Exam 1 Flashcards

(112 cards)

1
Q

AST/ALT

A

Hepatocellular pattern when these transaminases predominate

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2
Q

Alk phos

A

If GGT elevated also, then hepatic

Associated with obstruction, “cholestatic pattern”

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3
Q

Conjugation of bilirubin

A

Made to be more polar so that it can be absorbed better

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4
Q

Painless jaundice

A

Pancreatic/biliary cancer until proven otherwise

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5
Q

Jaundice levels

A

Total bili >2

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6
Q

Conjugated jaundice

A

Dark, tea colored urine (because direct bili can be excreted)

Light clay colored stools (no bili in the gut)

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7
Q

First imaging for the liver

A

Ultrasound

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8
Q

Reasons for nonpathologic increase in unconjugated bilirubin in a newborn

A

High HCT and short lifespan of fetal RBC

Low bilirubin clearance in first week

Increased enterohepatic circulation of bilirubin

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9
Q

Face vs feet jaundice in a newborn

A

Feet jaundice is a much higher level of bilirubin

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10
Q

Kernicterus

A

Bilirubin is neurotoxic to basal ganglia

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11
Q

Conjugated hyperbilirubinemia in a newborn

A

Abnormal and requires work up

Usually cholestasis

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12
Q

Kasai procedure

A

Remove damages bile duct to create roux en Y in neonatal jaundice from cholestasis

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13
Q

Gilbert syndrome general

A

Benign, asymptomatic jaundice

Autosomal dominant

UGT gene promoter defect

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14
Q

Criggler-Najjar syndrome general

A

Inherited unconjugated hyperbilirubinemia

Complete loss of UGT, autosomal recessive

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15
Q

Type 1 criggler-najjar

A

Persistent hyperbilirubinemia after birth, normal liver otherwise

Usually fatal from kernicterus

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16
Q

Type 2 crigler najjar

A

Later onset than type 1, milder elevations, traetment often not needed

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17
Q

Reye’s syndrome general

A

Usually pediatric and postinfections

Triad of encephalopathy, fatty liver/failure, transaminitis

Avoid ASA!!

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18
Q

Hemochromatosis general

A

Autosomal recessive HFE gene

Commonly white patients

Increased Fe uptakeas hemosiderin in liver, pancreas, heart, etc.

