03-10 Liver Structure and Fxn Flashcards

• Describe the gross and microscopic anatomy of the liver • Discuss the normal physiologic functions of the liver including: Bilirubin production and excretion; the metabolism of drugs and toxins; the metabolism of carbohydrate, lipid and protein; and the synthesis of albumin and clotting factors • List the different laboratory tests used to assess liver function, discuss their significance in assessing patients with liver disease • Describe the different imaging modalities and invasi

1
Q

<p>Major cell types (+ function) in the liver</p>

A

<p>Three major cell categories:</p>

<ol>
<li>&ndash; Hepatocytes PRODUCTION
<ul>
<li>Organized in lamina of cell plates</li>
<li>metab fxns involving CHOs, fats and prots</li>
<li>bile production</li>
<li>biotransform Rx &amp; toxins (make hydro<u>philic</u>)</li>
<li>gets rid of bilirubin</li>
<li>storage</li>
</ul>
</li>
<li>&ndash; Cholangiocytes EXCRETION
<ul>
<li>Intercellular channels > bile canaliculi</li>
</ul>
</li>
<li>&ndash; Non-parenchymal cells FILTRATION
<ol>
<li>Kuppfer cells</li>
<li>Sinusoidal epithelial cells (leaky)</li>
<li>Hepatic stellate cells, a.k.a. Ito cells (collagen synth)</li>
</ol>
</li>
</ol>

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2
Q

<p>Describe the gross anatomy of the liver</p>

<ul>
<li>Gross</li>
<li>Blood Supply</li>
<li>Biliary Tree</li>
<li>Lymphatics</li>
</ul>

A

<p>GROSS:</p>

<ul>
<li>Capsule (peritoneal): surrounds liver except “bare spot” of posterior aspect - continuity w/ retro-peritoneum</li>
<li>organ divided into segments by blood supply</li>
</ul>

<p>BLOOD SUPPLY: Dual hepatic a. + portal vein</p>

<ul>
<li>aorta→ celiac artery→ common hepatic a.→ r & L hep a.
<ul>
<li>OR</li>
</ul>
</li>
<li>aorta→SMA→RHA +</li>
<li>left gastric→LHA
<ul>
<li>R hep art→ cystic aa. to G.B.</li>
</ul>
</li>
<li>L, mid, and R hepatic vv.</li>
</ul>

<p>BILIARY TREE</p>

<ul>
<li>Canals of Hering→ bile ductules→ terminal bile ducts→ segmental bile ducts→ R + L lobar ducts→ common hepatic bile duct (see image)</li>
</ul>

<p>LYMPHATICS</p>

<ul>
<li>lymph forms in space of Disse</li>
<li>
<p>Pleural effusion in the presence of massive ascites may be explained by lymph flow in trans-diaphragmatic lymphatics</p>
</li>
</ul>

<p></p>

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3
Q

<p>Describe the microscopic anatomy of the liver.</p>

A

<ul>
<li>Divided into ~hexagonal "classic lobules with CV at center and 6 peripheral hepatic triads OR</li>
<li>Divided into acina, the area surrounding a portal "triad" which contains:
<ul>
<li>proper hepatic artery</li>
<li>hepatic portal vein</li>
<li>common bile duct</li>
<li>lymphatic vessels</li>
<li>branch of thevagus nerve</li>
</ul>
</li>
<li>Blood supply diminishes as you go to outside of acinus</li>
</ul>

<p>Hepatocyte arrangement</p>

<ul>
<li>
<p>Basal surface faces sinusoidal space, microvilli</p>

<p>Apical face adjacent cells, enclose bile canaliculi</p>
</li>
<li>
<p>Lateral from bile canaliculi > Disse’s space</p>
</li>
</ul>

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4
Q

<p>Kartagener&#39;s syndrome involves what findings?</p>

A

<ol>
<li>situs inversus</li>
<li>Bronchiectasis
<ul>
<li>&nbsp;</li>
</ul>
</li>
<li>chronic sinusitis</li>
</ol>

