π Essential for Anatomy & Physiology, Hematology, and Pathology Nursing
Bone marrow is the soft, spongy tissue found inside bones, responsible for hematopoiesis β the production of blood cells.
β βBone marrow is the site where all types of blood cells (RBCs, WBCs, platelets) are formed from pluripotent stem cells.β
𧬠Type | 𩸠Function |
---|---|
Red Marrow | Actively produces RBCs, WBCs, and Platelets |
Yellow Marrow | Mainly fat storage; can convert to red marrow during stress or blood loss |
πΉ Infants β mostly red marrow
πΉ Adults β red marrow in flat bones (sternum, pelvis), yellow marrow in long bones
π Bone | π¬ Type of Marrow |
---|---|
Sternum | Red marrow |
Ribs | Red marrow |
Vertebrae | Red marrow |
Pelvis (Iliac crest) | Red marrow (common for biopsy) |
Femur (shaft) | Yellow marrow |
Humerus | Yellow marrow |
π’ 1. Hematopoiesis:
πΉ Produces RBCs (carry oxygen), WBCs (fight infection), platelets (clotting)
π’ 2. Immune Function:
πΉ Lymphoid stem cells mature into B-lymphocytes
π’ 3. Stem Cell Storage:
πΉ Contains hematopoietic stem cells for regenerative potential
π’ 4. Fat Storage (Yellow Marrow):
πΉ Energy reserve during starvation or stress
β Disorder | π Effect |
---|---|
Aplastic anemia | Failure to produce blood cells |
Leukemia | Malignant proliferation of WBC precursors |
Myelofibrosis | Replacement with fibrous tissue |
Multiple Myeloma | Plasma cell cancer β bone pain, anemia, renal issues |
Bone marrow suppression | Caused by chemo, radiation β pancytopenia |
β’ Withdraws fluid portion
β’ Common site: Posterior iliac crest
β’ Diagnoses: Leukemia, anemia, infections
β’ Core of bone taken for histological study
β’ Assesses: Cellularity, infiltration, fibrosis
π©Ί Pre: Consent, explain procedure
π©Ί During: Aseptic technique, local anesthesia
π©Ί Post: Apply pressure, monitor for bleeding/infection, give analgesics
π© Assessment:
πΉ Monitor CBC, infection signs, bleeding risk
πΉ Evaluate fatigue, pallor, fever, bone pain
π¨ During Procedures:
πΉ Support patient physically and emotionally
πΉ Ensure sterile technique during aspiration
π₯ Post-procedure Care:
πΉ Pressure on site for 5β10 mins
πΉ Apply sterile dressing
πΉ Monitor VS, bleeding, and pain
π‘ Bone marrow is the primary site for blood cell production
π‘ Red marrow = active; Yellow marrow = fat storage
π‘ Iliac crest is the preferred site for bone marrow biopsy
π‘ Aplastic anemia β bone marrow failure
π‘ Leukemia originates in bone marrow
Q1. Which of the following bones is commonly used for bone marrow aspiration?
π
°οΈ Sternum
β
π
±οΈ Iliac crest
π
²οΈ Femur
π
³οΈ Tibia
Correct Answer: π
±οΈ Iliac crest
Q2. What is the primary function of red bone marrow?
π
°οΈ Fat storage
β
π
±οΈ Blood cell production
π
²οΈ Hormone synthesis
π
³οΈ Bone growth
Correct Answer: π
±οΈ Blood cell production
Q3. Yellow marrow primarily contains:
π
°οΈ Plasma cells
β
π
±οΈ Adipose tissue
π
²οΈ Cartilage
π
³οΈ Osteoblasts
Correct Answer: π
±οΈ Adipose tissue
Q4. Which condition is characterized by replacement of marrow with fibrous tissue?
π
°οΈ Leukemia
π
±οΈ Aplastic anemia
β
π
²οΈ Myelofibrosis
π
³οΈ Multiple myeloma
Correct Answer: π
²οΈ Myelofibrosis
Q5. Which blood cell is not formed in the bone marrow?
π
°οΈ RBC
π
±οΈ Platelet
β
π
²οΈ T-Lymphocyte
π
³οΈ Neutrophil
Correct Answer: π
²οΈ T-Lymphocyte (formed in marrow, matures in thymus)
π Important for Anatomy & Physiology, Hematology, and Nursing Pathology
The spleen is a soft, vascular lymphoid organ located in the left upper quadrant (LUQ) of the abdomen, beneath the diaphragm and behind the stomach.
β βThe spleen is a blood-rich organ that functions in immune surveillance, blood filtration, and destruction of old red blood cells (RBCs).β
π Feature | π Details |
---|---|
Location | Left hypochondriac region (LUQ) |
Shape & Size | Fist-sized, oval, ~12 cm long |
Blood Supply | Splenic artery (from celiac trunk) |
Drainage | Splenic vein β portal circulation |
Peritoneal Covering | Completely covered by peritoneum |
π¬ Part | π§ Function |
---|---|
White Pulp | Contains lymphocytes β involved in immune response |
Red Pulp | Contains macrophages β responsible for phagocytosis of old RBCs and platelets |
β’ Removes aged, damaged, or abnormal RBCs and platelets
β’ Clears microorganisms and cellular debris
β’ Activates B and T lymphocytes
β’ Produces antibodies and traps pathogens
β’ Produces blood cells during fetal development
β’ Can restart in adults under extreme anemia (extramedullary hematopoiesis)
β’ Stores up to 30% of bodyβs platelets
β’ Contracts during bleeding to release stored blood
β’ Recycles iron from hemoglobin for reuse in bone marrow
β Disorder | π Description |
---|---|
Splenomegaly | Enlarged spleen due to infections (malaria, typhoid), leukemia, liver disease |
Hypersplenism | Overactive spleen β causes anemia, leukopenia, thrombocytopenia |
Asplenia | Absence or surgical removal of spleen (splenectomy) |
Ruptured Spleen | Trauma-related emergency β internal bleeding |
Accessory Spleen | Small, extra spleen seen in some individuals |
πΉ Done in cases of trauma, rupture, or severe hypersplenism
πΉ After splenectomy:
β’ β Risk of infection (esp. pneumococcus, meningococcus)
β’ Patient needs lifelong vaccinations and prophylactic antibiotics
π© Assessment:
πΉ Palpate LUQ for splenic enlargement
πΉ Monitor for signs of anemia, infection, bleeding
π¨ Post-splenectomy Care:
πΉ Monitor VS and signs of internal bleeding
πΉ Administer vaccines (e.g., pneumococcal, meningococcal)
πΉ Educate on infection prevention and early reporting of fever
π₯ Patient Education:
πΉ Avoid contact sports (rupture risk in splenomegaly)
πΉ Maintain hygiene to prevent infections
πΉ Long-term follow-up if splenectomy done
π‘ Spleen is the largest lymphoid organ in the body
π‘ White pulp = immune function; Red pulp = phagocytosis
π‘ Spleen filters blood and recycles iron from RBCs
π‘ Splenectomy β increased infection risk (vaccinate early)
π‘ LUQ pain or trauma β suspect splenic injury
Q1. The spleen is located in which abdominal quadrant?
π
°οΈ Right lower
β
π
±οΈ Left upper
π
²οΈ Right upper
π
³οΈ Left lower
Correct Answer: π
±οΈ Left upper
Q2. The white pulp of the spleen is involved in:
π
°οΈ Iron recycling
π
±οΈ Platelet storage
β
π
²οΈ Immune response
π
³οΈ RBC destruction
Correct Answer: π
²οΈ Immune response
Q3. Which of the following is a common complication after splenectomy?
π
°οΈ Hypertension
π
±οΈ Hyperglycemia
β
π
²οΈ Increased infection risk
π
³οΈ Anaphylaxis
Correct Answer: π
²οΈ Increased infection risk
Q4. What does the red pulp of the spleen mainly do?
π
°οΈ Antibody production
β
π
±οΈ Destroys old RBCs
π
²οΈ Stores bile
π
³οΈ Produces hormones
Correct Answer: π
±οΈ Destroys old RBCs
Q5. Splenomegaly may occur in all of the following EXCEPT:
π
°οΈ Malaria
π
±οΈ Leukemia
π
²οΈ Liver cirrhosis
β
π
³οΈ Diabetes mellitus
Correct Answer: π
³οΈ Diabetes mellitus
π Essential for A&P, Hematology, Pathology, and Clinical Nursing
Hematopoiesis is the physiological process of formation, development, and maturation of all types of blood cells from stem cells.
β βHematopoiesis is the process through which multipotent hematopoietic stem cells differentiate into mature red blood cells (RBCs), white blood cells (WBCs), and platelets.β
πΆ Stage | π₯ Primary Site of Hematopoiesis |
---|---|
Embryonic (1β2 months) | Yolk sac |
Fetal (3β7 months) | Liver and spleen |
Late fetal and birth onwards | Red bone marrow (especially in flat bones) |
Adult | Skull, vertebrae, sternum, ribs, pelvis, proximal femur/humerus |
πΉ Resides in bone marrow
πΉ Capable of self-renewal and differentiation into two major lineages:
π Lineage | π Develops Into |
---|---|
Myeloid Stem Cell | RBCs, Platelets, Monocytes, Neutrophils, Eosinophils, Basophils |
Lymphoid Stem Cell | B-lymphocytes, T-lymphocytes, Natural Killer (NK) cells |
π©Έ Blood Cell | π§ Function | π Origin |
---|---|---|
RBCs (Erythrocytes) | Carry oxygen via hemoglobin | Myeloid stem cell β Erythroblast |
WBCs (Leukocytes) | Immunity and defense | Myeloid & Lymphoid pathways |
Platelets (Thrombocytes) | Blood clotting | Myeloid stem cell β Megakaryocyte |
1οΈβ£ Hematopoietic stem cell
2οΈβ£ Myeloid progenitor
3οΈβ£ Erythroblast
4οΈβ£ Normoblast
5οΈβ£ Reticulocyte (immature RBC)
6οΈβ£ Erythrocyte (mature RBC)
πΉ Erythropoietin (EPO): Hormone secreted by kidney β stimulates RBC production
πΉ Thrombopoietin: Stimulates platelet formation
πΉ Cytokines & Interleukins: Regulate WBC differentiation
πΉ Nutrients Required:
β’ Iron β for hemoglobin synthesis
β’ Vitamin B12 & Folic Acid β for DNA synthesis
β’ Protein β for globin production
β Disorder | π Effect |
---|---|
Aplastic Anemia | Bone marrow failure β β all blood cell types |
Leukemia | Uncontrolled WBC formation β crowding out normal cells |
Myeloproliferative Disorders | Overproduction of myeloid cells |
Thalassemia / Sickle Cell | Defective RBC production or shape |
π© Assessment:
πΉ Monitor CBC, hemoglobin, reticulocyte count
πΉ Observe for anemia (pallor, fatigue), bleeding, infections
π¨ Interventions:
πΉ Administer hematinics (iron, folic acid, vitamin B12) as ordered
πΉ Provide safe environment (β injury risk in thrombocytopenia)
πΉ Infection control in neutropenic patients
π₯ Education:
πΉ Encourage balanced diet rich in iron, B12, protein
πΉ Importance of hydration and follow-up for hematologic conditions
π‘ Hematopoiesis occurs in red bone marrow in adults
π‘ Pluripotent stem cells β myeloid or lymphoid lines
π‘ Erythropoietin = hormone that stimulates RBC formation
π‘ RBCs, WBCs, and platelets come from common stem cells
π‘ Vitamin B12 and folate are essential for DNA synthesis in RBCs
Q1. Which organ is the primary site of hematopoiesis in adults?
π
°οΈ Liver
π
±οΈ Spleen
β
π
²οΈ Red bone marrow
π
³οΈ Kidney
Correct Answer: π
²οΈ Red bone marrow
Q2. Which hormone stimulates red blood cell production?
π
°οΈ Insulin
π
±οΈ Thyroxine
β
π
²οΈ Erythropoietin
π
³οΈ Estrogen
Correct Answer: π
²οΈ Erythropoietin
Q3. Which blood cells are produced from lymphoid stem cells?
π
°οΈ Platelets
π
±οΈ Erythrocytes
β
π
²οΈ B and T lymphocytes
π
³οΈ Neutrophils
Correct Answer: π
²οΈ B and T lymphocytes
Q4. Which vitamin is essential for DNA synthesis in RBC maturation?
π
°οΈ Vitamin C
π
±οΈ Vitamin D
β
π
²οΈ Vitamin B12
π
³οΈ Vitamin A
Correct Answer: π
²οΈ Vitamin B12
Q5. Reticulocytes are:
π
°οΈ White blood cells
π
±οΈ Immature platelets
β
π
²οΈ Immature red blood cells
π
³οΈ Stem cells
Correct Answer: π
²οΈ Immature red blood cells
π Important for Anatomy & Physiology, Medical-Surgical Nursing, and Pathology
Blood is a specialized connective tissue that circulates through the cardiovascular system and performs vital functions such as transport, protection, and regulation.
β βBlood is a fluid connective tissue composed of plasma and formed elements, which transports gases, nutrients, hormones, and waste products.β
π§ͺ Component | π Percentage | π Function |
---|---|---|
Plasma | ~55% | Liquid portion β carries proteins, nutrients, waste |
Formed Elements | ~45% | RBCs, WBCs, Platelets (cellular components) |
π©Έ Element | π¬ Scientific Name | π Function |
---|---|---|
RBCs | Erythrocytes | Carry oxygen via hemoglobin |
WBCs | Leukocytes | Immunity and defense |
Platelets | Thrombocytes | Blood clotting (hemostasis) |
π Property | π Normal Value |
---|---|
pH | 7.35 β 7.45 (slightly alkaline) |
Temperature | ~38Β°C (warmer than body temp) |
Volume | 5 β 6 L (male); 4 β 5 L (female) |
Color | Bright red (oxygenated), dark red (deoxygenated) |
π§ Plasma Component | π Function |
---|---|
Water (~90%) | Solvent, temperature regulation |
Proteins (7β8%) | Albumin (osmotic pressure), Globulins (antibodies), Fibrinogen (clotting) |
Electrolytes | NaβΊ, KβΊ, CaΒ²βΊ, Clβ» β maintain osmotic balance, pH |
Hormones, nutrients, waste | Transported for metabolism and excretion |
πΉ Oβ from lungs to tissues
πΉ COβ from tissues to lungs
πΉ Nutrients from GIT to cells
πΉ Hormones and enzymes to target organs
πΉ Waste products to kidneys for excretion
πΉ WBCs fight infection
πΉ Platelets form clots to prevent blood loss
πΉ Antibodies neutralize pathogens
πΉ Body temperature
πΉ pH and acidβbase balance
πΉ Fluid and electrolyte balance
π§ͺ System | 𧬠Types |
---|---|
ABO Grouping | A, B, AB, O |
Rh Factor | RhβΊ (positive) or Rhβ» (negative) |
π§ͺ Universal Donor: Oβ»
π§ͺ Universal Recipient: ABβΊ
β Condition | π Description |
---|---|
Anemia | β RBC or hemoglobin β fatigue, pallor |
Leukemia | Malignant β WBC count |
Thrombocytopenia | β Platelet count β bleeding risk |
Polycythemia | β RBC count β β viscosity β thrombosis risk |
Hemophilia | Genetic clotting disorder (β factor VIII/IX) |
π© Assessment:
πΉ Monitor CBC, hemoglobin, hematocrit
πΉ Check for bleeding, bruising, signs of infection or anemia
π¨ Interventions:
πΉ Administer blood products as prescribed
πΉ Use aseptic technique during invasive procedures
πΉ Educate about nutrition (iron, B12, folate for hematopoiesis)
π₯ Precautions:
πΉ Crossmatch blood before transfusion
πΉ Monitor for transfusion reactions
πΉ Prevent injury in thrombocytopenic patients
π‘ Blood is a connective tissue
π‘ RBC = transport oxygen; WBC = defense; Platelets = clotting
π‘ Normal pH = 7.35β7.45
π‘ Plasma = 55%, Formed elements = 45%
π‘ Oβ» = universal donor, ABβΊ = universal recipient
Q1. Which component of blood is responsible for transporting oxygen?
