Air Brake Endorsement Test | CDL Practice

Fatty infiltration means triglycerides accumulate inside hepatocytes. It is typically benign and reversible if the driver is removed, such as alcohol, obesity, or insulin resistance. On ultrasound, fat increases liver echogenicity, and the liver often looks larger. The key reasoning is that “fat deposition” changes tissue reflectivity, not cellular destruction or uncontrolled growth, so autoimmune, malignant, and genetic protein disorders do not fit.

Cirrhosis is defined by irreversible fibrosis and architectural distortion. Hepatocyte injury triggers collagen deposition, forming regenerative nodules and impaired function. Clinically and on imaging, this progresses from enlargement in earlier phases to a nodular, shrunken liver later, often with ascites and portal hypertension. The logic is permanence and scarring. Acute hepatitis can improve; bile overproduction is not the core mechanism; benign tissue growth does not explain failure and portal pressure rise.

Portal hypertension is increased pressure within the portal venous system. Mechanistically, resistance rises inside the liver (cirrhosis, fibrosis) or in portal flow pathways, so pressure upstream increases. That produces predictable downstream signs such as splenomegaly and collaterals. The “calculation” is hemodynamic: Pressure equals flow times resistance, so if resistance increases while flow persists, pressure climbs. Low pressure and cystic duct problems do not match this vascular definition.

Hepatitis here refers to inflammatory liver disease that may be acute or chronic and can progress to cirrhosis. “Starry night” occurs when liver parenchyma becomes relatively hypoechoic while portal triads remain echogenic, making them stand out. Hepatosplenomegaly reflects systemic inflammation and portal changes. Hearing and vision symptoms are unrelated. Pure duct dilation suggests biliary obstruction instead. The correct cluster ties clinical course with a classic ultrasound pattern and organ enlargement.

Budd-Chiari syndrome is hepatic venous outflow obstruction, often from thrombosis. When hepatic veins are blocked, sinusoidal pressure rises, causing hepatomegaly, ascites, and collateral formation. Doppler may show absent or reversed venous flow and intrahepatic collaterals. The reasoning is drainage failure, not bile blockage or infection. Gallstones mainly affect biliary ducts, and primary biliary infection affects duct walls. Outflow occlusion uniquely explains rapid congestion plus fluid accumulation.

A cavernous hemangioma is the most common benign liver tumor, composed of vascular channels. Ultrasound often shows a small, well-defined echogenic lesion, sometimes with posterior enhancement due to its vascular composition. The logic is frequency and benign behavior: hemangiomas do not invade like cancer. They are also reported more often in women. A claim that it is always malignant or restricted to one lobe is incorrect because distribution varies, and malignancy features are absent.

Hepatic adenomas are benign hepatocellular tumors with a known association to estrogen exposure, including oral contraceptives. Imaging appearance varies, so they can be hyperechoic or hypoechoic, which is why risk-factor reasoning matters. They are not congenital duct anomalies, which would affect ducts, not hepatocytes. They are not parasitic, and calcification is not a defining feature. The analytical step is linking lesion type to epidemiology, then checking if imaging variability supports it.

FNH is a benign hyperplastic response, not a true neoplasm, and is more common in women. The central scar is a classic clue because fibrous tissue radiates from a central point, especially visible on some imaging phases. It does not behave like metastasis or autoimmune disease. The reasoning is pattern recognition plus behavior: benign lesions are usually well-defined and stable. Malignancy usually shows invasive features or systemic spread, which FNH lacks.

Hepatocellular carcinoma is most strongly linked to chronic liver disease, especially cirrhosis, and is more common in men. It can be solitary, multifocal, or infiltrative, and may invade the portal vein, creating thrombosis-like appearances. The analytical point is that vessel invasion is a hallmark of aggressive tumors. A “never invades” option is therefore wrong. Female predominance is also wrong epidemiologically. A cystic-only pattern conflicts with the range of echogenic and complex presentations.

