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Lab Medicine > LFTs > Flashcards

LFTs Flashcards

1
Q

Functions of the Liver

A
  1. Involved in amino acid, albumin, angiotensinogen, and cholesterol biosynthesis as well as carbohydrate metabolism (Gluconeogenesis; Glycogenolysis; Glycogenesis)
  2. Produces thrombopoeitin, coag factors (I, II, V, VII, IX, X, and XI) as well as protein C and S and antithrombin
  3. Main site of RBC production during the first 32 weeks of fetal development (then bone marrow takes over)
  4. Converts ammonia to urea.
  5. Stores glycogen, vitamin A (1-2 years supply), vitamin D (1-4 months supply), vitamin B12, iron, and copper
  6. Contains many immunologically active cells, acting as a “sieve” for antigens carried to it via the portal system.
  7. Facilitates the catabolism of hemoglobin and excretes bile.
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2
Q

This is the term for the breakdown of glycogen into glucose.

A

Glycogenolysis

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3
Q

This is the term for the formation of glycogen from glucose.

A

Glycogenesis

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4
Q

This is the term for the synthesis of glucose from certain amino acids, lactate or glycerol.

A

Gluconeogenesis

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5
Q

T/F: The pancreas has exocrine and endocrine functions.

A

True;
Proteases, Amylases, and Lipases allow for exocrine function.

Insulin and Glucagon allow for endocrine function.

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6
Q

What tests check for Synthetic Function of the Liver?

A

Total Protein
Albumin
Prealbumin
PT-INR

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7
Q

What tests check for Excretory Function of the Liver?

A

ALP
GGT
Total and Direct Bilirubin
5’-Nucleotidase

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8
Q

What tests check for Hepatocellular Injury of the Liver?

A

ALT and AST

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9
Q

What tests check for Detoxification of the Liver?

A

Ammonia

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10
Q

The Comprehensive Metabolic Panel (CMP) is a combination of ______ and ______. What individual tests does this include?

A

BMP and HFP (LFTs)

  1. Na
  2. K
  3. Cl
  4. CO2
  5. BUN
  6. Cr
  7. Glucose
  8. Ca
  9. Total Protein
  10. Albumin
  11. AST
  12. ALT
  13. ALP
  14. Total Bilirubin

**Direct BR and Globulins not typically included in the CMP.

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11
Q

This synthetic product of the liver is a protein that binds free HgB released from RBCs and inhibits its oxidative activity. The complex with HgB is then removed by the spleen.

A

Haptoglobin

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12
Q

This synthetic product of the liver is used to screen for hemolytic anemia along with LDH.

A

Haptoglobin

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13
Q

This synthetic product of the liver is a glycoprotein that transports ferric ions (Fe3+). It CAN measure synthetic function BUT is rarely used.

A

Transferrin

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14
Q

What is the normal range of Albumin?

A

4.0-5.0 g/dL

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15
Q

_____ grams of albumin are synthesized and excreted daily by the normal liver.

A

10

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16
Q

As liver damage progresses, albumin synthesis ___________.

A

Progressively declines

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17
Q

Half life of Albumin is?

A

18-20 days (with 4% degraded daily)

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18
Q

Albumin levels may be normal in cases of ____________ and ______________.

A
  • Acute Viral Hepatitis

- Drug-Related Hepatotoxicity Jaundice

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19
Q

A patient with chronic liver disease (cirrhosis) will have albumin levels that are _____.

A

Low (< 4.0) called Hypoalbuminemia

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20
Q

An albumin levels less than 2.5 g/dL gives a ______ prognosis.

A

Poor

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21
Q

Someone with Hypoalbuminemia could present with…?

A
  • Peripheral Edema
  • Ascites
  • Pulmonary Edema
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22
Q

Non-hepatic Causes of Hypoalbuminemia

A
  • Protein Malnutrition/Malabsorption
  • Loss from the Kidneys or Gut
  • Burns
  • Trauma
  • EtOH Abuse
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23
Q

A patient with dehydration (as noted with BUN and HCt), would have ____ albumin levels.

A

High (>5.0) called Hyperalbuminemia

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24
Q

Causes of Hyperalbuminemia

A
  • Anabolic Steroids

- False Elevation if pt on Heparin or Ampicillin

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25
Q

Patients with hyperlabuminemia commonly present with what symptom(s)?

A

None, often asymptomatic.

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26
Q

Normal Range of Prealbumin (Transthyretin)

A

17.0-34.0 mg/dL

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27
Q

Half life of Prealbumin

A

~2 days

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28
Q

Prealbumin binds to _________ and _______.