π
°οΈ WBCs
β
π
±οΈ RBCs
π
²οΈ Platelets
π
³οΈ Plasma
Correct Answer: π
±οΈ RBCs
Q2. What percentage of blood volume is made up of plasma?
π
°οΈ 25%
π
±οΈ 65%
β
π
²οΈ 55%
π
³οΈ 85%
Correct Answer: π
²οΈ 55%
Q3. Which plasma protein helps in clotting of blood?
π
°οΈ Albumin
π
±οΈ Globulin
β
π
²οΈ Fibrinogen
π
³οΈ Hemoglobin
Correct Answer: π
²οΈ Fibrinogen
Q4. Which blood group is known as the universal recipient?
π
°οΈ AβΊ
π
±οΈ Oβ»
π
²οΈ BβΊ
β
π
³οΈ ABβΊ
Correct Answer: π
³οΈ ABβΊ
Q5. The normal pH of human blood is:
π
°οΈ 6.8β7.2
π
±οΈ 7.0β7.3
β
π
²οΈ 7.35β7.45
π
³οΈ 7.5β8.0
Correct Answer: π
²οΈ 7.35β7.45
π Essential for Anatomy, Physiology, Medical-Surgical Nursing & Hematology
Blood cells (also called formed elements) are the cellular components of blood suspended in plasma and responsible for oxygen transport, immune defense, and clotting.
β βBlood cells are specialized cells including RBCs, WBCs, and platelets, each with distinct structure and function in circulation.β
π¬ Type | π§ͺ Scientific Name | π― Primary Function |
---|---|---|
Red Blood Cells | Erythrocytes | Oxygen and carbon dioxide transport |
White Blood Cells | Leukocytes | Immunity and defense |
Platelets | Thrombocytes | Clotting and prevention of blood loss |
πΉ Shape: Biconcave disc
πΉ Nucleus: Absent in mature form
πΉ Lifespan: ~120 days
πΉ Production Site: Red bone marrow (stimulated by Erythropoietin)
β
Carry oxygen using hemoglobin (Hb)
β
Carry COβ from tissues to lungs
β β RBC = Anemia
β β RBC = Polycythemia
πΉ Nucleated and larger than RBCs
πΉ Lifespan: Hours to days
πΉ Normal Count: 4,000β11,000/mmΒ³
βͺ WBC Type | π§ Category | π Function |
---|---|---|
Neutrophils | Granulocyte | First responders to infection (phagocytosis) |
Eosinophils | Granulocyte | Allergy & parasite defense |
Basophils | Granulocyte | Release histamine in allergic reactions |
Lymphocytes (B & T) | Agranulocyte | Specific immunity (antibodies & cytotoxicity) |
Monocytes | Agranulocyte | Become macrophages β phagocytose pathogens |
β β WBC = Infection, leukemia
β β WBC = Leukopenia, bone marrow suppression
πΉ Cell fragments from megakaryocytes
πΉ Lifespan: 7β10 days
πΉ Normal Count: 1.5β4 lakh/mmΒ³
β
Form platelet plugs
β
Release chemicals for blood clotting (coagulation)
β β Platelets = Thrombocytopenia β Bleeding
β β Platelets = Thrombocytosis β Clot formation risk
π¬ Parameter | π Normal Range |
---|---|
RBC (Male) | 4.7β6.1 million/mmΒ³ |
RBC (Female) | 4.2β5.4 million/mmΒ³ |
WBC | 4,000β11,000/mmΒ³ |
Platelets | 1.5β4 lakh/mmΒ³ |
Hemoglobin (Hb) | M: 13β17 g/dL; F: 12β16 g/dL |
Hematocrit (PCV) | M: 40β54%; F: 37β47% |
π© Assessment:
πΉ Monitor CBC, hemoglobin, WBC differential
πΉ Watch for signs of anemia (fatigue), infection (fever), or bleeding (bruises)
π¨ Intervention:
πΉ Administer hematinics, antibiotics, or blood products
πΉ Practice infection control for immunocompromised patients
πΉ Bleeding precautions in thrombocytopenia (no IM injections, soft toothbrush)
π₯ Education:
πΉ Encourage iron-rich diet (RBC support)
πΉ Explain signs of infection, anemia, or bleeding to patients
πΉ Adherence to medication and follow-up
π‘ RBCs lack nucleus and transport oxygen
π‘ Neutrophils are first to arrive at infection site
π‘ Platelets help in clot formation
π‘ Lymphocytes mediate specific immunity
π‘ Normal WBC count = 4,000β11,000/mmΒ³
Q1. What is the lifespan of red blood cells?
π
°οΈ 7β10 days
π
±οΈ 30 days
β
π
²οΈ 120 days
π
³οΈ 365 days
Correct Answer: π
²οΈ 120 days
Q2. Which WBCs are involved in allergic reactions and parasite defense?
π
°οΈ Neutrophils
π
±οΈ Lymphocytes
β
π
²οΈ Eosinophils
π
³οΈ Monocytes
Correct Answer: π
²οΈ Eosinophils
Q3. Platelets are derived from which cells?
π
°οΈ Erythroblasts
β
π
±οΈ Megakaryocytes
π
²οΈ Lymphocytes
π
³οΈ Myeloblasts
Correct Answer: π
±οΈ Megakaryocytes
Q4. Which of the following cells produce antibodies?
π
°οΈ T-cells
π
±οΈ Neutrophils
β
π
²οΈ B-lymphocytes
π
³οΈ Basophils
Correct Answer: π
²οΈ B-lymphocytes
Q5. A decrease in WBC count is known as:
π
°οΈ Leukocytosis
π
±οΈ Polycythemia
β
π
²οΈ Leukopenia
π
³οΈ Thrombocytopenia
Correct Answer: π
²οΈ Leukopenia
π Important for Anatomy, Physiology, Transfusion Nursing, and Lab Technology
Blood grouping is the process of classifying blood based on the presence or absence of specific antigens on the surface of RBCs (red blood cells).
β βBlood typing determines an individual’s blood group according to the ABO and Rh systems, essential for safe transfusion practices.β
πΈ Based on presence/absence of A and B antigens on RBC surface
πΈ Corresponding antibodies are present in plasma
π©Έ Blood Group | π§ͺ Antigen on RBC | π§ͺ Antibody in Plasma |
---|---|---|
A | A | Anti-B |
B | B | Anti-A |
AB | A and B | None |
O | None | Anti-A and Anti-B |
β
O = Universal Donor
β
AB = Universal Recipient
πΈ Based on presence of Rh (D) antigen
π§ͺ Rh Status | π Description |
---|---|
Rh Positive (RhβΊ) | D antigen present |
Rh Negative (Rhβ») | D antigen absent |
π Rh Incompatibility: If Rhβ» mother carries RhβΊ fetus β risk of Hemolytic Disease of the Newborn (Erythroblastosis fetalis)
β’ Mix patientβs RBCs with anti-A and anti-B sera
β’ Agglutination = presence of corresponding antigen
β’ Mix patientβs plasma with known RBC antigens
β’ Agglutination = presence of antibodies
π¬ Agglutination = reaction β helps identify blood group
β’ Patient’s serum + donor’s RBCs β check for agglutination
β’ Donorβs serum + patientβs RBCs (less common)
β Must be done before blood transfusion to prevent hemolytic reactions
πΈ Ensures safe transfusions
πΈ Prevents hemolytic transfusion reactions
πΈ Vital in organ transplant, pregnancy, surgery
π© Before Transfusion:
πΉ Verify patientβs name, ID, blood type
πΉ Ensure compatibility (ABO & Rh match)
πΉ Crossmatch report must be reviewed
πΉ Explain procedure and obtain consent
π¨ During Transfusion:
πΉ Start slowly and monitor vitals every 15 mins
πΉ Observe for chills, fever, hypotension, or rash
πΉ Keep emergency drugs ready (e.g., antihistamines)
π₯ After Transfusion:
πΉ Document date, time, volume, reaction (if any)
πΉ Monitor hemoglobin and hematocrit
π‘ ABO & Rh are the most important blood group systems
π‘ Oβ» = universal donor; ABβΊ = universal recipient
π‘ Agglutination indicates antigen-antibody reaction
π‘ Rh incompatibility causes erythroblastosis fetalis
π‘ Crossmatching is mandatory before transfusion
Q1. Which blood group is considered the universal donor?
π
°οΈ ABβΊ
π
±οΈ OβΊ
β
π
²οΈ Oβ»
π
³οΈ AβΊ
Correct Answer: π
²οΈ Oβ»
Q2. A person with blood group AB has which antibodies in plasma?
π
°οΈ Anti-A
π
±οΈ Anti-B
π
²οΈ Anti-A and Anti-B
β
π
³οΈ None
Correct Answer: π
³οΈ None
Q3. Which test is used to ensure compatibility before blood transfusion?
π
°οΈ ELISA
π
±οΈ CBC
β
π
²οΈ Crossmatch
π
³οΈ ESR
Correct Answer: π
²οΈ Crossmatch
Q4. Rh incompatibility is a concern in which situation?
π
°οΈ RhβΊ mother and Rhβ» baby
β
π
±οΈ Rhβ» mother and RhβΊ baby
π
²οΈ Both RhβΊ
π
³οΈ Both Rhβ»
Correct Answer: π
±οΈ Rhβ» mother and RhβΊ baby
Q5. What indicates a positive blood typing reaction?
π
°οΈ No color change
β
π
±οΈ Agglutination
π
²οΈ Hemolysis
π
³οΈ Clotting
Correct Answer: π
±οΈ Agglutination
π Essential for A&P, Hematology, Pathology & Clinical Nursing Practice
Blood coagulation (clotting) is the bodyβs natural defense mechanism to prevent blood loss after injury by forming a stable clot over the wound.
β βCoagulation is a complex process involving platelets, clotting factors, and the vascular endothelium to form a fibrin clot and stop bleeding.β
πΈ Immediate response
πΈ Blood vessel constricts to reduce blood flow
πΈ Platelets adhere to the damaged endothelium
πΈ Platelets aggregate and form a temporary plug
πΈ Release chemicals (ADP, thromboxane A2)
πΈ Involves clotting factors I to XIII
πΈ Converts fibrinogen (Factor I) into fibrin β stable clot
π Pathway | π Trigger | π§ͺ Involves |
---|---|---|
Intrinsic Pathway | Trauma inside vessel (slow) | Factors XII, XI, IX, VIII |
Extrinsic Pathway | Tissue injury outside vessel (fast) | Tissue factor (Factor III), Factor VII |
Common Pathway | Final steps to clot formation | Factor X, V, Prothrombin β Thrombin, Fibrinogen β Fibrin |
π§ͺ Name | π’ Factor No. | π©Έ Function |
---|---|---|
Fibrinogen | I | Converted to fibrin |
Prothrombin | II | Converted to thrombin |
Tissue Thromboplastin | III | Activates extrinsic pathway |
Calcium ions (CaΒ²βΊ) | IV | Required for all pathways |
Anti-hemophilic factor A | VIII | Deficient in Hemophilia A |
Anti-hemophilic factor B | IX | Deficient in Hemophilia B (Christmas disease) |
πΈ Plasminogen is activated to plasmin
πΈ Plasmin dissolves fibrin β clot removed after healing
β Condition | π Description |
---|---|
Hemophilia A | Deficiency of Factor VIII |
Hemophilia B | Deficiency of Factor IX |
Von Willebrand Disease | Deficiency of vWF + Factor VIII abnormality |
Vitamin K Deficiency | β Synthesis of factors II, VII, IX, X |
DIC (Disseminated Intravascular Coagulation) | Widespread clotting β bleeding |
π§ͺ Test | π Assesses |
---|---|
PT (Prothrombin Time) | Extrinsic pathway (Factor VII) |
APTT (Activated Partial Thromboplastin Time) | Intrinsic pathway (Factors VIII, IX, XI, XII) |
BT (Bleeding Time) | Platelet function |
CT (Clotting Time) | Overall clot formation |
INR (International Normalized Ratio) | Standardized PT β for warfarin monitoring |
π© Assessment:
πΉ Monitor signs of bleeding (bruises, gums, hematuria)
πΉ Check lab reports: PT, APTT, platelet count
π¨ Intervention:
πΉ Administer vitamin K or clotting factors as prescribed
πΉ Avoid IM injections or invasive procedures in bleeding patients
πΉ Apply pressure after venipuncture
π₯ Patient Education:
πΉ Teach bleeding precautions
πΉ Avoid NSAIDs, aspirin if at risk of bleeding
πΉ Compliance with anticoagulant monitoring (if on warfarin/heparin)
π‘ Clotting involves vascular, platelet, and coagulation phases
π‘ Calcium is essential for all pathways of coagulation
π‘ Hemophilia A = β Factor VIII; Hemophilia B = β Factor IX
π‘ PT = extrinsic; APTT = intrinsic
π‘ Fibrinolysis dissolves clot via plasmin
Q1. Which clotting factor is deficient in Hemophilia A?
π
°οΈ Factor IX
β
π
±οΈ Factor VIII
π
²οΈ Factor II
π
³οΈ Factor V
Correct Answer: π
±οΈ Factor VIII
Q2. What is the function of fibrinogen in coagulation?
π
°οΈ Activates platelets
π
±οΈ Forms thrombin
β
π
²οΈ Forms fibrin mesh
π
³οΈ Breaks down clot
Correct Answer: π
²οΈ Forms fibrin mesh
Q3. Which ion is essential for all steps in blood clotting?
π
°οΈ Sodium
π
±οΈ Potassium
β
π
²οΈ Calcium
π
³οΈ Magnesium
Correct Answer: π
²οΈ Calcium
Q4. Which test evaluates the intrinsic pathway of coagulation?
π
°οΈ PT
β
π
±οΈ APTT
π
²οΈ ESR
π
³οΈ Bleeding time
Correct Answer: π
±οΈ APTT
Q5. Von Willebrand disease involves:
π
°οΈ Platelet overproduction
π
±οΈ Vitamin K excess
β
π
²οΈ Defective vWF and Factor VIII
π
³οΈ Fibrinolysis defect
Correct Answer: π
²οΈ Defective vWF and Factor VIII
π Essential for Hematology, Medical-Surgical Nursing & Staff Nurse Exams
Hematological diagnostic tests are used to evaluate the quantity, quality, and functionality of blood cells and components, helping to detect disorders like anemia, leukemia, bleeding disorders, and infections.
