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GI > GI Final Exam > Flashcards

GI Final Exam Flashcards

1
Q

What is the fibrous connective tissue capsule covering the liver?

A

Glisson’s capsule

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2
Q

What is contained within the hilum of the liver?

A

• portal vein
• hepatic artery
• common bile duct
• lymphatic vessels
• nerves

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3
Q

What is a classic liver lobule?

A

• hexagonal shape with portal canals at the corners of the hexagon and a central vein at the center

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4
Q

What are the components of the portal canal?

A

• portal vein
• hepatic artery
• bile duct

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5
Q

What is the space of Disse?

A

A space that lies between sinusoidal lining and surface of parenchymal cells: this is where blood can interact directly with the Enterocyte surface

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6
Q

What is the appearance of liver hepatocytes?

A

• cells arranged in cords lining the sinusoids
• many Golgi and sER (eosinophilic)
• many ribosomes and rER (basophilic)
• glycogen and lipid (untrained)
• this creates the appearance of an eosinophilic cell with basophilic stippling

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7
Q

Direction of blood flow in the liver

A

Portal vein —> central vein through hepatic sinusoids

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8
Q

What are the bile canaliculi?

A

• located between adjacent hepatocytes, formed by their tight junctions
• contain small microvilli that extend into cannular lumen
• collect bile produced by hepatocytes

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9
Q

What is the flow of bile through the liver?

A

Parenchyma (hepatocytes) —> bile canaliculi —> bile ducts (canal of Hering) —> hepatic duct —> cystic duct —> gallbladder

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10
Q

What are the three perspectives for liver lobule microarchitecture?

A
  1. Classic lobule
  2. Portal lobule
  3. Acinus lobule
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11
Q

The concepts of a classic liver lobule:

A
  • blood flows from periphery of lobule to the center
  • bile flows from the center of the lobule to the periphery
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12
Q

The concepts of a portal liver lobule:

A
  • portal Canal is the lobule center
  • blood flows from the center of the lobuleto the periphery
  • bile flows from the periphery of the lobule to the center
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13
Q

The concepts of a liver acinus lobule:

A
  • the center of the lobule is the terminal branch of the portal vein and hepatic artery
  • blood flows from the center of the acinus to the periphery
  • bile flows from the periphery of the acinus to the center
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14
Q

What muscles make up the pelvic musculature?

A

• walls: piriformis, obturator internus
• floor: levator ani (pubococcygeus and iliococcygeus, puborectalis), coccygeus

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15
Q

What muscles make up the pelvic musculature?

A

• walls: piriformis, obturator internus
• floor: levator ani, coccygeus

Levator ani= pubococcygeus and iliococcygeus

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16
Q

Why does prolapse typically occur?

A

Injury to the perineal body

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17
Q

What runs through the greater sciatic foramen?

A

• piriformis
• superior to piriformis: superior gluteal nerve, artery, vein
• inferior to piriformis: inferior gluteal artery, nerve, vein, sciatic nerve, pudendal nerve, internal pudendal artery/vein, posterior femoral cutaneous nerve, nerve to obturator internus and quadratus femoris

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18
Q

What runs through the lesser sciatic foramen?

A

• pudendal nerve, internal pudendal artery and vein

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19
Q

What runs through the obturator foramen?

A

• obturator nerve, artery, vein

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20
Q

What LFTs indicate hepatocyte injury?

A

• AST, ALT, LDH
• all involved in gluconeogenesis pathway
• all increase during liver injury/disease

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21
Q

Where is AST present?

A

In cytosol and mitochondria of the liver, cardiac muscle, skeletal muscle, kidney, brain, pancreas, lungs, WBC and RBC

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22
Q

Where is ALT present?

A

In the cytosol, mostly in the liver

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23
Q

Where is LDH present?

A

In the cytosol everywhere: participates in glucogenesis in the liver and glycolysis everywhere else

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24
Q

What LFTs indicate biliary damage/function?

A

• bilirubin, alkaline phosphatase, 5’-nucleotidase, and GGT (gammaglutamyl transferase)

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25
Q

Where is alkaline phosphatase located?

A

• microvilli of the bile canaliculus
• also present in bone, intestine, placenta, kidney, WBC (non-specific)

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26
Q

Where is 5’-nucleotidase localized?

A

• in the microvilli of the bile canaliculus (more specific to the liver than alk phos)

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27
Q

Where is GGT located?

A

• found in hepatocytes and bile duct cells
• sensitive for hepatobiliary disease, but not specific

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28
Q

What LFTs indicate hepatocyte function?

A

• albumin
• clotting factors (PT/PTT)
• these labs decrease in disease (albumin, clotting factors), therefore PT/PTT increase in disease

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29
Q

Mild ALT predominant elevation indicates:

A

• hepatitis B
• hepatitis C
• acute viral hepatitis (A-E, EBV, CMV)
• steatosis
• hemachromatosis/auto immune
• alpha one antitrypsin
• Wilsons disease
• celiac disease

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30
Q

Mild AST predominant elevation indicates:

A

• alcohol related liver injury
• cirrhosis
• steatosis

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31
Q

What are non-hepatic reasons for mild ALT/AST elevation?

A

Hemolysis, myopathy, thyroid disease, strenuous exercise, macro AST

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32
Q

What are the common causes of severe elevations of ALT/AST (15x the upper limit of normal)?

A
  1. Drug induced (acetaminophen)
  2. Occupational/environment (toluene, CCl4)
  3. Ischemic hepatitis (Budd Chiari syndrome)
  4. Viral hepatitis (A-E, herpes)
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33
Q

When do you typically see an elevated alkaline phosphatase that is physiologic and not pathologic?

