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Drug Action II > Block 1: Pancreas, Hepatobiliary, and Liver Disorders > Flashcards

Block 1: Pancreas, Hepatobiliary, and Liver Disorders Flashcards

1
Q

What are the functions of the liver?

A
  1. Produces bule
  2. Synthesizes plasma proteins
  3. Metabolize and eliminates drugs and toxins
  4. Stores vitamin, glucose, and blood
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2
Q

What is hepatomegaly?

A

Abnormally enlarged liver

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3
Q

Where is the liver located?

A

right upper quadrant

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4
Q

What are the structural units that contain hepatocytes?

A

Liver lobule

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5
Q

What are hepatocytes?

A

Specialized cells of liver that produce enzymes that catalyze various chemical reactions

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6
Q

What are sinusoids?

A

Capillaries of liver lobule located between hepatocytes, receives blood from hepatic artery and portal vein and remove foreign materials from blood

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7
Q

Why does hepatic differ from standard blood supply?

A

75% from vein
25% from artery

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8
Q

What is the difference between hepatic artery and vein?

A

Artery: brings oxygen rich blood from abdominal aorta
Vein: Brings nutrient rich blood from digestive system

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9
Q

What are the types of hepatic portal vein?

A
  1. Superior mesenteric: brings blood from small intestine, ascending and transverse of large intestine and stomach
  2. Splenic vein: brings blood from spleen and pancrease
  3. Inferior mesenteric vein: collects blood from descending region of large intestine and rectum
  4. Central vein: move blood out of liver to heart
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10
Q

What are the Kupffer cells?

A

Phagocytic cells lining sinusoids that remove bacterial and foreign materials from blood

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11
Q

What clotting factors are synthesized by the liver?

A

I, II, VII, IX, X

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12
Q

What proteins are synthesized by the liver?

A

Albumin, globulin

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13
Q

What is bile?

A

Yellow-green thick fluid that breaks fat into small globules

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14
Q

What is bilirubin?

A

Brownish-yellow substance produced when liver breaks down red blood cells

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15
Q

What is biliverdin?

A

Pigment that gives bile its greenish color

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16
Q

Where does bile go once leaving the hepatic duct?

A
  1. Stored and concentrated in gallbladder
  2. Released via common bile duct to duodenum
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17
Q

What hormone produces bile?

A

Secretin from the duodenum

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18
Q

What is the process of excretion?

A

Bilirubin secreted and transported to feces

Liver breakdowns and detoxifies substances

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19
Q

What are the downside of hepatic detox?

A

Damages to hepatocytes

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20
Q

What is checked in a liver function test?

A
  1. Albumin
  2. Bilirubin
  3. AST
  4. ALT
  5. GGT
  6. Prothrombin
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21
Q

What happens when liver damage prevent albumin production?

A
  1. Causes body fluid leaks to interstitial spaces and peritoneal cavity
  2. Caused by edema, ascites
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22
Q

What happens when liver damage prevent ammonia conversion?

A

Ammoniamo accumulates → systemic damage

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23
Q

How do we test for liver disorders?

A

Bilirubin levels: Indicator of liver and pancreatic dysfunction
Elevated pancreatic pancreatic amylase and lipase

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24
Q

What is jaundice?

A

Yellowish discoloration of whites of eyes, skin, or mucous membranes caused by bile salts in tissues

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25
Q

What gives feces its dark color?

A

Bilirubin

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26
Q

What is amylase?

A

Breaks down starch to disaccharides

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27
Q

What is lipase?

A

Fat digestion to produce fatty acids and glycerol from triglycerides

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28
Q

What causes jaundice in newborns?

A

Takes several days to produce enzyme needed for conjugation of bilirubin (glucoronyltransferase)

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29
Q

What is cause of cirrhosis?

A
  1. Alcohol consumption → alcoholic liver disease → alcoholic hepatitis → hepatocellular damage, inflammation, obstruction → damages in hepatocytes and surrounding tissue
  2. Replacement of hepatocytes with scar tissue
  3. Constriction of blood and bile flow
  4. Enlarged spleen damages → leukopenia, anemia, thrombocytopenia
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30
Q

Cirrhosis rates are higher in ___?

A

Males

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31
Q

What is a fatty liver?

A

Alcohol catalyzes enzymes → enzymes make fatty acids → fatty acid accumulates in liver as fat → steatosis (early stage)

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32
Q

What system is used by the liver when consuming large amounts of alcohol?