β βHematological tests include a series of blood investigations to analyze red cells, white cells, platelets, hemoglobin, coagulation profile, and bone marrow function.β
β
Most basic and essential test
Includes:
π¬ Component | π Normal Range (approx.) | π Clinical Relevance |
---|---|---|
Hemoglobin (Hb) | M: 13β17 g/dL, F: 12β16 g/dL | Low = anemia, High = polycythemia |
Total WBC Count | 4,000β11,000/mmΒ³ | β = infection/leukemia; β = leukopenia |
Platelet Count | 1.5β4 lakh/mmΒ³ | β = thrombocytopenia; β = thrombocytosis |
RBC Count | M: 4.5β6.1, F: 4.2β5.4 mill/mmΒ³ | β = anemia; β = dehydration/polycythemia |
Hematocrit (PCV) | M: 40β54%, F: 37β47% | Indicates blood viscosity and cell volume |
MCV, MCH, MCHC | Indicates RBC size and content | For classifying types of anemia |
π¬ Microscopic examination of stained blood film
πΉ Detects abnormal shapes (poikilocytosis), sizes (anisocytosis), immature cells
πΉ Important in diagnosing leukemia, malaria, anemia
π Measures immature RBCs
πΉ Used to assess bone marrow activity and response to anemia
π Rate at which RBCs settle in 1 hour
πΉ β ESR = inflammation, infection, autoimmune disease, TB
π Measures clotting time via extrinsic pathway
πΉ Prolonged in vitamin K deficiency, liver disease, warfarin therapy
π Measures intrinsic pathway of coagulation
πΉ Prolonged in hemophilia, heparin therapy
π BT β time to stop bleeding (platelet function)
π CT β time to form clot (coagulation function)
π From posterior iliac crest
πΉ Diagnoses leukemia, aplastic anemia, multiple myeloma
πΉ Assesses cellularity and morphology
πΉ Evaluates iron levels, storage, and transport
πΉ For diagnosing iron deficiency anemia
π¬ Detects antibodies against RBCs
πΉ Used in autoimmune hemolytic anemia, transfusion reactions
π¬ Identifies abnormal hemoglobins
πΉ Used in thalassemia, sickle cell disease
πΉ Detects fibrin degradation products
πΉ Elevated in DVT, PE, DIC
π© Before Test:
πΉ Explain the purpose and obtain consent
πΉ Ensure patient fasting if required (e.g., iron studies)
πΉ Avoid invasive procedures before coagulation tests
π¨ During Test:
πΉ Maintain aseptic technique during blood collection
πΉ Label specimens properly
π₯ After Test:
πΉ Monitor site for bleeding, especially in thrombocytopenic patients
πΉ Inform patient about follow-up and reports
π‘ CBC is the most basic hematological test
π‘ ESR β in chronic infections & inflammation
π‘ PT = extrinsic; APTT = intrinsic pathway
π‘ Bone marrow biopsy is gold standard for leukemia
π‘ Coombs test detects autoimmune hemolysis
Q1. Which test evaluates the extrinsic pathway of coagulation?
π
°οΈ APTT
β
π
±οΈ PT
π
²οΈ ESR
π
³οΈ BT
Correct Answer: π
±οΈ PT
Q2. Which test is used to diagnose thalassemia?
π
°οΈ ESR
β
π
±οΈ Hemoglobin electrophoresis
π
²οΈ Reticulocyte count
π
³οΈ APTT
Correct Answer: π
±οΈ Hemoglobin electrophoresis
Q3. Bone marrow aspiration is commonly done from:
π
°οΈ Sternum
β
π
±οΈ Posterior iliac crest
π
²οΈ Femur
π
³οΈ Tibia
Correct Answer: π
±οΈ Posterior iliac crest
Q4. Reticulocyte count is used to assess:
π
°οΈ Platelet function
π
±οΈ Liver function
β
π
²οΈ Bone marrow activity
π
³οΈ Blood sugar
Correct Answer: π
²οΈ Bone marrow activity
Q5. Which of the following is prolonged in heparin therapy?
π
°οΈ PT
π
±οΈ ESR
β
π
²οΈ APTT
π
³οΈ BT
Correct Answer: π
²οΈ APTT
π Essential for Hematology, Medical-Surgical Nursing & Pathology
Hematological disorders are diseases that affect the blood cells, bone marrow, clotting mechanisms, or hemoglobin function. These conditions can lead to anemia, infections, bleeding, or malignancy.
β βHematological disorders involve abnormalities in the quantity or function of red cells, white cells, platelets, or plasma components.β
Anemia is a condition in which the number of red blood cells (RBCs) or the hemoglobin concentration is below normal, resulting in reduced oxygen-carrying capacity of the blood.
π¬ WHO Definition:
πΉ Hb <13 g/dL in men
πΉ Hb <12 g/dL in women
πΉ Hb <11 g/dL in pregnant women
𧬠A. Blood Loss Anemia:
β’ Acute: Trauma, surgery
β’ Chronic: GI bleeding, menstruation
𧬠B. Decreased RBC Production:
β’ Iron deficiency anemia
β’ Vitamin B12 or folic acid deficiency (megaloblastic anemia)
β’ Aplastic anemia
β’ Chronic disease anemia
𧬠C. Increased RBC Destruction (Hemolytic Anemia):
β’ Hereditary: Sickle cell, Thalassemia
β’ Acquired: Autoimmune hemolytic anemia, infections, drugs
πΈ Microcytic Hypochromic: Small, pale cells (Iron deficiency)
πΈ Macrocytic: Large RBCs (Vitamin B12/Folic acid deficiency)
πΈ Normocytic Normochromic: Normal size/color but reduced number (Aplastic anemia, Acute blood loss)
πΊ Poor nutritional intake (iron, B12, folate)
πΊ Blood loss (menstruation, ulcers, hemorrhoids)
πΊ Chronic infections (TB, renal failure)
πΊ Bone marrow suppression (chemotherapy, radiation)
πΊ Genetic disorders (thalassemia, sickle cell)
πΊ Alcoholism (folate deficiency)
πΉ Fatigue, weakness
πΉ Pallor (pale skin, mucosa)
πΉ Shortness of breath (dyspnea)
πΉ Palpitations, tachycardia
πΉ Dizziness, fainting
πΉ Brittle nails, hair loss
πΉ Glossitis (smooth tongue)
πΉ Angular cheilitis (cracked corners of mouth)
πΉ Cold intolerance
π§ͺ CBC (β Hb, β Hct, β RBCs)
π§ͺ Peripheral smear (RBC morphology)
π§ͺ Serum iron, ferritin, TIBC
π§ͺ Vitamin B12 and folate levels
π§ͺ Reticulocyte count
π§ͺ Bone marrow aspiration (in severe/aplastic anemia)
β’ Oral iron (Ferrous sulfate)
β’ Parenteral iron (Iron sucrose) if not tolerated orally
β’ Diet rich in iron: green leafy veg, meat, jaggery
β’ Vitamin B12 injections
β’ Oral folic acid supplements
β’ Treat underlying cause
β’ Blood transfusion if needed
β’ Corticosteroids in autoimmune cases
β’ Bone marrow transplant
β’ Immunosuppressive therapy
π© Assessment:
πΉ Monitor signs of anemia (pallor, breathlessness)
πΉ Check dietary history and menstrual history
πΉ Monitor lab values (Hb, RBCs)
π¨ Care and Monitoring:
πΉ Administer iron, B12, folic acid as prescribed
πΉ Give iron with vitamin C (improves absorption)
πΉ Monitor for side effects (nausea, constipation)
πΉ Educate about iron-rich diet
πΉ Manage fatigue: encourage rest
πΉ Watch for complications (heart failure in severe anemia)
π‘ Hb <12 g/dL in women = anemia
π‘ Iron deficiency anemia is the most common type
π‘ Glossitis and angular stomatitis are seen in nutritional anemia
π‘ Megaloblastic anemia shows macrocytic RBCs
π‘ Bone marrow transplant is used in aplastic anemia
Q1. Which is the most common type of anemia worldwide?
π
°οΈ Sickle cell anemia
π
±οΈ Aplastic anemia
β
π
²οΈ Iron deficiency anemia
π
³οΈ Hemolytic anemia
Correct Answer: π
²οΈ Iron deficiency anemia
π Rationale: Nutritional iron deficiency is the most prevalent cause globally.
Q2. Which vitamin deficiency causes megaloblastic anemia?
π
°οΈ Vitamin A
β
π
±οΈ Vitamin B12
π
²οΈ Vitamin D
π
³οΈ Vitamin K
Correct Answer: π
±οΈ Vitamin B12
π Rationale: B12 and folic acid deficiencies lead to large RBCs (macrocytes).
Q3. Which of the following is a symptom of anemia?
π
°οΈ Jaundice
π
±οΈ Constipation
β
π
²οΈ Fatigue
π
³οΈ Diarrhea
Correct Answer: π
²οΈ Fatigue
π Rationale: Low oxygen supply to tissues leads to tiredness and weakness.
Q4. What should be given with oral iron to enhance its absorption?
π
°οΈ Milk
π
±οΈ Tea
β
π
²οΈ Vitamin C
π
³οΈ Calcium
Correct Answer: π
²οΈ Vitamin C
π Rationale: Vitamin C (ascorbic acid) boosts iron absorption in the gut.
Q5. The characteristic RBCs in iron deficiency anemia are:
π
°οΈ Macrocytic
π
±οΈ Normocytic
β
π
²οΈ Microcytic hypochromic
π
³οΈ Sickle shaped
Correct Answer: π
²οΈ Microcytic hypochromic
π Rationale: Iron deficiency leads to small and pale red blood cells.
Iron Deficiency Anemia (IDA) is a condition where iron levels in the body are insufficient to produce adequate hemoglobin, resulting in reduced oxygen-carrying capacity of blood.
π§ͺ Hemoglobin production depends on iron β β iron = β hemoglobin = anemia
πΈ Inadequate dietary intake of iron (poor nutrition)
πΈ Chronic blood loss (e.g., menstruation, GI bleeding, hemorrhoids)
πΈ Increased iron requirement (pregnancy, growth spurts in children)
πΈ Malabsorption (e.g., celiac disease, chronic diarrhea)
πΈ Parasitic infestations (hookworm)
𧬠β Iron β β Hemoglobin synthesis β β RBC oxygen transport
β¬οΈ RBCs become microcytic (small) and hypochromic (pale)
β¬οΈ Tissue hypoxia β clinical symptoms of anemia
πΉ General weakness and fatigue
πΉ Pallor of skin, nail beds, conjunctiva
πΉ Dizziness, headache
πΉ Shortness of breath
πΉ Palpitations, tachycardia
πΉ Brittle nails (koilonychia β spoon-shaped nails)
πΉ Glossitis (smooth, shiny tongue)
πΉ Angular cheilitis (cracked corners of mouth)
πΉ Poor concentration and irritability (especially in children)
π§ͺ Hemoglobin: β (<12 g/dL in females, <13 g/dL in males)
π§ͺ MCV (Mean Corpuscular Volume): β (Microcytic)
π§ͺ MCH/MCHC: β (Hypochromic)
π§ͺ Serum Iron: β
π§ͺ Serum Ferritin: β
π§ͺ TIBC (Total Iron Binding Capacity): β
π§ͺ Peripheral smear: Microcytic, hypochromic RBCs
β
Oral Iron: Ferrous sulfate, Ferrous fumarate
β’ Give on an empty stomach or with orange juice (Vit. C enhances absorption)
β’ Avoid giving with milk or tea (inhibits absorption)
β
Parenteral Iron:
β’ Iron sucrose or iron dextran (for those intolerant to oral iron or with malabsorption)
β
Blood Transfusion:
β’ For severe anemia (Hb <7 g/dL or symptomatic)
π’ Iron-Rich Foods:
β’ Animal: Liver, red meat, egg yolk
β’ Plant: Green leafy vegetables, jaggery, beans, lentils, dry fruits (dates, raisins)
β’ Fortified foods (iron-fortified cereals)
π© Assessment:
πΉ Monitor signs: Pallor, fatigue, tachycardia
πΉ Check dietary habits and menstrual history
π¨ Interventions:
πΉ Administer oral/parenteral iron as prescribed
πΉ Give iron with vitamin C to increase absorption
πΉ Educate to avoid tea/coffee with iron supplements
πΉ Monitor for side effects: Nausea, constipation, black stools
πΉ Encourage iron-rich diet
πΉ Teach prevention: deworming, nutrition, hygiene
π‘ Iron deficiency causes microcytic hypochromic anemia
π‘ Serum ferritin is the best indicator of iron stores
π‘ Ferrous sulfate is the most commonly used oral iron
π‘ Vitamin C improves iron absorption
π‘ Koilonychia and glossitis are classic signs of IDA
Q1. What is the most common cause of iron deficiency anemia worldwide?
π
°οΈ Vitamin B12 deficiency
π
±οΈ Chronic kidney disease
β
π
²οΈ Inadequate dietary iron
π
³οΈ Thalassemia
Correct Answer: π
²οΈ Inadequate dietary iron
π Rationale: Poor nutrition is the leading cause, especially in developing countries.
Q2. What does the peripheral blood smear show in iron deficiency anemia?
π
°οΈ Macrocytic RBCs
π
±οΈ Normocytic normochromic RBCs
β
π
²οΈ Microcytic hypochromic RBCs
π
³οΈ Sickle cells
Correct Answer: π
²οΈ Microcytic hypochromic RBCs
π Rationale: Due to impaired hemoglobin synthesis, RBCs are small and pale.
Q3. Which lab value is increased in iron deficiency anemia?
π
°οΈ Serum iron
π
±οΈ Hemoglobin
π
²οΈ Serum ferritin
β
π
³οΈ TIBC
Correct Answer: π
³οΈ TIBC
π Rationale: Total iron-binding capacity rises as the body tries to bind more iron.
Q4. Which food should be avoided while taking iron supplements?
β
π
°οΈ Tea
π
±οΈ Orange juice
π
²οΈ Lemon water
π
³οΈ Guava
Correct Answer: π
°οΈ Tea
π Rationale: Tannins in tea inhibit iron absorption.
Q5. Which of the following is a side effect of oral iron therapy?
π
°οΈ Diarrhea
β
π
±οΈ Constipation
π
²οΈ Hypoglycemia
π
³οΈ Insomnia
Correct Answer: π
±οΈ Constipation
π Rationale: Iron supplements may cause GI disturbances, especially constipation.
Megaloblastic anemia is a type of macrocytic anemia caused by deficiency of Vitamin B12 and/or folic acid, leading to the production of abnormally large, immature red blood cells (megaloblasts) in the bone marrow.
𧬠It results from impaired DNA synthesis β delayed cell division β large RBCs
π§ͺ Poor dietary intake (vegetarians)
π§ͺ Malabsorption (pernicious anemia, gastric surgery, Crohnβs disease)
π§ͺ Lack of intrinsic factor (autoimmune destruction of gastric parietal cells)
π₯¦ Inadequate dietary intake (alcoholism, malnutrition)
π Drug-induced (methotrexate, phenytoin)
πΆ Increased requirement (pregnancy, lactation)
π¬ Deficiency of B12 or folate β impaired DNA synthesis
β¬οΈ Delayed nuclear maturation but normal cytoplasm β megaloblasts
β¬οΈ Ineffective erythropoiesis β anemia
β¬οΈ May lead to neurological complications (in B12 deficiency)
πΉ General symptoms of anemia:
β’ Fatigue, pallor, breathlessness, palpitations
πΉ Neurological symptoms (B12 deficiency):
β’ Tingling/numbness in hands and feet
β’ Gait disturbances (ataxia)
β’ Memory loss, confusion
β’ Irritability, depression
πΉ GI symptoms:
β’ Glossitis (smooth tongue)
β’ Anorexia, nausea, diarrhea
β’ Weight loss
π§ͺ CBC: β Hemoglobin, β MCV (>100 fL), low reticulocyte count
π§ͺ Peripheral smear: Macrocytic RBCs, hypersegmented neutrophils
π§ͺ Serum B12 level: β
π§ͺ Serum folate level: β
π§ͺ Schilling test: To check B12 absorption
π§ͺ Bone marrow: Hypercellular with megaloblasts
π IM Cyanocobalamin 1000 mcg
β’ Daily for 1 week β Weekly for 1 month β Monthly for life (if cause is pernicious anemia)
π Oral folic acid 1β5 mg/day
β’ Dietary sources: Green leafy vegetables, legumes, fortified cereals
β οΈ Always rule out B12 deficiency before starting folate alone (folate corrects anemia but not neurological damage)
π© Assessment:
πΉ Monitor for anemia and neurological signs
πΉ Dietary history and medication use
π¨ Intervention:
πΉ Administer prescribed supplements
πΉ Educate on B12- and folate-rich foods
πΉ Monitor response to therapy (RBC count, symptoms)
πΉ Provide safety for patients with neuropathy (fall precautions)
πΉ Coordinate Schilling test or GI workup if needed
π₯ Education:
πΉ Emphasize lifelong B12 therapy if cause is irreversible
πΉ Avoid alcohol, promote good nutrition
πΉ Explain importance of medication compliance
π‘ Megaloblastic anemia is macrocytic with hypersegmented neutrophils
π‘ Neurological symptoms are specific to B12 deficiency
π‘ Folic acid alone can mask B12 deficiency
π‘ B12 needs intrinsic factor for absorption in the ileum
π‘ MCV >100 fL is typical of macrocytic anemia
Q1. Which of the following causes megaloblastic anemia?