A

In the third trimester of pregnancy (placenta), and adolescence (bone)

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34
Q

If alkaline phosphatase is chronically elevated, evaluate for:

A
  • cholestatic liver disease
  • infiltrative liver disease (cancer, sarcoidosis)
  • biliary obstruction
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35
Q

When you have an elevated alkaline phosphatase, what confirms hepatic source?

A

Gammaglutamyl transferase (GGT) found in hepatocytes and bile duct cells

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36
Q

What drugs can cause an elevated GGT?

A

Carbamazepine, phenytoin, barbiturates

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37
Q

Blood from the G.I. system goes directly to the liver via what?

A

The portal vein

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38
Q

What are hepatic pit cells?

A

Liver associated lymphocytes. These natural killer cells protect against viruses and tumor cells

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39
Q

What are Kupfer cells?

A

Endocytic, phagocytic, macrophages

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40
Q

The liver converts excess protein and carbohydrates to what?

A

Blood proteins, glucose, and VLDL

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41
Q

How does the liver work to detoxify xenobiotics and metabolites?

A

• two phase reactions, where the first phase is to change the oxidation state to polar/reactive to induce higher solubility and then the second phase adds polar group to increase solubility

1.) reduction, oxidation, hydroxylation, hydrolysis
2.) conjugation, sulfuration, methylation, glucuronidation

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42
Q

What makes up phase 1 of the livers detoxifying capacity?

A

Cytochrome P450 enzymes using NADPH, sometimes NADH, and O2

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43
Q

What is an important class of phase 2 enzymes for liver detoxification?

A

Glutathione conjugation by glutathione S transferases

~ this is why depletion of the pool of reduced glutathione can exacerbate toxicity

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44
Q

What is the clinical presentation of acetaminophen toxicity?

A
  1. Early: nausea, vomiting
  2. 24-48 hours: ALT/AST increase, LDH increase, PTT/PT increase
  3. 72-96 hours: jaundice, hepatomegaly, increased bilirubin, encephalopathy, hypotension, hypoglycemia, metabolic acidosis, death by organ failure
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45
Q

In acetaminophen poisoning, CYP2E1 converts acetaminophen to what?

A

NAPQI: this creates adducts on cell proteins and kills cells

~ maintaining a pool of reduced glutathione (N-acetyl cysteine) allows for shuttling of the pathway to create mercapturic acid and safe excretion through the kidneys

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46
Q

Which cells are most affected by NAPQI cell destruction?

A

Perivenal (near the central vein, zone 3)

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47
Q

What induces CYP2E1 expression, and increases the rate of NAPQI production?

A

Alcohol. This depletes NADPH, which is required to maintain the pool of reduced glutathione

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48
Q

What is the hallmark symptom of a glycogen storage disease?

A

Fasted hypoglycemia

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49
Q

Excess nitrogen that result from amino acid catabolism must be converted to urea for excretion. Where does urea’s nitrogen come from?

A

Free ammonia, and aspartate

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50
Q

The majority of excess nitrogen is transported from peripheral tissue to the liver in what form?

A

Amino acids: glutamine and alanine

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51
Q

What hepatocytes secrete Wnt?

A

Central vein endothelial cells

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52
Q

To avoid liver toxicity, how is glutamine handled in the liver?

A

• High concentrations of glutaminase and CPS1 at the periportal hepatocytes
• high concentrations of glutamine synthetase at perivenal hepatocytes

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53
Q

How does a gradient of Wnt concentration create a safe zone for a free ammonia?

A

It all allows free ammonia to be a substrate for the urea cycle, without free ammonia being released into the general circulation

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54
Q

What are the most common causes of acute hepatitis?

A

• hepatitis A, hepatitis E
• fecal-oral route, transmitted through food or water

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55
Q

What does hepatitis A look like?

A

ssRNA+ virus, non-envelope, icosahedral nucleocapsid, single-stranded positive genome, non-segmented (picornavirus)

~ incubation of 15 to 50 days

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56
Q

What does hepatitis look like?

A

RNA virus, icosahedral nucleocapsid, non-enveloped, single-stranded positive genome, non-segmented, hepeviridae

~ incubation of 15 to 60 days

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57
Q

What are the diagnostic criteria of hepatitis A?

A
  1. Lab: Immunoglobulin M (IgM) for hepatitis A virus RNA
  2. Case classification confirmed: clinical criteria for IgM anti-HAV or hepatitis A RNA detected by PCR/genotyping

~ also qualifies if clinical criteria in a person who had contact with a confirmed hepatitis A case 15-50 days prior to onset of symptoms

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58
Q

What is the treatment/post exposure prophylaxis for hepatitis A?

A

• treatment is symptomatic
• exposure prophylaxis is hepatitis A vaccine administered within two weeks of exposure, occasionally co-administration of GamaSTAN S/D immunoglobulin

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59
Q

Who is most at risk for hepatitis E severity?

A

• pregnant women, particularly in the third trimester
• undercooked pork, bear, deer meat eaters

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60
Q

What is hepatitis B?

A

• liver infection caused by interaction with infected body fluids that can lead to chronic viral hepatitis
• liver damage via host immune response mediated by cytotoxic T lymphocytes
• only 5% of cases become chronic

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61
Q

What is hepatitis C?

A

• liver infection caused by interaction with infected body fluids that can lead to chronic viral hepatitis
• liver damage via host immune response mediated by cytotoxic T lymphocytes
• 50% of cases become chronic

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62
Q

Which has a vaccine: hepatitis B or hepatitis C?

A

Hepatitis B. It is recommended for all children, commonly co-administered in a DTaP, or IPV

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63
Q

What does hepatitis B look like?

A
  • dsDNA virus, Icosahedral nucleocapsid, enveloped, double-stranded partial genome (circular), hepadnaviridae

~ incubation time of 2 to 5 months

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64
Q

What does hepatitis C look like?