A

Microsomal ethanol-oxidizing system → fatty deposits and TG

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33
Q

What are causes of liver blood flow constriction?

A

Portal hypertension forces blood out of the liver→ shunts blood to spleen → splenomegaly

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34
Q

How does ascites from portal HTN cause dyspnea?

A
  1. Increased abdominal fluid place pressure on diaphragm
  2. Difficulty breathing
  3. Swollen abdomen
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35
Q

What are the factors that increase the severity of cirrhosis?

A
  1. Pattern of drinking
  2. Amount of alcohol
  3. Number of years drinking
  4. Liver damaging
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36
Q

How can you fix progression of cirrhosis from alcohol?

A

Elimination of alcohol can repair damages

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37
Q

What leads to irreversible liver damage from alcohol?

A

Liver shrinks and takes on nodular appearance → liver failure that is irreversible

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38
Q

What delays liver damage diagnosis?

A
  1. Vascular and regenerative capacities of liver
  2. Deep location of liver in abdominal cavity
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39
Q

What are the sx in patients with steatosis?

A

1, Asymptomatic
2. Elevated LFT
3. Palpitation
4. RUQ discomfort

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40
Q

Continual drinkers may experience what kind of sx?

A
  1. N/W
  2. Anorexia
  3. Weight loss
  4. Jaundice and icterus
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41
Q

What are the labs associated with metabolic liver disease?

A

Damage to hepatocytes

Prolonged prothrombin time

Portal HTN shifts fluids to body compartment

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42
Q

How can hypoalbumnemia and hyperaldosteronism contribute to ascites?

A

Hypoalbumnemia: loss of colloid osmotic pressure
Hyperaldosteronism: retention of sodium and water to elevate blood pressure

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43
Q

Sx of increased cerebral edema?

A
  1. Confusion
  2. Disorientation
  3. Decreased cognition
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44
Q

What builds up do to dysfunctional liver metabolism?

A

Ammonia and unmetabolized medications → toxicity

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45
Q

What is gynecomastia?

A

Inability of liver to degrade estrogens in males from phytoestrogens in alcohol → breast enlargement from testosterone and estrogen imbalances

46
Q

What are signs of further liver failure from portal HTN?

A
  1. Asterixis
  2. Spider angioma
  3. Caput medusa
  4. Esophageal varices
47
Q

What is asterixis?

A

Muscle tremor causing downward flap of hand when arm is extended

48
Q

What is spider angioma?

A

Dilated arteriole seen as small red dot with tiny, fragile veins surrounding the skin’s surface caused by unmetabolized estrogen

49
Q

What is caput medusa?

A

Bluish veins under the skin that radiate out across umbilicus → ascites and abdominal pressure

50
Q

What is esophageal varices?

A

Swollen esophageal veins → increased pressure in vessels due to portal HTN from liver scarring

51
Q

How many lobes are there in the liver?

A

2

52
Q

What does normal liver function look like?

A

Dual blood supply from hepatic artery and portal vein

Hepatic vein moves blood to heart

53
Q

What is classification of liver failure? Leading cause?

A

80-90% of hepatic function must be compromised

  1. Excessive alcohol
  2. Hepatitis C virus
54
Q

What is acute liver failure?

A
  1. Elevated liver test due to inflammation
  2. Prolong coagulation time
  3. Mental state alterations
55
Q

What is cirrhosis?

A

Scarring of the liver associated with poor liver function → systemic changes due to portal HTN

56
Q

What are the complications of chronic liver failure?

A
  1. Portal hypertension
  2. Esophageal varices
  3. Ascites
  4. Hepatic encephalopathy
57
Q

What are the complications of acute liver failure?

A
  1. Hepatic encephalopathy
  2. Coagulopathy (decreased clotting factor production)
58
Q

What is Portal HTN?

A

Increased portal venous pressure:
Increased resistance to blood flow through the portal venous system and pressure gradient over 5 mmHg

59
Q

What is the most common cause for cirrhosis?

A

Portal HTN

60
Q

What are the non cirrhotic causes of portal HTN?

A

Prehapatic: portal thrombosis, narrowing of portal veins
Posthepatic: severe right-sided congestive heart failure, hepatic vein outflow obstruction

61
Q

What are the Problems associated with increasing portal pressure?

A
  1. Hyperdynamic circulation
  2. Esophageal varices and hemorrhage
  3. Rectal varices
  4. Splenomegaly
62
Q

What are the problems associated with systemic circulatory abnormalities or portosystemic shunt?