A

Thryoxine; Retinol

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29
Q

Prealbumin levels respond to nutritional changes ____more/less____ frequently than albumin.

A

More

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30
Q

Normal Range of Total Protein

A

6.0 - 8.3 g/dL

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31
Q

Total Protein reflects the sum of ______ and ____.

A

Albumin and Globulins

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32
Q

How do you find Globulin levels on LFTs?

A

Total Protein - Albumin = Globulin

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33
Q

What would elevated Globulin Levels cause you to screen for?

A

Multiple Myeloma (serum urine protein electrophoresis, BM biopsy, etc.)

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34
Q

Normal Range of Serum Globulins

A

2-3 g/dL

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35
Q

These are larger proteins than albumin and important for immunologic responses (IgA, IgG, IgM, and IgE) but produced by B-lymphocytes.

A

Globulins

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36
Q

What do Globulins carry?

A
  • Hormones
  • Lipids
  • Metals
  • Antibodies
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37
Q

What would elevated Globulin levels indicate?

A
  • Chronic Infections
  • Liver Dz
  • Rheumatoid Arthritis
  • Myelomas
  • Lupus
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38
Q

What would low levels of Globulins indicate?

A
  • Immune Compromised
  • Protein Malnutrition/Malabsorption
  • Kidney dz
  • Protein Losing Enteropathy
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39
Q

The liver must be able to use Vitamin K in the Coagulation Cascade to produce what Factors?

A

II, VII, IX, and X

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40
Q

This test is used to screen for INTRINSIC pathway factor inhibitors (Factors VIII, IX, XI, and XII) as well as common pathway factors (Factors II, V, and X)

A

Activated Partial Thromboplastin Time (aPTT)

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41
Q

This test is used to screen for EXTRINSIC pathway of coagulation (Factors I, II, V, VII, and X). It also measures the Vitamin K Status (Factors II, VII, IX, and X)

A

Prothrombin Time (PT)

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42
Q

Normal Range for PT

A

12.7-15.4 seconds

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43
Q

This test accounts for variations between different manufacturer lots of tissue factor.

A

INR

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44
Q

Normal Range for INR

A

0.9-1.1

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45
Q

Meaning of Prolonged PT-INR

A

> 80% of liver synthetic capacity is lost

- Clotting Factors made by the liver are low (Factor VII has a half-life of about 6 hours)

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46
Q

In Acute Liver Dz, the PT may be _______ and as the patient recovers, the PT becomes _______.

A

Prolonged; normal

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47
Q

Causes of Prolonged PT

A
  • Chronic Cholestasis or Fat Malabsorption from Pancreatic or SB Dz
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48
Q

Bilirubin Metabolism Process

A
  1. Macrophages break down senescent RBCs in the spleen into globin and heme moieties
  2. Globin is catabolized to amino acids and the heme (porphyrin) to biliverdin and unconjugated bilirubin, which uses albumin as carriers
  3. In liver, there are three steps
    a. Uptake by the liver hepatocytes after dissociation with albumin
    b. Conjugation with glucoronic acid
    c. Excretion of conjugated bilirubin into the bile
    d. Conjugate bilirubin can be excreted unchaged in the stool
    e. It can also be converted to urobilinogen by commensal bacteria in the distal SB and will:
    - - be reabsorbed and enter portal circulation
    - - be reabsorbed into portal circulation and by the liver and re-excreted into the bile
    - - bypass the liver and be excreted by the kidneys as urine.
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49
Q

Normal Range of TBR (Total Bilirubin)

A

0.3 - 1.3 mg/dL

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50
Q

Two forms of Bilirubin

A
  1. Unconjugated (Indirect)

2. Conjugated (Direct)

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51
Q

Normal Range of Unconjugated Bilirubin

A

0.2 - 0.9 mg/dL

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52
Q

Normal Range of Conjugated Bilirubin

A

0.1 - 0.4 mg/dL

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53
Q

How do you calculate Indirect/Unconjugated Bilirubin?

***LFTs only show Conjugated/Direct and Total BR

A

IBR = TBR - DBR

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54
Q

T/F: Hyperbilirubinemia can occur as Indirect or Direct

A

True

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55
Q

T/F: Only Indirect/Unconjugated Hyperbilirubinemia can cause Jaundice.

A

False, Indirect or Direct Hyperbilirubinemia can cause Jaundice

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56
Q

When you see someone with Jaundice, what are you thinking?