A

• RNA virus, icosahedral nucleocapsid, enveloped, linear single-stranded positive genome, flaviviridae family (just like yellow fever, dengue fever and tickborne encephalitis)

~ incubation time of 2 weeks to 6 months

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65
Q

What are the two most common routes of transmission for hepatitis B?

A

• percutaneous (puncture through the skin) with infectious blood/body fluid

• mucosal contact with infectious blood/body fluids

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66
Q

What makes hepatitis B so difficult to clear?

A

Covalently closed circular DNA (cccDNA) as the template for viral messenger RNA transcription

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67
Q

What are Dane particles?

A

Hepatitis B virus (HBV) virions — seen on EM

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68
Q

What are the three serological tests required for laboratory diagnosis of hepatitis B?

A

• hepatitis B surface antigen [HBsAg]
• hepatitis B surface antibody [anti-HBs]
• total hepatitis B core antibody [anti-HBc]

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69
Q

What indicates a chronic infection with hepatitis B?

A

• presence of HBsAg (surface antigen) for longer than six months

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70
Q

What is the treatment for hepatitis B?

A
  • supportive, no alcohol
  • antivirals: entecavir, tenofovir, iamivudine, adefovir, telbivudine
  • interferons: Intron A, Peg-IFN
  • liver transplant in severe cases

~ complete cure not possible, functional cure (undetectable serum antigen and HBV DNA, with residual cccDNA POSSIBLE)

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71
Q

Which hepatitis is most likely to cause hepatocellular carcinoma?

A

Hepatitis B— 12-300x greater risk

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72
Q

What is hepatitis D?

A

• only a viral genome, not virus
• ORF transcribed— encodes HDAg
• Super infection with HBV is required (replication tools from HBV needed for HDV)

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73
Q

Why is hepatitis C a “quasi species”?

A

It’s RNA dependent RNA polymerase (3’-5’ repair inffective) is highly error prone— creating many subtypes

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74
Q

Where does hepatitis C replication occur?

A

All occurs in the cytosol, nucleus not required. Virus enters via pH dependent and/or clathrin-mediated endocytosis

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75
Q

What is a unique feature of hepatitis C replication?

A

• membranous Web: includes double membrane vesicles containing HCV nonstructural proteins, HCV RNA, ER membranes, and lipid droplets

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76
Q

What are the complications of chronic hepatitis C?

A

Fibrosis, cirrhosis, liver cancer (hepatocellular carcinoma)

Non-hepatic complications: diabetes, glomerulonephritis, cryoglobulinemia, porphyria cutanea tarda, non-Hodgkin’s lymphoma

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77
Q

What are the treatment options for hepatitis C?

A
  1. Older: interference on plus the antiviral ribavirin
  2. Newer: DAA therapy (90% cure rate)
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78
Q

What is direct acting antiviral (DAA) therapy?

A
  • hepatitis C treatment targeting specific nonstructural virus proteins disrupting viral replication and infection
  • PIs (protease inhibitor), NPIs (nucleoside polymerase inhibitor), NNPIs, and NS5A inhibitors
  • (sofosbuvir, velpatasvir, and voxilaprevir)
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79
Q

What are common symptoms of yellow fever due to hepatic dysfunction?

A

Jaundice and councilman bodies

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80
Q

What enzyme is responsible for the conjugation of bilirubin?

A

UGT1A1: uridine diphosphate-glucuronyltransferase (peptide 1A) in the hepatocyte

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81
Q

Which enzymes are important for transporting conjugated bilirubin from the liver?

A

• MRP2: multi drug resistant protein 2
• OATP: organic anion transporting polypeptide

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82
Q

What are the causes of unconjugated (indirect) hyperbilirubinemia?

A

1. Increased production: hemolysis, ineffective erythropoiesis (folate deficiency, iron deficiency, anemia)

2. Defects and conjugation, UGT1A1 activity: defect (Gilbert syndrome, Crigler Najjar syndrome)

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83
Q

What is Gilbert syndrome?

A
  • common clinically innocuous, unconjugated hyperbilirubinemia with otherwise normal liver chemistries
  • polymorphism of gene encoding bilirubin UGT1A1 (unable to conjugate bilirubin)
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84
Q

What is Crigler Najjar syndrome?

A

• type one: severe UGT1A1 deficiency, fatal in neonatal period

• type two (rare): similar to Gilbert syndrome, milder UGT1A1 deficiency

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85
Q

What is bilirubin encephalopathy/Kernicterus?

A

• hyperbilirubinemia leading to babies who are lethargic, hypotonic/hypertonic, high-pitched cry, opisthotonos, and have seizures
• permanent neurological symptoms such as choreoathetosis, spasticity, hearing loss, ataxia, mental retardation may occur

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86
Q

What are the common causes of conjugated (direct) hyperbilirubinemia?

A

Parenchymal disease or obstruction:

• hepatitis, cirrhosis, medication/toxins
• defects in canalicular transport (MRP2, OATP)
• bile duct obstruction

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87
Q

What is the name of the disease due to decreased MRP2 activity, causing blackening of the liver?

A

Dubin Johnson syndrome

~ elevated conjugated bilirubin

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88
Q

What disease process results due to a decreased OATP activity?

A

Rotor syndrome

~ elevated conjugated bilirubin

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89
Q

What are the notable features of fulminant hepatitis?

A

Mental status changes, bleeding/easy bruising, ascites and edema

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90
Q

Which is more mild, acute or chronic hepatitis?

A

Chronic: however, it is more likely to lead to hepatic failure or hepatocellular cancer

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91
Q

(Acute/chronic) hepatitis is more likely to have cholestatic findings compared to only hepatocellular

A

Chronic is more likely to have cholestatic findings of elevated alkaline phosphatase, elevated GGT, and elevated bilirubin

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92
Q

What does ballooning degeneration in acute hepatitis look like?