π
°οΈ Iron deficiency
β
π
±οΈ Vitamin B12 deficiency
π
²οΈ Aplastic anemia
π
³οΈ Hemolytic anemia
Correct Answer: π
±οΈ Vitamin B12 deficiency
π Rationale: B12 and folate are essential for DNA synthesis and RBC maturation.
Q2. What is a unique feature of B12 deficiency anemia?
π
°οΈ Hematuria
π
±οΈ Koilonychia
β
π
²οΈ Neuropathy
π
³οΈ Petechiae
Correct Answer: π
²οΈ Neuropathy
π Rationale: B12 deficiency affects nerve conduction and causes tingling/numbness.
Q3. Which test confirms poor absorption of Vitamin B12?
π
°οΈ ELISA
π
±οΈ Mantoux test
β
π
²οΈ Schilling test
π
³οΈ Coombs test
Correct Answer: π
²οΈ Schilling test
π Rationale: Schilling test measures B12 absorption with and without intrinsic factor.
Q4. What should be monitored after starting folic acid therapy?
π
°οΈ Platelet count
β
π
±οΈ Neurological symptoms
π
²οΈ Bleeding time
π
³οΈ PT/INR
Correct Answer: π
±οΈ Neurological symptoms
π Rationale: Folate improves anemia but not neurological damage from B12 deficiency.
Q5. What does a peripheral smear in megaloblastic anemia show?
π
°οΈ Microcytic RBCs
π
±οΈ Sickle cells
β
π
²οΈ Macrocytic RBCs and hypersegmented neutrophils
π
³οΈ Normocytic cells
Correct Answer: π
²οΈ Macrocytic RBCs and hypersegmented neutrophils
π Rationale: These are hallmark findings in megaloblatic anemia
Pernicious anemia is a type of megaloblastic anemia caused by vitamin B12 (cobalamin) deficiency due to the absence of intrinsic factor, a protein necessary for B12 absorption in the terminal ileum.
π It is autoimmune in nature β the body attacks the gastric parietal cells that produce intrinsic factor.
πΉ Autoimmune gastritis (most common)
πΉ Gastrectomy or gastric bypass surgery
πΉ Long-term use of proton pump inhibitors (β stomach acid)
πΉ Chronic alcohol use
πΉ Elderly individuals
πΉ Genetic predisposition (family history)
πΈ General symptoms of anemia:
β’ Fatigue, pallor, dizziness, breathlessness, palpitations
πΈ Neurological symptoms (due to demyelination):
β’ Tingling and numbness in hands and feet
β’ Ataxia (gait disturbance)
β’ Loss of proprioception and vibration sense
β’ Confusion, memory loss, irritability
πΈ Gastrointestinal symptoms:
β’ Glossitis (beefy red tongue)
β’ Anorexia, weight loss
β’ Diarrhea or constipation
π§ͺ CBC: β Hemoglobin, β MCV (>100 fL), β Reticulocyte count
π§ͺ Peripheral smear: Macrocytic RBCs, hypersegmented neutrophils
π§ͺ Serum Vitamin B12: β
π§ͺ Serum Intrinsic Factor Antibodies: β
Positive
π§ͺ Schilling Test (historical): Confirms B12 malabsorption due to intrinsic factor deficiency
π§ͺ Gastric biopsy: May show atrophic gastritis
π IM Cyanocobalamin (Vitamin B12) 1000 mcg
β’ Daily Γ 1 week β Weekly Γ 1 month β Monthly for life
β’ Oral B12 is not effective (due to absorption defect)
π© Assessment:
πΉ Observe for anemia and neurological deficits
πΉ Assess dietary intake and GI symptoms
π¨ Intervention:
πΉ Administer IM B12 injections as ordered
πΉ Provide safety support for patients with ataxia
πΉ Educate on lifelong B12 therapy and follow-up
π₯ Education:
πΉ Explain autoimmune nature of disease
πΉ Emphasize adherence to monthly B12 therapy
πΉ Encourage a B12-rich diet (though oral B12 wonβt be absorbed properly)
π‘ Pernicious anemia = B12 deficiency due to lack of intrinsic factor
π‘ It causes macrocytic anemia and neurological symptoms
π‘ IM B12 is the lifelong treatment
π‘ Common in elderly and post-gastrectomy patients
π‘ Glossitis and ataxia are hallmark symptoms
Q1. Pernicious anemia is caused by a deficiency of which factor?
π
°οΈ Folic acid
π
±οΈ Iron
β
π
²οΈ Vitamin B12
π
³οΈ Erythropoietin
Correct Answer: π
²οΈ Vitamin B12
π Rationale: Pernicious anemia is a form of B12 deficiency anemia.
Q2. The intrinsic factor needed for B12 absorption is produced by:
π
°οΈ Liver
β
π
±οΈ Gastric parietal cells
π
²οΈ Pancreas
π
³οΈ Small intestine
Correct Answer: π
±οΈ Gastric parietal cells
π Rationale: These cells are located in the stomach and help absorb B12 in the ileum.
Q3. A hallmark neurological symptom of pernicious anemia is:
π
°οΈ Nystagmus
β
π
±οΈ Tingling and numbness
π
²οΈ Diarrhea
π
³οΈ Diplopia
Correct Answer: π
±οΈ Tingling and numbness
π Rationale: Neuropathy is caused by demyelination due to B12 deficiency.
Q4. Which test helps detect the absorption problem in pernicious anemia?
π
°οΈ ELISA
π
±οΈ Mantoux test
β
π
²οΈ Schilling test
π
³οΈ Coombs test
Correct Answer: π
²οΈ Schilling test
π Rationale: This test identifies whether B12 absorption is impaired due to intrinsic factor deficiency.
Q5. How is vitamin B12 given in pernicious anemia?
π
°οΈ Oral tablets
π
±οΈ Nasal spray
β
π
²οΈ Intramuscular injection
π
³οΈ Sublingual drops
Correct Answer: π
²οΈ Intramuscular injection
π Rationale: IM B12 bypasses the need for intrinsic factor.
Folic Acid Deficiency Anemia is a type of megaloblastic anemia caused by inadequate levels of folic acid (Vitamin B9) in the body, leading to the formation of abnormally large, immature RBCs (megaloblasts) and impaired oxygen transport.
𧬠Folic acid is essential for DNA synthesis and cell division, especially in bone marrow.
πΈ Inadequate dietary intake (common in malnourished or elderly)
πΈ Alcoholism (impairs absorption and utilization)
πΈ Malabsorption syndromes (e.g., celiac disease)
πΈ Increased demand (pregnancy, infancy, cancer, burns)
πΈ Long-term use of certain drugs (e.g., phenytoin, methotrexate, sulfa drugs)
πΈ Chronic hemodialysis (folate loss)
πΉ General symptoms of anemia:
β’ Fatigue, weakness, pallor
β’ Shortness of breath, palpitations
β’ Headache, dizziness
πΉ Gastrointestinal symptoms:
β’ Glossitis (inflamed tongue)
β’ Anorexia
β’ Nausea, diarrhea
πΉ Special Note:
β No neurological signs (differentiates from B12 deficiency)
π§ͺ CBC: β Hb, β MCV (>100 fL), β Reticulocyte count
π§ͺ Peripheral Smear: Macrocytic, megaloblastic RBCs
π§ͺ Serum Folate Level: β (<2 ng/mL)
π§ͺ Serum Vitamin B12: Normal (to rule out combined deficiency)
π§ͺ Bone marrow biopsy: Megaloblastic changes (if needed)
π Oral folic acid 1β5 mg/day
β’ Continued until normal levels are restored
β’ Long-term supplementation in chronic conditions (e.g., dialysis, pregnancy)
π₯¦ Folate-rich foods:
β’ Green leafy vegetables (spinach, kale)
β’ Legumes (beans, lentils)
β’ Liver, eggs, bananas
β’ Fortified cereals and grains
π© Assessment:
πΉ Monitor signs of anemia and GI complaints
πΉ Dietary history review (vegetarian, alcohol use)
π¨ Interventions:
πΉ Administer folic acid as prescribed
πΉ Educate about folate-rich foods
πΉ Monitor CBC and patient response to therapy
πΉ Avoid over-replacement without ruling out B12 deficiency
π₯ Special Precautions:
πΉ If neurological symptoms are present, rule out B12 deficiency before giving folic acid
π‘ Folic acid is essential for DNA synthesis
π‘ Deficiency causes megaloblastic anemia without neurological symptoms
π‘ Alcoholism is a common cause
π‘ Green leafy vegetables are rich in folate
π‘ Always rule out B12 deficiency before folate therapy
Q1. What type of anemia is caused by folic acid deficiency?
π
°οΈ Microcytic
π
±οΈ Normocytic
β
π
²οΈ Megaloblastic
π
³οΈ Hemolytic
Correct Answer: π
²οΈ Megaloblastic
π Rationale: Folic acid deficiency leads to macrocytic megaloblastic anemia due to impaired DNA synthesis.
Q2. Which of the following is NOT a cause of folic acid deficiency?
π
°οΈ Malnutrition
π
±οΈ Pregnancy
π
²οΈ Alcoholism
β
π
³οΈ Hemorrhage
Correct Answer: π
³οΈ Hemorrhage
π Rationale: Hemorrhage causes iron loss, not folate depletion.
Q3. Which drug can interfere with folic acid metabolism?
π
°οΈ Paracetamol
β
π
±οΈ Methotrexate
π
²οΈ Omeprazole
π
³οΈ Ibuprofen
Correct Answer: π
±οΈ Methotrexate
π Rationale: Methotrexate is a folate antagonist and can induce folate deficiency.
Q4. Which of the following is a rich source of folic acid?
π
°οΈ Cheese
π
±οΈ Red meat
β
π
²οΈ Spinach
π
³οΈ Fish
Correct Answer: π
²οΈ Spinach
π Rationale: Green leafy vegetables like spinach are high in folate.
Q5. Folic acid deficiency does NOT cause which of the following?
π
°οΈ Fatigue
π
±οΈ Glossitis
β
π
²οΈ Neuropathy
π
³οΈ Diarrhea
Correct Answer: π
²οΈ Neuropathy
π Rationale: Neuropathy is specific to vitamin B12 deficiency, not folic acid.
Hemolytic anemia is a condition characterized by premature destruction of red blood cells (RBCs), leading to anemia and increased erythropoiesis (RBC production) in bone marrow to compensate.
π§ͺ Normally, RBCs live ~120 days β in hemolytic anemia, lifespan is drastically reduced.
πΈ Sickle Cell Anemia
πΈ Thalassemia
πΈ Hereditary Spherocytosis
πΈ G6PD Deficiency (Glucose-6-phosphate dehydrogenase)
πΈ Autoimmune Hemolytic Anemia
πΈ Drug-induced hemolysis
πΈ Infections (e.g., malaria)
πΈ Mechanical trauma (prosthetic heart valves, burns)
πΈ Hypersplenism
πΈ Intravascular Hemolysis: Occurs inside blood vessels
πΈ Extravascular Hemolysis: Occurs in spleen or liver
πΊ Genetic defects (sickle cell, thalassemia)
πΊ Autoimmune diseases (SLE, RA)
πΊ Certain medications (penicillin, quinidine)
πΊ Infections (EBV, malaria)
πΊ Blood transfusion mismatch
πΊ Exposure to oxidant stress (e.g., fava beans in G6PD deficiency)
πΉ Fatigue, pallor, weakness
πΉ Jaundice (due to bilirubin from RBC breakdown)
πΉ Dark-colored urine (hemoglobinuria)
πΉ Splenomegaly, hepatomegaly
πΉ Tachycardia, shortness of breath
πΉ Leg ulcers (in chronic hemolysis)
π§ͺ CBC: β Hb, β Reticulocyte count
π§ͺ Peripheral smear: Fragmented RBCs, spherocytes, sickle cells
π§ͺ LDH (Lactate dehydrogenase): β (cell destruction marker)
π§ͺ Bilirubin (indirect): β
π§ͺ Haptoglobin: β (binds free hemoglobin)
π§ͺ Coombs Test (Direct & Indirect): Positive in autoimmune hemolytic anemia
π§ͺ Hemoglobin electrophoresis: For thalassemia and sickle cell
π§ͺ G6PD assay (if suspected)
πΈ Treat the underlying cause (infection, drug, immune disorder)
πΈ Folic acid supplements (to support RBC production)
πΈ Immunosuppressive therapy (e.g., steroids in autoimmune cases)
πΈ Blood transfusion (if anemia is severe)
πΈ Splenectomy (if spleen causes excessive RBC destruction)
πΈ Avoid triggers (e.g., oxidant drugs in G6PD patients)
πΈ Hydroxyurea (in sickle cell anemia)
π© Assessment:
πΉ Monitor signs of anemia and jaundice
πΉ Observe for dark urine and fatigue
πΉ Evaluate spleen and liver enlargement
π¨ Interventions:
πΉ Administer medications as prescribed (folic acid, steroids)
πΉ Monitor CBC, bilirubin, and LDH levels
πΉ Educate to avoid triggers (in G6PD or autoimmune cases)
πΉ Ensure safe transfusion practices
πΉ Provide psychosocial support for chronic anemia patients
π₯ Patient Education:
πΉ Regular follow-up
πΉ Maintain hydration
πΉ Avoid certain medications and foods (e.g., sulfa drugs, fava beans in G6PD)
πΉ Importance of immunizations (post-splenectomy)
π‘ Hemolytic anemia = premature destruction of RBCs
π‘ Jaundice and dark urine are classic signs
π‘ G6PD anemia is triggered by certain foods and drugs
π‘ Coombs test is used in autoimmune hemolytic anemia
π‘ Splenectomy may be required in chronic hemolysis
Q1. Hemolytic anemia is characterized by:
π
°οΈ Low bilirubin
π
±οΈ Increased haptoglobin
β
π
²οΈ Premature destruction of RBCs
π
³οΈ Macrocytic anemia
Correct Answer: π
²οΈ Premature destruction of RBCs
π Rationale: The defining feature of hemolytic anemia is RBC destruction before 120 days.
Q2. Which test is commonly positive in autoimmune hemolytic anemia?
π
°οΈ Widal test
β
π
±οΈ Coombs test
π
²οΈ Mantoux test
π
³οΈ ELISA
Correct Answer: π
±οΈ Coombs test
π Rationale: Coombs detects antibodies against RBCs in autoimmune hemolysis.
Q3. A common complication of chronic hemolytic anemia is:
π
°οΈ Liver cirrhosis
β
π
±οΈ Splenomegaly
π
²οΈ Kidney stones
π
³οΈ Appendicitis
Correct Answer: π
±οΈ Splenomegaly
π Rationale: The spleen overworks to destroy defective RBCs, leading to enlargement.