Hepatoblastoma is the most common primary malignant liver tumor in infants and young children. AFP rises because the tumor cells often produce fetal proteins. Ultrasound may show a highly vascular mass, sometimes with calcifications. The reasoning is age plus biomarker plus vascularity. Adults more often get HCC, not hepatoblastoma. A simple cyst has no AFP rise and lacks vascular solid tissue. Metastases depend on a primary elsewhere, which is not typical in infants for this pattern.

Metastases are very common because the liver filters blood from the GI tract and receives systemic circulation, making it a frequent landing site. Their appearance varies by primary tumor and tumor biology: some are hypoechoic, others echogenic, some calcify, and some show target signs. The calculation is distribution logic: higher blood flow and dual supply increase exposure. Claims that they are rare or always one echogenic pattern ignore the known variability that is used diagnostically.

Simple hepatic cysts are fluid-filled spaces that may be congenital or acquired. They can be single or multiple, and ultrasound usually shows anechoic content, thin wall, and posterior enhancement. Unusual shapes can occur, but the key is fluid behavior, not solid tissue. Infections like abscesses typically have thick walls, internal echoes, and systemic symptoms. Tumors have solid components and vascularity. The analytical approach is identifying fluid physics on ultrasound and matching it to a cyst.

Hydatid disease is caused by Echinococcus, with dogs as a key host, and is more frequent in sheep and cattle regions. The “cyst within cyst” or floating membranes (water lily sign) reflect daughter cysts and detached membranes. Lab signs like elevated WBC may occur but are not the primary identifier. The reasoning is epidemiology plus signature morphology. High cat populations and fish-only diets do not match the parasite life cycle, and bird-flu linkage is unrelated.

Pyogenic abscesses are bacterial collections, often secondary to intraabdominal infections or biliary disease such as diverticulitis, appendicitis, and cholecystitis. Ultrasound often shows a complex fluid collection with irregular thick walls and good through transmission, consistent with pus and fluid content. Viral infections do not create purulent cavities. Vitamin intake is irrelevant. The analytical logic is source tracing: bacteria travel via portal blood or biliary tree, then form localized necrotic collections.

Amebic abscess is caused by Entamoeba histolytica, strongly associated with poor sanitation and tropical or resource-limited settings. Ultrasound may show a round lesion that can appear hypoechoic or sometimes more echogenic depending on stage and contents. The reasoning is etiologic: protozoa invade intestinal mucosa, then reach the liver via portal circulation. Lung bacterial disease, viral skin disease, and alcohol-related cancer do not match the transmission path or the lesion’s abscess nature.

Fungal abscesses are most common in immunocompromised patients because reduced immunity allows opportunistic organisms like Candida to disseminate. Lesions can be small and numerous, and the echo pattern changes by stage: early hypoechoic centers and later echogenic or calcified centers during healing. The analytical reasoning is time-course: tissue necrosis, then inflammation, then fibrosis and calcification. Healthy individuals can get fungal infections, but disseminated hepatic abscesses are far less likely without immunosuppression.

In AIDS, Pneumocystis-related hepatic findings may present as multiple small echogenic foci without shadowing, reflecting microcalcifications or infiltrates. As severity increases, lesions can calcify and enlarge. The reasoning is progression: mild disease creates small deposits; chronicity can increase calcified burden. “Shadowing in mild cases” contradicts the physics of tiny nonshadowing foci. Skin predominance is incorrect for this hepatic imaging clue. Healthy individuals rarely show this pattern without immunodeficiency.

Schistosomiasis is a parasitic disease that affects the portal system, especially around the porta hepatis, causing periportal fibrosis. Fibrosis increases echogenicity around portal tracts and raises vascular resistance, which can lead to portal hypertension and even portal vein thrombosis. The calculation is hemodynamic: fibrosis increases resistance, and pressure increases upstream. Viral, bacterial, or fungal labels do not fit the organism class or the hallmark periportal fibrotic pattern that differentiates it on imaging.

A hepatic hematoma is a blood collection after trauma or procedural injury. Its echogenicity evolves over time because clot organization changes acoustic properties: acute blood may look more echogenic, then become hypoechoic as it liquefies. Shape can be irregular and blend with liver tissue, making margins challenging. Subcapsular hematomas may curve along the liver surface and displace parenchyma. The analytical approach is time-dependent imaging. RBC count changes are systemic lab findings, not imaging definitions.