A
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93
Q

When do you see ground glass cells?

A

Typically hepatitis B

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94
Q

What histological changes are seen in hepatitis C?

A

• fatty changes
• bile ducts maintained, not destroyed

95
Q

What are the common causes of fulminant hepatitis/massive hepatic necrosis?

A

• acute viral hepatitis
• drug or toxin induced hepatitis (acetaminophen)
• vascular liver disease
• autoimmune hepatitis
• Wilson’s disease

96
Q

What is the pattern of necrosis for viral hepatitis and autoimmune hepatitis?

A

Focal, random necrosis with inflammatory infiltration

97
Q

What is the pattern of necrosis for drug toxicity or ischemic liver injury?

A

Zonal necrosis, non-inflammatory (primarily effects zone 3, near the central vein)

98
Q

Ground glass hepatocytes in hepatitis B look like what?

A

Their appearance is due to the accumulation of HBV surface antigen within the hepatocyte

99
Q

What are common morphological findings of hepatitis C?

A
  • progressions to chronic hepatitis in 80 to 90%
  • non-specific, variable fibrosis and cirrhosis
  • lymphoid aggregates and steatosis can be seen
100
Q

What does hepatitis D require in order to be infectious?

A

Coinfection or superinfection with hepatitis B

101
Q

Hepatitis E has a mortality rate in 20% of what patient population?

A

Pregnant people

102
Q

What are the genetic predispositions to autoimmune hepatitis?

A

• white: HLADR3
• Japanese: HLADR4
• South Americans: HLADRB1

~ female predominant (78%)

103
Q

What are the autoantibodies that can be seen in autoimmune hepatitis?

A

Type 1: adults, most common-
• anti-nuclear antibodies (ANA)
• anti-smooth muscle actin antibodies (ASMA)

Type 2: children-
• anti-liver kidney microsome-1 (LKM-1)

104
Q

What are the common pathological histology findings of autoimmune hepatitis?

A

• combination of lobular and portal/Periportal inflammation, often robust
• plasma cells numerous

105
Q

How do you diagnose autoimmune hepatitis?

A

Clinical evidence of hepatitis +

  1. Autoantibodies (ANA/ASMA or LKM)
  2. Elevated serum IgG
  3. Exclusion of viral/drug or toxic causes
  4. Supportive histological findings
106
Q

What’s the difference between steatosis and steatohepatitis?

A

Steatosis is only the fat deposition within hepatocytes, steatohepatitis is fat deposition with evidence of hepatocyte injury (biochemical and histologic)

107
Q

What is the pattern of fatty deposits for alcoholic and non-alcoholic fatty liver disease?

A

Macrovesicular with some microvesicular steatosis

108
Q

What generates a lot of NADH, leading to lipogenesis and reduced hepatocyte fatty acid oxidation?

A

Ethanol metabolism by alcohol dehydrogenase and acetaldehyde dehydrogenase

109
Q

Is steatosis reversible with the cessation of alcohol consumption?

A

Yes

110
Q

What are the microscopic features of alcoholic steatohepatitis?

A

• liver cell injury: swelling (ballooning degeneration) and necrosis
• Mallory bodies (cytokeratin aggregates)
• neutrophilic inflammation, clustered around degenerating hepatocytes

111
Q

Progressive alcohol liver disease can lead to what?

A

Cirrhosis and deposition of collagen/fibrosis typically beginning in perivenular zone 3 region

~ TGF-beta responsible for collagen deposition

112
Q

AST is typically 2x higher than ALT in what type of hepatitis?

A

Alcoholic hepatitis (every other hepatitis typically presents with a relatively higher ALT)

113
Q

What is nonalcoholic fatty liver disease and what is it associated with?

A

• steatosis with little or no alcohol consumption
• associated with: obesity, DM2, hyper lipidemia, hypertension

~ currently the most common cause of chronic liver disease in the United States

114
Q

What is cirrhosis?

A

• common end stage of chronic liver disease— extreme liver destruction replaced by fibrosis
• TGF-beta activates stellate cells in the space of Disse and they begin to lay down collagen

115
Q

What is the lab evaluation of cirrhosis?

A

• cholestasis: elevated alkaline phosphatase, elevated bilirubin
• reduced synthetic function: low albumin and clotting factors (PT/PTT)
• AST/ALT maybe low/normal, due to loss of liver parenchyma

116
Q

In cirrhosis, a combination of fibrosis and regeneration of hepatocytes leads to what?

A

Diffuse scarring and nodularity (typically irreversible, some reversibility with total cessation of alcohol consumption and eradication of hepatitis C)

117
Q

What are the complications of cirrhosis?

A

• hypoalbuminemia: edema
• clotting factor deficiencies: bleeding
• estrogen accumulation: gynecomastia, Palmar erythema, spider angiomata
• bilirubin accumulation: jaundice
• ammonia accumulation: hepatic encephalopathy, AMS, asterixis and coma

118
Q

What are the three portal hypertension/restrictions of blood flow through the liver, and which is the most common for cirrhosis?

A

• prehepatic: thrombosis/structural
• intrahepatic: cirrhosis
• posthepatic: hepatic vein obstruction, Budd-Chiari syndrome, right sided heart failure

119
Q

What are the complications of portal hypertension?

A

• hepatic encephalopathy (ammonia)
• ascites
• formation of portosystemic venous shunts
• congestive splenomegaly

120
Q

What is ascites?

A

• increased fluid in extravascular space with accumulation and abdominal cavity (increased hydrostatic pressure in hepatic sinusoids due to fibrosis, decreased oncotic pressure due to loss of albumin production)

121
Q

What is spontaneous bacterial peritonitis?

