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Pathophysiology Exam 4 > Hematology > Flashcards

Hematology Flashcards

1
Q

Erythropoiesis: In bone marrow

A
  1. ) Decreased blood oxygen
  2. ) Kidneys secrete erythropoietin
  3. ) Bone marrow stimulated
  4. ) Creates new blood cells

A man with renal failure would develop anemia because of the non-secretion of erythropoietin

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2
Q

Anemia

A

Decreased Hgb &/or RBC

Causes:
Blood loss
Impaired erythrocyte production
Increased erythrocyte destruction (hemolysis)

Signs and Symptoms
Gradual vs. sudden
Magnitude

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3
Q

Classic signs of Anemia:

A

Pallor
Fatigue
Dyspnea on Exertion (DOE)
Dizziness

Compensatory Manifestations:
CV: Tachycardia, palpitations, & vasoconstriction
Respiratory: Tachypnea & increased depth of breathing

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4
Q

Classification of Anemia

A

Based on Size - MCV
Normocytic
Macrocytic (large)
Microcytic (small)

Based on Color – MCHC (Hgb content)
Normochromic
Hyperchromic- (increased Hgb)
Hypochromic – (decreased Hgb)

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5
Q

MCV- Mean corpuscular Volume

A

Normally 80-90

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6
Q

MCHC- Mean Corpuscular Hemoglobin Concentration

A

Normally 32-36%

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7
Q

Iron Deficiency Anemia

A

Microcytic- Hypochromic

Etiology
Inadequate intake
Increased demand (growth, pregnancy)
Bleeding

Signs & symptoms
Classic signs of anemia PLUS…
Angular cheilosis. (cracking lips), brittle hair & nails, smooth tongue (“glossitis”), pica (craving non-foods), koilonychia (moon-shaped)

Evaluation
CBC analysis
Serum Iron profile
Total Fe, TIBC, Ferritin

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8
Q

Iron Deficiency Anemia Treatment

A 
Control chronic blood loss
Bleeding/GI losses are the most common cause 
Increase dietary intake
Iron Supplements
Types
ferrous sulfate
iron dextran
Blood transfusion if necessary
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9
Q

Vitamin B12 Deficiency

A

Macrocytic- Normochromic or “megaloblastic” anemia

Etiology
Defective gastric secretion of intrinsic factor (IF)
Interference of IF binding to B12 caused by chronic conditions of malabsorption and atrophic gastritis; gastrectomy.
Dietary deficiency (rare)

Signs and Symptoms
Classic signs of anemia
Glossitis
Neuro changes!
Vit. B12 is necessary for the synthesis of myelin
Paresthesias, loss of vibratory & position sense, ataxia, dementia

Evaluation
CBC analysis
Schilling test
Antibodies to intrinsic factor and gastric parietal cells

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10
Q

Folate Deficiency Anemia

A

Macrocytic- Normochromic

Etiology
Dietary deficiency & malnutrition
Commonly seen in alcoholism (ETOH interferes w/ folate metabolism)
Malabsorption

Symptoms
similar to B12 def. but NO neuro manifestations
Classic signs of anemia

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11
Q

Anemia of Chronic Disease

A

Normocytic - Normochromic

Decreased lifespan of erythrocyte & ↓ response to erythropoietin
In response to cell injury-
Macrophages sequester iron in the spleen
Lymphocytes release cytokines that ↓ erythropoetin response

Etiology
Chronic infections (HIV/AIDS)
Chronic inflammatory diseases (RA, SLE, CRF)
Malignancies

Clinical manifestations
Classic signs of anemia

Evaluation
CBC analysis
Screening for malignancies if chronic infection or inflammation is not present

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12
Q

Hemolytic Anemia

A

Premature, accelerated destruction of RBCs

Erythropoiesis is normal & often accelerates in an effort to compensate for the increased destruction

Elevated bilirubin as result of increased destruction
Jaundice & icterus

Elevated reticulocytes as result of hyperactive bone marrow

Acquired
Immune mediated (autoimmune; transfusion reaction, hemolytic disease of the newborn);  physical trauma; drugs
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13
Q

Hemolytic Anemia Manifestations/Treatment

A

Clinical manifestations
Classic signs of anemia
Jaundice
Splenomegaly

Treatment
Removing the cause
Treat underlying disorder
Blood transfusions
Splenectomy if this is site where hemolysis is occurring
Corticosteroids if immune mediated hemolysis

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14
Q

Sickle Cell Disease

A

Sickle cell disease is inherited in an autosomal recessive pattern.

Offspring inherit one recessive allele (S) and one normal allele (heterozygous expression) they become unaffected carriers and are said to have sickle cell trait (clinically silent).

Sickle cell disease is caused by a mutation in the hemoglobin beta (HBB) gene, leading to a single change in amino acid sequence.

The abnormal gene product (hemoglobin S) is not stable.

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15
Q

Heterozygote Advantage for SCD

A

When a person inherits only one allele for Hemoglobin S, they do not express disease.

