Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

First Aid > Gastroenterology 2 > Flashcards

Gastroenterology 2 Flashcards

1
Q

What are the 2 blood supplies to the liver? What is the percentage of each?

A

Portal veins (80%) and Hepatic artery (20%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the venous drainage of the liver?

A

Central vein → Interlobular vein → Hepatic veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does the portal triad consist of?

A

Portal vein, hepatic artery, bile duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What liver zone is closest to the portal triad?

A

Zone 1 (periportal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What liver zone is closest to the central vein?

A

Zone 3 (centrilobular zone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Zone 1 of the liver is affected by which disease first?

A

Viral hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Zone 3 of the liver is most vulnerable to what?

A

Ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Zone 3 of the liver has a high concentration of what enzymes?

A

P450 enzymes in hepatocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Alcoholic liver disease commonly affects what zone of the liver?

A

Zone 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

The pancreas is formed from the fusion of what 2 structures? Where do they bud off from?

A

Ventral and dorsal bud; Bud off from endodermal lining of duodenum (foregut)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

The Ventral bud of the pancreas forms what?

A

Part of head, uncinate process, Main pancreatic duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

The Dorsal bud of the pancreas forms what?

A

Rest of head, Body, tail, accessory duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why is the pancreas described as Secondarily retroperitoneal?

A

Forms covered in peritoneum (intraperitoneal); Later fuses with posterior wall → retroperitoneal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is an annular pancreas?

A

Congenital anomaly of ventral bud → 2 lobes wrap around the duodenum in opposite directions forming a ring of pancreatic tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Annular pancreas can cause what?

A

Bowel obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is Pancreas Divisum?

A

Dorsal and ventral ducts do not fuse leading to 2 separate ducts (accessory duct drains majority of pancreas)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the presentation of Pancreas Divisum? What complication can it cause?

A

Often asymptomatic; Pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the 3 major salivary glands?

A

Submandibular, Parotid, Sublingual

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Where are the 3 major salivary glands located?

A

Submandibular and Sublingual: floor of mouth; Parotid: Behind angle of the jaw, below and in front of ears

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

The Submandibular gland secretes saliva into what duct?

A

Wharton’s duct → mouth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Saliva is made of what 6 components?

A

Mostly water (>90%), Mucin, glycoproteins, IgA antibody, Lysozymes, Lactoferrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are 2 functions of Mucin and glycoproteins in saliva?

A

Lubricate food; Bind bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Saliva is important for what type of immunity?

A

Innate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

2 important enzymes for digestion found in saliva are?

A

α amylase (digests carbohydrates) and Lingual lipase (digests lipids)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Where is amylase produced?

A

Saliva and pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

The optimal pH for salivary amylase is?

A

> 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Lipid digestion is carried out by what 2 enzymes in adults? Which plays a more important role?

A

Salivary lipase: Minor contributor; Pancreatic lipase: Main lipase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Salivary lipase plays an important role in which demographic?

A

Newborns (they lower pancreatic enzyme levels)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Salivary fluid is produced by what type of cell and modified by what type of cell?

A

Acinar cells; Ductal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Initial salivary fluid contains what 4 electrolytes? Is it hypotonic, isotonic, or hypertonic compared to plasma?

A

Na, Cl, K, HCO3-; Isotonic (same concentration as plasma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How do the ductal cells modify salivary fluid? Are they permeable to water?

A

Remove Na, Cl; Secrete K, HCO3-; Impermeable to water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

As salivary fluid passes the ductal cells, the saliva becomes what?

A

Hypotonic from removal of Na, Cl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Composition of salivary electrolytes varies with what?

A

Flow rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What happens to the composition of salivary electrolytes when there is a higher flow rate? What happens to the [Bicarb]?

A

Fluid becomes more like plasma because there is less time for ductal modification; [Bicarb] goes up at high flow rates because higher flow = more metabolism = more CO2 in glandular cells → more bicarbonate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are 2 effects of aldosterone on the salivary glands?

A

↑ Na absorption; ↑ K secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Secretion of saliva is increased by what 2 systems? Which one has a greater effect?

A

Sympathetic AND parasympathetic; PNS has a greater effect (activated by food, smell, etc.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What receptors are important in the regulation of saliva?

A

Muscarinic receptors (M1 and M3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the effects of Muscarinic antagonists on saliva secretion?

