may occur in alcoholics who rely on gluconeogenesis to maintain blood glucose levels.

Alcohol (ethanol) is rapidly oxidized in the liver, producing an increase in NADH relative to NAD+ in liver cells.

Increased levels of NADH shift the lactate dehydrogenase reaction toward lactate and the cytosolic malate dehydrogenase reaction toward malate, thus preventing pyruvate and oxaloacetate from entering the gluconeogenesis pathway

This causes an imbalance between the NADH and NAD+ and impairs gluconeogenesis

39
Q

Why can alcoholics show signs of ketoacidosis?

A

Ketones build up in blood with lots of alcohol and no food

Alcoholic ketoacidosis is caused by the combined effects of alcohol and starvation on glucose metabolism;
it is characterized by hyperketonemia

As NADH builds up, needs to be consumed → lactic acid would be produced (as NADH increases so does lactic acid)

40
Q

How does ethanol get metabolized in the liver?

A

Ethanol is metabolized in the liver by alcohol dehydrogenase oxidized to acetate via acetaldehyde

acetate = source for lipid synthesis

41
Q

How can folate and vitamins B6 and B12 deficiencies in alcoholics cause oxidative liver injury?

A

B12 - cobalamin
B6 - pyridoxine

Methionine metabolism is impaired
-Cysteine to glutathione doesn’t happen → environment = oxidized
-Overload ETC → too much electrons from ethanol = ROS produced

Deficiency in vit B6 and B12 will lead to hyperhomocysteinemia and homocystinuria

42
Q

How can alcoholic liver cirrhosis affect the function of red blood cells?

A

-alcohol-induced cirrhosis, leads to decreased red blood cell (RBC) production

-Liver that can produce a lot of cholesterol → in membranes of RBC = fragile membrane

-spur cell anemia is associated with advanced stages of alcoholic cirrhosis

-decreased liver function from cirrhosis causes decreased B12 absorption

43
Q

What are therapeutic opportunities for alcoholic liver disease?

A

-Corticosteroids can be used to reduce inflammation of the liver

-Treat insulin resistance (adjust diet, nutrition, meds) -> GLP-1 enhances insulin secretion improving lipolysis reducing free fatty acid overload in the liver. GLP-1 receptor agonists reduce liver steatosis and inflammation.

-Prevent fatty acid accumulation

-Acetyl carboxylase blocked → fatty acid synthesis blocked

-GLP → deals with insulin insensitivity (manipulate drug to last longer)

-Block malonyl coA

-FXR → switched off during fatty liver disease (agonist to activate it → can help with disease)

-Peroxisome → activate them → can assist with the disease

-Block symporter

44
Q

Why can ammonia be toxic to the central nervous system in patients with acute liver failure?

A

When excessive amounts of ammonia enter the CNS, the brain’s defenses are severely challenged.

A complex molecular chain reaction is triggered when the brain is exposed to excessive levels of ammonia.

Ammonia short-circuits the transport of potassium into the brain’s glial cells

ammonia must be disposed of because even small amounts can be toxic to the CNS

Detoxification of ammonia is accomplished through its conversion to urea by the liver

An increase in circulating ammonia to about 400 uM causes alkalosis and neurotoxicity

In the brain, increased ammonia leads to pH imbalance

It also affects energy metabolism by depleting alpha-KG (a TCA cycle intermediate) and by depleting levels of Glu, a neurotransmitter

Increased ammonia in astrocytes results in the formation of reactive oxygen species (ROS), mitochondrial dysfunction and brain edema

The brain removes excess ammonium ions as either Glu or Gln using the enzymes glutamate dehydrogenase and glutamine dehydrogenase, respectively

45
Q

T/F:

NAFLD (nonalcoholic fatty liver disease) is one of the most common causes of chronic disease globally

A

true

46
Q

NAFLD (nonalcoholic fatty liver disease) is the development of hepatic steatosis in the ___________ of secondary causes

A

absence

47
Q

NAFLD (nonalcoholic fatty liver disease) can range from simple steatosis to extensive _________ to __________. Progression might not be linear as there can be periods of stability or regression

A

fibrosis to cirrhosis

48
Q

What does NASH stand for and what does it mean?

A

nonalcoholic steatohepatitis

inflammation and hepatocyte ballooning with or without fibrosis

49
Q

How does NAFLD (nonalcoholic fatty liver disease) compare to liver damage caused by alcohol abuse?