Instead, heterozygous expression of Hgb S is correlated with lower rates of mortality among carriers who are of African and Mediterranean descent,

Because the HbS allele decreases the risk of infection by malarial parasites endemic in those areas. (“heterozygote advantage”)

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16
Q

Phenotypic Features for SCD

A

Blood vessel occlusion**
Acute pain
Infarctions cause chronic damage to liver, spleen, heart, kidneys, eyes, bones
Pulmonary infarction acute chest syndrome (PNA)
Cerebral infarction  stroke
Marrow infarcts painful bone crisis
Splenic injury functional aspenia

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17
Q

Management & Treatment for SCD

A 
Avoid factors that trigger sickling and vessel occlusion
Stress
Cold
Infection
Dehydration
Hypoxia
Acidosis
Pain Management 
Hydration

Hydroxyurea is the most commonly prescribed therapy for sickle cell disease & has been shown to reduce the number of painful episodes, acute chest syndrome, and transfusions as well as to improve overall survival

Bone marrow or stem cell transplant if a suitable donor is found

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18
Q

Thalassemias: Alpha

A 
Defective gene for alpha-chain synthesis
May have 1–4 defective genes
Severity depends on how many genes deleted 
Affects both fetal and adult Hgb
Most common among Asians
Also Africans & African Am
19
Q

Thalassemias: Beta

A 
Defective gene for beta-chain synthesis
May have 1–2 defective genes
Affects only adult Hb
Most common among Mediterranean population
Also Africans & African Am
20
Q

Aplastic Anemia

A

Caused by bone marrow failure
Reduction of hematopoietic cells (RBCs, WBCs, platelets)
Pancytopenia (other name)

Etiology
Acquired:
Primary- idiopathic 
Secondary- Chemicals; chemotherapy; ionizing radiation; complication of AIDS 
Hereditary: rare

Clinical Manifestations
Classic signs of anemia
If WBCs low- infection
If platelets low- bleeding. Petechiae & echymoses

21
Q

Polycythemia

A

Abnormally high RBC mass with a Hct > 50%

Relative
Loss of plasma volume

Absolute
Increase in total red cell mass
Classified as primary or secondary

22
Q

Primary Polycythemia

A

“Polycythemia Vera”

Neoplastic disorder characterized by an abnormal proliferation of pluripotent cells of bone marrow
causes an increase in total red cell mass, WBC, and platelets.

Clinical manifestations
r/t ↑blood volume & viscosity
Decreased cerebral blood flow: headache, inability concentrating, hearing & visual difficulties
Venous stasis: plethoric (dusky red appearance)
Thromboembolism
Pruritis - r/t increased mast cells in the skin
Hemorrhage r/t platelet abnormalities

Treatment
Periodic phlebotomy
Chemotherapy

23
Q

Secondary Polycythemia

A

A physiologic response to hypoxia caused by an appropriate secretion of erythropoietin

High risk groups:
Living at high altitudes
Smokers
Persons with CHF
Persons with COPD
Persons w/ neoplasms that develop the ability to secrete erythropoietin

Clinical manifestations- Similar to polycythemia vera

Treatment
Relieving hypoxia

24
Q

Platelets (Thrombocytes)

A

Megakaryocytes formed in bone marrow
Break apart to form platelets

Thrombopoietin
Made in liver, kidney, smooth muscle, bone marrow

Platelets live 8–9 days in circulation
Many are stored in spleen
Released when needed
150,000 – 400,000 platelets/μL

25
Q

Hemostasis

A

1.) Vasoconstriction/ Vasospasm
2.) Platelet plug
Requires von Willbrand Factor (vWF) produced by endothelial cells

  1. ) Activation of clotting cascade: Formation of fibrin from fibrinogen, Intrinsic, Extrinsic & Final common pathway, Results in fibrin meshwork that stabilizes the plug
  2. ) Blood clot formation

5.) Clot retraction
6.) Clot lysis- mediated by plasmin.
plamin splits fibrinogen into Fibrin Degredation Product (FDPs), which dissolve the clot.

If blood vessel injury is minor, platelet plugs may be sufficient to result in hemostasis w/o the clotting cascade

26
Q

Coagulation Monitoring

A

Platelet count 150,000- 400,000

Partial Thromboplastin Time (PTT)
Measures activity of Intrinsic & Final common pathway
Normal= 21-35 sec

Prothrombin Time (PT)
Measures activity of the Extrinsic and Final common pathways
Normal= ~11-13 sec

International Normalized Ratio (INR)
Standardizes evaluation of extrinsic pathway
Normal= 1.0

27
Q

Coagulation Factors

A

Plasma proteins
Most are synthesized by liver
von Willebrand factor made by endothelium
Circulate as inactive procoagulation factors

Calcium
Required for clotting process

28
Q

Manifestations of Bleeding Disorders

A

Ecchymosis
Purpura- > 0.5 cm diameter
Petechiae- < 0.5 cm diameter

Hemorrhage
Epistaxis
Hemoptysis
Hematemesis
Coffee Ground emesis
Hematechezia
Melena
29
Q

