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Clin Med 2 > Exam 1 > Flashcards

Exam 1 Flashcards

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
Q

Primary biliary cirrhosis general

A

Chronic autoimmune destruction of bile ducts leading to cholestasis

Usually women 40-60

Overlaps with autoimmune disease

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26
Q

Primary biliary cirrhosis presentation

A

Asymptomatic for years

Xanthomas, jaundice, steatorrhea, portal HTN because fats aren’t getting broken down and the liver’s ability to expand is lessened

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27
Q

Primary biliary cirrhosis diagnostics

A

Highly increased alk phos, GGT

Antibody testing for AMA

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28
Q

Ursodeoxycholic acid

A

Only drug shown to have benefit in slowing progression of primary biliary cirrhosis

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29
Q

Liver abscess symptoms

A

FUO, RUQ pain, cough/hiccup, anorexia, right shoulder pain

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30
Q

Liver abscess traetment

A

Inpatient, drain fluid collects and aggressive antibiotics

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31
Q

Benign neoplasm of the liver general

A

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

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32
Q

Cavernous hemangioma

A

Vascular lesion with no increased risk of bleed

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33
Q

Focal nodular hyperplasia

A

Hypervascular mass with stellate appearance on imaging

Proliferation of bile ducts

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34
Q

Hepatocellular adenoma

A

20-40 age women on OCP

Risk of hemorrhage

Small risk of malignant transformation

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35
Q

Hepatocellular carcinoma general

A

Usually cirrhotic liver

Aflatoxin exposure is significant

Increased incidence from hep C and fatty liver dz

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36
Q

Hepatocellular carcinoma presentation

A

Often asymptomatic

Weakness, weight loss, ascites, tender HM, mass(?)

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37
Q

HCC labs

A

Sudden and sustained increase in alk phos (from blocked bile ducts)

AFP, helpful in monitoring

Leukocytosis

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38
Q

HCC imaging

A

Exaggerated washout with CT or MRI because HCC derives blood supply from hepatic artery, not vein

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39
Q

Treatment of HCC

A

Resection if possible, chemo and XRT are not helpful

**monitor cirrhotics

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40
Q

Acute liver failure fulminant vs sub

A

Fulminant- within 8 weeks of onset of acute liver disease

Subfulminant- 8 weeks to 6 months from onset

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41
Q

Acute liver failure manifestations

A

Hepatic encephalopathy

Impaired synthetic function

Increased transaminases

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42
Q

Acute liver failure common causes

A

APAP toxicity, viral hepatitis

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43
Q

Hepatic encephalopathy general

A

Complex, multifactorial impairment of brain function

Ammonia is commonly elevated

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44
Q

Cirrhosis general & stages

A

Fibrosis of liver with generative nodules

Stages: compensated (asymptomatic), compensated with varices, and decompensated (ascites, bleeding, jaundice)

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45
Q

Asterixis

A

Most specific exam finding for hepatic encephalopathy

Flapping of outstretched, dorsiflexed hands

46
Q

Stigmata of liver disease

A 
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
Q

Child pugh score parts and stages

A

Classes A B and C

Encephalopathy, ascites, bilirubin, albumin, and prothrombin time

48
Q

Portal hypertension general

A

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
Q

Varices from portal HTN

A

Can rupture in the esophagus, causing severe and life threatening bleeds

50
Q

Ascites watch…

A

Blood pressure

Puddle sign, shifting dullness

51
Q

TIPS

A

Transjugular intrahepatic portosystemic shunt

Placed between portal and hepatic veins to bypass the liver, decreasing portal venous pressure

52
Q

Hepatorenal syndrome

A

Renal failure in setting of advanced liver dz due to intense renal vasoconstriction and decreased renal blood flow

53
Q

Spontaneous bacterial peritonitis general, criteria and treatment

A

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
Q

Alcoholic liver disease presentation

A

Can be asymptomatic HSM to fatal acute hepatitis or cirrhosis

Jaundice, anorexia/nausea, hepatomegaly

55
Q

Alcoholic liver disease labs

A

AST 2x ALT (another scotch and tonic)

56
Q

Alcoholic liver disease traetment

A

Alcohol cessation, cornerstone of treatment because it can be reversible

57
Q

Drug/toxin induced liver disease

A

Clinically indistinguishable, history is the key!

Antibiotics and NSAIDs

58
Q

Non alcoholic fatty liver disease general/risks

A

Likely affects 24-40% of US population

Obesity, diabetes are risks, metabolic syndrome increases the risk 4-11 fold

Fatty infiltration without inflammation

59
Q

NAFLD diagnostics

A

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
Q

NAFLD treatment

A

Correct modifiable risk factors

Benign and readily reversible

61
Q

Cholelithiasis general

A

Gallstones

More common in hispanic women and very common in women over 70

Best seen on US

62
Q

Stones in cholelithiasis.

A

Black- hemolytic

Brown- infection, cholangitis, or post cholecystectomy

Cholesterol stones- most common, supersaturation and crystallization within biliary sludge

63
Q

Cholelithiasis presentation

A

Nausea, belching, bloating, RUQ pain, biliary pain/colic (within 30 minutes after eating)

