Session 1: Group Work Flashcards Preview

Immunology > Session 1: Group Work > Flashcards

Flashcards in Session 1: Group Work Deck (23)
Loading flashcards...
1

What are the main blood groups defined by the ABO system?

A

B

0

AB

2

Describe the role of antibodies involved in blood transfusion reactions.

E.g. blood group A has the 'A' antigen on the RBC where as B has the 'B' antigen.

AB has both antigens and 0 has none.

This means that person with blood group A will have antibodies against antigen B.

B will have antibodies against antigen A.

AB will no antibodies.

0 will have both antibodies for antigen A and antigen B.

 

If you give B blood to someone with blood group A -> The antibodies of the recepient which will have antibodies B will attack the B blood.

0 can only get from 0 because they will attack both otherwise.

AB don't have any so can get from anyone.

3

What is the other common antigen group present on red blood cells?

The Rhesus

Most common is Rhesus D also called Rhesus +.

There is also C, c, E and e.

4

Describe the symptoms or signs of jaundice.

Yellowish skin and sclera

Pruritus if post-hepatic

Can have pale stool and dark urine

Usually painful (can however be painless)

5

Describe how lysis of red blood cells cause jaundice in newborn.

Lysis of red blood cells leads to release of haemoglobin and breakdown of Haem.

This turns into biliverdin and then further into bilirubin.

The bilirubin then overloads in the liver (or too young to conjugate) and is not conjugated.

This leads to increased unconjugated bilirubin. 

Bilirubin turns skin and sclera yellow.

6

What is the main complication of increased bilirubin levels for a baby?

Kernicterus which is a bilirubin induced brain-damage.

7

Which lab tests could be performed during pregnancy to confirm destruction of red blood cells?

Doppler scan of middle cerebral artery to check for anaemia

Amniotic fluid (amniocentesis)

8

Explain the type of hypersensitivity reaction responsible for HDN.

Type II IgG driven.

Antibodies develop against Rhesus D antigen and attack the red blood cells and destroys them.

 

9

How could the medical team predict the development of HDN?

Check blood group of mum and dad

Ask if they have had a kid before

10

Explain why the couple's first baby was born with no complications.

Because the mother has not been exposed to the Rh+ antigen until partum (where the blood almost always mixes)

It is first after first exposure that sensitation will occur.
IgG is created vs Rh+. And IgG antibodies can cross the placenta in second pregnancy and end up in the foetal blood.

11

Why does a mismatch of the ABO system rarely cause HDN?

Anti-A and Anti-B antibodies are IgMs and can therefore not cross the placenta.

12

RhoGam is a purified polyclonal antibody against the rhesus D antigen and is now being given to rhesus D antigen negative women carrying a rhesus D antigen positive baby. This is in order to prevent HDN.

Explain why RhoGam works.

It destroys the rhesus D antigen so is given within 72h after birth of the baby.

This is given to the mother and prevents sensitisation and production of IgG antibody vs. rhesus D antigen.

13

A 31 year old woman who was in good health has been lately suffering from diplopia which has gradually worsened over the course of four months. The examination reveals that the patient had ptosis of both eyelids with marked limiations of the ocular movements of both eyes.

Chewing and swallowing difficulties were also present. The neurologist noted that the patient had weakness of the facial muscles, tongue and upper arms and had problem breathing properly.

 

What are the symptoms that point toward a neuromuscular problem?

Weakness of muscles

Difficulty swallowing

Difficulty chewing

Diplopia

Ptosis

14

Clinical diagnosis of myasthenia gravis was made.

Which serology tests will confirm the diagnosis?

Antibody to the acetylcholine receptor

15

Describe the type of hypersensitivity reaction involved in the pathophysiology of the myasthenia gravis.

Type II hypersensitivity where there is receptor blockade.

16

Write down the basic pathophysiology of myasthenia gravis.

Antibodies are produced vs. nACh receptors and degradation of the nACh receptors ensue.

This means that less Na+ can enter to cause action potential.

17

Newborn infants from mothers with myasthenia gravis exhibit symptoms of myasthenia gravis at birth. Describe the immune mechanism responsible for the disease in the infant and explain why the disease eventually disappear.

The antibodies are not made by the baby but by the mother. The antibodies can cross the placenta and end up in the foetal circulation. On birth the antibodies will still be in the baby but will disappear as time passes and the baby will not have myasthenia gravis anymore.

18

How would you treat this patient knowing the immunopathology of the disease? 

Acetylcholine esterase inhibitors suchs as pyridostigmine

Also corticosteroids

19

Side effects of pyridostigmine.

Salivation

Lacrimation

Urination

Diarrhoea/Diaphoresis

GI upset

Emesis

20

Side effects of corticosteroids

Cataracts

Ulcers

Skin/Striae

Hypertension/glycaemia

Infection

Necrosis of femoral head

Glycosuria

Osteoporosis/Obesity

Immunosuppresion

Diabetes

21

Explain how plasmapheresis can be used for the treatment of a life-threatening myasthenic crisis.

Blood is filtered (1st) and then the plasma is also filtered (2nd). 

Antibodies against nACh are removed and plasma with saline is added.

Since it is an antibody driven disease the stimulus will subside for the time being.

22

Give examples of two other diseases caused by type II hypersensitivity reactions associated with change in receptor function.

Anti-GBM syndrome

Graves' syndrome

23