Choledochal cysts are congenital dilations of the common bile duct. Imaging often shows a cystic structure at the porta hepatis, separate from the gallbladder, with a dilated duct entering it. The reasoning is anatomic continuity: if the CBD feeds into the cystic dilatation, it confirms duct origin rather than a gallbladder abnormality. Lifestyle and old age are not core drivers. A focal congenital duct dilatation explains early presentation, especially in children, and female predominance is commonly reported.

Biliary atresia is an infant disease with progressive obstruction or absence of extrahepatic bile ducts, causing cholestasis and rapid liver damage. Early intervention is critical because fibrosis accelerates. The logic is time-sensitive: without bile flow, hepatocytes are injured, leading to cirrhosis. The Kasai procedure reroutes bile drainage via bowel anastomosis, and transplant is needed if it fails. Adult viral infection does not match the age group or the obstructive anatomy. Intestinal degeneration and inherited splenomegaly are off-topic.

Hydrops of the gallbladder means marked distension, often from biliary obstruction, inflammation, or trauma. The gallbladder enlarges because bile cannot drain effectively, so volume increases and dimensions expand. The analytic reasoning is blockage leading to accumulation. Medication and alcohol are not typical primary drivers, and “genetic mutation” is not the clinical model for acute distension. Imaging focuses on size criteria and cause evaluation, including cystic duct obstruction or post-inflammatory narrowing, which better explains a massively enlarged gallbladder.

Caroli disease is a congenital disorder with focal saccular dilatation of intrahepatic bile ducts. The key reasoning is location and morphology: it involves intrahepatic ducts and has a saccular, segmental pattern, unlike choledochal cysts that primarily involve extrahepatic ducts. It can predispose to stones, cholangitis, and biliary complications because stagnant bile forms a “storage” environment. Chronic cirrhosis is not the defining feature, though chronic complications can affect liver health. Rectal cancer and pancreatitis are unrelated etiologies.

Primary sclerosing cholangitis is a chronic inflammatory process that causes bile duct strictures and scarring, often associated with ulcerative colitis. Thickened duct walls and narrowed lumens reflect fibrosis and chronic inflammation. The analytical step is pattern matching: chronic scarring causes alternating strictures and dilation, rather than uniform dilation. Elevated inflammatory markers may occur. Acute viral infection does not create progressive duct scarring. Low platelets can happen secondarily in advanced liver disease but is not a defining diagnostic feature of PSC itself.

Biliary calculi form primarily in the gallbladder but can migrate into the bile ducts, including the common hepatic duct and distal CBD near the sphincter of Oddi. The reasoning is flow-based: bile movement and gravity can carry stones, and narrow points become obstruction sites. Stones do not originate in the stomach or colon in this context. Obstruction risk is a “bottleneck” problem: smaller duct diameters increase blockage probability. This explains jaundice, cholangitis, and pancreatitis depending on where the stone lodges.

AIDS cholangitis reflects opportunistic infection or inflammation involving bile ducts in immunocompromised patients. Imaging may show smooth or irregular thickening of duct walls and ductal abnormalities, consistent with inflammatory injury rather than purely pancreatic duct obstruction or isolated gallbladder disease. The analytical reasoning is localization: cholangitis targets bile ducts. Liver enlargement is nonspecific and can occur for many reasons. Thickened walls are a direct structural sign that supports the diagnosis when combined with immunodeficiency context and cholestatic symptoms or lab patterns.

Klatskin tumor is a hilar cholangiocarcinoma located at the junction of the right and left hepatic ducts. Because it sits high, it often causes peripheral intrahepatic duct dilation while the distal CBD may remain nondilated. The reasoning is plumbing: obstruction upstream dilates upstream ducts, not downstream structures. It can be small and hard to see directly, so the “calculation” is inference from duct patterns. Abscess and benign polyps do not explain selective intrahepatic dilation with poor prognosis and a hilar origin.