A

A life-threatening bacterial infection of the ascitic fluid

122
Q

What are the portosystemic shunts?

A

• esophageal varies
• hemorrhoids
• Caput medusae

123
Q

Why does congestive splenomegaly occur in cirrhosis?

A

• decrease in clotting factors, increased bleeding—> massively expanded red pulp leading to sequestration of cellular blood elements
• thrombopenia can exacerbate bleeding tendencies, pancytopenia possible

124
Q

What is Budd-Chiari syndrome?

A
  • A hypercoagulable state (polycythemia vera) leading to obstruction of the hepatic veins
  • presents with pain, hepatomegaly, and ascites
  • hepatocellular pattern with transaminases up to 5x normal
125
Q

In what condition would you see thrombi in the hepatic veins?

A

Budd-Chiari syndrome

126
Q

How does right sided heart failure lead to liver failure?

A

• right sided heart failure causes passive congestion with dilated sinusoids and a progressive loss of centrilobular hepatocytes —> long-standing can lead to hepatic fibrosis

127
Q

How does left sided heart failure cause liver failure?

A

Left sided heart failure causes hypoperfusion and ischemic and necrosis of centrilobular hepatocytes —> long-standing can lead to hepatic fibrosis (cardiac sclerosis)

128
Q

What is the common gross finding of passive congestion/systemic circulatory compromise in the liver?

A

nutmeg liver creating a mottled appearance

129
Q

What is the difference between right sided and left sided heart failure creating centrilobular (zone 3) congestion and necrosis?

A

• right sided heart failure: congestion > necrosis
• left sided heart failure: necrosis > congestion

130
Q

What powers biosynthetic and detoxification reactions in the liver?

A

NADPH from the pentose phosphate pathway

131
Q

How does glycosylation occur?

A

In the lumen of the endoplasmic reticulum of hepatocytes: the chain begins assembly on a molecule of dolichol and then transported to the Golgi for additional modification

132
Q

What is phosphoglucomutase 1 deficiency?

A

• PGM1 is an enzyme essential for glycogenolysis and glycogen synthesis. Also important for generating UDP-galactose, glycosylation intermediate
• symptoms: hepatopathy, bifid uvula, dilated cardiomyopathy, hypoglycemia, myopathy, mental retardation

133
Q

Without proper glycosylation, what happens to transferrin?

A

It cannot be created, iron cannot be transported. It is normally glycosylated with two identical glycol chains that terminate with two sialic acids

134
Q

What works as treatment for PGM1 deficiency?

A

Dietary galactose supplementation

135
Q

What hormone has three glycosylation sites, required for maturation of puberty in females?

A

Leutinizing hormone (LH): glycosylation stabilizes it in circulation and increases its affinity for its receptor (without glycosylation, luteinizing hormone does not efficiently stimulate estrogen production)

136
Q

What hepatocytes are most susceptible to damage from acetaminophen toxicity?

A

Centrilobular (zone 3), where there is maximum CYP450 enzymes

137
Q

What is a genetic variant that leads to increased susceptibility to liver toxicity when being treated for tuberculosis with isoniazid?

A

Variant of N-acetyltransferase (NAT2)

~ ALT > 5x normal, or ALT/alk phos ratio >5 (hepatocellular pattern)

138
Q

What is hemachromatosis, and why does it lead to liver toxicity?

A

• Excessive iron absorption (or blood transfusion) leading to excess iron accumulating in the liver, pancreas, heart, joints
• classic tetrad of: cirrhosis, hepatomegaly, abnormal skin pigmentation, diabetes, cardiac dysfunction

139
Q

Hemachromatosis can lead to what neurological symptoms?

A

Cognitive decline, gait difficulties, cerebellar ataxia, extrapyramidal dysfunction

~ all likely due to iron deposition in the basal ganglia

140
Q

Iron deposition in the anterior pituitary and testicles due to hemachromatosis leads to what?

A

Hypogonadism; amenorrhea
in females, impotence in males

141
Q

What are the most common genetic disorders leading to hereditary primary hemachromatosis?

A

Adults: HFE, usually C282Y
Children: HAMP, and HJV

142
Q

What binds to a ferroportin (the iron influx channel at the basal surface of intestinal cells) and causes its degradation?

A

Hepcidin (produced by the HAMP gene)

143
Q

Hemachromatosis will look like what histologically?

A

• iron deposits (brown cytoplasmic granules or positive Prussian blue stain)
• fibrosis with cirrhosis in advanced cases

144
Q

What is the treatment of hemachromatosis?

A

Regular phlebotomy

145
Q

What are the clinical manifestations of Wilson’s disease?

A

• liver hepatitis and failure
• tremors, muscle stiffness, troubles speaking, personality changes, anxiety, auditory or visual hallucinations (psychosis)
• Kaiser Fleischer ringed eyes

146
Q

Mutation in what gene leads to Wilson’s disease?

A

ATP7B gene (a trans transmembrane copper transporting ATPase)

~ lab values will show a decreased serum ceruloplasmin and copper

147
Q

What does the histology look like in a person with Wilson disease?

A

Similar to steatohepatitis, fatty change with focal hepatocyte necrosis, ballooning degeneration, and Mallory hyaline (+ copper accumulation)

148
Q

What is the treatment of Wilson disease?

A

Copper chelation therapy with penicillamine and trientine

149
Q

What is alpha-1 antitrypsin deficiency?

A

• autosomal recessive disorder caused by mutations in alpha-1 AT (typically an active protest inhibitor— inhibits neutrophil elastase)
• leads to: pulmonary disease (destruction), liver disease (accumulation of misfolded alpha-1 AT the endoplasmic reticulum causing apoptosis of hepatocytes)

150
Q

Of the four genotypes for alpha-1 antitrypsin (M, S, Z, Null), which is the most pathogenic?

