ORAL REVALIDA Flashcards

1
Q

What is Streptolysin O?

A

Streptolysin O is a hemolytic toxin produced by Group A beta-hemolytic Streptococcus (S. pyogenes). It is oxygen-labile, meaning it is inactivated by oxygen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the difference between Streptolysin O and Streptolysin S?

A

• Streptolysin O is oxygen-labile, only active in a reduced state, and is antigenic (stimulates ASO antibodies).
•Streptolysin S is oxygen-stable, active in both reduced and oxidized conditions, and is non-antigenic (no antistreptolysin S test).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the three types of hemolysis in Streptococcus species?

A
  1. Beta-hemolysis – Complete hemolysis (clear zone on blood agar).
    1. Alpha-hemolysis – Partial hemolysis (greenish discoloration).
    2. Gamma-hemolysis – No hemolysis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How do you differentiate Group A from Group B beta-hemolytic streptococci?

A

• Group A (S. pyogenes): Bacitracin-sensitive, CAMP-negative.
• Group B (S. agalactiae): Bacitracin-resistant, CAMP-positive.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What test differentiates S. pneumoniae from Viridans Streptococcus?

A

Optochin Test:
• S. pneumoniae: Optochin-sensitive, bile-soluble.
• Viridans Strep: Optochin-resistant, bile-insoluble.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why is the ASO test important?

A

The Anti-Streptolysin O (ASO) test detects antibodies against Streptolysin O. It helps diagnose post-streptococcal complications like rheumatic fever and post-streptococcal glomerulonephritis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does a high ASO titer indicate?

A

A recent or past Streptococcus pyogenes infection, which could lead to complications such as rheumatic fever or glomerulonephritis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What enzymes are produced by Group A Streptococcus?

A
  1. DNAse – Breaks down DNA, aids in chromatin breakdown during apoptosis/necrosis.
    1. Streptokinase – Causes complete hemolysis on blood agar by breaking down blood clots.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is Anti-Streptolysin O (ASO)?

A

ASO is a neutralizing antibody produced after a Streptococcus pyogenes infection. It binds to and neutralizes the hemolytic activity of Streptolysin O (SLO).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

When does ASO appear in the blood after infection?

A

ASO appears in serum 1 week to 1 month after a streptococcal infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the normal values (NV) for ASO titer?

A

• Children: <150 U/mL
• Adults: <200 U/mL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the incubation period for ASO production?

A

Around 2 weeks after infection. It peaks at 5 weeks.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the ASO test used for?

A

To diagnose post-streptococcal conditions such as:
• Rheumatic fever
• Glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the timeline for ASO antibody levels?

A

• Rises after 1 to 3 weeks of infection.
• Peaks at 3 to 5 weeks.
• Declines to insignificant levels by 6 months.
• Persistent high levels suggest recurrent or chronic infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does ASO inhibit Streptolysin O?

A

ASO binds to Streptolysin O and prevents its hemolytic activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How is ASO titer estimated?

A

By diluting the patient’s serum in the presence of a constant amount of Streptolysin O until hemolysis is completely prevented.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What does the ASO level depend on?

A

The amount of Streptolysin O produced by Streptococcus pyogenes in the infected host.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the commercially available ASO tests?

A
  1. ASO Latex Slide Test – Used for rapid screening of high ASO titers.
    1. ASO Titration Test – Determines the exact titer of ASO antibody.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the principle of the Rapid ASO Latex Agglutination Test?

A

ASO antibodies in the patient’s serum react with latex particles coated with Streptolysin O antigen, causing visible agglutination.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What type of specimen is required for the ASO test?

A

Clear, hemolysis-free serum. because the test measures antibodies specifically anti streptolysin O which are present in the serum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How should ASO reagents be stored?

A

• Keep refrigerated at 2–8°C.
• DO NOT freeze.
• Reagents are stable until the expiration date.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What should ASO latex reagent look like after shaking?

A

It should be uniform without visible clumping. Slight sedimentation when refrigerated is normal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

When should ASO reagents or controls not be used?

A

When they show contamination or visible clumping after shaking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How should the serum sample be stored?

A

• If testing the same day → Keep at 2–8°C.
• If not tested within 7 days → Store at -20°C.
• For longer periods → Must be frozen.

25
Q

What types of serum should not be used in ASO testing?

A

Hemolytic or contaminated serum should not be used.

26
Q

What types of ligands can CRP recognize?

A

Self ligands (from damaged cells):
• Plasma lipoproteins
• Damaged cell membranes
• Phospholipids
• Small nuclear ribonucleoprotein components
• Apoptotic cells

Extrinsic ligands (pathogens):
• Phospholipids
• Capsular/cell body components of bacteria fungi or parasites

27
Q

What are positive acute-phase proteins (APPs)?

A

• C-reactive protein (CRP)
• Serum Amyloid A (SAA)
• Haptoglobin (Hp)
• Ceruloplasmin
• α2-Macroglobulin
• α1-Acid glycoprotein (AGP)
• Fibrinogen
• Complement proteins (C3, C4)

28
Q

What are negative acute-phase proteins?

A

These decrease during inflammation. Examples:
• Albumin
• Transferrin
• Transthyretin
• Retinol-binding protein

29
Q

What does a high CRP level indicate?

A

It indicates inflammation, which may be due to infection, autoimmune disease, or tissue damage.

30
Q

Is CRP disease-specific?