Pancreatic head cancer commonly blocks the CBD as it passes through or near the pancreatic head. This produces painless jaundice and may enlarge the gallbladder (Courvoisier sign) because bile backs up without the inflammation typical of stones. The analytic reasoning is anatomy: CBD obstruction location predicts ductal dilation patterns. Thyroid hormones and lung consolidation are unrelated. High fever suggests infection, not classic malignancy presentation. Dilation of both CBD and pancreatic duct (double-duct sign) supports an obstructing mass even when the mass is subtle.

Gallbladder polyps are small intraluminal growths arising from the gallbladder wall. They are typically immobile, unlike gallstones which move with position changes. The reasoning uses physics and attachment: a wall-based lesion stays fixed, while free stones shift. Most polyps are benign, though size and growth rate influence malignancy risk. Inflammation is a separate process that affects wall thickness diffusely, not a discrete immobile mass. “Always cancerous” is incorrect because the majority are cholesterol polyps and benign adenomas.

Adenomyomatosis is a benign hyperplastic condition of the gallbladder wall with Rokitansky-Aschoff sinuses. Cholesterol crystals trapped in these sinuses create characteristic comet-tail artifacts on ultrasound, which is a physics-based clue from reverberation. The analytic reasoning is artifact interpretation: bright reflections plus comet-tail from the wall points toward adenomyomatosis rather than stones in the lumen. CBD obstruction is a different pathway. Malignancy would more often show irregular mass-like invasion. Pancreatitis is anatomically separate and does not produce classic gallbladder wall sinuses.

Fatty liver typically increases liver echogenicity because fat scatters ultrasound more than normal hepatocytes. This also causes posterior beam attenuation, so deeper structures look less bright. The analytical reasoning is ultrasound physics: increased reflectivity reduces penetration. Decreased echogenicity is more typical in acute hepatitis relative patterns. Shadowing is classically from calcified structures or gas, not diffuse fat. Thick septated cyst patterns point to cystic disease or abscess, not steatosis. The correct choice matches both tissue composition and expected acoustic effect.

Hepatopetal flow means portal venous blood moves toward the liver, which is the normal physiologic direction for the portal vein. Hepatofugal is the reverse, often seen with portal hypertension and collateralization. The reasoning is directional terminology: “petal” aligns with “toward,” while “fugal” aligns with “away.” This is clinically useful because reversed flow suggests elevated portal pressures and altered hemodynamics. The other terms are non-flow descriptors or toxicity-related words and do not describe blood direction on Doppler.

Portal hypertension creates a predictable chain: increased portal pressure causes splenic congestion and collateral venous pathways. Therefore, splenomegaly plus collateral veins is a strong supportive imaging combination. The analytic reasoning is vascular redistribution: the body “bypasses” high resistance by opening collateral channels, and the spleen enlarges due to backpressure. Gallbladder wall thickening is nonspecific and may relate to cholecystitis or systemic edema. Isolated pancreatic duct dilation points to pancreatic obstruction. Renal enlargement is unrelated to portal venous pressure.

Gallstones typically appear as echogenic foci that are mobile with position changes and produce posterior acoustic shadowing because the dense stone strongly reflects and absorbs sound. The “calculation” is signal behavior: high reflectivity plus blocked beam equals shadow. A fixed hypoechoic mass is more consistent with a polyp or wall lesion. Diffuse calcification is a different pattern. Splenic nonshadowing echogenic foci relate to other entities, not gallstones. Mobility plus shadowing remains the classic combined discriminator for stones.

Courvoisier sign describes painless jaundice with a palpable or enlarged gallbladder, suggesting malignant obstruction rather than gallstones. The reasoning is chronicity and inflammation: stones usually cause repeated inflammation and scarring, which prevents marked gallbladder enlargement, while a slowly growing tumor can obstruct flow without the same fibrosis, allowing distension. The analytic inference links symptom quality (painless) to mechanism (malignancy). Appendicitis and viral hepatitis do not produce this specific obstructive biliary pattern, and kidney stones cause colic, not jaundice.