A

Causes dry mouth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the effects of Muscarinic agonists on saliva secretion?

A

Increase saliva production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the drug class of Atropine and Scopolamine?

A

Muscarinic antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the drug class of Pilocarpine? What condition is it used to treat?

A

Muscarinic agonist; Sjogren’s syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Cholinesterase poisoning will have what effect on saliva production?

A

Increase salivation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is sialolithiasis?

A

Salivary duct stones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Sialolithiasis is most common in what gland?

A

Submandibular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are 3 risk factors for Sialolithiasis?

A

Dehydration, Diuretics, Anticholinergic medication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is the treatment for Sialolithiasis?

A

Hydration, NSAIDs; rarely surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Sialadenitis often occurs secondary to what?

A

Obstructing stone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What pathogen most often causes Sialadenitis? It often contains what type of pathogen as well?

A

S. Aureus; Anaerobes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the common treatment for Sialadenitis caused by S. Aureus and anaerobes?

A

Nafcillin (Staph coverage); Metronidazole or Clindamycin (anaerobes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is a key feature of mumps?

A

Parotitis, often bilateral causing facial swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Salivary tumors are usually present in which gland? How does it present?

A

Parotid; Presents as facial swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

How does a benign salivary tumor present vs an invasive one?

A

Benign: mobile, painless (not invading the nerve); Invasive: painful (may involve facial nerve → paralysis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is the most common salivary gland tumor? How does it usually present?

A

Pleomorphic Adenoma (benign mixed tumor, rarely undergoes malignant transformation); Painless, mobile mass at the angle of the jaw

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What types of cells are found in a Pleomorphic Adenoma?

A

Epithelial and stromal tissue cells; Epithelial: Glandular cells (left); Stromal: Cartilage, sometimes bone (right)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is a risk factor for Pleomorphic Adenoma? What is the treatment?

A

Risk factors: Prior radiation; Treatment: Surgery +/- radiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Reoccurrence is uncommon in Pleomorphic Adenoma [T/F]. Why?

A

F; Tumor often has irregular margins and cells are left behind after surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is the second most common salivary tumor?

A

Warthin’s tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is another name for Warthin’s tumor?

A

Papillary Cystadenoma Lymphomatosum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Warthin’s tumor usually occurs in what gland?

A

Parotid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is a key risk factor for Warthin’s tumor?

A

Smoking (8x more common)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are 2 key histological findings seen in Warthin’s tumor?

A

Cysts surrounded by dense lymphoid infiltrate; Lymph tissue can aggregate into germinal centers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is the most common malignant salivary tumor?

A

Mucoepidermoid Carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is the key risk factor for Mucoepidermoid Carcinoma? What gland is it normally found?

A

Prior radiation; Parotid (can cause paralysis and pain)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What 3 cell types are found in Mucoepidermoid Carcinoma?

A

Squamous (epidermoid) cells, Mucus-secreting cells, Intermediate hybrid cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Where do hernias commonly occur?

A

In areas of discontinuity of the abdominal wall i.e. inguinal canal, esophagus, umbilicus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is the mnemonic for the femoral vessels? What does it stand for?

A

NAVeL (lateral to medial); Nerve-artery-vein-lymphatics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What are the anatomic borders for the femoral triangle?

A

Superior: Inguinal ligament; Medial: Adductor longus; Lateral: Sartorius

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What is the femoral sheath? What does it contain?

A

Tunnel of fascia below the inguinal ligament; Femoral vein, artery, and ring (Does not contain nerve)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is found within the femoral canal?

A

Lymph vessels and deep inguinal nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is the femoral ring? What is the importance of this landmark?

A

Opening to femoral canal; Site of femoral hernias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Testes descend through what structure to the scrotum?

A

Inguinal canal (processus vaginalis)

72
Q

What is found in the spermatic cord?

A

Vas deferens, arteries, veins, nerves

73
Q

What are the 3 fascial layers of the spermatic cord?

A

External spermatic fascia, Cremasteric fascia, Internal spermatic fascia

74
Q

The inguinal canal contains what key structure in males vs females?

A

Males: spermatic cord; Females: round ligament

75
Q

What structure forms the floor of the inguinal canal?

A

Inguinal ligament

76
Q

What is an Indirect Inguinal Hernia? What is the origin in relation to the epigastric vessels?