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5
Q

<p>Describe bilirubin production and excretion.</p>

A

<ol>
<li>RBC breakdown: Hgb →Heme →<strong>Biliverdin</strong> →Bilirubin</li>
<li>Bilirubin transported in blood bound to albumin (unconjugated, lipidsoluble)</li>
<li>Bili taken up by hepatocytes</li>
<li>Bound to glutathione-s-transferase and then conjugated by <strong>bilirubinUDP-glucuronosyltransferase</strong></li>
<li>conj bili (water soluble) →bile ducts via MRP2 transporter (or some back to blood)
<ul>
<li>some: bili—intest. bacteria→ urobilinogen→ reabsorb'd = <strong>eneterohepatic circulation</strong> (99%)​
<ul>
<li>will be secreted by kidney</li>
<li>or urobilinogen —reduction→ stercobilin (gives poop brown color)</li>
</ul>
</li>
</ul>
</li>
</ol>

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6
Q

<p>DDx for jaundice</p>

<ul>
<li>framework for thinking</li>
<li>DDx for unconjugated hyperbilirubinemia</li>
<li>DDx for conjugated hyperbilirubinemia</li>
</ul>

A

<ul>
<li>Pre-Hepatic
<ul>
<li>e.g. hemolysis</li>
</ul>
</li>
<li>Hepatic
<ul>
<li>viral/toxic hepatic impairment</li>
</ul>
</li>
<li>Post-Hepatic
<ul>
<li>bile duct obstruction</li>
</ul>
</li>
</ul>

<p>UNCONJUGATED</p>

<ul>
<li>&uarr; production (hemolysis)</li>
<li>Liver cell damage (no uptake)</li>
<li>&darr;<span> conjugation (</span>&darr;<span> UDP-glucuronosyltransferase)</span></li>
<li><span>Congenital</span>
<ul>
<li>Gilbert&rsquo;s (5% of people)</li>
<li><span>&raquo; Crigler-Najjar</span></li>
</ul>
</li>
<li><span>Acquired: drug effect</span></li>
</ul>

<p>CONJUGATED</p>

<ul>
<li>Liver cell damage (<span>limited MRP2 activity)</span></li>
<li>Obstruction (stone or tumor)</li>
<li>Decreased excretion (limited MRP2 activity)</li>
<li>Congenital:
<ul>
<li>&raquo; Dubin-Johnson</li>
<li>&raquo; Rotor</li>
</ul>
</li>
</ul>

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7
Q

<p>Describe liver metab of Rx</p>

A

<ul>
<li><span>Phase I: cytochrome P-450 monooxygenase system (many) &ndash; Oxidation, Reduction, Hydrolysis, Hydration, Decarboxylation,</span>

<ul>
<li>Isomerization</li>
<li>Variability: drug-drug, host factors, environmental factors</li>
</ul>
</li>
<li><span>Phase II: other enzymes</span>
<ul>
<li>Glucuronidation, Sulfation, Methylation, Acetylation, Glutathoine conjugation</li>
</ul>
</li>
</ul>

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8
Q

<p>Describe liver metab of carbs</p>

A

<p>Carbs</p>

<ul>
<li>Recall that G-6-P has 3 fates→
<ul>
<li>glycogen (2 days supply)</li>
<li>breakdown→ TCA</li>
<li>Pentose-Phosphate shunt</li>
</ul>
</li>
</ul>

<p>Liver Makes Glucose via Gluconeogenesis</p>

<ul>
<li>
<p>glycogenolysis → glucose(liver has enough glycogen for two days' energy needs)</p>
</li>
<li>
<p>pyruvate, AAs, and FAs→ glucose</p>
</li>
<li>
<p>Lactatefrom muscle, intestine, liver, or RBCs→<strong>Cori cycle </strong>(see image here)</p>
</li>
<li>
<p><strong>Alanine Cycle</strong>:</p>

<ul>
<li>
<p><span>Ala made by catab of muscle (muscle wasting during prolonged fasting)→ liver→ glucose→ back to muscle</span></p>
</li>
</ul>
</li>
</ul>

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9
Q

<p>Describe liver metab of fats</p>

A

<ul>
<li>the liver is the main site of fatty acid synthesis from excess glucose (mammary gland and to a lesser extense adipose do this, too [Wiki])</li>
<li>
<p>the liver synthesizes and extracts a large number of apolipoproteins* to transport these lipids</p>