A

Hyperbilirubinemia

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57
Q

What are the best places to look for Jaundice?

A
  • Sclera (first)
  • Skin
  • Mucous Membranes (under tongue, hard palate)
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58
Q

TBR in Jaundice is about

A

2.0 - 3.0 mg/dL (2-3 x nl)

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59
Q

What is the first step in approaching jaundice?

A

Determine whether the hyperbilirubinemia is primarily unconjugated (indirect) or conjugated (direct).

60
Q

Possible Causes of Indirect (Unconjugated) Hyperbilirubinemia

A
  1. Increased production of unconjugated bilirubin:
    - - Hemolytic Anemia
    - - Diserythropoiesis
    - - Internal Hemorrhage
  2. Decreased Bilirubin Uptake:
    - - HF
    - - Sepsis
    - - Meds (Rifampin, Probenecid)
    - - Fasting
  3. Impaired Bilirubin Conjugation
    a. Hereditary
    - - Gilbert Syndrome
    - - Crigler-Najjar Syndrome
    b. Acquired
    - - Neonates
    - - Hyperthyroidism
    - - Ethinyl Estradiol
    - - Sepsis
61
Q

This is a rare disorder affecting the metabolism of bilirubin. It causes a non-hemolytic jaundice, which results in high levels of unconjugated bilirubin and often leads to brain damage in infants.

A

Crigler-Najjar Syndrome

62
Q

Presentation of Hemolytic Anemia

Increased Production of Unconjugated BR

A
  • Symptoms of Anemia
  • Jaundice
  • Splenomegaly
  • Gallstones
  • Dark Urine
63
Q

Lab Findings of Hemolytic Anemia

A
  • Elevated serum unconjugated BR
  • Elevated serum reticulocyte count
  • Dec. haptoglobin and elevated LDH
64
Q

Possible Causes of Direct (Conjugated) Hyperbilirubinemia

**Elevated Liver Enzymes

A
  1. Hepatocellular Injury (Transaminase > ALP)
    - - Acute Viral, Alcoholic and Non-Alcoholic Hepatitis
    - - Chronic Hepatitis
    - - Cirrhosis
    - - Drug/Toxins
  2. Extrahepatic and Intrahepatic Obstruction (ALP > Transaminases) – Cholestasic Problems
    - - Extrahepatic = Biliary obstruction
    - - Intrahepatic = Impaired excretion
  3. Defects in Canalicular Excretion
    - - Dubin-Johnson Syndrome
    - – Rotor Syndrome
65
Q

Causes of Intrahepatic Obstruction causing Direct/Conjugated Hyperbilirubinemia

A
  • Viral and Alcoholic hepatitis
  • Drugs and Toxins (Steroids)
  • Sepsis
  • TPN
  • Post-liver transplant
  • Granulomatous/Infiltrative diseases (sarcoidosis, TB, amyloidosis, lymphoma)
  • PSC (associated with UC)
  • PBC
66
Q

Causes of Extrahepatic Obstruction causing Direct/Conjugated Hyperbilirubinemia

A
  1. Choledocholithiasis (stones)
  2. Tumors – benign & malignant
    a) Intrinsic to the biliary system (ie: cholangiocarcinoma)
    b) Extrinsic to the biliary system (ie: pancreatic head cancer)
    - - Primary sclerosing cholangitis (PBC – also fits here too)
    - - Strictures (post-procedure)
    - - Parasitic infections
    - - Ascaris lumbricoides
    - - Liver flukes
    - - AIDS cholangiopathy
67
Q

This is an autosomal recessive disorder that causes an increase of conjugated BR in the serum without elevation of liver enzymes (ALT, AST). It is assc with a defect in the ability of hepatocytes to secrete conjugated BR int the bile. It is usually asymptomatic but may be diagnosed in early infancy based on laboratory tests.

  • Has dark pigmented liver cells
  • GB not visualized
  • Normal Total Urine Coproporhyrin Content with 80+% being isomer 1
A

Dubin-Johnson Syndrome

68
Q

This is a rare, relatively benign autosomal recessive BR disorder. The main symptom is non-itching jaundice. Mainly elevation of conjugated BR.

