Type 2 HSR

Question 1

Type 2 HSR, also known as

Answer 1

Cytolytic Hypersensitivity Reaction

Question 2

3 types of HSR2

Answer 2

1) Inflammation type (involves complement activation)
2) Opsonization and phagocytosis (Antibody induced tissue
damage) ——— Erythroblastosis fetalis
3) Antibody induced tissue dysfunction (Not damage. Just dysfunction)
——— Graves dse

Question 3

Thyroid hormone depends on which amino acid for it’s production?

Answer 3

Tyrosine

Question 4

More potent thyroid hormone? Which is produced in higher amounts?

Answer 4

More potent/active form: T3

More production: T4

Question 5

Examples of HSR2

Answer 5

MY - Myasthenia Gravis
Blood - Blood transfusion rxn (mismatching)
Is - Immune hemolytic anemia, ITP
R - Rheumatic fever, Rh incompatibility (erythroblastosis fetalis)
H - Hyperacute transplant rejection (transplant rejection w/in/ a very few
time (mins to hours)
Positive - Pernicious anemia, Pemphigus vulgaris

Question 6

Most common cause of hyperthyroidism

Answer 6

Graves disease

Question 7

Pathophysiology of Graves dse.

Answer 7

Formation of autoimmune antibodies, TSIg —- binds to the receptor for TSH on thyroid hormone, resulting in subsequent increase in the production of thyroid hormones

Question 8

Triad of manifestations in Graves dse.

Answer 8

Triad includes: 1) thyroid manifestations: due to inc. thyroid
hormone production (sinus tavhy,
palpitations, heat intolerance,
oligomenorrhea, diarrhea)
Rx. Antithyroid Drugs (Propylthiouracil), Propranolol
2) Skin manifestations: Pretibial Myxedema (non pitting
edema on the shin)
Rx. Steroids
3) Eye manifestations: Proptosis (exophthalmus)
Rx. Steroids and Radiotx.

• Myxedema - S.I HypOthyroidism; Pretibial Myxedema - S.I
  HypERthyroidism
• Most common cause of U/L & B/L proptosis in adults - Graves Dse.

Question 9

M.C blood group system used.

Answer 9

ABO blood group system, aka. Landsteiner Blood Group System

Question 10

Chromosome where ABO antigens are present.

Answer 10

Short arm of chromosomes 9 (chr. 9p)

Question 11

Mechanism of inheritance in ABO blood group system

Answer 11

Codominance

Question 12

Antigens present in Rhesus Blood group system

Answer 12

C,D & E

“D” being the most important and most commonly seen in Rh antigen exposures

Question 13

Pathophysiology of Erythroblastosis fetalis.

Answer 13

Rh (-) mother, Rh (+) fetus

1st pregnancy: At around 37 weeks AOG, the mother’s and fetus’ blood mixes across the placental barrier. As the fetus’ RBC enters the maternal circulation, as part of the primary immune response, IgM antibodies are created against it as the fetal RBCSs have Rh antigen. This IgM antibodies can’t cross the placental barrier due to their size. So, these antibodies can’t affect the fetus. Later, after about 2 weeks (39 wks. AOG), IgG antibodies are produced as part of the secondary immune response. These antibodies can cross the placental barrier but by that time the baby has already reached term and so is delivered. But the IgG antibodies still remain in the maternal circulation.

2nd pregnancy: Same thing happens at the 37wk AOG, but this time the mother has preformed IgG antibodies against the Rh antigen. And since IgG can cross the placenta and reach the fetal circulation, hemolysis of the fetal blood takes place and the fetus suffers from anemia and jaundice.

Question 14

Minimum amount of blood required for sensitization of maternal blood with fetus’ Rh antigen in Erythroblastosis fetalis?

Answer 14

0.1mL

Question 16

How does Erythroblastosis fetalis manifest as kernicterus?

Answer 16

Increased hemolysis of the fetal Hb cause increase in unconjugated bilirubin, which is lipid soluble, meaning it can cross the BBB. Once it crosses the BBB, it gets deposited in the basal ganglia and cause irreversible brain damage.

Question 17

Consequences of severe anemia and jaundice in px. w/ erythroblastosis fetalis

Answer 17

Severe anemia causes hypoxia which damages cardiac and hepatic tissue, causing CHF ——— Death

Question 18

First manifestation of px. w/ erythroblastosis fetalis

Answer 18

Scalp Edema

Question 19

Manifestations of erthroblastosis fetalis

Answer 19

1) Scalp edema
2) Ascitis
3) Pleural effusion
4) Placentomegaly
5) HALO sign (Buddha’s sign)
6) Golden yellow colored liquor (Amniotic fluid)

1,2 & 3 ——— d/t CHF

Question 20

Diagnosis of Erthroblastosis fetalis

Answer 20

Coombs Test (CT)
           i) Direct CT: done with fetus blood
          ii) Indirect CT: done with maternal blood (Fetal Hb 
                                   detected)

Question 21

1) Golden Yellow AF S.I?
2) Green AF S.I?
3) Saffron AF S.I?

Answer 21

1) Golden Yellow AF: Erythroblastosis Fetalis
2) Green AF: Fetal distress (Meconium stained)
3) Saffron AF: >42 wks. AOG (Post maturity)