Q4. Which condition causes hemolysis after eating fava beans?
π
°οΈ Iron deficiency anemia
π
±οΈ Aplastic anemia
β
π
²οΈ G6PD deficiency
π
³οΈ Pernicious anemia
Correct Answer: π
²οΈ G6PD deficiency
π Rationale: Fava beans can trigger hemolysis in individuals with G6PD deficiency.
Q5. What is a classic lab finding in hemolytic anemia?
π
°οΈ Decreased LDH
π
±οΈ Increased haptoglobin
β
π
²οΈ Increased indirect bilirubin
π
³οΈ Decreased reticulocyte count
Correct Answer: π
²οΈ Increased indirect bilirubin
π Rationale: Breakdown of hemoglobin leads to elevated indirect (unconjugated) bilirubin.
Sickle Cell Anemia (SCA) is a genetic disorder of the blood in which red blood cells become abnormally shaped like a sickle (crescent) due to the presence of abnormal hemoglobin S.
π¬ This leads to chronic hemolytic anemia, vaso-occlusion, and multiple organ complications.
𧬠It is an autosomal recessive inherited disorder.
πΉ Genetic inheritance (both parents carry sickle cell trait)
πΉ Most common in African, Indian, Middle Eastern ancestry
πΉ Triggered by:
β’ Dehydration
β’ Infection
β’ High altitude
β’ Stress
β’ Extreme cold or heat
πΈ General symptoms of anemia:
β’ Fatigue, pallor, weakness
β’ Jaundice
πΈ Vaso-occlusive (Pain) Crises:
β’ Sudden severe pain in limbs, chest, abdomen, joints
β’ Due to blocked blood flow
πΈ Other signs:
β’ Swelling of hands/feet (dactylitis in infants)
β’ Delayed growth and puberty
β’ Repeated infections (due to splenic dysfunction)
β’ Vision problems
β’ Shortness of breath
π¨ Stroke
π¨ Acute chest syndrome
π¨ Splenic sequestration crisis
π¨ Avascular necrosis (bone death)
π¨ Leg ulcers
π¨ Priapism (prolonged painful erection)
π¨ Pulmonary hypertension
π¨ Chronic organ damage (kidney, liver, retina)
π§ͺ CBC: β Hemoglobin, β Reticulocytes
π§ͺ Peripheral smear: Sickle-shaped RBCs
π§ͺ Hemoglobin electrophoresis: Confirms HbS
π§ͺ Sickling test: Positive
π§ͺ Bilirubin: β (due to hemolysis)
π Oxygen therapy
π Pain control: NSAIDs, opioids (morphine)
π§ IV fluids (to reduce sickling)
π Antibiotics for infection
π Blood transfusion (for severe anemia or stroke)
π Hydroxyurea β increases fetal hemoglobin (HbF)
π Folic acid supplementation
π Routine vaccinations (Pneumococcal, HIB, Meningococcal)
𧬠Bone marrow transplant β only curative option
π©Ί Genetic counseling for families
π© Assessment:
πΉ Monitor for signs of anemia and crisis
πΉ Assess for pain, swelling, jaundice
πΉ Evaluate hydration status and infection signs
π¨ Intervention:
πΉ Administer prescribed pain meds and hydration
πΉ Provide oxygen during crisis
πΉ Monitor vital signs and labs
πΉ Prevent infection (handwashing, vaccinations)
πΉ Educate about avoiding triggers (cold, dehydration)
π₯ Patient Education:
πΉ Lifelong condition β adherence to medications and follow-up
πΉ Importance of hydration and nutrition
πΉ Genetic counseling for future pregnancy
πΉ Prompt treatment for fever or infection
π‘ Sickle cell anemia = inherited HbS mutation
π‘ Sickle cells cause vaso-occlusion and pain crises
π‘ Hydroxyurea β fetal hemoglobin and reduces crises
π‘ Hemoglobin electrophoresis confirms diagnosis
π‘ Only cure = bone marrow transplant
Q1. Sickle cell anemia is caused by:
π
°οΈ Vitamin B12 deficiency
β
π
±οΈ Inherited abnormal hemoglobin gene
π
²οΈ Iron overload
π
³οΈ Viral infection
Correct Answer: π
±οΈ Inherited abnormal hemoglobin gene
π Rationale: It’s a genetic disorder due to hemoglobin S mutation.
Q2. Which test confirms sickle cell anemia?
π
°οΈ Coombs test
β
π
±οΈ Hemoglobin electrophoresis
π
²οΈ Schilling test
π
³οΈ ELISA
Correct Answer: π
±οΈ Hemoglobin electrophoresis
π Rationale: It identifies abnormal hemoglobin types like HbS.
Q3. Which of the following is used to manage sickle cell crisis?
π
°οΈ Iron supplements
π
±οΈ Antihypertensives
β
π
²οΈ IV fluids and pain management
π
³οΈ Diuretics
Correct Answer: π
²οΈ IV fluids and pain management
π Rationale: Hydration and analgesia help relieve vaso-occlusive episodes.
Q4. Which drug increases fetal hemoglobin in sickle cell anemia?
π
°οΈ Folic acid
β
π
±οΈ Hydroxyurea
π
²οΈ Prednisone
π
³οΈ Warfarin
Correct Answer: π
±οΈ Hydroxyurea
π Rationale: HbF reduces sickling and frequency of crises.
Q5. A common early sign in infants with sickle cell disease is:
π
°οΈ Clubbing
π
±οΈ Weight gain
β
π
²οΈ Hand-foot swelling (dactylitis)
π
³οΈ Petechiae
Correct Answer: π
²οΈ Hand-foot swelling (dactylitis)
π Rationale: It’s a classic early symptom due to small vessel occlusion
Polycythemia Vera (PV) is a rare chronic myeloproliferative disorder in which the bone marrow produces too many red blood cells, and often excess WBCs and platelets as well.
𧬠It is a primary polycythemia, usually due to mutation in the JAK2 gene, and is not caused by hypoxia.
πΈ Primary (Polycythemia Vera):
β’ Bone marrow disorder (JAK2 mutation)
β’ Independent of erythropoietin levels
πΈ Secondary Polycythemia:
β’ Due to β erythropoietin from chronic hypoxia
β’ Seen in COPD, high altitude, tumors
πΈ Relative Polycythemia:
β’ Due to plasma volume loss (e.g., dehydration, burns)
πΉ Genetic mutation (JAK2 V617F in 90β95% cases)
πΉ Age >60 years
πΉ Male > Female
πΉ No known external cause (idiopathic)
π΄ Due to Increased Blood Viscosity:
β’ Headache
β’ Dizziness
β’ Blurred vision
β’ Tinnitus
β’ Hypertension
π΄ Due to Hypervolemia & Clotting Risk:
β’ Red/purple facial flushing (plethora)
β’ Thrombosis: DVT, stroke, MI
β’ Itching after hot bath (aquagenic pruritus)
π΄ Other Symptoms:
β’ Splenomegaly (abdominal fullness)
β’ Gout (due to uric acid elevation)
β’ Fatigue, night sweats, weight loss
π§ͺ CBC: β RBCs, β Hematocrit (>60%), β Hemoglobin
π§ͺ Erythropoietin level: β (in primary PV)
π§ͺ JAK2 mutation analysis: Positive
π§ͺ Bone marrow biopsy: Hypercellular
π§ͺ Serum uric acid: β
π§ͺ Oxygen saturation: Normal (to rule out secondary polycythemia)
πΉ Phlebotomy:
β’ First-line treatment
β’ Remove 300β500 mL of blood every few weeks
β’ Goal: Hematocrit <45%
πΉ Hydroxyurea:
β’ Myelosuppressive drug to reduce RBC production
πΉ Aspirin (low dose):
β’ To reduce thrombosis risk
πΉ Interferon-alpha:
β’ For younger or pregnant patients
πΉ Antihistamines:
β’ For pruritus management
π© Assessment:
πΉ Monitor signs of thrombotic or hemorrhagic complications
πΉ Assess for itching, vision changes, fatigue
π¨ Intervention:
πΉ Assist in regular phlebotomy
πΉ Administer medications (hydroxyurea, aspirin)
πΉ Educate to avoid dehydration and smoking
πΉ Encourage exercise to improve circulation
πΉ Monitor CBC and uric acid levels regularly
π₯ Education:
πΉ Lifelong follow-up is required
πΉ Maintain hydration to reduce viscosity
πΉ Report symptoms of clots (pain, swelling, confusion, chest pain)
π‘ PV is a primary bone marrow disorder causing β RBCs
π‘ JAK2 mutation is present in most PV cases
π‘ Phlebotomy is first-line therapy
π‘ Aquagenic pruritus is a classic sign
π‘ Aspirin reduces thrombosis risk in PV
Q1. Which genetic mutation is most commonly associated with polycythemia vera?
π
°οΈ BRCA1
π
±οΈ CFTR
β
π
²οΈ JAK2
π
³οΈ TP53
Correct Answer: π
²οΈ JAK2
π Rationale: JAK2 mutation drives the overproduction of RBCs in PV.
Q2. What is the hallmark symptom of polycythemia vera?
π
°οΈ Petechiae
β
π
±οΈ Itching after hot shower
π
²οΈ Mouth ulcers
π
³οΈ Cyanosis
Correct Answer: π
±οΈ Itching after hot shower
π Rationale: Aquagenic pruritus is a classic symptom due to histamine release.
Q3. Which test is used to reduce hematocrit in PV?
π
°οΈ Bone marrow transplant
β
π
±οΈ Phlebotomy
π
²οΈ Dialysis
π
³οΈ Blood transfusion
Correct Answer: π
±οΈ Phlebotomy
π Rationale: Removing blood lowers hematocrit and reduces viscosity.
Q4. What is the usual erythropoietin level in primary polycythemia vera?
π
°οΈ High
β
π
±οΈ Low
π
²οΈ Normal
π
³οΈ Absent
Correct Answer: π
±οΈ Low
π Rationale: Bone marrow produces RBCs independently of erythropoietin.
Q5. Which of the following is NOT a typical complication of PV?
π
°οΈ Stroke
π
±οΈ Myocardial infarction
π
²οΈ Deep vein thrombosis
β
π
³οΈ Hemophilia
Correct Answer: π
³οΈ Hemophilia
π Rationale: Hemophilia is a genetic bleeding disorder unrelated to PV.
Hemochromatosis is a disorder in which the body absorbs and stores too much iron, leading to iron overload in various organs, especially the liver, heart, pancreas, joints, and skin.
𧬠It can lead to organ damage, especially liver cirrhosis, diabetes, heart disease, and arthritis.
πΉ Primary (Hereditary) Hemochromatosis:
β’ Genetic mutation (usually HFE gene β C282Y)
β’ Autosomal recessive inheritance
πΉ Secondary Hemochromatosis:
β’ Due to chronic blood transfusions, iron supplements, liver disease, or anemia (e.g., thalassemia)
πΈ Hereditary mutation (especially C282Y mutation in HFE gene)
πΈ Male > Female (due to menstrual iron loss in females)
πΈ Age > 40 years
πΈ Chronic liver disease
πΈ Multiple blood transfusions
πΈ Excessive iron supplementation
π€ Often asymptomatic early (detected on routine iron testing)
π΄ General Symptoms:
β’ Fatigue, weakness
β’ Joint pain (arthralgia)
β’ Loss of libido
β’ Weight loss
π΄ Organ-Specific Symptoms:
π§ Memory loss
β€οΈ Cardiomyopathy (heart failure, arrhythmia)
𧬠Diabetes mellitus (“bronze diabetes”)
π§ Hypogonadism (erectile dysfunction, amenorrhea)
π‘ Liver: Hepatomegaly, fibrosis, cirrhosis
π€ Skin: Hyperpigmentation (“bronze skin”)
π§ͺ Serum ferritin: β
π§ͺ Serum iron: β
π§ͺ Transferrin saturation: β (>45%)
π§ͺ Total iron-binding capacity (TIBC): β or normal
π§ͺ Liver function tests: May be abnormal
π§ͺ Genetic testing for HFE mutation (C282Y, H63D)
π§ͺ Liver biopsy (if cirrhosis is suspected)
π©Έ Therapeutic Phlebotomy
β’ Remove 500 mL blood once or twice weekly
β’ Goal: Maintain ferritin <50 ng/mL and transferrin saturation <50%
π Deferoxamine, Deferasirox
πΉ Manage diabetes, liver disease, heart failure
πΉ Avoid alcohol and iron-rich foods
πΉ Avoid vitamin C supplements (increase iron absorption)
π© Assessment:
πΉ Monitor for signs of iron overload: fatigue, skin changes, liver enlargement
πΉ Monitor blood pressure, glucose, liver function
π¨ Intervention:
πΉ Assist with phlebotomy procedures
πΉ Administer prescribed chelation therapy
πΉ Educate to avoid alcohol, iron supplements, raw shellfish (infection risk)
π₯ Education:
πΉ Encourage family screening (genetic counseling)
πΉ Teach about low-iron diet and hydration
πΉ Regular follow-up for ferritin and liver function
π‘ Hemochromatosis = iron overload disorder
π‘ HFE gene mutation (C282Y) is the most common cause
π‘ First-line treatment is therapeutic phlebotomy
π‘ βBronze diabetesβ = diabetes + skin pigmentation
π‘ Transferrin saturation >45% is diagnostic clue
Q1. Hemochromatosis is a disorder of:
π
°οΈ Copper metabolism
β
π
±οΈ Iron overload
π
²οΈ Vitamin B12 deficiency
π
³οΈ Platelet destruction
Correct Answer: π
±οΈ Iron overload
π Rationale: Excessive iron absorption and storage cause tissue damage.
Q2. Which gene is commonly mutated in hereditary hemochromatosis?
π
°οΈ BRCA1
π
±οΈ JAK2
β
π
²οΈ HFE
π
³οΈ TP53
Correct Answer: π
²οΈ HFE
π Rationale: HFE gene mutation (especially C282Y) disrupts iron absorption control.
Q3. The most effective initial treatment for hemochromatosis is:
π
°οΈ Iron supplements
π
±οΈ Liver transplant
β
π
²οΈ Therapeutic phlebotomy
π
³οΈ Blood transfusion
Correct Answer: π
²οΈ Therapeutic phlebotomy
π Rationale: Removing blood helps reduce excess iron levels.
Q4. Which organ is NOT typically affected by iron overload?
π
°οΈ Liver
π
±οΈ Pancreas
π
²οΈ Heart
β
π
³οΈ Lungs
Correct Answer: π
³οΈ Lungs
π Rationale: Iron deposits mainly affect liver, pancreas, heart, joints, skin.
Q5. A classic skin sign of hemochromatosis is:
π
°οΈ Cyanosis
π
±οΈ Jaundice
β
π
²οΈ Bronze pigmentation
π
³οΈ Erythema
Correct Answer: π
²οΈ Bronze pigmentation
π Rationale: Iron deposits in skin cause a bronze or grayish tone.
Agranulocytosis (also called Granulocytopenia or Malignant Neutropenia) is a severe and acute reduction in granulocytes, especially neutrophils, leading to increased risk of life-threatening infections.