A
  1. Ascites
  2. Encephalopathy
63
Q

What is esophageal varices?

A

Increased portal hypertension → flow through the liver drops → increased pressure in blood vessels lining the esophagus

64
Q

What are the sx of acute bleeding in esophageal varices?

A
  1. Melena
  2. Hematemesis
  3. Bright red blood from rectum
65
Q

What are ascites?

A

Abnormal collection of excess fluid in the abdominal cavity → poor prognosis

66
Q

What causes ascites?

A

Peripheral arterial vasodilation → decreased systemic vascular resistance

67
Q

How do spontaneous portosystemic shunts cause ascites?

A

redirection of blood flow and vasodilators → Capillary permeability and lymph formation increase → Ascites develop when the body can not longer absorb this fluid

68
Q

What are the sx of ascites?

A
  1. Increased abdominal girth
  2. Weight gain
  3. Bulging flanks
  4. Shifting dullness
  5. Decreased appetite
69
Q

What is icterus?

A

Yellowing of the sclerae of eyes

70
Q

What is cholestasis?

A

Systemic retention of excess bilirubin and other bile solutes

71
Q

What is the difference between unconjugated and conjugated bilirubin?

A

Unconjugated: Cannot be excreted in urine because it is tightly bound to albumin and is insoluble in water
Conjugated: Can be excreted in urine because it is loosely bound to albumin and is water soluble; nontoxic

72
Q

How is bilirubin eliminated from the body?

A

Extrahepatic bilirubin binds with albumin and is delivered to the liver → glucoronidation in ER → Water-soluble, nontoxic bilirubin glucuronides (direct bilirubin) are excreted in bile → Gut bacteria deconjugate the bilirubin into urobilinogens that are excreted in the feces (stercobilin) and enterohepatic circulation → Some products may be reabsorbed and then excreted in urine

73
Q

How can Extrahepatic obstructive cholestasis develop?

A

Obstruction of common bile duct due to tumor, gallstone, or compression

74
Q

What are signs of bilirubin levels increase?

A
  1. Urine becomes tea colored
  2. Stools become clay colored
  3. Pruritis occurs.
  4. Serum alkaline phosphatase levels increase.
  5. Gamma glutamyl transpeptidase (GGT) levels increase
75
Q

What are the signs of reduced bile flow?

A
  1. Decreases intestinal absorption and leads to deficiencies of fat-soluble vitamins A, D, E, and K
  2. Fever, chills, and RUQ pain
  3. Xanthomas
76
Q

What is alcoholic liver disease?

A

Damage to the liver and its function due to alcohol abuse

77
Q

What are the causes of alcoholic liver disease?

A
  1. Steatosis: accumulation of lipid droplets in liver cell cytoplasm
  2. Steatohepatisis: Multifactorial inflammation seen in setting of steatosis
  3. Ballooning degeneration: swelling of hepatocytes due to severe cell injury
  4. Mallory body formation: Damaged filaments in the liver that accumulate
  5. Fibrosis → cirrhosis
78
Q

Why is alcohol so damaging?

A
  1. Affects CYP450 system
  2. CYP2EI inducer
  3. Catabolism in the ER increases
  4. ROS ↑ (lipid per oxidation and acetaldehyde protein adducts, methionine metabolism impaired, glutathione levels ↓
79
Q

How does alcoholic liver disease ↑ gut permeability?

A
  1. Hepatic exposure to gut bacterial degradation releasing endotoxins
  2. Kupffer cell activate
  3. Proinflammatory cytokines release

Hepatocellular death occurs due to damage to and disruption of proteins and DNA

Accumulation of cells

80
Q

What are the labs of alcoholic liver disease?

A

2:1 ratio of AST/ALT
Leukocytosis
Elevated GGT

81
Q

What is the physical sx of alcoholic liver disease?

A
  1. Hepatomegaly
  2. Jaundice
  3. Ascites
  4. Encephalopathy
  5. Spider angiomata
82
Q

What is NAFLD?

A

Spectrum of liver diseases ranging from simple steatosis to nonalcoholic steatohepatitis (NASH) caused by a deposit of lipids in liver

83
Q

What is the NAFLD spectrum?

A

Simple steatosis: Mild liver disease, 5% lipid accumulation
NASH: inflammation and hepatocyte damage → cirrhosis

84
Q

What are the important components of NASH and how is it associated with NAFLD?