  • Normal Histology and Appearance
  • GB can be visualized by oral cholecystogram
  • High Total Urine Coproporhyrin Content with 70+% being isomer 1
A

Rotor Syndrome

69
Q

Labs to check for Hyperbilirubinemia

A
  1. CBC (Hgb and Hct)
  2. BMP (BUN)
  3. LFTs (all)
  4. GGT
  5. Coag Study (PT)
  6. UA (RBCs and everything else)
70
Q

Two broad categories of Liver Disease

A
  1. Hepatocellular (Hepatocytes are inflamed or damaged)
  2. Cholestatic (Primary interference with metabolism or secretion of BR any from conversion to conjugated form to secretion into duodenum
71
Q

What lab tests measures Hepatocellular Injury?

A
  1. ALT (Alanine Aminotransferase)
  2. AST (Aspartate Aminotransferase)
  3. GGT (Gamma-Glutamyl Transpeptidase)
72
Q

Normal Range of ALT

A

7 - 41 units/L

Men usually < 30
Women usually < 20

73
Q

Function of ALT

A

Catalyzes the transfer of an amino group from alanine to alpha-ketoglutarate (transamination)

Glutamate + Pyruvate alpha-ketoglutarate + Alanine

74
Q

Half life of ALT

A

17 - 47 hours

75
Q

Why is ALT a measure of Hepatocellular Injury?

A

ALT leaks into bloodstream as hepatocytes are damaged. So it correlates with the degree of cell death or inflammation.

76
Q

T/F: ALTs can give us an accurate estimate of inflammatory activity or the amount of cell death.

A

False, only Liver Biopsy can do that.

77
Q

Normal Range of AST

A

12 - 38 units/L

Men: < 30
Women: < 20

78
Q

Function of AST

A

Catalyzes the transfer of an amino group from aspartate to alpha-ketoglutarate (transamination)

Glutamate + Pyruvate alpha-ketoglutarate + Aspartate

79
Q

T/F: AST is similar to ALT but ALT is less specific for Liver Dz because it is also produced in Skeletal and Cardiac Muscle

A

False.

AST is similar to ALT but AST is less specific for Liver Dz because it is also produced in Skeletal and Cardiac Muscle

80
Q

T/F: In many cases of liver inflammation, the ALT and AST activities are elevated roughly in a 1:1 ratio.

A

True

81
Q

In some conditions, such as _________, the elevation in the serum AST level may higher than the elevation in the serum ALT level (> 2-3:1and AST < 400).

A

Alcoholic Hepatitis

82
Q

Drug Sources of Hepatocellular Injury

A
  • Acteominophen
  • Allopurinol
  • Amiodarone
  • Cisplatin
  • Dapsone
  • Ketoconazole
  • Isoniazid
  • NSAIDs
  • Methotrexate
  • Lovastatin
83
Q

Non-Drug Sources of Hepatocellular Injury

A
  • Alcoholic Liver Dz
  • Autoimmune Hepatitis
  • Celiac Sprue
  • CHF
  • NAFLD
  • Hemochromatosis
  • Wilson’s Dz
84
Q

Viral Sources of Hepatocellular Injury

A
  • Hep A
  • Hep B
  • Hep C
  • Hep D
  • Hep E
  • EBV
  • CMV
85
Q

What lab tests measures Cholestasis?

A
  1. Alkaline Phosphatase
  2. GGT
  3. 5’-Nucleotidase
86
Q

Normal Range of Alkaline Phosphatase

A

33 - 96 units/L

87
Q

What is Alkaline Phosphatase?

A

A family of related enzymes (isoenzymes), produced in the bile ducts, small intestine, kidney, placenta and bone (usually ~80% in liver & bone).

88
Q

Variability with Alkaline Phosphatase

A
  • Adolescents may have 3X adult levels
  • May be increased late in pregnancy due to placental ALP
  • Bile accumulation increases hepatic ALP by hepatocytes
  • Generally associated with cholestatic D/Os (though cannot distinguish this with ALP alone.
89
Q

Hepatic Sources of ALP Elevation

A
  • Bile Duct Obstruction
  • Primary Biliary Cirrhosis
  • Primary Sclerosing Cholangitis
90
Q

Non-Hepatic Sources of ALP Elevation

A
  • Bone (Healing Fractures, Osteomalacia, Tumors)
  • Metabolic (Hyperthyroidism, Renal Failure, Acromegaly)
  • Drug Related (Anticonvulsants, Lithium, OCP)
91
Q

Normal Range of GGT

A

9 - 58 Units/L

92
Q

Where does GGT come from?

A

Bile Ducts (just like ALP)

93
Q

T/F: Elevations of GGT with ALP suggests Bile Duct Disease

A

True

94
Q

T/F: GGT maybe be elevated in virutally any liver dz and sometimes in normal individuals.