π¬ Neutropenia:
Absolute Neutrophil Count (ANC) <1500/mmΒ³
π Severe Neutropenia / Agranulocytosis: ANC <500/mmΒ³
πΈ Drug-induced (most common):
β’ Antipsychotics (Clozapine)
β’ Antibiotics (Chloramphenicol, Sulfonamides)
β’ Antithyroid drugs (Methimazole, Propylthiouracil)
β’ Chemotherapy agents
πΈ Autoimmune diseases: SLE, RA
πΈ Infections: Hepatitis, HIV, EBV
πΈ Bone marrow disorders: Aplastic anemia, leukemia
πΈ Radiation or toxic chemical exposure
β οΈ Often sudden and severe, especially in drug-induced agranulocytosis
πΈ High-grade fever
πΈ Sore throat, mouth ulcers (oral mucositis)
πΈ Gingival swelling, bleeding gums
πΈ Fatigue, malaise
πΈ Chills, rigors
πΈ Signs of sepsis: hypotension, confusion
π§ͺ CBC with Differential:
β’ β WBC count
β’ β Neutrophils (ANC <500/mmΒ³)
π§ͺ Bone Marrow Aspiration/Biopsy:
β’ β Myeloid precursors
π§ͺ Blood cultures, throat swab, urine culture:
β’ To identify infection source
π§ͺ Serology:
β’ To rule out viral causes (HIV, EBV, hepatitis)
πΉ Discontinue offending drug immediately
πΉ Broad-spectrum antibiotics (empiric therapy in febrile neutropenia)
πΉ Antifungals (if fever persists >72 hrs)
πΉ G-CSF (Granulocyte-Colony Stimulating Factor)
β’ e.g., Filgrastim, to stimulate neutrophil production
πΉ Isolation precautions (protective reverse isolation)
π© Assessment:
πΉ Monitor temperature every 4 hours
πΉ Watch for signs of infection (mouth ulcers, throat pain, chills)
π¨ Interventions:
πΉ Strict hand hygiene and aseptic technique
πΉ Initiate protective isolation (neutropenic precautions)
πΉ Avoid fresh fruits, flowers, and visitors with infections
πΉ Administer antibiotics, G-CSF as prescribed
πΉ Educate patient on avoiding crowds and infection risks
π₯ Emergency Care:
πΉ Notify physician if temp >100.4Β°F (38Β°C)
πΉ Initiate sepsis protocol if signs of shock or confusion
π‘ ANC <500/mmΒ³ = Agranulocytosis
π‘ Clozapine and chemotherapy are common causes
π‘ Oral ulcers and fever are early warning signs
π‘ G-CSF (Filgrastim) stimulates neutrophil production
π‘ Isolation and prompt antibiotics are critical
Q1. Which lab finding confirms agranulocytosis?
π
°οΈ RBC <3 million
π
±οΈ Platelet <50,000
β
π
²οΈ ANC <500/mmΒ³
π
³οΈ Hemoglobin <10 g/dL
Correct Answer: π
²οΈ ANC <500/mmΒ³
π Rationale: Absolute neutrophil count under 500 is diagnostic of agranulocytosis.
Q2. Which drug is most commonly associated with agranulocytosis?
π
°οΈ Paracetamol
β
π
±οΈ Clozapine
π
²οΈ Ibuprofen
π
³οΈ Aspirin
Correct Answer: π
±οΈ Clozapine
π Rationale: Clozapine is known to cause severe agranulocytosis as a side effect.
Q3. First action when a neutropenic patient develops a fever?
π
°οΈ Give antipyretic
π
±οΈ Notify dietician
β
π
²οΈ Start broad-spectrum antibiotics
π
³οΈ Start iron therapy
Correct Answer: π
²οΈ Start broad-spectrum antibiotics
π Rationale: Fever in neutropenia is treated as an emergency due to sepsis risk.
Q4. Which medication helps increase neutrophil production?
π
°οΈ Erythropoietin
π
±οΈ Warfarin
β
π
²οΈ Filgrastim
π
³οΈ Folic acid
Correct Answer: π
²οΈ Filgrastim
π Rationale: Filgrastim is a G-CSF that boosts bone marrow production of neutrophils.
Q5. A nurse should avoid giving which to an agranulocytosis patient?
π
°οΈ Cooked vegetables
π
±οΈ Bottled water
β
π
²οΈ Fresh fruits and flowers
π
³οΈ Warm blankets
Correct Answer: π
²οΈ Fresh fruits and flowers
π Rationale: These may carry bacteria and fungi that can be harmful to immunocompromised patients.
π Important for Medical-Surgical Nursing, Pathology, Pediatrics & Staff Nurse Exams
Aplastic anemia is a rare but serious condition in which the bone marrow fails to produce sufficient blood cells, resulting in pancytopenia β β RBCs, WBCs, and platelets.
π¬ It is due to bone marrow failure β marrow becomes hypocellular or empty (fatty infiltration).
πΉ Idiopathic (Unknown) β ~70% of cases
πΉ Drug-induced:
β’ Chemotherapy, antibiotics (chloramphenicol), NSAIDs
πΉ Radiation exposure
πΉ Toxins: Benzene, insecticides
πΉ Viral infections: Hepatitis, HIV, EBV
πΉ Autoimmune disorders
πΉ Congenital: Fanconi anemia (in children)
β’ Fatigue, pallor
β’ Dyspnea on exertion
β’ Weakness, tachycardia
β’ Recurrent infections
β’ Fever, sore throat
β’ Oral ulcers
β’ Bleeding gums, nosebleeds
β’ Petechiae, ecchymosis
β’ Heavy menstruation
π΄ Other signs:
β’ No lymphadenopathy or splenomegaly (distinguishes from leukemia)
β’ Bone tenderness rare
π§ͺ CBC:
β’ β RBCs, β WBCs, β Platelets (pancytopenia)
β’ Low reticulocyte count
π§ͺ Bone Marrow Biopsy:
β’ Hypocellular marrow with fatty infiltration
π§ͺ Serum iron: Normal or β (due to low RBC use)
π§ͺ Viral studies (Hepatitis, HIV)
π§ͺ Chromosomal analysis (for Fanconi anemia)
π Blood transfusions (RBCs, platelets)
π Antibiotics for infections
β οΈ Avoid NSAIDs, aspirin
β’ ATG (Anti-thymocyte globulin)
β’ Cyclosporine A
β’ Prednisolone
π G-CSF or EPO to stimulate marrow (in some cases)
𧬠Bone Marrow Transplant (BMT) β for young patients with matched donor
π© Assessment:
πΉ Monitor for signs of bleeding, infection, fatigue
πΉ Check skin for petechiae, bruises
π¨ Interventions:
πΉ Apply bleeding precautions (no IM injections, soft toothbrush)
πΉ Ensure neutropenic precautions
πΉ Administer transfusions, antibiotics, and immunosuppressants as prescribed
πΉ Provide emotional support and nutrition counseling
π₯ Patient Education:
πΉ Avoid crowds, raw foods (infection risk)
πΉ Importance of hygiene and hand washing
πΉ Need for regular follow-up and blood counts
πΉ Inform about bone marrow transplant eligibility
π‘ Aplastic anemia = Pancytopenia + hypocellular marrow
π‘ Bone marrow biopsy is the confirmatory test
π‘ Common cause = idiopathic or drug-induced
π‘ Bone marrow transplant is potentially curative
π‘ Avoid live vaccines and NSAIDs in these patients
Q1. Aplastic anemia is primarily due to failure of:
π
°οΈ Liver function
π
±οΈ Kidney function
β
π
²οΈ Bone marrow function
π
³οΈ Heart function
Correct Answer: π
²οΈ Bone marrow function
π Rationale: Bone marrow fails to produce all blood cell lines.
Q2. Which of the following findings is most characteristic of aplastic anemia?
π
°οΈ Leukocytosis
π
±οΈ Lymphadenopathy
β
π
²οΈ Pancytopenia
π
³οΈ Polycythemia
Correct Answer: π
²οΈ Pancytopenia
π Rationale: Aplastic anemia presents with deficiency of all 3 blood cell types.
Q3. The definitive test for diagnosing aplastic anemia is:
π
°οΈ CBC
π
±οΈ ESR
β
π
²οΈ Bone marrow biopsy
π
³οΈ Reticulocyte count
Correct Answer: π
²οΈ Bone marrow biopsy
π Rationale: Shows hypocellular marrow with fatty replacement.
Q4. Which therapy is curative in young patients with aplastic anemia?
π
°οΈ Iron therapy
π
±οΈ Steroids
π
²οΈ Blood transfusions
β
π
³οΈ Bone marrow transplant
Correct Answer: π
³οΈ Bone marrow transplant
π Rationale: BMT replaces defective marrow with healthy stem cells.
Q5. What precaution is important in nursing care for aplastic anemia patients?
π
°οΈ Apply cold compresses
β
π
±οΈ Use strict infection control and bleeding precautions
π
²οΈ Encourage high-impact exercise
π
³οΈ Administer iron routinely
Correct Answer: π
±οΈ Use strict infection control and bleeding precautions
π Rationale: Due to low WBCs and platelets, infection and bleeding are major risks.
π Important for Pediatrics, Medical-Surgical Nursing, Hematology, & Staff Nurse Competitive Exams
Thalassemia is a group of inherited blood disorders characterized by reduced or absent synthesis of one or more globin chains of hemoglobin, leading to chronic hemolytic anemia.
π§ͺ Hemoglobin = Globin (Ξ± and Ξ² chains) + Heme
𧬠Defect in globin chain production β ineffective erythropoiesis and hemolysis
β’ Defective or absent alpha-globin chains
β’ Common in Southeast Asia
β’ Severity depends on number of defective genes (1β4)
β’ Defective or absent beta-globin chains
β’ Common in Mediterranean, Indian, Middle Eastern populations
β’ Types:
β
Thalassemia Minor (Trait) β Carrier, mild anemia
β
Thalassemia Major (Cooleyβs Anemia) β Severe, transfusion-dependent
β
Thalassemia Intermedia β Moderate severity
πΉ Autosomal recessive inheritance
πΉ Consanguineous marriages
πΉ Both parents are carriers (trait)
πΉ Common in malaria-endemic regions (protective trait)
β’ Mild anemia
β’ Often asymptomatic
β’ Detected during routine testing
β’ Severe anemia by 6 months of age
β’ Failure to thrive, poor feeding
β’ Bone deformities (frontal bossing, chipmunk face)
β’ Hepatosplenomegaly
β’ Jaundice
β’ Delayed growth and puberty
β’ Iron overload due to repeated transfusions
π§ͺ CBC: β Hemoglobin, β MCV (microcytic anemia)
π§ͺ Peripheral smear: Target cells, anisopoikilocytosis
π§ͺ Reticulocyte count: β
π§ͺ Serum ferritin: β (in transfused patients)
π§ͺ Hemoglobin electrophoresis: Confirms diagnosis (β HbF and β HbA in beta-thalassemia major)
π§ͺ DNA testing: To detect gene mutation
β’ Usually no treatment needed
β’ Folic acid supplements
β’ Maintain Hb >9β10 g/dL
β’ Every 2β4 weeks
β’ To prevent iron overload from transfusions
β’ Drugs: Deferoxamine (IV), Deferasirox (oral)
β’ Curative in children with HLA-matched sibling donor
β’ If hypersplenism causes severe anemia or transfusion requirement
π© Assessment:
πΉ Monitor for signs of anemia, jaundice, infections
πΉ Assess for transfusion reactions
π¨ Intervention:
πΉ Administer transfusions and monitor vitals
πΉ Educate on iron chelation compliance
πΉ Provide psychological support
πΉ Promote nutrition: high protein, folate-rich diet
πΉ Prevent infections: hand hygiene, vaccinations
π₯ Patient Education:
πΉ Genetic counseling for families
πΉ Importance of regular follow-up
πΉ Avoid iron-rich foods and supplements in major cases
πΉ Encourage sibling HLA typing for transplant eligibility
π‘ Thalassemia = inherited disorder of abnormal hemoglobin synthesis
π‘ Beta-thalassemia major = severe anemia by 6 months of age
π‘ Repeated transfusions β iron overload
π‘ Iron chelation therapy is essential in thalassemia major
π‘ Hemoglobin electrophoresis is the confirmatory test
Q1. Thalassemia is primarily a disorder of:
π
°οΈ Platelets
π
±οΈ WBCs
β
π
²οΈ Hemoglobin chain synthesis
π
³οΈ Coagulation factors
Correct Answer: π
²οΈ Hemoglobin chain synthesis
π Rationale: Thalassemia affects production of alpha or beta globin chains of hemoglobin.
Q2. Which type of thalassemia requires regular transfusions?
π
°οΈ Alpha trait
π
±οΈ Thalassemia minor
β
π
²οΈ Thalassemia major
π
³οΈ Thalassemia intermedia
Correct Answer: π
²οΈ Thalassemia major
π Rationale: Thalassemia major causes life-threatening anemia.
Q3. Which test confirms thalassemia?
π
°οΈ Coombs test
π
±οΈ Blood culture
β
π
²οΈ Hemoglobin electrophoresis
π
³οΈ Serum bilirubin
Correct Answer: π
²οΈ Hemoglobin electrophoresis
π Rationale: It identifies abnormal hemoglobin patterns.
Q4. Iron chelation therapy is required to prevent:
π
°οΈ Infection
π
±οΈ Bleeding
β
π
²οΈ Iron overload
π
³οΈ Hemolysis
Correct Answer: π
²οΈ Iron overload
π Rationale: Chronic transfusions increase body iron stores.
Q5. Thalassemia is inherited in which pattern?
π
°οΈ Autosomal dominant
β
π
±οΈ Autosomal recessive
π
²οΈ X-linked recessive
π
³οΈ Mitochondrial
Correct Answer: π
±οΈ Autosomal recessive
π Rationale: Both parents must carry the gene for the child to be affected.
π Important for Pediatrics, Hematology, Medical-Surgical Nursing & Staff Nurse Exams
G6PD Deficiency is a genetic, X-linked recessive disorder characterized by deficiency of the enzyme Glucose-6-Phosphate Dehydrogenase in red blood cells, making them vulnerable to oxidative damage.
π§ͺ It causes hemolytic anemia when exposed to certain drugs, infections, or foods.
𧬠X-linked recessive
πΉ Mostly affects males
πΉ Females can be carriers (may have mild symptoms)
πΊ Drugs:
β’ Sulfonamides, Nitrofurantoin
β’ Antimalarials (Primaquine)
β’ Aspirin (high doses)
β’ NSAIDs
πΊ Infections:
β’ Viral or bacterial infections increase oxidative stress
πΊ Foods:
β’ Fava beans (broad beans) β “Favism”
πΊ Chemicals:
β’ Naphthalene (mothballs)
πΈ Triggered hemolysis (within hours to days):
β’ Sudden onset of fatigue, pallor
β’ Jaundice
β’ Dark tea-colored urine (hemoglobinuria)
β’ Rapid heartbeat (tachycardia)
β’ Splenomegaly in recurrent attacks
πΈ Neonatal jaundice:
β’ May occur within first few days of life
β’ Risk of kernicterus if untreated
π§ͺ CBC: β Hemoglobin, β Reticulocyte count
π§ͺ Peripheral smear: Bite cells, Heinz bodies
π§ͺ G6PD enzyme assay: Confirms diagnosis
π§ͺ Serum bilirubin: β indirect
π§ͺ LDH: β
π§ͺ Haptoglobin: β
πΉ Avoid triggering agents (mainstay of management)
πΉ Hydration and supportive care
πΉ Blood transfusion in severe cases
πΉ Phototherapy or exchange transfusion for neonatal jaundice
πΉ Oxygen if needed
π© Assessment:
πΉ Monitor for signs of anemia and hemolysis
πΉ Check urine color and jaundice
π¨ Intervention:
πΉ Educate family about drugs and foods to avoid
πΉ Monitor for infection (fever, chills)
πΉ Prepare for blood transfusion if indicated
πΉ Administer IV fluids to prevent kidney damage
πΉ Follow phototherapy protocol in neonates
π₯ Patient Education:
πΉ Lifelong avoidance of triggers
πΉ Importance of medical alert ID
πΉ Inform every healthcare provider about G6PD deficiency
πΉ Neonatal screening in high-risk populations
π‘ G6PD deficiency = X-linked recessive enzyme defect
π‘ Triggered by drugs, infections, or fava beans
π‘ Heinz bodies and bite cells seen in smear
π‘ Confirmed by G6PD enzyme assay
π‘ Main treatment = avoid oxidant exposure
Q1. G6PD deficiency is inherited as:
π
°οΈ Autosomal dominant
π
±οΈ Autosomal recessive
β
π
²οΈ X-linked recessive
π
³οΈ Mitochondrial
Correct Answer: π
²οΈ X-linked recessive
π Rationale: This explains why males are predominantly affected.