A

No, CRP is a nonspecific marker of inflammation. it is produced in response to a wide range of inflammatory conditions but it doesn’t indicate the specific cause or location of the inflammation

31
Q

How can CRP help in disease monitoring?

A

• Tracks disease progression and flares (e.g., autoimmune diseases).
• Helps differentiate between bacterial vs. viral infections (high CRP → bacterial infection).
• Monitors treatment effectiveness and postoperative complications.

32
Q

Which interleukins regulate CRP production?

A

• IL-1: Primary inducer of inflammation.
• IL-2: Regulates acute-phase protein production.

33
Q

CRP vs. ESR

A

CRP
- rapidly produced
- more sensitive
- more specific

ESR
- delayed
- moderate sensitivity
- less specific

34
Q

What is the normal value (NV) for CRP?

35
Q

What are the main functions of CRP?

A
  1. Anti-infective actions
    • Opsonizes particles for phagocytosis
    • Activates complement via the classical pathway
  2. Anti-inflammatory actions
    • Prevents systemic inflammation
    • Aids in neutrophil release from blood vessels
    • Prevents white cell adhesion in non-inflamed tissue
  3. Scavenging action
36
Q

Does CRP bind to normal cell membranes?

A

No, CRP only binds to cells undergoing apoptosis or necrosis.

37
Q

What happens when CRP binds to damaged cells?

A

• Activates complement
• Initiates an inflammatory reaction
• Attracts neutrophils and monocytes to the site

38
Q

Processes Induced by CRP

A
  1. Complement Activation – Enhances immune response by opsonization and cell lysis.
    1. RAAS Activation – Increases blood pressure and fluid retention, contributing to inflammation.
    2. Vascular Wall Damage – Inflammatory cells infiltrate, smooth muscle proliferates, increasing atherosclerosis risk.
    3. Prothrombotic State – activation of completion cascade. Promotes clot formation by increasing thrombin, adhesion molecules, and platelet stickiness.
    4. Endothelial Dysfunction – Reduces nitric oxide, impairing vasodilation and damaging blood vessel lining or glycocalyx
    5. Opsonization of Oxidized LDL – easier macrophage uptake, formation of foam cells.
39
Q

Factors Affecting CRP Levels & its effects

A

• Gender – Higher in women than men.
• Body Mass – Weight loss decreases CRP.
• Ethnicity – Higher in Black individuals than in White individuals.
• Exercise – Lowers CRP levels.
• Alcohol Consumption – Decreases CRP levels.

40
Q

what happens in complement activation and RAAS activation

A
  1. Complement Activation - Enhances immune response by opsonization and cell lysis.
  2. RAAS Activation - Increases blood pressure and fluid retention, contributing to inflammation.
41
Q

what happens in Vascular Wall Damage

A

Inflammatory cells infiltrate, smooth muscle proliferates, increasing atherosclerosis risk.

42
Q

what happens in Prothrombotic State

A

activation of completion cascade.
Promotes clot formation by increasing thrombin, adhesion molecules, and platelet stickiness.

43
Q

what happens in endothelial dysfunction

A

Reduces nitric oxide, impairing vasodilation and damaging blood vessel lining or glycocalyx

44
Q

what happens in Opsonization of Oxidized LDL

A

easier macrophage uptake, formation of foam cells.

45
Q

Methods for CRP Detection

A

• ELISA
• Immunoturbidimetry
• Rapid Immunodiffusion
• Visual Agglutination

46
Q

Clinical Importance of CRP

A
  • Elevated CRP
  • Mild CRP Elevation
  • Normalization of CRP
  • Transplant Cases
  • Cerebral Vein Thrombosis
  • Giant Cell Arteritis
  • Pancreatitis
47
Q

What are the methods for CRP detection?

A

• ELISA
• Immunoturbidimetry
• Rapid Immunodiffusion
• Visual Agglutination

48
Q

What conditions are associated with elevated CRP levels?

A

Elevated CRP is seen in osteoarthritis, coronary events, and prothrombotic states.

49
Q

What conditions are associated with mild CRP elevation?

A

Mild CRP elevation is found in SLE, scleroderma, Sjogren’s syndrome, and dermatomyositis/polymyositis.

50
Q

How is CRP used to assess antibiotic therapy response?

A

Normalization are a helpful tool in determining response to antibiotic therapy because it indicates a positive response to antibiotic therapy.

51
Q

What is the significance of CRP in transplant cases?

A
  • Elevated CRP is seen in kidney and heart transplants, with highly increased levels in graft-versus-host disease (GVHD).
  • Changes in levels are not organ specific, like other inflammatory conditions
52
Q

How does CRP relate to cerebral vein thrombosis?

A

High CRP levels are linked to a poor short-term prognosis in cerebral vein thrombosis.

53
Q

How is CRP used in diagnosing giant cell arteritis?

A

A CRP level >2.45 mg/dL along with thrombocytosis (pc >400,00/uL) predicts a positive temporal artery biopsy.

54
Q

What is the CRP pattern in pancreatitis?

A

CRP peaks 3 days post-onset, and levels >150 mg/L suggest severe disease.

55
Q

What is high-sensitivity CRP (hs-CRP)?

A

hs-CRP is a more sensitive marker than CRP, especially for detecting cardiovascular injury.

56
Q

What is the normal range for hs-CRP?

A

The normal range is <0.3 mg/dL

57
Q

What are the uses of hs-CRP?

A

• Cardiovascular risk assessment (predicts CVD, stroke, peripheral vascular disease).
• Identifies risk for hypotension.