<ul>
<li>
<p>*contain&nbsp;TGs, phospholipids, cholesterol and its esters, and lecithins</p>
</li>
</ul>
</li>
<li>
<p>Recall that&nbsp;Cholesterol from food or made by liver is not a fuel source but a structural component of membranes and a steroid hormone precursor</p>
</li>
</ul>

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10
Q

<p>Describe liver synthesis of albumin and clotting factors</p>

<ul>
<li>What proteins are synthesized in the liver</li>
</ul>

A

<ul>
<li>Coagulation</li>
<li>Transport, such as albumin and iron binding</li>
<li>Protease inhibitors</li>
<li>Acute-phase reactants
<ul>
<li>group of proteins expressed during acute and chronic systemic inflammation</li>
<li>These proteins are assumed to play an important role in the host defense against tissue damage and infection.</li>
<li>Example:&nbsp;<span>Fibrinogen aids in clot formation</span></li>
<li><span>Anti-proteases serve to protect normal cells from proteases that are released from&nbsp;</span><span>necrotic tissues.</span></li>
</ul>
</li>
</ul>

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11
Q

<p>Interpret elevated AST (SGOT) and ALT (SGPT)</p>

<ul>
<li>Ref Range</li>
<li>Basis</li>
<li>Assoc Dzs</li>
<li>Extrahep sources</li>
</ul>

A

<p>Both Aminotransferaseselevated in "hepatic pattern"</p>

<p><strong>Ref Ranges</strong></p>

<ul>
<li>ALT/SGPT <strong>10-55</strong> U/L</li>
<li>AST/SGOT <strong>10-40</strong> U/L</li>
<li>part of gluconeogenic pathway</li>
</ul>

<p><strong>Basis</strong></p>

<ul>
<li>
<p>Leakage from damaged tissue into circulation (hepatocellular necrosis)</p>
</li>
</ul>

<p><strong>Assoc Dzs</strong></p>

<ul>
<li>
<p>Viral, autoimmune, toxic, Wilsons, ischemia, acohol, NASH etc.</p>
</li>
</ul>

<p><strong>Extrahepatic Sources</strong></p>

<ul>
<li>ALT, relatively specific for hepatocyte necrosis AST: muscle (skeletal and cardiac), kidney, brain, pancreas, RBC</li>
</ul>

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12
Q

<p>Interpret alk phos (AP, AF) findings.</p>

A

<p>High alk phos + GGT is a<strong> biliary pattern</strong></p>

<p><strong>Ref Ranges</strong></p>

<ul>
<li>(ALP, AF 45-115 U/L: Catalyze hydrolysis of phosphate esters</li>
<li><span>3x higher in children due to bone growth</span></li>
</ul>

<p><strong>Basis</strong></p>

<ul>
<li>
<p>Overproduction and leakage into serum (rise is delayed due to need for induction of enzyme)</p>
</li>
</ul>

<p><strong>Assoc Dzs</strong></p>

<ul>
<li>
<p>Marked elevations: extra- and intrahepatic cholestasis, infiltrating disease (e.g., tumor, MAC), occasionally alcoholic hepatitis</p>
</li>
</ul>

<p><strong>Extrahepatic Sources</strong></p>

<ul>
<li>
<p>Bone growth or disease (e.g., tumor, fracture, Paget's disease), placenta, intestine, tumors</p>
</li>
</ul>

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13
Q

<p>Interpret bilirubin labs</p>

A

<p><strong>Ref Ranges</strong></p>

<ul>
<li>
<p>Total Bilirubin&nbsp;(0.0-1.0 mg/dL, 0,)</p>
</li>
</ul>

<p><strong>Basis of elevation</strong></p>

<ul>
<li>
<p>Decreased hepatic clearance</p>
</li>
</ul>

<p><strong>Assoc Dzs</strong></p>

<ul>
<li>
<p><u>Unconjugated</u>:&nbsp;liver cell damage (no uptake, e.g. viral/drug/EtOH hepatitis), increase production (hemolysis), decreased conjugation (congenital: Gilbert&#39;s and Crigler-Najjar or acquired: drug effect), vascular (decreased flow to liver), or starvation</p>
</li>
<li>
<p><u>Conjugated</u>: liver cell damage, obstruction (stone or tumor), or congenital (Dubin-Johnson and Rotor)</p>
</li>
</ul>

