liver masses Flashcards

1
Q

Most common benign liver tumor,Hemartomatous outgrowths of endothelium; some express estrogen receptors so accelerated growth is associated with high estrogen states

A

Cavernous Hemangiomas

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2
Q

how do u diagnose cavernous hemangiomas

A

Biopsy is contraindicated because of the risk of hemorrhage

• CT and MRI are specific. On contrast CT, hepatic hemangiomas have a characteristic pattern of enhancement, with early peripheral nodular
enhancement, followed by centripetal filling in of the lesion on delayed phases.

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3
Q

Histologically the lesion is composed of abnormal vessels, and cholangial proliferation. normal hepatocytes. Bile ductules are usually found. Kupffer cells
are present.

A

Focal nodular hyperplasia

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4
Q

Imaging: CT in focak nidular hyperplasia

A

bright homogeneous arterial contrast enhancement
except for the central scar which remains hypoattenuating

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5
Q

Hormone induced benign liver tumor

A

Hepatocellular adenoma

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6
Q

risk factors of Hepatocellular adenoma:

A

OCP and anabolic steroid use

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7
Q

what type of benign tumor where MRI is the best

A

Hepatocellular adenoma

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8
Q

Histologically, hepatocytes without normal lobular architecture. They are traditionally described as being devoid of bile ducts and Kupffer cells.

A

Hepatocellular adenoma

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9
Q

where is most common site of mestasis in HEPATOCELLULAR CARCINOMA

A

lungs

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10
Q

risk factors of HEPATOCELLULAR CARCINOMA

A

HBV, HCV, cirrhosis, aflatoxins (in peanuts), hemochromatosis, AAT, anabolic steroids, liver flukes, carbon tetrachloride.

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11
Q

diagnosis in HCC

A

Abnormal LFTs and tumor markers (α-fetoprotein)

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12
Q

tx of hepatocellular adenoma depend on size

A

o Small <5cm = follow up with imaging; cessation of OCP/steroids
o Large > 5 cm =surgical resection

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13
Q

Histology: degeneration of bile duct epithelium and diffuse infiltration of portal tracts with periductal concentric fibrosis (onion skin appearance)

A

PRIMARY SCLEROSING CHOLANGITIS

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14
Q

what causes destruction of both intra and extrahepatic bile ducts, 75% of patients have inflammatory bowel disease (usually UC), and Associated with HLA-A1-B8-DR3.

A

PRIMARY SCLEROSING CHOLANGITIS

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15
Q

what is the antibody in PSC

A

60% of patients have pANCA antibodies

• 70% of patients are men and average age is 40 years

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16
Q

diagnosis of PSC

A

High serum ALP, GGT, bilirubin

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17
Q

Chronic disorder w/ progressive destruction of small bile ducts (intrahepatic) leading to cirrhosis.

A

PRIMARY BILIARY CHOLANGITIS (PBC)

18
Q

PRIMARY BILIARY CHOLANGITIS (PBC) affects who mostly

A

Most commonly (90%) affects women aged 40-50 years old; usually in association with other autoimmune disorders ex: SS/RA.

19
Q

Why Does PBC Happen? (The Root Cause)

A

• Autoimmune attack → The immune system targets the small bile ducts.
• Bile can’t flow properly, leading to bile acid buildup, which damages liver cells.
• Over time, this leads to scarring (fibrosis) and cirrhosis (severe liver damage).

20
Q

How is PBC Diagnosed?

A
  1. Liver Function Tests (LFTs)
    • High Alkaline Phosphatase (ALP) → Most important marker
    • High Gamma-GT (GGT), AST, ALT
  2. Anti-Mitochondrial Antibody (AMA) – Key Test
    • Positive in 95% of PBC patients → Confirms autoimmune cause
  3. Liver Biopsy (Sometimes Needed)
    • Shows bile duct inflammation and scarring
21
Q

tx of pbc

A
  1. Ursodeoxycholic Acid (UDCA) – First-Line Treatment
    • Improves bile flow, slows disease progression
  2. Obeticholic Acid (OCA) – For Patients Who Don’t Respond to UDCA
    • Helps reduce bile buildup in the liver
  3. Symptom Management
    • Itching (Pruritus): Cholestyramine, Rifampin, Antihistamines
22
Q

what is shown in MRCP in PSC

A

MRCP (Magnetic Resonance Cholangiopancreatography) shows bile duct strictures (“beaded appearance”)

23
Q

PSC or PBC have high chance of cancer

A

PBC has a better prognosis; PSC has a higher risk of bile duct cancer.