A

M is normal. Z is more pathogenic than S, however Null mutation results in no alpha1-AT expression (bad)

151
Q

How does Alpha-1 anti-trypsin present in neonates?

A

• typically symptomatic with ZZ mutation
• neonatal hepatitis
• cholestasis

152
Q

What is intrahepatic cholestasis?

A

• obstruction of the intrahepatic bile ducts
• caused by colon hepatitis, intra-hepatic atresia, contraceptive pills, antibiotics, pregnancy, tumors, sickle cell disease, or ductopenia

153
Q

What is extrahepatic cholestasis?

A

• obstruction/stasis of the common bile duct and below
• caused by choledocolithiasis, benign bile duct structures, tumors, primary sclerosing colitis, and biliary atresia

154
Q

Lack of bilirubin excretion (such as cholestasis), lead to what exam findings?

A

• icterus and jaundice
• dark urine (excess unconjugated bilirubin excreted by the kidneys)
• light colored, pale stool (pigment from conjugated bilirubin not present)

155
Q

Lack of bile acid secretion, such cholestasis, leads to what clinical findings?

A

• pruritis
• fatigue and easy bruising/bleeding

156
Q

Cholestasis sepsis

A
  • inflammatory mediators such as LPS affect bile acid transporters leading to cholangitis
  • effect is reduced bile flow, with predominant bile plugs at the portal-parenchymal interface
157
Q

What is seen in an acute large bile duct obstruction?

A

• portal tract edema with neutrophil at the interface between portal tract and hepatocytes

• prolonged obstruction: ascending cholangitis and periportal fibrosis

158
Q

What is a hallmark of ascending cholangitis?

A

• intestinal tract bacteria migrating up into the biliary tract due to stasis
• neutrophils within the epithelial cell lining of the portal tract

159
Q

Chronic biliary obstruction (biliary cirrhosis) causes what types of nodules of the liver cells?

A

Puzzle piece rather than lobular

160
Q

What is neonatal cholestasis? (non-obstructive)

A

• Present clinically at 1-2 months of age with prominent cholestatic signs and symptoms such as Icterus, jaundice, pale stool, dark urine, failure to thrive, hepatomegaly
• imaging studies will show normal biliary tree (distinguishing between biliary atresia)
• biopsy shows giant cell hepatitis pattern

161
Q

What is extrahepatic biliary atresia (obstructive neonatal cholestasis)

A

• complete or partial obstruction of the extra hepatic biliary tree within the first three months of life

1.) perinatal form (80%) biliary tree develops normally, subsequently destroyed
2.) fetal form (20%) failure of normal development of the extrahepatic biliary tree

162
Q

What is the pathology of extrahepatic biliary atresia?

A

• inflammation and fibrosis of the hepatic or common bile ducts
• extension to involve intrahepatic ducts is possible
• cirrhosis by 3-6 months of age
• Tx: Kasai procedure

163
Q

What is primary biliary cholangitis (PBC)?

A
  • autoimmune disorder with T cell mediated inflammatory destruction of intrahepatic bile ducts
  • more common females, 40-50yo
  • associated with other autoimmune disorders, risk for hepatocellular carcinoma following cirrhosis is increased
164
Q

How is PBC diagnosed?

A

• LFTs: prominent cholestatic pattern
• serology: positive AMA, positive ANA
• florid duct lesion (chronic and granulomatous inflammation damaging bile ducts)
• diagnosis established with elevated alkaline phosphatase for greater than six months, positive AMA, and characteristic histological findings

165
Q

What is the treatment of primary biliary cholangitis (PBC)?

A

• Ursodeoxycholic acid (UDCA)

~ stimulates biliary secretion, protects injured bile duct epithelial cells from acid, promotes detoxification, inhibits hepatocyte apoptosis, slows fibrosis

166
Q

What is primary sclerosing cholangitis (PSC)?

A

• autoimmune inflammatory and fibrosing disease of large bile ducts affecting extrahepatic and large intrahepatic ducts
• more common in males
• highly associated with ulcerative colitis, increased risk of cholangiocarcinoma

167
Q

How is PSC diagnosed?

A
  • elevated alkaline phosphatase
  • imaging: beading of large bile duct on ERCP/MRCP
  • MHC association: HLA-B8
  • positive at typical perinuclear anti-neutrophil cytoplasmic antibodies (AP-ANCA)
168
Q

What is the histopathology of PSC?

A
  • large intrahepatic bile duct and extrahepatic duct show epithelial injury and inflammation
  • periductal onion skinning
  • small intrahepatic bile ducts are spared
169
Q

What is a choledochal cyst?

A

• congenital dilation of the common bile duct
• usually presents before age 10, more common in females
• presents with jaundice and abdominal pain
• complications: stones, pancreatitis, obstructive biliary liver disease, choleangiosarcoma

170
Q

What is fibropolycystic disease?

A
  • a variety of lesions that are due to congenital malformations of the biliary tree (ductal plate malformations)
  • Von Meyenburg = innocuous lesion
  • congenital hepatic fibrosis = presents in late childhood hepatosplenomegaly, portal hypertension, and NO hepatocellular dysfunction w/ increased risk for choleangiosarcoma
171
Q

What does a von Meyenburg complex/bile duct hamartoma look like?

A

• irregular glands in a fibrotic stroma

172
Q

What is Caroli disease?

A

Multifocal cystic dilation of the large intrahepatic bile duct seen in fibropolycystic disease.

Combined with congenital hepatic fibrosis = Caroli syndrome

173
Q

What does congenital hepatic fibrosis look like histopathologically?

A
  • portal tracts are expanded with fibrous tissue and irregular shaped bile ducts
  • resembles cirrhosis, patients are at risk for portal hypertension
174
Q

What bacteria from dental caries leads to pulmonary abscesses?

A

Actinomycosis (Gram + bacilli, annular and branching, yellow pigment sulfur clusters)

175
Q

What pulmonary infectious agents are associated with alcoholism?

A

• Klebsiella pneumonia
• Myobacterium tuberculosis

176
Q

What antibiotic typically causes closterioides difficile?

A

Clindamycin (metronidazole and vancomycin are used to treat c. Diff)

177
Q

What is used to treat Trichinosis spiralis?

A

Albendazole and mebendazole

178
Q

Determination of alcoholic hepatitis via labs includes what?

A

• AST: ALT ratio is 2:1
• AST is never >500
• elevated total bilirubin and PT

~ Tx: prednisolone reduces inflammation and improves mortality

179
Q

What best describes the formation of ascites?

A

Increased capillary hydrostatic pressure

~ in combination with decreased capillary oncotic pressure

180
Q

What is the most appropriate agent to treat ascites?

A
  1. Start with spironolactone (potassium sparing diuretic)
  2. Add furosemide (loop diuretic)
181
Q

How is cirrhosis diagnosed?

A

Biopsy

• lab test include: elevated PT, decreased albumin. Can have normal LFTs

182
Q

What are the physical findings of cirrhosis?

A

• Icterus
• palmar erythema
• muscle wasting
• spider angiomas
• portal hypertension
• dupuytren’s contracture
• gynecomastia
• parotid enlargement
• clubbing of digits

183
Q

Portal hypertension causes what vascular change?

A

Increased splanchnic capillary hydrostatic pressure

184
Q

Cirrhosis/ascites can cause what secondary problem?

A

Secondary hyperaldosteronism: increased RAAS activation causing volume retention and worse ascites

185
Q

What is the pathophysiology of hepatorenal syndrome?

A

Decreased hepatic clearance of nitric oxide leading to kidney vasculature vasodilation (hypoperfusion)

186
Q

What medication is given for hepatic encephalopathy (excess ammonia)?

A

Lactulose: a drug that creates an acidic environment in the intestinal lumen (osmotic laxative) NH3 is trapped as NH4 and excreted in feces

Rifamixin: RNA polymerase inhibitor, select gut bacteria that produces less NH3

187
Q

What mushroom contains a chemical that inhibits RNA polymerase II?

A

Amanitin mushroom (produces alpha-amanitin)

188
Q

Nausea and vomiting in children can lead to what?

A

Hypochloremia, hypokalemic metabolic alkalosis

189
Q

What are the signs and symptoms of diabetic ketoacidosis and children?

A

• Kussmaul respirations
• weight loss
• polyuria/polydipsia
• acetone breath
• AMS and dehydration
• hyperglycemia
• metabolic acidosis

190
Q

A patient that has bilious vomiting without abdominal distention on the first day of life typically has what GI problem?

A

Duodenal atresia

191
Q

What is the primary cause of diarrhea in North America?

A

Viral gastroenteritis

192
Q

What are the most common causative agents of infectious diarrhea?

A
  • rotavirus
  • norovirus
  • Campylobacter
193
Q

What can be the sole symptom of a child with COVID-19?

A

G.I. symptoms, diarrhea

194
Q

What are the clinical history features that are atypical of viral gastroenteritis?

A

• fever
• abdominal pain
• blood/mucus in stool
• bilious/projectile vomiting
• duration >7 days
• increased your output
• altered consciousness
• international travel
• exposure to food, unsafe water, farm animals, reptiles

195
Q

What are clinical exam features that are atypical of viral gastroenteritis?

A

• moderate to severe dehydration
• bulging fontanelle
• hyponatremia with hyperkalemia
• respiratory abnormalities
• abdominal distention/focal tenderness/mass
• petechiae

196
Q

What are clinical lab values that are atypical of viral gastroenteritis?

A

• abnormal CBC
• elevated CRP
• fecal leukocytes
• persistent diarrhea

197
Q

What are the organisms that cause bloody diarrhea?

A

SSCCEEYAA, bloody diarrhea

• salmonella
• Shigella
• campylobacter
• c. diff
• EIEC
• EHEC
• Yersinia enterocolitis
• amoeba
• aeromonas

198
Q

What is an objective measure when a evaluating dehydration of children?

A

percentage of weight loss

  • mild: 3-5%
  • moderate: 6-9%
  • severe: >10%
199
Q

What is the typical IV treatment of diarrhea in children?

A

• typically in children >10% dehydrated based on weight
• 20mL/Kg of NS or D5NS

200
Q

What is colic in infants?

A
  • inconsolable crying associated with drawing up the legs and gaseous distention (due to hypomotility, constipation)
  • diagnosis of exclusion, no treatment
  • starts at 3 weeks, and peaks at week 6
201
Q

What is recurrent abdominal pain syndrome?

A

• two distinct peaks of frequency (first between 5-7 and second between 8-12) due to separation anxiety
• Tx: emphasize normality by remaining in school, continuing activities and resuming normal diet

202
Q

What is the number one genetic disorder of all time?

A

Lactose intolerance (lactase deficiency)

203
Q

What are the treatments of constipation in children?

A
  • polyethylene glycol (MiraLAX)
  • milk of magnesia (1-3mL/Kg/day)
  • mineral oil
  • sorbitol
204
Q

What is a liver hemangioma?

A

• most common benign liver mass
• commonly small and subcapsular, with Caverness histology and large thin walled vessels
• incidental detection

205
Q

What is focal nodular hyperplasia?

A

• common benign liver mass found an adult women age 20-50
• arterial malformation causing altered blood flow (both hyperperfusion and hypoperfusion triggering regeneration/reactive hyperplasia of hepatocytes)

206
Q

What hereditary disorder has a high incidence of focal nodular hyperplasia?

A

Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome)

207
Q

What does focal nodular hyperplasia look like?

A
  • homogenous enhancing mass with a central scar (scar contains thick walled arterial vessels without corresponding bile ducts)
  • benign regenerative nodules of hepatocytes separated by thick fibrous bands that radiate from the central scar
208
Q

What causes a hepatic abscess?

A

• majority are bacteria (pyogenic) can be amoebic, parasitic, fungal
• most common etiology is biliary: ascending infection, cholangitis usually associated with obstructive cholestasis

209
Q

What typically causes hepatocellular adenoma (benign neoplasm more often seen in young women)?

A

• oral contraceptives, anabolic steroids, obesity, metabolic syndrome
• typically detected in incidentally- tumors >5cm have risk for hemorrhage/malignancy

210
Q

When is hepatocellular adenoma excised?

A
  1. > 5cm due to risk of intra-abdominal hemorrhage
  2. If beta-catenin mutation due to risk of malignant transformation

Only monitored: If small, with cessation of OCP/anabolic steroids

211
Q

What are the pathological features of hepatocellular adenoma?

A

• discrete mass, sometimes hemorrhagic, sometimes multiple
• Unpaired arteries are seen, no portal triads— only artery, no bile duct or vein associated

212
Q

What are the variant types of hepatocellular adenoma?

A
  1. HNF1A: diffuse change, LFABP1 negative, associated with diabetes, females, minimal risk for HCC
  2. Beta-catenin: Similar to well differentiated HCC, Associated with males, anabolic steroids, HCC
  3. Inflammatory: dilated sinusoid and inflammatory cells, CRP stain and serum amyloid A stain, associated with obesity, females
213
Q

What is hepatoblastoma?

A

• malignant liver tumor of early childhood, less than three years old
• presents with abdominal swelling, occasionally cholestatic symptoms (jaundice, pruritus)
• activation of WNT signaling and nuclear beta-catenin expression (fetal and embryonal hepatocytes)

214
Q

What are the associated syndromes with hepatoblastoma?

A

• familial adenomatous polyposis (FAP)
• Beckwith- Wiedeman syndrome

~ tumor can present with embryonal/fetal liver cells and mesenchymal tissue such as bone

215
Q

What is associated with hepatocellular carcinoma?

A

• chronic hepatitis B
• cirrhosis
• males
• hemachromatosis
• alpha-1 anti-trypsin
• pathways: TERT/telomerase overexpression, beta-catenin, TP53
• increased alpha-fetoprotein (AFP)

216
Q

What is a fibrolamellar hepatocellular carcinoma?

A

• adolescent and young adult tumor
• no known risk factors
• normal serum AFP

• presents as a solid tumor in otherwise normal liver, thick plates and nests of malignant hepatocytes separated by dense bands of lamellar fibrous tissue

217
Q

What is cholangiocarcinoma, and what is it associated with?

A

• malignant adenocarcinoma of the bile duct epithelium
• intrahepatic: intrahepatic cholangiocarcinoma
• extrahepatic: biliary adenocarcinoma, Klatskin tumor
• risk factors: liver flukes, primary sclerosing cholangitis, hepatolithiasis, HCC

218
Q

Which tumors are found sooner, intrahepatic or extrahepatic?

A

Extrahepatic: they are more likely to completely obstruct flow of bile even with a small tumor. May cause jaundice and pruritus earlier at a resectable stage

219
Q

What causes angiosarcoma of the liver?

A
  1. Vinyl chloride
  2. Arsenic
  3. Thorotrast
220
Q

What is the most common malignancy found in the liver?

A

Metastasis from somewhere else: colon, lung, breast, pancreas. Typically multiple nodules, presents with isolated elevation of alkaline phosphatase

221
Q

Malrotation in development of the G.I. tract leads to what?

A

• ligament of Treitz on the right side of the abdomen and does not cross the midline
• bilious emesis, lethargy, toxic
• Ladd’s procedure to fix

222
Q

What is the diagnostic test of choice for pyloric stenosis?

A

Ultrasound: shows a 3 mm thick, 15 mm length obstruction

223
Q

What is the triad of symptoms for intussusception?

A
  1. Colicky abdominal pain
  2. Bilious emesis
  3. Currant jelly stools
224
Q

What is the typical Management of intussusception?

A

Barium enema: 80% success rate, can be done twice if needed. Third time occurrence is indication for surgery

225
Q

Why are 12 to 18–year-olds most likely to get appendicitis?

A

That age is associated with the greatest number of lymphoid follicles present (lymphoid hyperplasia)

226
Q

What are common labs that can be seen with appendicitis?

A

• high neutrophil count
• mild elevation in WBC (High, 15k+, indicates perforation)
• urinalysis may show sterile pyuria (WBC in urine without bacteria)

227
Q

Meckel diverticulum is associated with what type of hernia?

A

Littre’s hernia

228
Q

What is a common indication of Hirschsprung disease?

A

Failure to pass meconium in the first 24 hours

229
Q

Omphaloceles are associated with what karyotype abnormalities?

A

• Trisomy 13, 18, 21
• also associated with other malformations: cardiac, MS, G.I., GU, and with Beckwith-Wiedmann syndrome

~bad baby, healthy bowels

230
Q

What is seen in Beckwith-Wiedmann syndrome?

A

• omphalocele
• hyperinsulinemia
• macroglossia

231
Q

Do babies with Gastroschisis have other comorbidities?

A

Typically no, bad bowel, healthy baby

232
Q

The lining of the G.I. tract is from what embryological layer?

A

Endoderm

233
Q

Smooth muscle and connective tissue in the G.I. tract are derived from what embryological layer?

A

Splanchnic mesoderm

GI (3 decks)

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