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19
Q

Hemochromatosis symptoms

A

Fatigue, impotence, arthralgia, hepatomegaly, hyperpigmentation(common), DM

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20
Q

Hemochromatosis genetics

A

Test all 1st degree relatives of the person diagnosed

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21
Q

Hemochromatosis treatment

A

Phlebotomy if symptomatic

Fast iron/decrease intake

Avoid vitamin C supplements

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22
Q

Wilson disease general

A

Autosomal recessive, less than 40 years old

Disrupted copper transport

Deposited copper in the liver and brain

Looks like parkinson’s in a young patient

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23
Q

Kayser fleischer ring

A

Pathognomonic for wilson disease, granular. Copper deposits around iris

Low ceruloplasmin

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24
Q

Alpha 1 antitrypsin deficiency general

A

Can lead to cholestasis

Otherwise acts mostly in the lung, manifests as early onset of emphysema

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25
Primary biliary cirrhosis general
Chronic autoimmune destruction of bile ducts leading to cholestasis Usually women 40-60 Overlaps with autoimmune disease
26
Primary biliary cirrhosis presentation
Asymptomatic for years Xanthomas, jaundice, steatorrhea, portal HTN because fats aren't getting broken down and the liver's ability to expand is lessened
27
Primary biliary cirrhosis diagnostics
Highly increased alk phos, GGT Antibody testing for AMA
28
Ursodeoxycholic acid
Only drug shown to have benefit in slowing progression of primary biliary cirrhosis
29
Liver abscess symptoms
FUO, RUQ pain, cough/hiccup, anorexia, right shoulder pain
30
Liver abscess traetment
Inpatient, drain fluid collects and aggressive antibiotics
31
Benign neoplasm of the liver general
Asymptomatic, not a lot of risk Need to be distinguished from hepatocellular carcinoma or metastatic disease Don't necessarily need resection unless painful, rapidly growing, or ruling out cancer
32
Cavernous hemangioma
Vascular lesion with no increased risk of bleed
33
Focal nodular hyperplasia
Hypervascular mass with stellate appearance on imaging Proliferation of bile ducts
34
Hepatocellular adenoma
20-40 age women on OCP Risk of hemorrhage Small risk of malignant transformation
35
Hepatocellular carcinoma general
Usually cirrhotic liver Aflatoxin exposure is significant Increased incidence from hep C and fatty liver dz
36
Hepatocellular carcinoma presentation
Often asymptomatic Weakness, weight loss, ascites, tender HM, mass(?)
37
HCC labs
Sudden and sustained increase in alk phos (from blocked bile ducts) AFP, helpful in monitoring Leukocytosis
38
HCC imaging
Exaggerated washout with CT or MRI because HCC derives blood supply from hepatic artery, not vein
39
Treatment of HCC
Resection if possible, chemo and XRT are not helpful **monitor cirrhotics
40
Acute liver failure fulminant vs sub
Fulminant- within 8 weeks of onset of acute liver disease Subfulminant- 8 weeks to 6 months from onset
41
Acute liver failure manifestations
Hepatic encephalopathy Impaired synthetic function Increased transaminases
42
Acute liver failure common causes
APAP toxicity, viral hepatitis
43
Hepatic encephalopathy general
Complex, multifactorial impairment of brain function Ammonia is commonly elevated
44
Cirrhosis general & stages
Fibrosis of liver with generative nodules Stages: compensated (asymptomatic), compensated with varices, and decompensated (ascites, bleeding, jaundice)
45
Asterixis
Most specific exam finding for hepatic encephalopathy Flapping of outstretched, dorsiflexed hands
46
Stigmata of liver disease
``` Asterixis Palmar erythema Fetor hepaticus (fecal sweet odor of breath) Caput medusum (dilation of periumbilical veins) HSM Ascites Spider angioma Depuytren's contracture Gynecomastia ```
47
Child pugh score parts and stages
Classes A B and C Encephalopathy, ascites, bilirubin, albumin, and prothrombin time
48
Portal hypertension general
Liver disease causes increased vascular system pressure, fibrosis leads to compression of vessels Engorgement of portal and related veins, backflow into splenic and mesenteric circulation
49
Varices from portal HTN
Can rupture in the esophagus, causing severe and life threatening bleeds
50
Ascites watch...
Blood pressure Puddle sign, shifting dullness
51
TIPS
Transjugular intrahepatic portosystemic shunt Placed between portal and hepatic veins to bypass the liver, decreasing portal venous pressure
52
Hepatorenal syndrome
Renal failure in setting of advanced liver dz due to intense renal vasoconstriction and decreased renal blood flow
53
Spontaneous bacterial peritonitis general, criteria and treatment
Infected ascites without clear intra abdominal source Need 1 or more of the criteria- fever, pain, changed mental status, fluid of ascites with >250 PMN Cefotaxime first line
54
Alcoholic liver disease presentation
Can be asymptomatic HSM to fatal acute hepatitis or cirrhosis Jaundice, anorexia/nausea, hepatomegaly
55
Alcoholic liver disease labs
AST 2x ALT (another scotch and tonic)
56
Alcoholic liver disease traetment
Alcohol cessation, cornerstone of treatment because it can be reversible
57
Drug/toxin induced liver disease
Clinically indistinguishable, history is the key! Antibiotics and NSAIDs
58
Non alcoholic fatty liver disease general/risks
Likely affects 24-40% of US population Obesity, diabetes are risks, metabolic syndrome increases the risk 4-11 fold Fatty infiltration without inflammation
59
NAFLD diagnostics
May have RUQ pain, or asymptomatic May have abnormal labs Need to biopsy to confirm, esp if it is someone where you suspect cirrhosis or have stigmata of chronic liver disease
60
NAFLD treatment
Correct modifiable risk factors Benign and readily reversible
61
Cholelithiasis general
