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Auto immune hemolytic Anemia

Auto immune Hemolytic anemia associated with 'warm' antibodies

  1. Antibodies directed against protein antigen are usually IgGQ
  2. These antibodies are active between 35° C and 40°C (warm)
  3. They do not require complement for there activityQ
  4. Spleen is usually enlarged and is the primary site for destruction IgG coated RBCs
  5. Glucocorticoids are the treatment of choiceQ
  6. Those who not respond to steroid splenectomy dose.

Auto immune Hemolytic anemia associated with 'Cold' antibodies

  1. RBC antibodies that are more active at low temperature and agglutinate RBC at temperature below 37°C have been called cold antibodies.
  2. They are primarily of the IgM class and require complement for activity. Q
  3. Destroyed in both the liver and spleen.
  4. Glucocorticoids are much less effective
  5. Splenectomy is not useful. 

Auto immune hemolytic Anemia

  1. A number of extrinsic agent and disorder may least to premature obstruction of red blood cells (RBC). The antibodies associated with immune hemolytic anemia. The hall mark of this group of disease is a positive direct Coombs test. Q
  2. Autoimmune hemolytic anemia due to warm reactive auto antibodies. 

A. Primary (idiopathic)


B. Secondary

  1. Lymphoproliferative disorder
  2. Connective tissue disorder (SLE)
  3. Non lymphoid neoplasm (e.g. ovarian tumors)
  4. Chronic inflammatory disease (e;g ulcerative colitis) 

Autoimmune hemolytic anemia due to cold reactive auto antibodies.

  1. Primary
  2. Secondary .
    1. Lymphoproliferative disorder
    2. Infection (Mycoplasma pneumoniae, Ebstein Barr virus) Q
    3. Paroxysmal cold hemoglobinuria
      1. Primary  
      2. Congenital or tertiary syphilis
    4. Drug induced immune hemolytic anemia
    5. Penicillin
    6. Immune
    7. Methyldopa 

Bleeding Disorder    

When a blood vessel is act or ruptured, the bleeding usually stops. Spontaneously after some time by the following mechanism

  1. Vascular spasm - The blood vessels contracts as a result of neurological reflex and local myogenic spasm. 

Table: Vascular causes of bleeding

  1. Henoch Schönlein purpura                            
  2. Connective tissue disease
  3. Scurvy                                          
  4. Prolonged steroid use/Cushing’s disease
  5. Hereditary hemorrhagic telangiectasia 

2. Platelet phase - The platelet comes in contact with the collagen fibers in the vessels wall become irregular and sticky and aggregate together to form a loose platelet plug.

3. Clotting phase-
Traumatized vessels and platelets liberate activating substances which initiate the clotting process.


Table: Classification of platelet dysfunction.


Quantitative disorders

  1. Decreased production          
  2. Increased destruction

Qualitative disorders


Inherited disorders
  1. Glanzmann thrombasthenia          
  2. Bernard Soulier syndrome
  3. Gray platelet syndrome        
  4. Wiskott Aldrich syndrome

Acquired disorders

  1. Medications                  
  2. Chronic renal failure                    
  3. Cardiopulmonary bypass



i) Patient with quantitative or qualitative deficiency in platelet or having defect in vascular integrity

  • Present with mucus or skin bleed (epistaxis, menorrhagia, hematuria, GIT bleed) and manifest as petechiae (small pinpoint haemorrhage) or echymosis (large superficial haemorrhage).



ii) Individual with a clotting factor deficiency having symptoms of deep bleeding into muscles and joint with muscles more extensive ecchymoses and hematoma formation.

