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Anemia

Prepared by: Rezhin Aryan Qadir –F190224


Introduction
Anemia, which is defined as a reduction in the oxygen carrying capacity
of the blood, usually is associated with

a decreased number an abnormality in the Hb


of circulating RBCs contained within the RBCs
Etiology
05
Infections
01 Genetic Disorders
produce aberrant RBCs that result
in RBC destruction

02 Nutritional Disorders
that limit the production of RBCs 06
Diseases of Bone Marrow
03 Immune-Mediated Disorders
that result in attacks on RBCs

04
Bleeding Disorders
07
Chronic Diseases (Rheumatoid Arthritis)
Types of Anemia
Iron Deficiency Anemia
Iron Deficiency Anemia is a microcytic anemia that can be caused by

Excessive Blood Loss Poor Iron Intake Poor Absorption Increased Iron Demand

Chronic Inflammation
Menstruation Insufficient Diet Gastrectomy
(Autoimmune Disease)

Bleeding from GIT Intestinal Disease


Duodenum
Absorption of Iron Decreases
Jejunum
Iron Deficiency Anemia
In women

Menstruation Pregnancy

Repeated Blood Loss Increased Demand for Additional Iron

Contribute to the Development of IDA


Pernicious Anemia Folate Deficiency Anemia

Vitamin B12 Vitamin B9


(Cobalamin) (Folic Acid)
Needed for
Cofactor in Enzymatic Reactions
Methionine-Associated Enzymatic Reaction

Required for the Synthesis of


Required for

Purines Pyrimidine
Protein
Synthesis

DNA RNA
RBC Protein
Maturation Synthesis

RBC
Maturation
Pernicious Anemia & Folate Deficiency Anemia

Vitamin B12
Formation
(Cobalamin)
RBC Within Bone Marrow
Vitamin B9
Growth
(Folic Acid)

Daily Intake

Vitamin B12
(Cobalamin)
Deficiency Vitamin B9 Anemia
(Folic Acid)

Absorption
Pernicious Anemia & Folate Deficiency Anemia
Q/ Where is Folate Found?
In Fruits & Leafy Vegetables.

Q/ Why is a Continual Dietary Supply of Folate Needed?


Because, it is not stored in the body in large amounts, so a continual dietary supply is needed.

Q/ What Interferes with the Absorption & Metabolism of Folate?


Alcohol Consumption & Certain Drugs (Methotrexate & Phenytoin).

Q/ Why Does Pernicious Anemia Usually Develop Late in Life?


Because Vitamin B12 may be stored for several years.

Q/ How Does Pernicious Anemia Develop?


Due to a Deficiency of Intrinsic Factor, that is Necessary for Absorption of Vitamin B12.

Parietal Cells Secretes Absorbs


Intrinsic Factor Vitamin B12
(Stomach)
Hemolytic Anemia
Caused by

1 Immune Attack

2 Extrinsic Factors Infection Splenomegaly Drugs

Disorders of
3 RBC Membrane
Spherocytosis

4 Enzymopathies G-6PD Deficiency

5 Hemoglobinopathies Sickle Cell Anemia Thalassemia


Hemolytic Anemia: G-6PD Deficiency
Glucose-6-Phosphate Dehydrogenase (G-6PD)
an Enzyme that Helps the RBC to turn Carbohydrates into Energy
(Needed for the Hexose Monophosphate Shunt Pathway)

Fava Bean Ingestion is the Most Common Dietary Cause of Hemolytic Anemia
(in Persons with G-6PD Deficiency)

Glucose

RBC

Hexose Monophosphate
90% Glycolytic Pathway Metabolized Shunt Pathway
10%

ATP NADPH

Provides Energy Reduce Various


for the Cell Cellular Oxidants
G-6PD Deficiency

Hexose Monophosphate Shunt Pathway

Accumulation of Harmful Oxidants

Methemoglobin Denatured Hb

Heinz Bodies

Attach to Cell Membranes

Hemolytic Anemia

Drugs that can Induce Hemolysis


(used in Dental Practice)

Acetophenetidin Ascorbic Acid Acetylsalicylic Acid Vitamin K. Dapsone


Hemolytic Anemia: Sickle Cell Anemia
• Sickle Cell Anemia: is a Hemoglobinopathy Caused by a Mutation in the β Globin Gene.

• More than 90% of Affected Individuals, have Single Amino Acid Substitutions in the Hb Chain.

• HbS Results from the Substitution of Valine for Glutamic Acid.

• Sickle Cell Anemia is the Homozygous State (Autosomal Recessive),


Resulting from Inheriting the HbS Gene from Both Parents.