<p><strong>Extrahepatic Sources</strong></p>

<ul>
<li>
<p>Increased breakdown of hemoglobin (hemolysis, ineffective erythropoiesis, resorption of hematoma) or myoglobin (resulting from muscle injury)</p>
</li>
</ul>

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14
Q

<p>Interpret elevated GGT</p>

A

<p>High alk phos + GGT is a<strong> biliary pattern</strong></p>

<p><strong>Ref Ranges</strong></p>

<ul>
<li>
<p>Gammaglutamyl transpeptidase (gamma-GT 0-30 U/L):</p>
</li>
</ul>

<p><strong>Enzyme Fxn</strong></p>

<ul>
<li>
<p>catalyzes the transfer of gamma glutamyl groups of peptides such as glutathione to other amino acids</p>
</li>
</ul>

<p><strong>Basis for Elevation</strong></p>

<ul>
<li>
<p>Overproduction and leakage into serum (inducible by alcohol and dilatin)</p>
</li>
</ul>

<p><strong>Assoc Dzs</strong></p>

<ul>
<li>
<p>Same as for high Alk P (Marked elevations: extra- and intrahepatic cholestasis, infiltrating disease (e.g., tumor, MAC), occasionally alcoholic hepatitis)</p>
</li>
</ul>

<p><strong>Extrahepatic Sources</strong></p>

<ul>
<li>
<p>Kidney, spleen, pancreas, heart, lung, brain</p>
</li>
</ul>

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15
Q

<p>Interpret <strong>low</strong> albumin labs.</p>

A

<p><strong>Ref Ranges</strong></p>

<ul>
<li>
<p>(4.0-6.0 g/dL = 40-60 g/L)</p>
</li>
</ul>

<p><strong>Basis for Low Alb</strong></p>

<ul>
<li>Decreased synthesis</li>
<li>?Increased catabolism</li>
<li><u>poor nutrition</u><u>​</u>&nbsp;(in that case, you&#39;d expect INR to be normal or correctable with vit k supp; if not, likely liver dz)</li>
</ul>

<p><strong>Assoc Dzs</strong></p>

<ul>
<li>
<p>chronic liver failure</p>
</li>
</ul>

<p><strong>Extrahepatic Cause</strong></p>

<ul>
<li>
<p>Malnutrition Nephrotic syndrome, Protein-losing enteropathy, vascular leak, , malignancy, and inflammatory states</p>
</li>
</ul>

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16
Q

<p>Interpret increased PT/INR labs in the case of suspected liver dz</p>

A

<p><span>PT/INR is a sign of the production capability of the liver (like albumin)</span></p>

<p><strong>Ref Ranges</strong></p>

<ul>
<li>Prothrombin time (10.9␣12.5 sec, PT)</li>
<li>International Normalized Ratio (INR) (0.9␣1.2)</li>
</ul>

<p><strong>Basis for Low Numbers</strong></p>

<ul>
<li>
<p>Decreased synthetic capacity</p>
</li>
</ul>

<p><strong>Assoc Dzs</strong></p>

<ul>
<li>Acute or chronic liver failure (unresponsive to vitamin K)</li>
<li>Biliary obstruction (usually responsive to vitamin K administration)</li>
</ul>

<p><strong>Extrahepatic Sources</strong></p>

<ul>
<li>Vitamin K deficiency (secondary to malabsorption, malnutrition, antibiotics)</li>
<li>consumptive coagulopathy</li>
</ul>