Gallstones More common in hispanic women and very common in women over 70 Best seen on US
62
Stones in cholelithiasis.
Black- hemolytic Brown- infection, cholangitis, or post cholecystectomy Cholesterol stones- most common, supersaturation and crystallization within biliary sludge
63
Cholelithiasis presentation
Nausea, belching, bloating, RUQ pain, biliary pain/colic (within 30 minutes after eating)
64
Acute cholecystitis presentation
Postprandial belching and abdominal pain N/v Murphy's sign Fever/leukocytosis Usually from stones
65
Biliary imaging
Ultrasound is very good , CT rules out other things, HIDA sees rate of output, Ttube cholangiogram is real time images ERCP and MRCP
66
If jaundice present in cholecystitis, consider...
Common duct stone
67
The F's and other risks
Acute cholecystitis, fat fertile female, forty Obesity or rapid weight loss
68
Acute cholecystitis labs/treatment
Alk phos increased US then HIDA Abx, pain management and fasting
69
Gangrenous gallbladder
Progressive pain, fever suggest necrosis, increased risk of perforation May not take out right away but let drain first Complication of acute cholecystitis
70
Chronic cholecystitis
Chronic. Inflammation from cholecystitis, usually stones Serous filling of GB with persistent cystic duct obstruction Porcelain or calcified gallbladder is associated with GB cancer, indication for ccx
71
Post cholecystectomy syndrome
RUQ pain, flatulence, intolerance to fatty foods after ccx Evaluate for common bile duct dz, residual stones, etc
72
Choledocholithiasis general and presentation
Bile duct stones Can arise in GB or the bile duct Biliary pain, jaundice, chills, fever
73
Choledocholithiasis labs and treatment
Significant transaminitis, hyperbilirubinemia ERCP, often followed by ccx
74
Ascending cholangitis general
Pus in the biliary system, gram negative sepsis Need ERCP emergently to assess
75
Ascending cholangitis presentation
Charcot's triad and reynold's pentad
76
Charcot's triad
Ascending cholangitis RUQ pain, fever, jaundice
77
Reynold's pentad
Ascending cholangitis RUQ pain, fever, jaundice, AMS, hypotension Emergency!!!
78
Primary sclerosing cholangitis
Rare inflammatory dz, fibrosis and stricture of biliary tract, usually men 20-50 Could also have IBD
79
Primary sclerosing cholangitis after...
Often get cholaniocarcinoma 12-17 year survival
80
Hep A general and presentation
Fecal oral, have a vaccine Anorexia, N/V, malaise, then fever and enlarged tender liver with jaundice
81
Hep A labs
Strikingly elevated AST and or ALT IgM anti HAV is acute hep A IgG anti HAV is exposure to HAV
82
Hep B general
Bodily fluids, insidious onset, common Some are asymptomatic, some are fulminant disease, mostly intermediate Can become chronic
83
Positive hep B e antigen
Actively infected/infectious
84
Hep B e antibody
Acute phase is over, infectivity reduced
85
Hep C general
Type 1 is the most common Very often injection drug use, other needle risks like tattoos 75% of infected people are varenicline
86
Hep C presentation
Illness is often mild and asymptomatic High rate of chronic hepatitis Can progress to cirrhosis or HCC
87
Cryoglobulinemia
Seen in Hep C, cold precipitating immune complexes
88
ITP
Hep C presentation, easy bleeding and bruising, petechiae and purpura
89
Porphyria cutaneous tarda
Hep C presentation, photosensitivity reaction with increased porphyrin levels
90
Autoimmune hepatitis
Often younger females ANA or ASMA Clue is presence of other autoimmune diseases Risk of cirrhosis and liver failure
91
Budd chiari syndrome
Hepatic vein obstruction, often thrombotic Polycythemia vera/myeloproliferative dz is 50% of cases Fulminant, acute, subacute or chronic Classic triad of abdominal pain, ascites and hepatomegaly
92
Budd chiari syndrome imaging
Doppler, sometimes need biopsy
93
Acute Pancreatitis
Deep boring pain in epigastrum that radiates to the back Caused by alcohol, biliary disease, hypertriglyceridemia
94
Acute pancreatitis patho
Inflammation and autodigestion of pancreas Loss of pancreatic function Formation of pseudocyst (autolyzed debris) or abscess (bacteria)
95
Acute pancreatitis exam
Epigastric tenderness Distension of bowel Obstructive jaundice Systemically ill with SRS (without sepsis)
96
Acute pancreatitis decrease in calcium
Saponification- fat necrosis complexes with calcium, white chalky deposits
97
Which pancreatic enzyme is more sensitive for pancreatitis?
Lipase
98
Sentinel loop
Air filled section of small intestine usually in LUQ
99
Colon cutoff sign
Gas filled section of transverse colon abruptly ending at pancreas
100
Apache II
Scoring system for critically ill patients, has good data for predicting mortality in pancreatitis patients
101
Stages of acute pancreatitis
Mild- no organfailure Moderate- transient organ failure or local/systemic complications Severe- persistent organ failure
102
Ranson's criteria
Admission- age, WBC, glucose, AST, LDH 48 hours- ca, hct, hypoxemia, BUN, base deficit, fluids
103
Pseudocysts
Fairly small, amylase rich fluid within or next to pancreas Can secondarily get infected "Walled off pancreatic necrosis"
104
Chronic pancreatitis
Common in patients with alcoholism, 80% will develop DM
105
Pancreatic cancer
Very lethal due to lack of early symptoms and proximity to other organs Cause cause new onset DM 1 after 45
106
Pancreatic cancer presentation
Epigastric pain, diarrhea, weight loss, fixed epigastric mass, sister mary joseph's nodule, painless jaundice***, courvoisier's sign
107
Sister mary joseph's nodule
Periumbilical nodule, metastatic from pancreatic cancer
108
Courvoisier's sign
Palpable gallbladder = neoplastic obstruction
109
Pancreatic cancer lab
CA 19-9
110
Double duct cutoff sign
ERCP for pancreatic cancer, dilation of CBD and pancreatic duct
111
Biliary cancer presentation
Hematemesis, jaundice, hemobilia, courvoisier's sign
112
Biliary and pancreatic cancer treatment
Resection were possible, chemo and XRT aren't great