• The RBCs in SCA become Sickle-Shaped due to:


1. Deoxygenation

2. Decreased pH

3. Dehydration

• Distorted Sickle-Shaped RBCs causes:


1. Erythrostasis
2. Increased Blood Viscosity
3. Reduced Blood Flow
4. Hypoxia
5. Vascular Occlusion
Hemolytic Anemia: Sickle Cell Anemia
Aplastic Anemia

Bone Marrow

Unable to Produce

RBC WBC Platelets

Most Common

Young Adults (15 - 30)yrs Persons Older than 60yrs


Aplastic Anemia
Causes

Drugs Viruses Organic Compounds Radiation Idiopathic

Antibacterials Viral Hepatitis Benzene 50 – 65%

Anticonvulsants Insecticides

Antidiabetic

Diuretics

Sulfonamides

Synthetic
Antithyroid
Aplastic Anemia

Based on Degree of Pancytopenia

Moderate Severe Very Severe

> 500 Neutrophils/µL < 500 Neutrophils/µL < 200 Neutrophils/µL

> 20,000 Platelets/µL < 20,000 Platelets/µL < 20,000 Platelets/µL

> 20,000 Reticulocytes/µL < 20,000 Reticulocytes/µL < 20,000 Reticulocytes/µL

Initial Sign & Weakness – Fatigue – Headaches - Dyspnea (with Exertion)


Symptoms Petechiae – Ecchymosis – Epistaxis - Metrorrhagia - Gingival Bleeding
Renal Disease & Organ Transplantation
Kidney
Erythropoietin

Erythropoietin Renal Damage Decreases Anemia

RBC Production

RBC Production

Transplantation

Kidney

Immunosuppression
Liver Anemia
(Bone Marrow)

Bone Marrow
Signs & Symptoms
Signs
Jaundice – Pallor – Cracking – Splitting & Spooning of the Fingernails
Hepatosplenomegaly – Lymphadenopathy – Blood in the Stool.

Symptoms
Fatigue – Lethargy – Palpitations – SOB - Abdominal Pain - Bone Pain
Tinnitus – Irritability – Dizziness - Tingling of Fingers & Toes - Muscular Weakness.

Pernicious Anemia Iron Deficiency Anemia

Premature Hair Graying Glossitis

Skin Yellowing
Smooth Tongue
(Due to Jaundice)

Cheilosis

Loss of Taste Sensation


Signs & Symptoms

Pernicious Anemia Iron Deficiency Anemia


Screening Laboratory Tests

Hematocrit MCV WBC Count Platelet Count

MCH
CBC RBC Indices
MCHC

Hb Level RDW Generalized Bone Marrow Defect


Screening Laboratory Tests
Female
Hb < 12g/dL
Anemia
Hb < 13g/dL
Male

Reticulocyte Count
(Based on Percentage of RBC)

< 0.5% > 1.5%

Decreased RBC Production Increased RBC Production


Screening Laboratory Tests
Anemia
(Based on Size of RBC)

Microcytic Normocytic Macrocytic


MCV < 80 fL MCV = (80 – 100) fL MCV > 100 fL

Iron Deficiency G-6PD Deficiency Folate Deficiency

Sickle Cell Anemia Pernicious Anemia

Aplastic Anemia
Screening Laboratory Tests
How to Distinguish between the Different Types of Anemia?
1. Microcytic Anemia
2. Low Serum Ferritin
Iron Deficiency Anemia
3. Low Serum Iron
4. High Total Iron Binding Capacity (TIBC)
1. Macrocytic Anemia
Folate Deficiency Anemia
2. Hypersegmented PMNLs (in Peripheral Blood Smear)
1. Serum Cobalamin Assay
Pernicious Anemia
2. Schilling Test
Screening Tests for:
Hemolytic Anemia: G-6PD Deficiency 1. Heinz Bodies
2. NADPH (Direct Fluorescent Measures of NADPH)

Hemolytic Anemia: Sickle Cell Anemia 1. Sickledex Test

1. Anemia (Normochromic, Normocytic)


2. Thrombocytopenia (Normal Sized Platelets)
Aplastic Anemia
3. Neutropenia
4. No Abnormal Cells (in Leukocyte Differential)
Medical Management
Microcytic Anemia • Iron Supplements for Children: Ferrous Sulfate (2 - 6 mg/kg/day)
(Iron Deficiency) • Iron Supplements for: Patients who have undergone Gastrectomy (Administered Long-Term Orally)
Folate Deficiency • Administer Folic acid Supplements.
Anemia • Increase Intake of Green, Leafy Vegetables & Citrus Fruits.

Pernicious Anemia • Treat with Cyanocobalamin Injections.

• For Infants: Routine Prophylactic Penicillin.


• Early use of Antibiotics: to Prevent Severe Infections.
Sickle Cell Anemia • Vaccination against Specific Pathogens.
• Daily Folic Acid Supplements.
• For Select Cases (Especially in Younger Patients): Stem Cell Transplantation.

Aplastic Anemia • Immunosuppression Therapy with Antithymocyte Globulin (ATG) Alone or with Cyclosporine.

Chronic Renal • Dialysis.


Failure Anemia • Long-Term use of Recombinant Erythropoietin: to Stimulate RBC Production.

Severe Anemia • Hospitalization: If Hematocrit Value < 20%.