17
Q

<p>Interpret ammonia labs.</p>

A

<p><strong>Ref Ranges</strong></p>

<ul>
<li>
<p>(0-50 uMOl/L NH3)</p>
</li>
</ul>

<p><strong>Basis</strong></p>

<ul>
<li>
<p>Decreased hepatic clearance</p>
</li>
</ul>

<p><strong>Assoc Dzs</strong></p>

<ul>
<li>
<p>Chronic liver failure</p>
</li>
</ul>

<p><strong>Extrahepatic Sources</strong></p>

<ul>
<li>
<p>Hepatocaval shunting, Protein metabolism defect</p>
</li>
</ul>

18
Q

<p>Liver imaging options.</p>

A

<ul>
<li>xray: only shows hepatosplenomegaly and calcifications</li>
<li>U/S: good general screening test, good especially for eval biliary tree, can show blood flow w/ doppler
<ul>
<li>not useful in obese pts</li>
</ul>
</li>
<li>CT:
<ul>
<li>w/o contrast: fat infiltration, Fe deposition, and focal ∆s e.g. subtle calcification or&nbsp;hemorrhage.</li>
<li>w/ contrast: tumors/focal lesions</li>
</ul>
</li>
<li>MRI: especially good for MRCP</li>
<li>Angio</li>
<li>ERCP</li>
<li>
<p>Percutaneous Transhepatic Cholangiography (PTC):&nbsp;contrasted fluoro w/ catheter directly&nbsp;in biliary tree</p>

<ul>
<li>
<p>Used if ERCP is impossible (after surgery or impaired access from small bowel, (e.g. tumor))</p>
</li>
<li>
<p>Disadvantages: cost, pain, rad, bleeding, perf,&nbsp;cholangitis</p>
</li>
</ul>
</li>
<li>Biopsy
<ul>
<li>percutaneous</li>
<li>via laparotomy</li>
<li>transjugular</li>
</ul>
</li>
<li>Fibroscan: gives a number relfecting the amount of fibrosis/scarring
<ul>
<li>Can be used in place of biopsy in for staging hepatitis/cirrhosis</li>
</ul>
</li>
</ul>

19
Q

<p>Important physical exam findings in liver disease</p>

A

<ul>
<li>Jaundice</li>
<li>Hepatomegaly</li>
<li>Splenomegaly</li>
<li>Spiders</li>
<li>Edema</li>
<li>Ascites</li>
<li>Asterixis etc.</li>
</ul>

20
Q

<p>Interpret what pattern you see here:</p>

<ul>
<li>Example AST 678 ALT 542 AP 126 gamma-GT 49</li>
</ul>

A

<p>High transaminases relative to alk phos and gamma-GT = <strong>hepatic pattern</strong></p>

<ul>
<li>predominantly damage to hepatocytes</li>
</ul>

21
Q

<p>Interpret pattern here:</p>

<ul>
<li>
<p>Example AST 47 ALT 23 AP 674 gamma-GT 499</p>
</li>
</ul>

A

<p>High alkaline phosphatase and gamma-GT relative to transaminases = <strong>cholestatic pattern</strong></p>

<ul>
<li>tends to reflectinjury to bile ducts</li>
</ul>

22
Q

<p>What does this pattern and time course suggest?</p>

<ul>
<li>
<p>Acute enormous elevation of transaminases (5000-10000), then lower 5 days later (300-500)</p>
</li>
</ul>

A

<p>Strong suggestion of ischemic liver injury (&quot;shock liver&quot;)</p>

<ul>
<li>Typical example: Patient after MVA with major bleeding and shock admitted to ICU</li>
</ul>

23
Q

<p>Patient has an acute elevation persistent for 2-3 weeks (transmainases 2000 - 4000), then coming down to 200 - 400, then after 2 months completely normal.</p>

<ul>
<li>This pattern is typical for...?</li>
</ul>

A

<p>Typical pattern in for example acute hepatitis A</p>

24
Q

<p>Example: Patient age 72, with general malaise, fever and abn liver tests, pain in back: ALT 76 AST 47 Alkaline phosphatase 760.</p>

<ul>
<li>What are your thoughts?</li>
<li>What lab would you check next?</li>
<li>How would you interpret those findings?</li>
</ul>

A

<ul>
<li>Unclear pattern, ?cholestatic?</li>
<li>Order GGT
<ul>
<li>If definitely high:&nbsp;a liver/biliary tract problem very likely. Could have cholangitis, a malignancy of pancreas or bile ducts</li>
<li>If normal could be bone fraction of AP with a bone metastasis of malignancy or an infiltrating process such as lymphoma</li>
</ul>
</li>
</ul>