PT - Prolong -suggest factor VU deficiency

PIT Prolong- suggest factor VIII IX, XI, XII deficiency


VIII IX deficiency- severe bleeding


XI deficiency- mild bleeding


XII deficiency- No bleeding

Both PT and PIT prolong- suggest deficiency off actor II, V, X

IT (throb in time) prolong


- Afibrinogenemia


- Dysfibrinogenemia


- PT, PIT, IT all prolong → DIC


Extra Edge
  1. In early Vitamin K deficiency - PT prolong                     
  2. In late Vitamin K deficiency- Both PT and PIT prolong'
  3. Oral anticoagulant therapy monitored by - PT                
  4. ​Parenteral heparin therapy monitored by- PIT


Clot solubility in 5m urea

  • Factor XIII deficiency

  1. Hemophilia
    1. X linked recessive disorders
    2. Hemophilia A    VIII
    3. Hemophilia B    IX
    4. Hemophilia C    XI
    5. Parahemophilia V 

Hemophilia is a group of hereditary genetic disorders that impair the body's ability to control blood clotting or coagulation.

  1. Hemophilia A (clotting factor VIII deficiency) is the most common form of the disorder, present in about 1 in 5,000–10,000 male births.
  2. Hemophilia B (factor IX deficiency) occurs in around 1 in about 20,000–34,000 male births.
  3. Hemophilia C due to coagulant factor XI deficiency, which can affect either sex.
  4. Haemophilia lowers blood plasma clotting factor levels of the coagulation factors needed for a normal   clotting process. Thus when a blood vessel is injured, a temporary scab does form, but the missing coagulation factors prevent fibrin formation, which is necessary to maintain the blood clot. A hemophiliac does not bleed more intensely than a person without it, but can bleed for a much longer time.
  5. In severe haemophiliacs even a minor injury can result in blood loss lasting days or weeks, or even never healing completely. In areas such as the brain or inside joints, this can be fatal or permanently debilitating. 



There are numerous different mutations which cause each type of haemophilia. Due to differences in changes to the genes involved, patients with haemophilia often have some level of active clotting factor.



Clotting factor VIII level


< 1 %


1 – 5 %


5 – 40 %


Sign & Symptoms

  1. Children with mild to moderate haemophilia may not have any signs or symptoms at birth. Their first symptoms are often frequent and large bruises and haematomas from frequent bumps and falls as they learn to walk. Swelling and bruising from bleeding in the joints, soft tissue, and muscles may also occur.
  2. Children with mild haemophilia may not have noticeable symptoms for many years. Often, the first sign in very mild haemophiliacs is heavy bleeding from a dental procedure, an accident, or surgery.
  3. Patients with more severe haemophilia suffer more severe and more frequent bleeds, while patients with mild haemophilia usually suffer more minor symptoms except after surgery or serious trauma. Moderate haemophiliacs have variable symptoms which manifest along a spectrum between severe and mild forms.
  4. The most characteristic type of internal bleed is a joint bleed where blood enters into the joint spaces. This is most common with severe haemophiliacs and can occur spontaneously (without evident trauma).
  5. If not treated promptly, joint bleeds can lead to permanent joint damage and disfigurement. Bleeding into soft tissues such as muscles and subcutaneous tissues is less severe but can lead to damage and requires treatment. 



Severe complications are much more common in severe and moderate haemophiliacs. Complications may be both directly from the disease or from its treatment:[

  1. Deep internal bleeding, e.g. deep-muscle bleeding, leading to swelling, numbness or pain of a limb.
  2. Joint damage from haemarthrosis (haemophilic arthropathy), potentially with severe pain, disfigurement, and even destruction of the joint and development of debilitating arthritis.
  3. Transfusion transmitted infection from blood transfusions that are given as treatment.
  4. Adverse reactions to clotting factor treatment, including the development of an immune inhibitor which renders factor replacement less effective.
  5. Intracranial haemorrhage is a serious medical emergency caused by the buildup of pressure inside the skull. It can cause disorientation, nausea, loss of consciousness, brain damage, and death. 



In both haemophilia A and B, there is spontaneous bleeding but a normal bleeding time, normal prothrombin time, normal thrombin time, but prolonged partial thromboplastin time.

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