Dental Management
Identify these Patients through History & Clinical Examination (Before Starting any Treatment)
 Obtain a Careful History (Include Questions Concerning):
• Dietary Intake – Malnutrition

• Alcohol or Drug Use – NSAIDs Use

• Menstrual Blood Loss – Pregnancies

• Hypothyroidism – Jaundice – Gallstones – Splenectomy

• Bleeding Disorders – Abnormal Hb - Organ Transplantation

 If the Patient is a Woman, ask about the Following:


1. Menstrual Cycle: Onset, Nature & Regularity.

2. Pregnancy: Experienced Excessive Bleeding & Duration between Pregnancies (Risk for Development of IDA)

3. Childbirth: May Lose Iron During Delivery & Breastfeeding (Once the Baby is Born)

 Identify Signs & Symptoms of Anemia (If Identified):


• Should be Referred Directly to a Physician.

• Screened by Appropriate Laboratory Tests.


Dental Management
Ensure that the Patient’s Underlying Condition is under Good Medical Control (Before Proceeding)
 Assessment of the Severity of a Patient’s Anemia (For Preventing Complications):
• Hb Levels should be: Above 11 g/dL.

• The Patient should be: Free from Symptoms.

Patients Who Are

SOB Hb Levels < 11 g/dL Abnormal Heart Rate Oxygen Saturation < 91%
Pulse Oximetry

Medically Unstable (Routine Treatment Should be Deferred; until Health Status Improves
Dental Management
Patients with G-6PD Deficiency
Increased Drug Sensitivity

Sulfonamides Penicillin

Aspirin Streptomycin

Chloramphenicol Isoniazid
Should be Avoided

Dental Infection

Hemolysis
Accelerated

Should be Avoided
Dental Management
Sickle Cell Anemia

Antibiotics Anesthesia
Prophylactic Antibiotics are often Recommended • For Routine Dental Care:
(Major Surgical Procedures) Use LA without Epinephrine
to Prevent Wound Infection or Osteomyelitis
• For Surgical Procedures:
Penicillin (Nonallergic Patients) Use LA with 1:100,000 Epinephrine
IM/IV Antibiotics (Acute Dental Infection)
Analgesics • Avoid General Anesthesia:
If Hb Level < 10 g/dL.
The Following Should Be Avoided:
1. Narcotics: Respiratory Suppression Leads to Hypoxia & Consultation
Acidosis, which may Precipitate an Acute Crisis. • Consultation with the Patient’s Physician is a Must
2. High Doses of Salicylates: The “Acid” Effect can Precipitate (Before any Surgical Procedure)
a Crisis.
Emergencies
For Pain Control Use: • Treat Acute Infection: with Incision & Drainage.
Acetaminophen, With or Without, Small Doses of Codeine
Equipment • Local Heat & High Doses of Appropriate Antibiotics
(Can Help Avoid a Crisis)
Use Pulse Oximeter
(Maintain Oxygen Saturation above 95%)
• Dehydration: Should be Avoided.

• If Sickling Crisis Occurs: Hospitalization is Indicated.


Dental Management
Sickle Cell Anemia

Drugs
• Avoid Barbiturates & Narcotics:
Respiratory Suppression Leads to Hypoxia & Acidosis, which
may Precipitate an Acute Crisis.

• Use Inhalational Sedation (Nitrous Oxide-Oxygen):


For Short Periods
With 50% Oxygen Concentration

• Intravenous Sedation:
Must be Used with Extreme Caution
(in Patients who have a History of SCA)

• Light Sedation:
Can be Provided with Midazolam
Dental Management
Oral Complications & Manifestations
Nutritional Causes of Anemia
(Vitamin B12 or Iron Deficiencies)

Aphthae Plummer-Vinson Syndrome


Iron Deficiency Anemia
Angular Cheilitis

Sore Mouth Increased Frequency of Carcinoma Dysphagia


Atrophic Changes
Oral Cavity & Pharynx
Oral Mucosa
Caused By:
Burning or Sore Tongue Muscular Degeneration

Loss of Papillae Esophageal Stenosis


Tongue
Tongue
Oral Complications & Manifestations
Hemolytic Anemia (Sickle Cell Anemia)

Pallor Dental Hypoplasia Delayed Teeth Eruption

Oral Evidence of Jaundice

Hyperbilirubinemia

Excessive RBC Destruction

Ischemic Necrosis (Mandible)

Asymptomatic Pulpal Necrosis


Vasoocclusive Events
Osteomyelitis

Peripheral Neuropathy
Oral Complications & Manifestations
Hemolytic Anemia (Sickle Cell Anemia)

Enlarged Bone Marrow Spaces


Dental Radiographs

Increased Widening Generalized Osteoporosis


Trabeculations Thinning Inferior Border Mandible
Decreased Numbers

Trabeculae Between Teeth

Horizontal Rows
Stepladder
Oral Complications & Manifestations

Sickle Cell Anemia


Plummer-Vinson Syndrome
Oral Complications & Manifestations

Aplastic Anemia

Petechiae Ecchymosis Mucosal Pallor Ulceration

Gingival Bleeding Necrotizing Gingivostomatitis Gingival Hyperplasia


Reference
● Rhodus, N.L., Miller, C.S., Falace, D.A., & Little, J.W. (2013). Little and
Falace's Dental Management of the Medically Compromised Patient,
8th Edition.
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