A

True

95
Q

Normal Range of 5’-Nucleotidase

A

0 - 11 units/L

96
Q

Where is 5’-Nucleotidase found?

A

Many Tissues (Liver, Brain, Heart, Vessels)

But most elevated in hepatic dzs.
Can also be elevated in RA and some cancers

97
Q

T/F: 5’-Nucleotidase responds similar to ALP.

A

True

98
Q

With the following Lab Results, what should be in your DDx?

ALP: Mildy Elevated
GGTP: Normal
ALT & AST: Normal

A
  • Preggo

- Non-Hepatic Causes

99
Q

With the following Lab Results, what should be in your DDx?

ALP: Moderately Elevated
GGTP: Markedly Elevated
ALT & AST: Normal

A

Cholestatic Syndromes

100
Q

With the following Lab Results, what should be in your DDx?

ALP: Mildy Elevated
GGTP: Mildly Elevated
ALT & AST: Markedly Elevated

A

Hepatocellular Dz

101
Q

This is produced by the breakdown of amino acides that are converted to urea by the liver. It is able to measure the liver’s ability to detoxify.

A

Ammonia

102
Q

In severe liver disease, what happens to serum ammonia levels? BUN levels?

A

Increase; Decrease

103
Q

Increasing ammonia may signal _____ with a high risk of hepatic encephalopathy or coma.

A

ESLD

104
Q

T/F: Measures of Ammonia are best in venous blood.

A

False, Arterial Blood

Venous blood levels may be elevated as a result of the metabolism of AAs in the muscles.

105
Q

When are ammonia levels most useful?

A

In patients with stupor or coma of unknown origin.

106
Q

Normal Range of Ammonia

A

10-80 microg/dL

107
Q

Urea is formed in the _____ and Eliminated in the _______.

A

Liver; Kidneys

108
Q

Facts about Hep A

A

Source: Feces

Route of Transmission: Fecal-Oral

Chronic Infection? No

Prevention: Pre-Exposure Immuization

109
Q

Facts about Hep B

A

Source: Blood/Blood-Derived Body Fluids

Route of Transmission: Percutaneous, Permucosal

Chronic Infection? Yes

Prevention: Pre-/Post-exposure Immunization

110
Q

Facts about Hep C

A

Source: Blood/Blood-Derived Body Fluids

Route of Transmission: Percutaneous, Permucosal

Chronic Infection? Yes

Prevention: Blood Donor Screening

111
Q

Facts about Hep D

A

Source: Blood/Blood-Derived Body Fluids

Route of Transmission: Percutaneous, Permucosal

Chronic Infection? Yes

Prevention: Pre-/Post-exposure Immunization

112
Q

Facts about Hep E

A

Source: Feces

Route of Transmission: Fecal-Oral

Chronic Infection? No

Prevention: Ensure safe drinking water

113
Q

Hepatitis A Antibody Testing for:

Acute Hep A

A

Anti HAV Total (IgG, IgM): Positive

IgM Anti-HAV: Positive

114
Q

Hepatitis A Antibody Testing for:

Resolved Hep A

A

Anti HAV Total (IgG, IgM): Positive

IgM Anti-HAV: Negative

115
Q

Hepatitis A Antibody Testing for:

Immunized Hep A

A

Anti HAV Total (IgG, IgM): Positive

IgM Anti-HAV: Negative

116
Q

Where is Hep B e antigen located?

A

Inside the first capsule.

117
Q

Where is Hep B surface antigen (HBsAg) located?

A

Outside the first capsule.

118
Q

Where is Hep B core antigen (HBcAg) located?

A

Inner capsule (Core capsule?)

119
Q

Hepatitis B Antibody Testing for:

Immunized Hep B

A

HBsAg: Negative

anti-HBc: Positive (or neg if long time ago)

Anti-HBs: Positive

Anti-HBc: Negative
HBsaAg: Negative

120
Q

Hepatitis B Antibody Testing for:

Acute Hep B

A

HBsAg: Positive

IgM anti-HBc: Positive

Anti-HBs: Negative

HBV DNA: Positive

HBeAg: May be either.

121
Q

Hepatitis B Antibody Testing for:

Chronic Hep B

A

HBsAg: Positive

IgG anti-HBc: Positive

Anti-HBs: Negative

HBV DNA: Positive

122
Q

Therapeutic Regimens for HBV

A
  1. lamivudine (Epivir)
  2. adefovir (Hepsera)
  3. tenofovir (Viread)
  4. telbivudine (Tyzeka)
  5. entecavir (Baraclude)

– Two Immune System Modulators = Interferon Alpha-2a and PEGylated Interferon Alpha-2A (Pegasys)

123
Q

T/F: Although none of the available drugs can clear the infection, they can stop the virus from replicating, thus minimizing liver damage.