Q2. Which food can trigger hemolysis in G6PD deficiency?
π
°οΈ Cheese
π
±οΈ Spinach
β
π
²οΈ Fava beans
π
³οΈ Apples
Correct Answer: π
²οΈ Fava beans
π Rationale: Fava beans contain oxidants that damage RBCs in G6PD deficiency.
Q3. Which of the following drugs should be avoided in G6PD deficiency?
π
°οΈ Paracetamol
π
±οΈ Ciprofloxacin
β
π
²οΈ Sulfonamides
π
³οΈ Amoxicillin
Correct Answer: π
²οΈ Sulfonamides
π Rationale: Sulfa drugs are known triggers of hemolysis.
Q4. A hallmark finding in the peripheral blood smear of G6PD patients is:
π
°οΈ Schistocytes
β
π
±οΈ Bite cells and Heinz bodies
π
²οΈ Target cells
π
³οΈ Spherocytes
Correct Answer: π
±οΈ Bite cells and Heinz bodies
π Rationale: Oxidative damage leads to Heinz body formation and removal of denatured hemoglobin.
Q5. Which is the best confirmatory test for G6PD deficiency?
π
°οΈ Hemoglobin electrophoresis
π
±οΈ Coombs test
β
π
²οΈ G6PD enzyme assay
π
³οΈ Reticulocyte count
Correct Answer: π
²οΈ G6PD enzyme assay
π Rationale: Enzyme level testing confirms deficiency.
π Important for Pediatrics, Hematology, Medical-Surgical Nursing & Staff Nurse Exams
Hemophilia is a genetic bleeding disorder characterized by deficiency or absence of specific clotting factors, leading to prolonged bleeding after injury or spontaneously.
𧬠It is an X-linked recessive disorder, usually affecting males, while females are carriers.
β’ Deficiency of Factor VIII
β’ Most common (80β85% cases)
β’ Deficiency of Factor IX
β’ Deficiency of Factor XI
β’ Affects both genders (autosomal recessive)
𧬠X-linked recessive pattern
πΉ Males affected
πΉ Females usually carriers
πΉ Each son of a carrier mother has 50% chance of being affected
πΈ Genetic mutation in factor VIII or IX gene
πΈ Family history of bleeding disorders
πΈ More common in males
β’ Prolonged bleeding after injury/surgery
β’ Spontaneous bleeding into joints (hemarthrosis)
β’ Easy bruising (ecchymosis)
β’ Bleeding into muscles and soft tissues
β’ Gum bleeding, nosebleeds (epistaxis)
β’ Hematuria (blood in urine)
β’ Pain, swelling, stiffness
β’ Most commonly in knees, ankles, elbows
β’ Recurrent episodes may lead to joint deformities
πΊ Anemia
πΊ Chronic joint damage
πΊ Intracranial hemorrhage (life-threatening)
πΊ Bloodborne infections (HIV, Hepatitis B/C from transfusions)
πΊ Development of inhibitors (antibodies against factor therapy)
π§ͺ Prolonged aPTT (activated partial thromboplastin time)
π§ͺ Normal PT, BT, platelet count
π§ͺ Clotting factor assay (Factor VIII/IX levels)
𧬠Genetic testing (for carrier detection and prenatal diagnosis)
π§ͺ Family history
π Factor VIII for Hemophilia A
π Factor IX for Hemophilia B
β’ Given IV during bleeding episodes or prophylactically
β’ May be plasma-derived or recombinant
β’ Stimulates release of stored Factor VIII (for mild Hemophilia A)
β’ Tranexamic acid for mucosal bleeding (e.g., dental work)
β’ Under research for long-term cure
π© Assessment:
πΉ Check for signs of bleeding: bruising, joint swelling, bleeding gums
πΉ Assess mobility, pain, and joint health
π¨ Intervention:
πΉ Administer factor replacement therapy as prescribed
πΉ Apply cold compress during bleeding
πΉ Use soft toothbrush, avoid IM injections
πΉ Avoid NSAIDs and aspirin (increase bleeding risk)
πΉ Prevent falls and injuries
π₯ Patient & Family Education:
πΉ Avoid contact sports and trauma
πΉ Educate on self-infusion of factor at home
πΉ Maintain good oral hygiene
πΉ Importance of medical alert ID
πΉ Genetic counseling for families
π‘ Hemophilia A = Factor VIII deficiency
π‘ Hemophilia B = Factor IX deficiency (Christmas disease)
π‘ X-linked disorder affecting males
π‘ Hemarthrosis = hallmark sign
π‘ aPTT prolonged, PT & platelets normal
Q1. Hemophilia A is caused by deficiency of:
π
°οΈ Factor IX
π
±οΈ Factor XI
β
π
²οΈ Factor VIII
π
³οΈ Factor VII
Correct Answer: π
²οΈ Factor VIII
π Rationale: Hemophilia A is due to deficiency of clotting factor VIII.
Q2. What is the most common bleeding manifestation in hemophilia?
π
°οΈ GI bleeding
π
±οΈ Hematuria
β
π
²οΈ Hemarthrosis
π
³οΈ Petechiae
Correct Answer: π
²οΈ Hemarthrosis
π Rationale: Joint bleeding is a classical feature in hemophiliacs.
Q3. Which lab finding is expected in hemophilia?
π
°οΈ Prolonged PT
β
π
±οΈ Prolonged aPTT
π
²οΈ Decreased platelet count
π
³οΈ Increased bleeding time
Correct Answer: π
±οΈ Prolonged aPTT
π Rationale: Hemophilia affects intrinsic clotting pathway.
Q4. Which drug is used to increase Factor VIII in mild cases?
π
°οΈ Furosemide
π
±οΈ Vitamin K
β
π
²οΈ Desmopressin
π
³οΈ Heparin
Correct Answer: π
²οΈ Desmopressin
π Rationale: DDAVP stimulates Factor VIII release from endothelial stores.
Q5. Hemophilia is inherited in what pattern?
π
°οΈ Autosomal dominant
π
±οΈ Autosomal recessive
β
π
²οΈ X-linked recessive
π
³οΈ Mitochondrial
Correct Answer: π
²οΈ X-linked recessive
π Rationale: It is typically passed from carrier mothers to male children.
π Important for Medical-Surgical Nursing, Hematology, Pediatrics & Staff Nurse Exams
Thrombocytopenia is a hematological condition characterized by a decrease in platelet count below 150,000/mmΒ³, resulting in increased risk of bleeding.
π¬ Normal platelet count: 150,000 β 450,000/mmΒ³
πΊ Severe thrombocytopenia: <50,000/mmΒ³
πΊ Life-threatening: <20,000/mmΒ³
β’ Aplastic anemia
β’ Leukemia, lymphoma
β’ Chemotherapy or radiation
β’ Viral infections (HIV, hepatitis, EBV)
β’ ITP (Idiopathic/Immune Thrombocytopenic Purpura)
β’ DIC (Disseminated Intravascular Coagulation)
β’ TTP (Thrombotic Thrombocytopenic Purpura)
β’ Drug-induced (e.g., heparin = HIT)
β’ Lupus, rheumatoid arthritis
β’ Hypersplenism
β’ Cirrhosis with portal hypertension
πΈ Petechiae (tiny pinpoint red spots)
πΈ Purpura (purple discoloration under skin)
πΈ Easy bruising (ecchymosis)
πΈ Bleeding gums, nosebleeds (epistaxis)
πΈ Prolonged bleeding after injury
πΈ Heavy menstrual bleeding
πΈ Hematuria (blood in urine)
πΈ GI bleeding or black stools (melena)
π§ͺ CBC: β Platelet count
π§ͺ Peripheral smear: Large or fragmented platelets
π§ͺ Bone marrow biopsy (if production issue suspected)
π§ͺ Coagulation profile: PT, aPTT (usually normal in ITP)
π§ͺ ANA, anti-platelet antibodies (if autoimmune cause)
π§ͺ HIV, hepatitis panel
β’ Monitor only
β’ Avoid triggers and trauma
π Corticosteroids (Prednisolone)
π IV Immunoglobulin (IVIG)
π§ͺ Anti-D immunoglobulin (if Rh+)
π Platelet transfusion (<20,000/mmΒ³ or active bleeding)
𧬠Splenectomy (if unresponsive to medical therapy)
π Immunosuppressants (Rituximab)
π TPO receptor agonists (Romiplostim)
π© Assessment:
πΉ Monitor for skin/mucosal bleeding
πΉ Assess for headache or neuro changes (sign of brain bleed)
π¨ Intervention:
πΉ Apply bleeding precautions
πΉ Avoid IM injections, rectal temps
πΉ Use soft toothbrush, electric razor
πΉ Monitor platelet count, report <50,000/mmΒ³
πΉ Administer meds and transfusions as prescribed
π₯ Patient Education:
πΉ Avoid NSAIDs, aspirin
πΉ Report unusual bleeding/bruising
πΉ Avoid contact sports
πΉ Wear medical alert bracelet
πΉ Importance of follow-up and regular CBC
π‘ Thrombocytopenia = platelet count <150,000/mmΒ³
π‘ Petechiae and purpura are early signs
π‘ ITP is immune-mediated platelet destruction
π‘ Platelet transfusion if count <20,000/mmΒ³ with bleeding
π‘ Avoid NSAIDs, trauma, and invasive procedures
Q1. What is the primary danger associated with thrombocytopenia?
π
°οΈ Infection
π
±οΈ High blood pressure
β
π
²οΈ Bleeding
π
³οΈ Fatigue
Correct Answer: π
²οΈ Bleeding
π Rationale: Platelets help in clot formation; their absence increases bleeding risk.
Q2. Which of the following is an autoimmune cause of thrombocytopenia?
π
°οΈ Hemophilia
β
π
±οΈ ITP
π
²οΈ Anemia
π
³οΈ DIC
Correct Answer: π
±οΈ ITP
π Rationale: In ITP, the body attacks its own platelets.
Q3. Which symptom is common in thrombocytopenia?
π
°οΈ Fever
β
π
±οΈ Petechiae
π
²οΈ Seizures
π
³οΈ Muscle cramps
Correct Answer: π
±οΈ Petechiae
π Rationale: Small pinpoint red spots under the skin from capillary bleeding.
Q4. Which lab test best confirms thrombocytopenia?
π
°οΈ ESR
π
±οΈ PT
β
π
²οΈ CBC
π
³οΈ BUN
Correct Answer: π
²οΈ CBC
π Rationale: CBC provides platelet count directly.
Q5. Which of the following is a priority nursing intervention?
π
°οΈ Encourage high-impact exercise
π
±οΈ Use of sharp instruments
β
π
²οΈ Implement bleeding precautions
π
³οΈ Offer iron supplements
Correct Answer: π
²οΈ Implement bleeding precautions
π Rationale: Bleeding precautions help prevent hemorrhage in low platelet states.
π Important for Medical-Surgical Nursing, Cardiovascular System, and Staff Nurse Competitive Exams
Thrombophlebitis is the inflammation of a vein associated with thrombus (blood clot) formation, usually in the superficial or deep veins, often in the legs.
π§ͺ βThromboβ = clot + βphlebitisβ = inflammation of a vein
π¬ Commonly occurs due to venous stasis, vessel wall injury, and hypercoagulability (Virchowβs triad)
β’ Affects veins near the skin surface (e.g., varicose veins)
β’ Less serious, localized inflammation
β’ Affects deep veins, especially in the legs (femoral, popliteal)
β’ Can lead to pulmonary embolism (PE)
πΈ Prolonged immobilization (e.g., surgery, bed rest, long flights)
πΈ Trauma or injury to the vein (e.g., IV catheter, cannula)
πΈ Pregnancy and postpartum period
πΈ Oral contraceptives or hormone therapy
πΈ Obesity
πΈ Smoking
πΈ History of varicose veins
πΈ Cancer and chemotherapy
πΈ Genetic clotting disorders
β’ Redness and warmth over vein
β’ Palpable, tender, cord-like vein
β’ Localized pain and swelling
β’ Swelling of affected limb (usually unilateral)
β’ Pain or tenderness (especially in calf)
β’ Warmth over vein
β’ Red or discolored skin
β’ Positive Homanβs sign (pain in calf on dorsiflexion of foot)
π¨ Pulmonary embolism (PE)
π¨ Chronic venous insufficiency
π¨ Post-thrombotic syndrome
π¨ Recurrent DVT or thrombophlebitis
π§ͺ Doppler ultrasound β primary diagnostic test
π§ͺ D-dimer β elevated if clot present
π§ͺ Venography (rarely used now)
π§ͺ CBC, coagulation profile
π§ͺ CT pulmonary angiography (if PE suspected)
πΉ For Superficial Thrombophlebitis:
β’ Warm compresses
β’ NSAIDs for pain and inflammation
β’ Compression stockings
πΉ For DVT:
π Anticoagulants (e.g., heparin, warfarin, rivaroxaban)
π Thrombolytics (e.g., alteplase in severe cases)
𧦠Graduated compression stockings
ποΈ Early ambulation and leg elevation
π Inferior vena cava (IVC) filter (in patients with recurrent DVT or PE risk)
π© Assessment:
πΉ Monitor for signs of DVT: swelling, warmth, pain
πΉ Watch for signs of PE: chest pain, dyspnea, hemoptysis
π¨ Interventions:
πΉ Apply warm compresses and compression stockings
πΉ Elevate affected limb
πΉ Administer anticoagulants as prescribed
πΉ Encourage early mobilization and leg exercises
πΉ Do not massage the affected area
π₯ Patient Education:
πΉ Avoid prolonged immobility
πΉ Stay hydrated and active
πΉ Take medications exactly as prescribed
πΉ Wear compression stockings if advised
πΉ Recognize signs of PE and seek immediate help
π‘ Thrombophlebitis = inflammation + clot in vein
π‘ DVT is more dangerous than superficial thrombophlebitis
π‘ Doppler ultrasound is the diagnostic test of choice
π‘ Homanβs sign may indicate DVT
π‘ Main treatment = anticoagulants and leg elevation
Q1. Thrombophlebitis is defined as:
π
°οΈ Inflammation of arteries
β
π
±οΈ Inflammation of a vein with clot formation
π
²οΈ Bleeding disorder
π
³οΈ Autoimmune vessel disease
Correct Answer: π
±οΈ Inflammation of a vein with clot formation
π Rationale: Thrombophlebitis combines thrombosis and phlebitis.
Q2. Which of the following is a serious complication of DVT?
π
°οΈ Liver failure
π
±οΈ Renal calculi
β
π
²οΈ Pulmonary embolism
π
³οΈ Myocardial infarction
Correct Answer: π
²οΈ Pulmonary embolism
π Rationale: A dislodged clot can travel to the lungs causing PE.
Q3. Which drug is used in the management of thrombophlebitis?
π
°οΈ Digoxin
π
±οΈ Aspirin only
β
π
²οΈ Heparin
π
³οΈ Ciprofloxacin
Correct Answer: π
²οΈ Heparin
π Rationale: Heparin is an anticoagulant used to prevent clot extension.