A

Abdominal contents travel through inguinal canal (covered by all layers of the spermatic fascia); Origin is lateral to epigastric vessels

77
Q

What is the Processus Vaginalis? What happens to it during the newborn period and during infancy?

A

Outpouching of peritoneum where testes descend; Remains open in newborn period and closes in infancy (replaced by fibrous tissue)

78
Q

After the processus vaginalis is replaced with fibrous tissue, it remains as the what?

A

Tunica vaginalis testis (serous covering of testes)

79
Q

If the processus vaginalis fails to close, it may result in what?

A

Indirect inguinal hernia

80
Q

Most common type of inguinal hernia is what?

A

Indirect

81
Q

Indirect Inguinal Hernia is most common on the what side?

A

Right (Persistent processus vaginalis more common on right)

82
Q

Indirect Inguinal Hernias are more common in what demographic?

A

Men

83
Q

What are 2 risk factors for indirect inguinal hernia in adulthood? In newborns?

A

Adults: Heavy lifting, Constipation; Newborns: Mechanical ventilation

84
Q

What is a Direct Inguinal Hernia? What is the origin in relation to the epigastric vessels?

A

Bowel bulges ‘directly’ through abdominal wall (Hesselbach’s triangle); Origin is medial to epigastric vessels

85
Q

What is another name for the external inguinal ring? Where is it located?

A

Superficial inguinal ring; Terminal end of the inguinal canal, just superior to the pubic tubercle

86
Q

Direct inguinal hernias are caused by breakdown of what?

A

Transversalis fascia

87
Q

Direct Inguinal Hernias are covered by what fascia?

A

External spermatic fascia only

88
Q

Direct Inguinal Hernias travel through the what ring?

A

Superficial/external ring

89
Q

What are the anatomic boundaries of Hesselbach’s triangle?

A

Inguinal ligament, Inferior epigastrics, Rectus abdominis; Floor: Transversalis fascia

90
Q

Direct Inguinal Hernias usually occur in what demographic?

A

Older men

91
Q

What is a femoral hernia?

A

Bowel protrudes through femoral ring below inguinal ligament

92
Q

Femoral hernias are more common in what demographic?

A

Women

93
Q

There is a high risk for what complication in femoral hernia?

A

Incarceration (bowel trapped in hernia sac since femoral ring is small opening)

94
Q

What are 2 complications of inguinal hernias?

A

Incarceration: bowel cannot be reduced; Strangulation: blood flow cut off, bowel becomes ischemic/necrotic → urgent surgery is indicated

95
Q

How are inguinal hernias usually diagnosed?

A

Clinically (US/CT sometimes used)

96
Q

What is the treatment for inguinal hernias?

A

Surgery: primary closure, mesh placement

97
Q

What is a ventral hernia? What are 2 subtypes?

A

Bowel protrusion through ventral abdominal wall; Umbilical, incisional hernias

98
Q

What is a major risk factor for hiatal hernia?

A

Obesity

99
Q

Hiatal hernia can lead to what condition?

A

GERD

100
Q

Majority of hiatal hernias are what type?

A

95% are Type I (sliding hiatal hernia)

101
Q

What is a Sliding hiatal hernia?

A

Herniation through hiatus; Displacement of GE junction above diaphragm, fundus remains below GE junction

102
Q

Sliding hiatal hernia has a what appearance?

A

Hourglass

103
Q

What is a Paraesophageal hiatal hernia?

A

Protrusion of stomach fundus due to defect in ‘phrenoesophageal membrane’; GE junction is in normal location

104
Q

What is a classic finding in Paraesophageal hiatal hernia?

A

Bowel sounds in lung fields

105
Q

What is the cause of congenital diaphragmatic hernia? In utero herniation can lead to what?

A

Defective formation of pleuroperitoneal membrane → hole in diaphragm; Pulmonary hypoplasia

106
Q

What is the prognosis of congenital diaphragmatic hernia?

A

Variable, often poor due to associated pulmonary complications

107
Q

What is a Paraesophageal hiatal hernia?

A

Protrusion of stomach fundus due to defect in the phrenoesophageal membrane. GE junction is in normal location.

108
Q

What is a classic finding in Paraesophageal hiatal hernia?

A

Bowel sounds in lung fields.