Thrombocytopenia

A

Platelet count <100,000
<50,000= Bleeding potential
<20,000= High risk for spontaneous bleeding

Causes
Decreased platelet production (bone marrow depression; HIV)
Increased platelet destruction (immune or nonimmune)
Disordered platelet distribution (pooling of platelets in spleen)

Examples
Immune Thrombocytopenia Purpura (ITP) – autoimmune
Drug-induced thrombocytopenia
Thrombotic Thrombocytopenia Purpura (TTP) –widespread platelet thrombi

30
Q

A woman with lupus develops breast cancer…
She is given radiation therapy
She begins to develop nosebleeds and bruising
Her menstrual period is abnormally heavy

Why did this happen?

A

Thrombocytopenia, Anemia (not enough platelets)

31
Q

Vitamin K Deficiency

A

Necessary for the production of Prothrombin, Factors II, VII, IX, & X
Fat soluble vitamin
#1 source: green leafy vegetables
Resident intestinal bacteria

Causes
Insufficient dietary intake
Absence of bile salts necessary for Vit K
Intestinal malabsorption syndromes
Oral antibiotics that kill resident intestinal bacteria
Neonates- immature liver & lack of normal intestinal flora

32
Q

Hemophilia A (Inherited Coagulation Disorders)

A

X-linked recessive, primarily affecting males
Possibly a new mutation of factor VIII gene
Mild, moderate, severe forms (<1% with severe forms)
Avoid ASA, NSAIDS
Factor VIII replacement
Gene replacement therapy being studied

33
Q

Von Willebrand Disease (Inherited Coagulation Disorders)

A

Deficiency of or defect in vWF
Autosomal dominant or rarely—several autosomal recessive variants identified (severe manifestations d/t severely ↓vWF)
Most cases mild
Clinical manifestations of spontaneous bleeding w/ normal platelet count

34
Q

DIC (Disseminated Intravascular Coagulation)

A

Acquired coagulopathy in which clotting & hemorrhage occur within the vascular system

Etiology
Clinical conditions that activate clotting mechanisms (infection, hemorrhage, shock).
Widespread clotting occurs → vessel occlusion, tissue ischemia
Consumption of platelets and coagulation factors results
Viscous cycle of clotting and bleeding results

Treatment:
Remove precipitating cause
Restore balance between coagulation & fibrinolysis
Maintain organ viability

35
Q

White Blood Cell Deficiencies

A

Leukopenia
Neutropenia (agranulocytosis)
Aplastic anemia
Infectious mononucleosis

36
Q

Neoplasms

A

Neoplasms arising here (bone marrow) cause leukemias or plasma cell dyscrasias

Neoplasms arising here (lymph nodes) are lymphomas

37
Q

Leukemias

A

Malignant neoplasms of hematopoietic stem cells
In bone marrow
Create abnormal white blood cells

Lymphocytic
immature lymphocytes originating in bone marrow, infiltrating spleen, lymph nodes, CNS, and other tissues

Myelogenous
Involve myeloid pluripotent stem cells in bone marrow, interfering w/ maturation of all blood cells (granulocytes, erythrocytes, thrombocytes).

38
Q

Myelocytic Leukemias

A

Mutation of myeloid cell line
Overproduction of abnormal monocytes or granulocytes
Production of other cell types decreases

39
Q

Lymphocytic Leukemias

A

Mutation of lymphoid cell line
Overproduction of abnormal immune cells
Production of other cell types decreases

40
Q

Leukemia

A

Definition- malignant neoplasms of the hematopoietic stem cells

Types:
Acute
ALL
AML

Chronic
CLL
CML

41
Q

Non-Hodgkin’s lymphoma

A

More common
Random, non-contiguous spread
B cell
T cell

42
Q

Hodgkin’s lymphoma

A

Malignancy of lymphoid tissue
Begins in a single lymph node then spreads contiguously
Characterized by presence of Reed-Sternberg cell (B cell origin)

43
Q

Multiple Myeloma

A

Abnormal B cells proliferation
Excessive production of monoclonal antibody
Can form tumors in bones & soft tissue

Produce abnormal antibodies
M protein or Bence Jones protein…toxic to renal tubules
Immune depression due to decreased levels of normal immunoglobulins
Proteins increase blood viscosity. Proteins may break into amyloid & cause heart failure and neuphropathy.
Proliferation and activation of osteoclasts

Osteolytic bone lesions- breakdown of bone…hypercalcemia
Compression fractures

44
Q

A child develops night sweats (usually lymphoma) and nosebleeds (thrombocytopenia)…
He appears pale (anemia), weak, and fatigued
Cervical lymph nodes are enlarged
Blast count is elevated
After chemotherapy, he develops hyperkalemia (Potassium floats intracellulary).

A

Lymphoma, Thrombocytopenia, Anemia, Potassium is now floating extracellularly

Pathophysiology Exam 4 (5 decks)

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