Q4. The best non-invasive test for DVT is:
π
°οΈ CT scan
β
π
±οΈ Doppler ultrasound
π
²οΈ Angiography
π
³οΈ MRI
Correct Answer: π
±οΈ Doppler ultrasound
π Rationale: It’s widely used, safe, and effective for visualizing veins.
Q5. A patient with thrombophlebitis should avoid:
π
°οΈ Leg elevation
π
±οΈ Walking
β
π
²οΈ Massaging the affected area
π
³οΈ Wearing compression stockings
Correct Answer: π
²οΈ Massaging the affected area
π Rationale: Massage may dislodge the clot and cause embolism.
π Important for Medical-Surgical Nursing, Hematology, Pediatrics & Staff Nurse Exams
von Willebrand Disease (vWD) is the most common inherited bleeding disorder, caused by a deficiency or dysfunction of von Willebrand factor (vWF) β a protein that helps platelets stick to injured blood vessels and also carries clotting factor VIII.
𧬠It results in prolonged bleeding time and defective platelet plug formation.
β’ Partial quantitative deficiency of vWF
β’ Most common (~75% of cases)
β’ Qualitative defect (vWF is present but defective)
β’ Subtypes: 2A, 2B, 2M, 2N
β’ Complete absence of vWF
β’ Rare and severe form
πΉ Inherited (autosomal dominant or recessive based on type)
πΉ Family history of bleeding disorders
πΉ More common in females (may notice during menstruation)
πΈ Easy bruising
πΈ Frequent nosebleeds (epistaxis)
πΈ Prolonged bleeding after injury or surgery
πΈ Heavy or prolonged menstrual bleeding (menorrhagia)
πΈ Prolonged bleeding after dental procedures
πΈ GI bleeding (in severe cases)
πΈ Hemarthrosis (rare, more in Type 3)
π¨ Anemia (due to chronic bleeding)
π¨ Hemorrhage during surgery or trauma
π¨ Excessive menstrual blood loss (may lead to fatigue and weakness)
π¨ Bleeding into joints in severe cases (rare)
π§ͺ Bleeding Time: β
π§ͺ aPTT: May be β (due to low Factor VIII)
π§ͺ PT: Normal
π§ͺ Platelet Count: Normal
π§ͺ vWF Antigen assay: β
π§ͺ Ristocetin Cofactor Assay: β (tests vWF activity)
𧬠Genetic testing (for confirmation and family screening)
π Desmopressin (DDAVP):
β’ Increases release of stored vWF and Factor VIII
β’ Used before surgery or dental work
π vWF/Factor VIII concentrates (e.g., Humate-P, Wilate)
π Antifibrinolytics (e.g., tranexamic acid) for mucosal bleeding
π Hormonal therapy (e.g., oral contraceptives) for menorrhagia
π© Assessment:
πΉ Monitor for signs of mucosal bleeding, bruising
πΉ Menstrual history in adolescent girls
πΉ Family bleeding history
π¨ Intervention:
πΉ Administer DDAVP or factor concentrates as prescribed
πΉ Avoid IM injections and invasive procedures
πΉ Use soft toothbrush and gentle oral hygiene techniques
πΉ Apply prolonged pressure after venipuncture
πΉ Ensure safe environment to prevent trauma
π₯ Patient Education:
πΉ Avoid aspirin and NSAIDs
πΉ Inform dentist and healthcare providers of diagnosis
πΉ Wear a medical alert ID
πΉ Educate females on managing heavy menstrual bleeding
πΉ Emphasize importance of follow-up and testing
π‘ vWD = Most common inherited bleeding disorder
π‘ Caused by deficiency/dysfunction of von Willebrand factor
π‘ Platelet count is normal, bleeding time is prolonged
π‘ DDAVP increases vWF release from endothelium
π‘ Type 3 is the most severe form
Q1. von Willebrand disease primarily affects which process?
π
°οΈ Coagulation factor synthesis
β
π
±οΈ Platelet adhesion
π
²οΈ Platelet count
π
³οΈ Vitamin K metabolism
Correct Answer: π
±οΈ Platelet adhesion
π Rationale: vWF helps platelets adhere to blood vessel walls during injury.
Q2. Which laboratory test is typically prolonged in vWD?
π
°οΈ PT
β
π
±οΈ Bleeding time
π
²οΈ Platelet count
π
³οΈ RBC count
Correct Answer: π
±οΈ Bleeding time
π Rationale: vWF deficiency impairs platelet plug formation, prolonging bleeding time.
Q3. Which medication helps raise vWF levels in mild cases?
π
°οΈ Folic acid
π
±οΈ Vitamin K
β
π
²οΈ Desmopressin
π
³οΈ Warfarin
Correct Answer: π
²οΈ Desmopressin
π Rationale: DDAVP promotes release of vWF and Factor VIII from endothelial cells.
Q4. What is the inheritance pattern of most forms of vWD?
π
°οΈ X-linked
β
π
±οΈ Autosomal dominant
π
²οΈ Autosomal recessive
π
³οΈ Multifactorial
Correct Answer: π
±οΈ Autosomal dominant
π Rationale: Most common types of vWD are inherited in an autosomal dominant manner.
Q5. Which symptom is most characteristic of von Willebrand disease?
π
°οΈ Hemarthrosis only
π
±οΈ Petechiae with low platelets
β
π
²οΈ Mucosal bleeding and menorrhagia
π
³οΈ Cyanosis
Correct Answer: π
²οΈ Mucosal bleeding and menorrhagia
π Rationale: These are hallmark features due to defective platelet plug formation.
π Important for Critical Care Nursing, Medical-Surgical Nursing, Obstetrics & Hematology Exams
Disseminated Intravascular Coagulation (DIC) is a life-threatening acquired bleeding and clotting disorder characterized by widespread activation of the clotting cascade, resulting in formation of microthrombi and subsequent consumption of clotting factors and platelets, leading to severe bleeding.
π¬ It is a secondary condition triggered by an underlying disease.
πΈ S β Sepsis (most common)
πΈ T β Trauma (e.g., burns, head injury)
πΈ O β Obstetric complications (e.g., abruption, eclampsia, retained placenta, amniotic fluid embolism)
πΈ P β Pancreatitis (acute)
πΈ M β Malignancy (leukemia, adenocarcinoma)
πΈ N β Nephrotic syndrome
πΈ T β Transfusion reactions
πΊ Bleeding symptoms (external & internal):
β’ Bleeding from IV sites, wounds, gums, nose
β’ Hematuria, GI bleeding, petechiae, ecchymosis
β’ Vaginal or uterine bleeding (obstetric DIC)
πΊ Clotting symptoms (organ ischemia):
β’ Cyanosis, gangrene
β’ Altered mental status (CNS thrombosis)
β’ Dyspnea (PE), chest pain (MI), oliguria (renal infarction)
πΊ Shock signs:
β’ Hypotension, tachycardia, pallor, cold clammy skin
π¨ Multiorgan failure
π¨ Severe hemorrhage
π¨ Hypovolemic shock
π¨ Death (if untreated)
π§ͺ CBC: β Platelets
π§ͺ PT / aPTT: Prolonged
π§ͺ D-dimer: ββ (marker of fibrinolysis)
π§ͺ Fibrinogen level: β
π§ͺ FDPs (Fibrin degradation products): β
π§ͺ Peripheral smear: Schistocytes (fragmented RBCs)
πΉ Treat underlying cause:
β’ Sepsis β Antibiotics
β’ Obstetric cause β Delivery of fetus/placenta
πΉ Control bleeding and support clotting:
π Fresh Frozen Plasma (FFP) β Replaces clotting factors
π Platelet transfusion β If count <50,000/mmΒ³ and bleeding
π Cryoprecipitate β If fibrinogen <100 mg/dL
π Heparin β In chronic DIC or thrombotic phase (caution)
πΉ Supportive care:
ποΈ Oxygen, IV fluids, vasopressors for shock
π©Ί ICU monitoring, maintain organ perfusion
π© Assessment:
πΉ Monitor for bleeding (gums, urine, puncture sites)
πΉ Monitor vitals, LOC, signs of organ dysfunction
πΉ Check lab values regularly (PT, aPTT, platelets, fibrinogen)
π¨ Intervention:
πΉ Apply pressure to bleeding sites
πΉ Avoid IM injections and invasive procedures
πΉ Administer blood products carefully as prescribed
πΉ Maintain IV lines with aseptic technique
πΉ Provide oxygen and fluid resuscitation
π₯ Education & Communication:
πΉ Inform family about critical condition
πΉ Update team about ongoing changes
πΉ Educate on prevention of infection and early sepsis recognition (in high-risk patients)
π‘ DIC = Clotting + bleeding at the same time
π‘ Most common trigger = Sepsis
π‘ D-dimer ββ, platelets β, PT/aPTT prolonged
π‘ Fibrinogen and clotting factors are consumed
π‘ Life-threatening emergency requiring rapid intervention
Q1. Which of the following best describes DIC?
π
°οΈ Platelet disorder
β
π
±οΈ Consumptive coagulopathy
π
²οΈ Hemolytic anemia
π
³οΈ Leukemia
Correct Answer: π
±οΈ Consumptive coagulopathy
π Rationale: DIC consumes clotting factors and platelets, leading to bleeding and thrombosis.
Q2. The most common cause of DIC is:
π
°οΈ Liver failure
β
π
±οΈ Sepsis
π
²οΈ Renal failure
π
³οΈ Malaria
Correct Answer: π
±οΈ Sepsis
π Rationale: Septicemia triggers widespread coagulation activation.
Q3. Which test is elevated in DIC due to fibrinolysis?
π
°οΈ Hematocrit
π
±οΈ ESR
β
π
²οΈ D-dimer
π
³οΈ LDL
Correct Answer: π
²οΈ D-dimer
π Rationale: D-dimer is a fibrin degradation product and a marker of clot breakdown.
Q4. Which blood component is used to replace clotting factors in DIC?
π
°οΈ RBCs
β
π
±οΈ Fresh Frozen Plasma
π
²οΈ Albumin
π
³οΈ Whole blood
Correct Answer: π
±οΈ Fresh Frozen Plasma
π Rationale: FFP contains all clotting factors needed to manage coagulopathy.
Q5. What type of anemia may be seen in DIC on peripheral smear?
π
°οΈ Spherocytes
π
±οΈ Microcytic cells
β
π
²οΈ Schistocytes
π
³οΈ Target cells
Correct Answer: π
²οΈ Schistocytes
π Rationale: Fragmented RBCs (schistocytes) occur due to mechanical destruction in microvasculature.
π Important for Medical-Surgical Nursing, Critical Care, Pathology, and Staff Nurse Exams
Blood transfusion is the intravenous administration of whole blood or its components (e.g., RBCs, plasma, platelets) to replace lost components, treat anemia, or support during surgery or critical illness.
𧬠It is a life-saving procedure, but carries risks if not done properly.
πΉ Acute blood loss (trauma, surgery)
πΉ Severe anemia (Hb <7 g/dL)
πΉ Thrombocytopenia
πΉ Coagulation disorders
πΉ Hemophilia, DIC
πΉ Bone marrow failure
πΉ Exchange transfusion in neonates
β’ Contains RBCs, WBCs, platelets, plasma
β’ Used in acute hemorrhage
β’ RBCs with minimal plasma
β’ Used to treat anemia without volume overload
β’ Given for thrombocytopenia (platelet count <20,000/mmΒ³ or active bleeding)
β’ Lifespan: 5β7 days
β’ Contains all clotting factors
β’ Used in DIC, liver disease, warfarin overdose
β’ Rich in Factor VIII, fibrinogen, vWF
β’ Used in Hemophilia A, DIC, hypofibrinogenemia
β’ Plasma protein used for hypovolemia, hypoalbuminemia
β’ For autoimmune diseases, immune deficiencies
πΈ Blood group and Rh factor must be matched
πΈ Cross-matching = donor RBCs + recipient serum tested for reaction
πΈ O negative = universal donor (RBCs)
πΈ AB positive = universal recipient (RBCs)
β’ Due to ABO incompatibility
β’ S/S: Fever, chills, back pain, chest pain, hypotension, hemoglobinuria
β’ Stop transfusion immediately
β’ Most common
β’ Due to recipient antibodies against donor WBCs
β’ S/S: Fever, chills
β’ Manage with antipyretics
β’ Due to plasma proteins
β’ S/S: Rash, itching, urticaria
β’ Treat with antihistamines
β’ Rare, life-threatening
β’ S/S: Hypotension, dyspnea, wheezing, shock
β’ Give epinephrine, stop transfusion
β’ Occurs days to weeks later
β’ S/S: Low-grade fever, jaundice, β Hb
β’ Monitor and report
β’ Rare but fatal; in immunocompromised
β’ Prevent with irradiated blood
β’ HIV, Hepatitis B/C, Malaria (rare due to screening)
πΉ Check doctorβs order, consent
πΉ Confirm blood type and cross-match
πΉ Verify identity of patient and blood unit (2 nurses)
πΉ Record baseline vital signs
πΉ Use 18β20 gauge IV cannula
πΉ Use blood administration set with filter
πΉ Start slowly (25β50 mL in first 15 mins)
πΉ Stay with patient for first 15 mins
πΉ Monitor vital signs frequently
πΉ Observe for any signs of transfusion reaction
πΉ Transfuse within 4 hours of starting
πΉ Stop transfusion immediately
πΉ Maintain IV line with normal saline
πΉ Notify physician and blood bank
πΉ Monitor vitals and symptoms
πΉ Send remaining blood and tubing for investigation
πΉ Document the reaction thoroughly
π‘ PRBCs are used for anemia without volume overload
π‘ Platelets are stored at room temp and used for thrombocytopenia
π‘ FFP contains all clotting factors, not platelets
π‘ Acute hemolytic reaction is most dangerous
π‘ Always start transfusion slowly and monitor first 15 minutes
Q1. Which blood product is preferred for a patient with low hemoglobin but normal volume?
π
°οΈ Whole blood
β
π
±οΈ PRBCs
π
²οΈ FFP
π
³οΈ Platelets
Correct Answer: π
±οΈ PRBCs
π Rationale: PRBCs raise hemoglobin without causing fluid overload.
Q2. Which transfusion reaction is life-threatening and caused by ABO incompatibility?
π
°οΈ Febrile reaction
β
π
±οΈ Acute hemolytic reaction
π
²οΈ Allergic reaction
π
³οΈ Delayed reaction
Correct Answer: π
±οΈ Acute hemolytic reaction
π Rationale: Incompatible RBCs cause hemolysis and severe systemic symptoms.
Q3. A patient develops itching and rash 15 minutes into transfusion. What is the nurseβs first action?
π
°οΈ Slow the transfusion
β
π
±οΈ Stop the transfusion
π
²οΈ Call the doctor
π
³οΈ Flush the line with heparin
Correct Answer: π
±οΈ Stop the transfusion
π Rationale: Immediate discontinuation is key to prevent progression of reaction.
Q4. Which component is rich in Factor VIII and used in Hemophilia A?
π
°οΈ Platelets
π
±οΈ PRBCs
β
π
²οΈ Cryoprecipitate
π
³οΈ Albumin
Correct Answer: π
²οΈ Cryoprecipitate
π Rationale: Cryoprecipitate contains high levels of Factor VIII and fibrinogen.
Q5. Which solution is used to flush IV before and after blood transfusion?
π
°οΈ Dextrose 5%
π
±οΈ Ringer lactate
β
π
²οΈ Normal saline (0.9% NaCl)
π
³οΈ Heparinized saline
Correct Answer: π
²οΈ Normal saline (0.9% NaCl)
π Rationale: Only normal saline is compatible with blood products.