109
Q

What is the cause of congenital diaphragmatic hernia?

A

Defective formation of pleuroperitoneal membrane leading to a hole in diaphragm.

110
Q

What can in utero hernation lead to?

A

Pulmonary hypoplasia.

111
Q

What is the prognosis of congenital diaphragmatic hernia?

A

Often fatal.

112
Q

What is bile made of?

A

Mostly water, phospholipids, electrolytes, bile salts, and bilirubin.

113
Q

What is a triglyceride made of?

A

1 glycerol and 3 fatty acids.

114
Q

Bile salts act as _____?

A

Surfactant.

115
Q

How are bile salts formed?

A

Taurine and glycine conjugated to bile acids (cholic acid, chenodeoxycholic acid) to form bile salts.

116
Q

Where are bile acids synthesized?

A

Only in liver (>90% classic pathway, <10% acidic pathway).

117
Q

What is the rate limiting enzyme in the classic pathway of bile acid synthesis?

A

7-α hydroxylase.

118
Q

What does 7-α hydroxylase require?

A

Cytochrome P450 enzymes, NADPH, and oxygen.

119
Q

Where does most lipid absorption occur?

A

In the jejunum.

120
Q

Bile salts undergo ______?

A

Enterohepatic circulation.

121
Q

What are the two outcomes of bile salts?

A

95% absorbed and recycled, 5% excreted in stool.

122
Q

Where are bile salts absorbed?

A

By active transporters in the terminal ileum.

123
Q

What are three functions of bile salts?

A

Emulsification of fats, excretion of cholesterol, and antimicrobial activity.

124
Q

How is cholesterol excreted from the body?

A

Convert cholesterol to bile salt (conjugated bile acid) and excrete in stool.

125
Q

What are three bile acid resins?

A

Cholestyramine, colestipol, colesevelam.

126
Q

What is the function of bile acid resins?

A

Retains bile acids in the stool to prevent reabsorption.

127
Q

What is the mechanism by which bile salts prevent bacterial overgrowth?

A

Disrupts bacterial cell membranes.

128
Q

What is cholestasis?

A

Disrupted bile flow to intestines.

129
Q

What are two lab findings in cholestasis?

A

Direct (conjugated) hyperbilirubinemia and elevated alkaline phosphatase (ALP).

130
Q

What are four symptoms of cholestasis?

A

Jaundice, pruritus, dark urine, and clay-colored stools.

131
Q

What are two long term consequences of cholestasis?

A

Fat malabsorption and decreased fat soluble vitamins.

132
Q

Alkaline Phosphatase is produced by what cells?

A

Bile duct epithelial cells.

133
Q

Bile obstruction leads to an increase or decrease in Alkaline Phosphatase?

A

Increase.

134
Q

What are the levels of alk phos and AST/ALT in cholestasis?

A

↑ alk phos&raquo_space; ↑ AST/ALT.

135
Q

What does ↑ AST/ALT&raquo_space; ↑ Alk Phos indicate?

A

Primary abnormality relates to hepatocytes.

136
Q

What does ↑ Alk Phos&raquo_space; ↑ AST/ALT indicate?

A

Primary abnormality relates to bile ducts.

137
Q

What is the best first test for cholestasis?

A

Right upper quadrant ultrasound.

138
Q

What are normal AST/ALT and Alk phos levels?

A

AST/ALT: ~50IU/L, Alk phos: ~100 IU/L.

139
Q

What are three extrahepatic causes of cholestasis?

A

Gallstone, pancreatic mass, biliary strictures.

140
Q

What are four intrahepatic causes of cholestasis?

A

Primary biliary cirrhosis, cholestasis of pregnancy, contraceptives, erythromycin.

141
Q

Describe Heme metabolism.

A

Heme is released from old RBCs, macrophages convert it to bilverdin, then to bilirubin.

142
Q

Bilirubin is carried by what protein in the blood?

A

Albumin.

143
Q

What enzyme conjugates bilirubin in the liver?

A

UDP glucuronyltransferase.

144
Q

What does UDP glucuronyltransferase add to unconjugated bilirubin?

A

Glucuronic acid, forming bilirubin monoglucuronide and bilirubin diglucuronide.

145
Q

What is conjugated bilirubin also called?

A

Bilirubin diglucuronide.

146
Q

What is the purpose of bilirubin conjugation?

