Anemia.pptx

NandishS19 1,403 views 52 slides Dec 10, 2023
Slide 1
Slide 1 of 52
Slide 1
1
Slide 2
2
Slide 3
3
Slide 4
4
Slide 5
5
Slide 6
6
Slide 7
7
Slide 8
8
Slide 9
9
Slide 10
10
Slide 11
11
Slide 12
12
Slide 13
13
Slide 14
14
Slide 15
15
Slide 16
16
Slide 17
17
Slide 18
18
Slide 19
19
Slide 20
20
Slide 21
21
Slide 22
22
Slide 23
23
Slide 24
24
Slide 25
25
Slide 26
26
Slide 27
27
Slide 28
28
Slide 29
29
Slide 30
30
Slide 31
31
Slide 32
32
Slide 33
33
Slide 34
34
Slide 35
35
Slide 36
36
Slide 37
37
Slide 38
38
Slide 39
39
Slide 40
40
Slide 41
41
Slide 42
42
Slide 43
43
Slide 44
44
Slide 45
45
Slide 46
46
Slide 47
47
Slide 48
48
Slide 49
49
Slide 50
50
Slide 51
51
Slide 52
52

About This Presentation

For 2nd year B.Sc Nursing students


Slide Content

ANEMIA Presented By: Mr. Nandish.S Asso. Professor Mandya Institute of Nursing Sciences

DEFINITION It is a deficiency in number of erythrocytes, the quantity of hemoglobin or the volume of packed RBC’s. It is a condition in which the hemoglobin concentration is lower than normal. It is a condition that develops when your blood produces lower than normal amount of healthy red blood cells. It is a blood disorder in which the blood has a reduced ability to carry oxygen due to lower number of RBC or reduction in the amount of hemoglobin .

INCIDENCE & PREVALENCE : It is one of the major killer disease in India. Research reveals that every second I ndian women is anemic . One in every menstrual deaths is directly due to anemia . It affects both adults and children of both sex. Pregnant women & Adolescent girls are more susceptible to this disease.

ETIOLOGIC CLASSIFICATION OF ANEMIA Decreased Erythrocyte Production Blood loss Increased Erythrocyte Destruction MORPHOLOGIC CLASSIFICATION OF ANEMIA Normocytic Normochromic (Normal size & color) Macrocytic Normochromic ( Large size & normal color) Microcytic Hypochromic (Small size & pale color)

Decreased Erythrocyte Production Decreased Hemoglobin Synthesis Iron deficiency Thalassemia (Decreased Globin synthesis) Sideroblastic anemia (decreased porphyrin ) Defective DNA Synthesis Vitamin B12 deficiency Folic Acid deficiency Decreased Number of Erythrocyte Precursors Aplastic Anemia Anemia of leukemia Chronic Diseases Chemotherapy

Blood Loss Acute Trauma Blood vessel rupture Persistent Hematuria Chronic Gastritis Menstrual Flow / Menorrhagia Regular blood Donors Hemorrhoids

Increased Erythrocyte Destruction Intrinsic Abnormal Hemoglobin (Sickle Cell Anemia ) Enzyme Deficiency (G6PD) Membrane abnormalities Extrinsic Physical Trauma Antibodies (Autoimmune) Infectious Agents & Toxins

Based on the severity of Signs & Symptoms : 1. Mild Hemoglobin : 10 to 14 gm/dl Palpitation Exertional Dyspnea Moderate Hemoglobin : 6 to10 gm/dl Dyspnea Increased Palpitation Fatigue Continued ………………

3. Severe : Hemoglobin : less than 6 gm/dl. Pallor, pruritus Icteric Conjunctiva, Blurred vision Glossitis , Smooth tongue Tachycardia, Murmur Tachypnea , O rthopnea , Dyspnea at rest Headache, Vertigo, irritability, Depression Anorexia, Dysphagia, Sore mouth, Hepato -splenomegaly Bone pain Weight loss, Lethargy, Sensitivity to cold.

IRON DEFICIENCY ANEMIA : DEFINITION : It is defined as anemia associated with either inadequate absorption or excessive loss of iron from the body.