A

Metabolic syndrome
1. Overproduction leads to components of metabolic syndrome: hyperglycemia, DLD, hyperinsulinemia
Insulin resistance:
1. Fatty liver is insulin resistant and overproduces LDL, glucose, CRP, IL6

85
Q

What are sx of NAFLD?

A
  1. Elevation of liver transaminases
  2. AST higher than ALT levels
  3. Obesity
  4. Diabetes
  5. DLD
86
Q

What is acute liver failure?

A

Loss of hepatocyte function affecting almost the entire liver without the presence of cirrhosis

87
Q

What is the leading cause of acute liver failure?

A

Drugs (Acetaminophen) → hepatic necrosis

88
Q

Describe the cell injury of acute liver failure?

A
  1. Direct toxic damage
  2. Combination of toxic damage and immune-related inflammation
89
Q

What is the treatment for severe acute liver failure ?

A

liver transplantation

90
Q

What are the hallmark signs of acute liver failure?

A
  1. Coagulopathy
  2. Altered mental status (encephalopathy)
  3. Jaundice can occur
  4. Hepatic coma or cerebral edema
91
Q

What is Cholelithiasis?

A

Stone formation in the gallbladder

92
Q

Why is a gallstone problematic?

A

Blockade of bile → inflammation and tissue damage

93
Q

What is a gallstone composed of?

A

Cholesterol (80%)
Pigment (20%)

→ Caused by excessive cholesterol from obesity and high fat diets

94
Q

What are the risk factors of Cholelithiasis?

A
  1. Femal
  2. Fair
  3. Fat
  4. Fertile
  5. Forty
95
Q

What are the sx of Cholelithiasis?

A
  1. Nonspecific complaints following consumption of fat: indigestion and mild gastric distress
  2. midepigastric pain in RUQ, right uubscapular pain, back
  3. Biliary colic: Painful spasms to RUQ that accompany obstruction in cystic duct by stone.
  4. Steatorrhea: Greasy, foul-smelling feces containing undigested fats
  5. Bile salts accumulated in blood
96
Q

What is the function of the pancreas?

A
  1. Digestive enzymes in exocrine cell
  2. Hormone in endocrine cells
97
Q

What is acute pancreatitis?

A

Inflammation or necrosis of the pancreas.

98
Q

What is the most common form of pancreatitis?

A

Edematous pancreatitis

99
Q

What are the causes of pancreatitis?

A
  1. Alcohol abuse
  2. Gallstones
  3. Virus
  4. Trauma/surgery
100
Q

How can gallstones cause pancreatitis?

A

Trap digestive enzymes (trypsin) → auto digestion og pancreas → inflammation

101
Q

What does inflammation of acute pancreatitis look like?

A
  1. Release of inflammatory mediators → ↑ vascular permeability and vessel dilation
  2. Leaking of fluid into peritoneal cavity → hypovolemia and decreased renal BF
  3. Systemic inflammatory response system (SIRS)
  4. Multiple organ failure (MOF)
102
Q

What are the sx of acute pancreatitis?

A
  1. Pain in upper abdomen
  2. Deep epigastric pain
  3. Abdominal dissension and tenderness
  4. Tachycardia
  5. Hypotension
  6. Fever
  7. Jaundice
  8. ↑ in amylase/lipase
103
Q

What is Parethesia?

A

Prickly pins-and-needles sensation in alcoholics or pernicious anemia

104
Q

What is cullen sign?

A

Bruising and edema to subcutaneous tissue from hemorrhagic pancreatitis

105
Q

What is grey-turner sign?

A

Bruising in flank area from bleeding behind the peritoneum

106
Q

What is steatorrhea?

A

From decreased or absent lipase

107
Q

What are the main clinical manifestation of acute pancreatitis?

A
  1. Parethesia
  2. Cullen sign
  3. Grey-turner sign
  4. Steatorrhea
108
Q

What are the warning signs of acute pancreatitis progression?

A
  1. Low UO
  2. Hypoxemia
  3. Restlessness
  4. Altered mental status
109
Q

What is chronic pancreatitis?

A

Tissue damage is irreversible even though chronic pain is less severe

110
Q

What are the causes of chronic pancreatitis?

A
  1. Alcoholism
  2. Genetics (familial HLD)
111
Q

What are sx of chronic pancreatitis?

A
  1. Weight loss
  2. Dull, constant abdominal pain
  3. Remove alcohol consumption
112
Q
A

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