A

Produces more water soluble compounds that facilitate excretion with bile.

147
Q

What are two functions carried out by bacteria in bilirubin metabolism?

A

Convert unconjugated bilirubin back and produce urobilinogen.

148
Q

What is the fate of the majority (80-90%) of urobilinogen?

A

Converted to stercobilin and excreted in feces.

149
Q

What happens to the urobilinogen not excreted in feces?

A

Reabsorbed by intestines and taken up by liver, small amount converted to urobilin.

150
Q

What is the Van den Bergh reaction?

A

Coupling of bilirubin with a diazonium salt to form a colored complex.

151
Q

Can serum conjugated bilirubin directly undergo the Van den Bergh reaction?

A

Can.

152
Q

Can serum unconjugated bilirubin directly undergo the Van den Bergh reaction?

A

Cannot.

153
Q

What are the levels of bilirubin (conjugated) and urobilinogen in a normal urine dipstick?

A

Bilirubin: Normal absent, Urobilinogen: Normally a small amount.

154
Q

What is the earliest sign of jaundice?

A

Scleral icterus.

155
Q

What is a normal total bilirubin level and at what level does jaundice appear?

A

Normal: <1.0 mg/dL, Jaundice: >3mg/dL.

156
Q

What are four possible causes of dark urine?

A

Hematuria, rhabdomyolysis, elevated conjugated bilirubin, dehydration.

157
Q

What are three general causes of increased bilirubin?

A

Hemolysis, biliary obstruction, liver disease.

158
Q

What three lab findings are present in hemolysis hyperbilirubinemia?

A

Increased unconjugated bilirubin, no urine bilirubin detected, increased urobilinogen.

159
Q

What are four lab findings present in biliary obstruction hyperbilirubinemia?

A

Elevated serum direct bilirubin, urine bilirubin detected, ↑ AlkP, absent urobilinogen.

160
Q

Why is bilirubin fractionation unreliable for liver disease?

A

Often mixed increase of direct/indirect.

161
Q

Name two primary liver diseases that can cause unconjugated hyperbilirubinemia.

A

Chronic hepatitis, advanced cirrhosis.

162
Q

Name three primary liver diseases that can cause conjugated hyperbilirubinemia.

A

Viral hepatitis, alcoholic hepatitis, NASH.

163
Q

How do urobilinogen levels present early vs late in primary liver disease?

A

Early: increase, Late: decrease.

164
Q

How does rifampin cause hyperbilirubinemia?

A

Competes with bilirubin for uptake by liver, blunt hepatic uptake of unconjugated bilirubin.

165
Q

What enzyme is defective in Gilbert’s Syndrome?

A

UDP-glucuronyltransferase.

166
Q

What is the clinical presentation of Gilbert’s Syndrome?

A

Jaundice can occur with increased bilirubin production, no serious clinical consequences.

167
Q

What is Crigler-Najjar Syndrome?

A

Severely reduced/absent UGT enzyme leading to inability to conjugate bilirubin.

168
Q

What is the clinical presentation of Crigler-Najjar Syndrome Type I?

A

Usually presents in infancy with jaundice and kernicterus.

169
Q

What type of bilirubin can cause Kernicterus?

A

Unconjugated.

170
Q

How does unconjugated bilirubin cause Kernicterus?

A

It is fat soluble and can cross the blood-brain barrier, acting as a neurotoxin.

171
Q

Crigler-Najjar Syndrome Type II is less severe compared to which type?

A

Crigler-Najjar Syndrome Type I.

172
Q

What is the treatment for Crigler-Najjar Syndrome Type II?

A

Phenobarbital or clofibrate to induce liver glucuronidation.

173
Q

What is Dubin-Johnson Syndrome?

A

Defective liver excretion of conjugated bilirubin due to an abnormal gene.

174
Q

What are three findings in Dubin-Johnson Syndrome?

A

↑ conjugated bilirubin, bilirubin in urine, liver turns black.

175
Q

What is the treatment for Dubin-Johnson Syndrome?

A

No treatment required, benign condition.

176
Q

What is Rotor’s syndrome?

A

Similar to Dubin-Johnson but milder with impaired liver excretion of conjugated bilirubin.

177
Q

What differentiates Rotor’s syndrome from Dubin-Johnson?

A

No black liver.

First Aid (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions