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IHO Week 5 > Reactive Oxygen Species & Antioxidants - Basem > Flashcards

Reactive Oxygen Species & Antioxidants - Basem Flashcards

1
Q

What are sources of ascorbic acid?

A

Sources of Vitamin C:

-Citrus fruits, green peppers, strawberries, tomatoes, broccoli, sweet & white potatoes

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2
Q

What symptoms does Vitamin C deficiency cause?

A
  • Impaired wound healing
  • Bleeding ecchymoses
  • Swollen gums
  • Anemia
  • Enlargement and keratosis of hair follicles
  • Lethargy
  • Depression
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3
Q

What symptoms are seen in scurvy (VitaC deficiency)?

A
  • Corkscrew hairs
  • Perifollicular Petechiae
  • Poorly healing wounds
  • Peridontal disease
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4
Q

When does Ischemia perfusion injury usually happen?

A

Can occur when tissue is interrupted during surgery or transplantation

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5
Q

What causes Ischemia perfusion injury?

A

Caused by cytotoxic ROS derived from oxygen in the blood that represses previously hypoxic cells

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6
Q

What does insufficient O2 in ischemia perfusion injury cause?

A

Decreased ATP

-Reduced ATP causes Increased Na+ and Ca2+ levels

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7
Q

What happens to electron carriers during ischemia perfusion injury that causes superoxide production?

A

Reduced state of electron carriers in the absence of oxygen and loss of mito gradients or membrane integrity leads to increased superoxide production when oxygen becomes available during reperfusion

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8
Q

What test is used for chronic granulomatous disease?

A

Nitro Blue-Tetrazolium Test (NBT)

  • Semiquantitative assay
  • Tests the phagocytic function of polymorphonuclear leukocytes (PMNL)
  • Cells reduce a colorless NBT into a blue-black deposit within the cell
  • In CGD, the PMNLs will not turn blue
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9
Q

What does a typical case of Chronic Granulatomous Disease look like?

A
  • History: 12 yr old boy admitted for fevers, chills, sweats, productive cough, nausea and vomiting
  • PE: febrile (symptoms of fever), tachycardic, tachypenic (fast resp. rate), diffuse rhonchi in both lungs, finger clubbing, splenomegaly, massive cervical, axillary, preauricular epitrochlear and inguinal lymphadenopathy
  • BCx: positive for S. aureus
  • CXR and CT show multiple lung abscesses bilaterally
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10
Q

What are the diagnostic tests and treatment for a patient diagnosed with Chronic Granulatomous Disease?

A

-Nitroblue tetrazolium reduction test and immunoblotting confirm dx of CGD
-Tx: with trimethoprim-sulfamethoxazole, levofloxacin, and voriconazole
-Received lifelong itraconazole and bactrum pox thereafter
[patient needed to be on these drugs his entire life to prevent these infections]

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11
Q

What is the incidence of chronic granulomatous disease?

A

1/200,000-250,000 live births

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12
Q

What is the Mechanism behind Chronic Granulomatous Disease?

A

-Phagocytes (neutrophils, eosinophils, monocytes/macrophages) have genetic defects in NADPH oxidase

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13
Q

Where can defects occur in NADPH oxidase in Chronic Granuloatous Disease?

A

NADPH oxidase:

  • Several isozymes
  • Generally has six different subunits (two in the cell membrane-alpha and beta) and four form the cytosol
  • Genetic defect can be in any of four of these genes that encode these subunits
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14
Q

What is CGD characterized by?

A

Recurrent life-threatening bacterial and fungal infections and granuloma formation

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15
Q

What are the most frequent infections in CGD? What is their unique property?

A

They are all Catalase positive:

  • Aspergillus (deadly infection - common in these cases)
  • S. aureus
  • Serratia
  • Nocardia
  • B. cepacia
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16
Q

What is the significance of Catalase positive organisms in CGD?

A
  • Catalase degrades small amount of H2O2 produced by infecting microbes, allowing them to survive in the phagosome
  • Catalase negative organisms generate enough H2O2 from which other highly reactive compounds are produced within the phagocytic vacuole of CGD neutrophils and macrophages, leading to effective microbial killing
17
Q

When are most patients with chronic granulomatous disease diagnosed?

A

Before age 5

18
Q

What is the prognosis for patients with CGD?

A
  • Only 21% lived beyond 5 years in 1967, now 92% live beyond 8 years
  • 50% live through the third decade
  • Median age of survivors in 1998 was 16 years
19
Q

What histology is associated with CGD?

A

Giant cells + caseous necrosis

20
Q

What types of treatments are available for CGD?

A
  • Vigilant surveillance
  • Anti-microbial ppx
  • Gene therapy - trying to give kids a gene for NADPH oxidase
  • Bone marrow transplant
  • Granulocyte transfusions - giving patient neutrophils form someone else
  • Compliance is an issue - kids don’t want to take their meds
21
Q

What must happen to hydrogen peroxide to prevent it from forming a hydroxyl radical?

A

Once a hydrogen peroxide molecule is formed, it must be reduced to water to prevent it from forming the hydroxyl radical in the Fenton reaction or the Haber-Weiss reaction.

22
Q

Where is catalase found?

A

Principally in peroxisomes, but is in cytosol and microsomal cell fraction

23
Q

Where in the body is catalase highest?

A

Highest in kidney an liver, where peroxisomal content is highest

24
Q

What reaction does catalase mediate?

A

2H2O2 –> 2H2O + O2

25
Q

What does catalase protect immune cells from?

A

It protects immune cells from respiratory burst

26
Q

What reaction does superoxide disputes regulate?

A

It turns a superoxide anion (O2-) into a hydrogen peroxide molecule (H2O2)

27
Q

What do defense/antioxidant defense enzymes do?

A

Antioxidant defense enzymes reaction with ROS and cellular products of free radical chain reactions to convert them to nontoxic products

28
Q

What reaction does superoxide dismutase catalyze?

A

2O2- (Superoxide) —- 2H+ —–> H2O2 (Hydrogen Peroxide) —> O2 is kicked off

29
Q

What are the two defense enzymes?

A
  1. Superoxide dismutase (SOD) removes the superoxide free radical
  2. Catalase and glutathione peroxidase remove hydrogen peroxide and lipid peroxides
30
Q

What does superoxide dismutase do?

A

Converts superoxide anion to hydrogen peroxide and O2 (called disputation)

31
Q

Why is superoxide dismutase called the primary defense against oxidative stress?

A

Because it is a strong initiator of chin reactions

32
Q

When is activity of superoxide dismutase increased?

A

It’s increased by chemicals and conditions, such as hyperbaric oxygen, which increase superoxide production

33
Q

What is a mutation in superoxide dismutase associated with?

A

ALS

-Implicated in familial ALS (5-10% of total ALS)

IHO Week 5 (7 decks)

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