25
Q

<p>You have a jaundiced patient with a bilirubin elevated at 3.4, but all other liver tests (AST, ALT, Alk Phos, albumin, PT/INR, NH3 etc.) are normal.</p>

<ul>
<li>DDx?</li>
</ul>

A

<p>It is usually predominantly unconjugated elevation that may reflect Gilbert&#39;s (silent t) syndrome</p>

<ul>
<li>could also be hemolytic process</li>
</ul>

26
Q

<p>DDx for elevated AFP</p>

A

<p>Ref range is < 19ng/mL</p>

<ul>
<li>HCC:&nbsp;<span>Classic = hypervascular mass&nbsp;</span><span>in cirrhotic liver and a high AFP of 34,000 ng/ml, pathognomonic for HCC</span><span>. AFP typically continues to rise.</span></li>
<li>Can also reflect a regenerating liver (e.g. pt w/ HCV w/ AFPs fluctuating up into the 300-500 range)</li>
<li>Can also reflect other germ cell tumors
<ul>
<li>But then you&#39;d expect not to find any liver dz findings</li>
</ul>
</li>
</ul>

27
Q

<p>DDx for Elevated CEA</p>

A

<p>Carcinoembryonic Antigen (CEA)</p>

<ul>
<li>Usually thought of as a colon cancer biomarker</li>
<li>sometimes associated w/ cholangiocarcinoma</li>
</ul>

28
Q

<p>Interpretation of an elevated &nbsp;<span>Carbohydrate Antigen 19-9 (CA 19-9)</span></p>

A

<ul>
<li>Associated w/ cholangioncarcinoma (as is CEA), but can also go up temporarily in cases of non-malignant cholangitis</li>
</ul>

29
Q

<p>LAbs to order for suspected hemochromatosis</p>

A

<ul>
<li>iron</li>
<li>TIBC</li>
<li>iron saturation</li>
<li>ferritin</li>
<li>HFE gene assay: C282Y and H63D mutations</li>
</ul>

30
Q

<p>Labs to order to suspected a1AT</p>

A

<ul>
<li>A-1-AT level</li>
<li>Phenotype (Pi type)</li>
</ul>

31
Q

<p>Test to order for suspected cases of Wilson&#39;s dz</p>

A

<ul>
<li>ceruloplasmin</li>
<li>24 hour urine copper (+/- penicillamine challenge)</li>
</ul>

32
Q

<p>Tests to order when working up NAFLD/NASH</p>

A

<ul>
<li>TSH</li>
<li>Lipid panel</li>
<li>HgbA1c</li>
<li>ferritin</li>
</ul>

33
Q

<p>Autoimmune liver disease work-up labs</p>

A

<ul>
<li><span>Autoimmune Hepatitis Type 1:</span>

<ul>
<li><span>​</span>ANA, SMA SPEP (globulins)</li>
</ul>
</li>
<li><span>Autoimmune Hepatitis Type 2:</span>
<ul>
<li><span>​</span>LKM (anti-liver kidney microsomal Ab)</li>
</ul>
</li>
<li><span>Primary Biliary Cirrhosis: </span>
<ul>
<li><span>​</span>AMA (anti-mitochondrial antibody) IgM)</li>
</ul>
</li>
<li><span>Primary Sclerosing Cholangitis:</span>
<ul>
<li><span>​pANCA</span></li>
</ul>
</li>
</ul>

34
Q

<p>Where in bodies do we get ammonia from?</p>

<p>What is it broken down into?</p>

<p>In which section of the liver (microscopic anatomy level) does this break down occur?</p>

<p>What happens to a patient w/ high NH3?</p>

A

<p>breakdown of AAs in our bodies&nbsp;&rarr; NH3</p>

<p>Periportal zone is where<span>&nbsp;urea cycle converts NH3 to urea</span></p>

<p>If not working: encephalopathy</p>

35
Q

<p>Why might you see thrombocytopenia in a patient w/ liver dz?</p>

A

<ul>
<li>increased resistance to portal flow&nbsp;&rarr;</li>
<li>diversion to spleen (also varices, etc.)&nbsp;&rarr;</li>
<li>splenomegaly&nbsp;&rarr;</li>
<li>splenic sequestration of platelets</li>
</ul>