64
Q

Acute cholecystitis presentation

A

Postprandial belching and abdominal pain

N/v

Murphy’s sign

Fever/leukocytosis

Usually from stones

65
Q

Biliary imaging

A

Ultrasound is very good ,

CT rules out other things,

HIDA sees rate of output,

Ttube cholangiogram is real time images

ERCP and MRCP

66
Q

If jaundice present in cholecystitis, consider…

A

Common duct stone

67
Q

The F’s and other risks

A

Acute cholecystitis, fat fertile female, forty

Obesity or rapid weight loss

68
Q

Acute cholecystitis labs/treatment

A

Alk phos increased

US then HIDA

Abx, pain management and fasting

69
Q

Gangrenous gallbladder

A

Progressive pain, fever suggest necrosis, increased risk of perforation

May not take out right away but let drain first

Complication of acute cholecystitis

70
Q

Chronic cholecystitis

A

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
Q

Post cholecystectomy syndrome

A

RUQ pain, flatulence, intolerance to fatty foods after ccx

Evaluate for common bile duct dz, residual stones, etc

72
Q

Choledocholithiasis general and presentation

A

Bile duct stones

Can arise in GB or the bile duct

Biliary pain, jaundice, chills, fever

73
Q

Choledocholithiasis labs and treatment

A

Significant transaminitis, hyperbilirubinemia

ERCP, often followed by ccx

74
Q

Ascending cholangitis general

A

Pus in the biliary system, gram negative sepsis

Need ERCP emergently to assess

75
Q

Ascending cholangitis presentation

A

Charcot’s triad and reynold’s pentad

76
Q

Charcot’s triad

A

Ascending cholangitis

RUQ pain, fever, jaundice

77
Q

Reynold’s pentad

A

Ascending cholangitis

RUQ pain, fever, jaundice, AMS, hypotension

Emergency!!!

78
Q

Primary sclerosing cholangitis

A

Rare inflammatory dz, fibrosis and stricture of biliary tract, usually men 20-50

Could also have IBD

79
Q

Primary sclerosing cholangitis after…

A

Often get cholaniocarcinoma

12-17 year survival

80
Q

Hep A general and presentation

A

Fecal oral, have a vaccine

Anorexia, N/V, malaise, then fever and enlarged tender liver with jaundice

81
Q

Hep A labs

A

Strikingly elevated AST and or ALT

IgM anti HAV is acute hep A

IgG anti HAV is exposure to HAV

82
Q

Hep B general

A

Bodily fluids, insidious onset, common

Some are asymptomatic, some are fulminant disease, mostly intermediate

Can become chronic

83
Q

Positive hep B e antigen

A

Actively infected/infectious

84
Q

Hep B e antibody

A

Acute phase is over, infectivity reduced

85
Q

Hep C general

A

Type 1 is the most common

Very often injection drug use, other needle risks like tattoos

75% of infected people are varenicline

86
Q

Hep C presentation

A

Illness is often mild and asymptomatic

High rate of chronic hepatitis

Can progress to cirrhosis or HCC

87
Q

Cryoglobulinemia

A

Seen in Hep C, cold precipitating immune complexes

88
Q

ITP

A

Hep C presentation, easy bleeding and bruising, petechiae and purpura

89
Q

Porphyria cutaneous tarda

A

Hep C presentation, photosensitivity reaction with increased porphyrin levels

90
Q

Autoimmune hepatitis

A

Often younger females

ANA or ASMA

Clue is presence of other autoimmune diseases

Risk of cirrhosis and liver failure

91
Q

Budd chiari syndrome

A

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
Q

Budd chiari syndrome imaging

A

Doppler, sometimes need biopsy

93
Q

Acute Pancreatitis

A

Deep boring pain in epigastrum that radiates to the back

Caused by alcohol, biliary disease, hypertriglyceridemia

94
Q

Acute pancreatitis patho

A

Inflammation and autodigestion of pancreas

Loss of pancreatic function

Formation of pseudocyst (autolyzed debris) or abscess (bacteria)

95
Q

Acute pancreatitis exam

A

Epigastric tenderness

Distension of bowel

Obstructive jaundice

Systemically ill with SRS (without sepsis)

96
Q

Acute pancreatitis decrease in calcium

A

Saponification- fat necrosis complexes with calcium, white chalky deposits

97
Q

Which pancreatic enzyme is more sensitive for pancreatitis?

A

Lipase

98
Q

Sentinel loop

A

Air filled section of small intestine usually in LUQ

99
Q

Colon cutoff sign

A

Gas filled section of transverse colon abruptly ending at pancreas

100
Q

Apache II

A

Scoring system for critically ill patients, has good data for predicting mortality in pancreatitis patients

101
Q

Stages of acute pancreatitis

A

Mild- no organfailure

Moderate- transient organ failure or local/systemic complications

Severe- persistent organ failure

102
Q

Ranson’s criteria

A

Admission- age, WBC, glucose, AST, LDH

48 hours- ca, hct, hypoxemia, BUN, base deficit, fluids

103
Q

Pseudocysts

A

Fairly small, amylase rich fluid within or next to pancreas

Can secondarily get infected

“Walled off pancreatic necrosis”

104
Q

Chronic pancreatitis

A

Common in patients with alcoholism, 80% will develop DM

105
Q

Pancreatic cancer

A

Very lethal due to lack of early symptoms and proximity to other organs

Cause cause new onset DM 1 after 45

106
Q

Pancreatic cancer presentation

A

Epigastric pain, diarrhea, weight loss, fixed epigastric mass, sister mary joseph’s nodule, painless jaundice***, courvoisier’s sign

107
Q

Sister mary joseph’s nodule

A

Periumbilical nodule, metastatic from pancreatic cancer

108
Q

Courvoisier’s sign

A

Palpable gallbladder = neoplastic obstruction

109
Q

Pancreatic cancer lab

A

CA 19-9

110
Q

Double duct cutoff sign

A

ERCP for pancreatic cancer, dilation of CBD and pancreatic duct

111
Q

Biliary cancer presentation

A

Hematemesis, jaundice, hemobilia, courvoisier’s sign

112
Q

Biliary and pancreatic cancer treatment

A

Resection were possible, chemo and XRT aren’t great

Clin Med 2 (8 decks)

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