24
Q

INTRAHEPATIC CHOLESTASIS OF PREGNANCY

A

generally seen in the third trimester.
• Most common liver disease of pregnancy.
• Presents as pruritus, often in the palms and soles, and no rash (although skin changes may be seen due to scratching) • Raised bilirubin
• Complications: increased rate of stillbirth; not generally associated with increased maternal morbidity

25
Hemolysis with a microangiopathic blood smear, ↑ liver enzymes, ↓ platelet count
HELLP SYNDROME
26
what are two main presentation in ots with HELLP SYNDROME
Hypertension and proteinuria are present in 85% of cases.
27
complications of hellp syndrome
abruptio placentae acute kidney injury subcapsular liver hematoma hepatic rupture pulmonary edema retinal detachment
28
Most cases of HELLP are diagnosed between
28 and 36 weeks of gestation
29
Obstruction of venous outflow of the liver owing to occlude the hepatic vein
BUDD CHIARI SYNDROME
30
what can cause budd chiari syndrome
hypercoagulable state, oral contraceptives, leukemia, and occlusion of hepatic vein
31
patients with chromic form of budd chiari syndrome
jaundice, caudate lobe enlargement, splenomegaly, portal hypertension, negative hepatojugular reflux.
32
ascetic tap in budd chiari syndrome
High protein in ascetic fluid and high SAAG
33
causes of acute pancreatitis
I Idiopathic (Unknown cause) G Gallstones (Most common cause) E Ethanol (Alcohol) T Trauma (Abdominal injury, post-surgery) S Steroids M Mumps & other infections (CMV, EBV, HIV) A Autoimmune (Lupus, IgG4-related disease) S Scorpion sting (Rare) H Hyperlipidemia & Hypercalcemia E ERCP (Endoscopic Retrograde Cholangiopancreatography) D Drugs (Diuretics, Azathioprine, Valproate, Sulfa drugs)
34
Signs of hemorrhagic pancreatitis:
o Gray turner = flanks o Cullen = umbilicus o Fox = inguinal region
35
symptoms of acute pancreatitis
• Low-grade fever • Acute, sharp, continuous, severe, epigastric pain that radiates to the back/interscapular region, with nausea and vomiting, relieved by leaning forward (tripod positioning) • Hypovolemia and hypovolemic shock (tachycardia, hypotension) • Hypoxia: ARDS and lung collapse • DIC signs (due to prothrombin activation by trypsin)
36
ransons criteria present on admission
G – Glucose > 200 mg/dL (11.1 mmol/L) A – Age > 55 years L – LDH (Lactate Dehydrogenase) > 350 IU/L A – AST (Aspartate Aminotransferase) > 250 IU/L W – WBC (White Blood Cell count) > 16,000/mm³
37
ranson criteria after 48 hrs
C – Calcium < 8.0 mg/dL (2.0 mmol/L) H – Hematocrit Drop > 10% decrease O – Oxygen (PaO₂) < 60 mmHg B – BUN (Blood Urea Nitrogen) Increase > 5 mg/dL (after IV fluids) B – Base Deficit > 4 mEq/L (Metabolic Acidosis) S – Sequestration of Fluids > 6 L (Severe third-spacing)
38
investigations of acute pancreatitis
Amylase (3X normal) & Lipase (very specific)
39
abdominal x ray in acute pancreatitis
Abdominal x-ray: -Rule out perforated peptic ulcer (air under the diaphragm) - Signs of pancreatitis: sentinel loop sign, colon cut off sign
40
chronic pancreatitis causes
T Toxic (Alcohol, Smoking, Hypercalcemia, Hyperlipidemia) I Idiopathic G Genetic (CFTR mutations, Hereditary pancreatitis, SPINK1, PRSS1 mutations) A Autoimmune (IgG4-related disease) R Recurrent acute pancreatitis (multiple attacks cause scarring) O Obstructive (Tumors, Strictures, Pancreas Divisum, Post-surgical)
41
Pancreatic insufficiency symptoms in chronic pancreatitis
o Endocrine: early onset diabetes o Exocrine = Malabsorption: Fat maldigestion: steatorrhea, fat-soluble vitamin deficiency, weight loss,
42
complication in chronic pancreatitis
Pancreatic pseudocyst