A

histologically there is no difference

50
Q

NAFLD (nonalcoholic fatty liver disease) is strongly associated with what?

A

metabolic syndrome

51
Q

NAFLD (nonalcoholic fatty liver disease) has ___________ circulating free fatty acids that can cause insulin resistance and low grade inflammation

A

elevated

52
Q

NAFLD (nonalcoholic fatty liver disease) has increased risk for…..

A

-vascular disease
-osteoarthritis
-PCOS
-kidney disease
-diabetes
-cardiac disease
-sleep apnea

53
Q

What is metabolic syndrome?

A

-excess body fat (obesity)
-insulin resistance (DM)
-high cholesterol
-HTN
-hyperlipidemia
-fatty liver = hepatic component of metabolic syndrome

54
Q

Systemic insulin resistance ___________ adiponectin and ___________leptin concentrations, while adipose tissue lipolysis is not suppressed, despite high circulating insulin levels, and plasma FFA concentration is increased. Increased glucagon levels have also been reported in NAFLD (nonalcoholic fatty liver disease)

A

reduces, increases

55
Q

What is adiponectin? How does adiponectin relate to insulin resistance?

A

its a protein hormone that stimulates insulin secretion

involved in regulating glucose levels as well as fatty acid breakdown

decreases insulin resistance by decreasing triglyceride content in muscle and liver

56
Q

What is leptin? How does leptin relate to insulin resistance?

A

its a hormone released from adipose tissue and helps regulate energy balance by inhibiting hunger

-decreases glycemia,
-decreases insulinemia
-decreases insulin resistance
-decreases adiposity and lipotoxicity
-plays a role in regulating glucose-insulin homeostasis through osteocalcin
-diminishes fat storage in adipocytes
-stimulates hepatic gluconeogenesis and hepatic insulin sensitivity via the hepatic branch of the vagus nerve

57
Q

fatty liver _________ adiponectin and ____________ leptin

A

decreases, increases

58
Q

NAFLD (nonalcoholic fatty liver disease) is usually suspected in patients with unexplained persistently ___________, asymptomatic elevation of aminotransferase levels and radiologic findings of fatty liver

A

hepatomegaly

59
Q

What is the best diagnostic tool/ “gold standard” for NAFLD (nonalcoholic fatty liver disease) confirmation? What are other tools you can use for diagnosing?

A

gold standard= liver biopsy

less invasive= serum and imaging

60
Q

Will you do a liver biopsy on every pt you suspect has NAFLD (nonalcoholic fatty liver disease)?

A

no because its invasive and cost prohibitive with insurance companies

61
Q

Primary care providers can expect to see growing numbers of patients with nonalcoholic fatty liver disease (NAFLD), given its increasing prevalence - fueled by the global epidemics of _________ and ____________

A

obesity and type 2 diabetes

62
Q

A significant risk of cardiovascular morbidity and mortality is associated with __________.

A

NAFLD

63
Q

The progressive form of NAFLD, nonalcoholic steatohepatitis (NASH), is a leading indication for _________

A

liver transplant.

64
Q

T/F:

Liver biopsy is the “gold standard” for diagnosis of NASH but has several disadvantages; thus, noninvasive biomarkers (serum and imaging) are used more frequently.

A

true!!!

65
Q

What is the treatment protocol for NAFLD?

A

*Lifestyle modification
*Treat the various conditions that are a part of NAFLD
*Weight loss and glycemic control
*Weight loss of 3-5% improves steatosis
*Weight loss of 10% reduces hepatic inflammation
*Metformin increases insulin sensitivity, but does not improve liver histology

66
Q

Hepatic encephalopathy due to severe liver disease has ____________ hepatocellular function and ___________ toxin metabolism

A

decreased, decreased

67
Q

Hepatic encephalopathy due to severe liver disease has disordered metabolism and ___________ protein synthesis. This results in what?

A

decreased

muscle atrophy and decreased extrahepatic ammonia removal

68
Q

Hepatic encephalopathy due to severe liver disease can cause electrolyte dysregulation. Explain

A

there will be increased conversion of NH4+ to NH3 (ammonia)

69
Q

A decompensated liver is at increased risk for……

A

developing HCC (hepatocellular carcinoma)

70
Q

Hepatic encephalopathy has _________ liver function

A

impaired

71
Q

In hepatic encephalopathy, the liver is not breaking down __________

A

ammonia

Health Studies (14 decks)

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