A

True

124
Q

This is a chronic disease involving progressive destruction of small intrahepatic bile ducts leading to cholestatis and progressive fibrosis over decades. It can necessitate transplantation.

  • Etiology is unknown, but may be autoimmune.
  • Occurs in F>M 9:1
  • Onset: Early 20 - late 80s

Clinical Presentation:
- Inc. ALP, GGT, and BR

A

Primary Biliary Cirrhosis (PBC)

125
Q

What is the most useful test for PBC?

A

AMA (AntiMitochondrial Antibody)

85% Sensitive

126
Q

Clinical Presentation of PBC

A
  • Fatigue
  • Cholestasic Symptoms (Jaundice, Generalized Pruritius, etc)
  • Fat-Soluble Vitamin Deficiencies
  • Xerostoma
127
Q

Sibling Dz of PBC

A
  • RA
  • Sjorgen Syndrome
  • Systemic Scleroderma
128
Q

Managements of PBC

A
  • Prednisone and Ursodiol

- Liver Transplant

129
Q

Tests to Assess Pancreatic Inflammation:

A
  1. Amylase
  2. Lipase
  3. Trypsin and Tysinogen
  4. CT or MRI
130
Q

Where does Amylase come from?

A

Originates from Pancreas and Salivary Glands

131
Q

How soon does Amylase rise after onset of pancreatitis?

A

2-6 Hours

Peaks: 12-30 hours

3-5x normal = Diagnostic for Pancreatitis

132
Q

How soon do Amylase levels return to normal?

A

3-5 days

133
Q

Half life of Amylase in blood

A

1-2 hours

134
Q

How soon does Lipase rise after onset of pancreatitis?

A

2-6 hours

Peaks: 12-3- hours

3-5x normal = Diagnostic for Pancreatitis

135
Q

How soon do Lipase levels return to normal?

A

8-14 days

136
Q

Half life of Lipase in blood

A

7-14 hours

137
Q

Pathogen causing Ulcer Dz

A

H. pylori

138
Q

Transmission of H. Pylori

A
  • Gram-negative, microaerophilic bacillus that is contracted via oral-fecal transmission during childhood.
  • Prevalence increases with age; most are asymptomatic but >90% of patients with duodenal ulcers and 80% with gastric ulcers is caused by H. pylori.
139
Q

H. pylori can cause

A

MALT (Lymphoma) that is cured when the pathogen is destroyed.

140
Q

How do you dx H. pylori?

A
  • Urea Breath Test and Fecal Ag

- EGD with bx

141
Q

Treatment of H. pylori

A

14 day:

  1. concomitant (PPI + 1 gram of Amoxicillin + 500 mg of Metronidazole or Tinidazole bid
  2. Bismuth quadruple (PPI bid + bismuth subsalicylate qid + tetracycline 500 mg qid + Metronidazole 500 mg tid
  3. hybrid-concomitant (PPI + Amoxicillin 1g for 14 days with Amoxicillin 1 gram + 500 mg Clarithromycin + 500 mg Metronidazole or Tinidazole for the last 7 days).
142
Q

This condition can be acute or chronic and often presents with profound bloody diarrhea, urgency and abdominal cramping. It is distinguished from non-inflammatory on the basis of physical signs (fever, abdomen, leukocytosis).

A

Colitis

143
Q

Causes of Colitis

A
  1. Infectious (C. jejuni, Shigella, Samonella, Hemorrhagic E. coli O157:H7)
  2. CMV, Herpes = immunocompromised
  3. Ischemic = Mesenteric colitis
  4. Drug-induced = NSAIDs
  5. IBD = CD, UC, Indeterminate
144
Q

This is a toxin-induced dz caused by facultative gram positive anaerobe with evolving antibiotic-resistant strains. It is most commonly assc. with fluoroquinolones, clindamycin, cephalosporins, and beta-lactams.

Depending on the carrier state would determine if it was chronic diarrhea or life-threatening Colitis with sepsis.

A

C. Difficile

145
Q

Dx of C. Diff

A
  • PCR

- Toxins A and B

146
Q

Management of C. Diff

A
  • Flagyl –> PO Vanc

- Fidaxomycin –> Fecal Transplant

Lab Medicine (7 decks)

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