Etiology : Inadequate dietary intake. Malabsorption After gastro intestinal surgery. Malabsorption syndrome Blood loss Chronic blood loss from GI (Peptic Ulcer, Gastritis, Esophagitis, Hemorrhoids ) & GU System (Menstrual bleeding) At the time of Delivery & Lactation Pregnancy (diversion of iron towards fetus ) Dialysis treatment

CLINICAL FEATURES : Fatigability Dizziness Irritability Headache Palpitation Glossitis Stomatitis Dry pale skin Spoon shaped nails Hair loss

DIAGNOSTIC STUDIES : History collection & Physical Examination Stool examination : for presence of occult blood Endoscopy or colonoscopy : to detect GI Bleeding. Blood examination : decreased Hemoglobin / RBC / Hematocrit Decreased or normal WBC Decreased or normal Platelets.

MANAGEMENT : 1. Parenteral Iron therapy : It is initiated during Malabsorption Intolerance to oral replacement (colitis) Needs in excess amount that cannot be given through oral route. Poor compliance patients & Hemodialysis patients. Iron is given either intramuscularly or intravenously. IM – given deep IM in the upper & outer quadrant of buttocks using 18 or 20 gauze needle. Iron Dextran or Iron sucrose contains 50 mg/dl. It is diluted while administration to patients. Test dose is given to rule out any allergy.

2. Oral therapy Oral Iron & Folic acid tablets are usually prescribed. Total daily dosage : 150 – 200 mg elemental iron. Give iron in divided dose. ( each dose of 50 – 100 mg) Taking Iron with vitamin C, enhances its absorption. Iron preparations cause stool to become dark due to excess excretion of iron. Constipation is common, hence stool softners can be advised.

3. Others : Advise the patient to consume Liver, muscle meat, Egg, Dry fruits, Legumes, Dark green leafy vegetables, bread, cereals, pototoes , etc.. Encourage to include fibre rich diet to handle constipation. If iron deficiency is from acute blood loss, it require transfusion of packed RBC. Hemoglobin returns to normal by 2 – 4 months. Replacement therapy is prolonged to 6 – 12 months if ongoing bleeding is present.

MEGALOBLASTIC ANEMIA : They are the group of disorders caused by impaired DNA Synthesis and characterized by presence of large RBC. When DNA synthesis is impaired, it results in defective RBC Maturation. Megaloblast represent large and abnormal RBC’s. They are easily destroyed because they have fragile cell membrane. Two common forms of Megaloblastic anemia are : Cobalamin Deficiency & Foloic Acid deficiency.

COBALAMIN DEFICIENCY ANEMIA : Intrinsic Factor (IF) is required for absorption of Cobalamin , which is secreted by parietal cells of gastric mucosa. Pernicious Anemia is a disease of insidious onset, caused by an absence of Intrinsic Factor from gastric mucosal atrophy or Autoimmune destruction of Parietal cells. The main cause for cobalamin deficiency is Pernicious anemia . Pernicious Anemia is usually seen in middle aged people (after 40 years).

Etiology : 1. Inborn errors of cobalamin metabolism. 2. Erythroleukemia 3. Malabsorption Inadequate production of Intrinsic Factor Pernicious Anemia Gastrectomy (Partial or Total) Inadequate releasing of Vitamin B 12 from blood Abnormal Stomach functioning, Chronic pancreatic Insufficiency Terminal ileum disease (Celiac disease, Crohn’s disease) Others (bacterial overgrowth, intestinal obstruction) Continued …..

4. Inadequate intake Pure vegetarians 5. Medications Neomycin Nitrous oxide Long term use of H2 receptor blockers

CLINICAL FEATURES : GI Manifestations Neurologic Manifestations Atrophic Glossitis / sore tongue Abnormal gait , Symmetric Neuropathy Weight loss Numbness & weakness Anorexia Parasthesia Abdominal pain Memory loss Nausea & vomiting Spasticity & incontinence

DIAGNOSTIC STUDIES : History collection & Physical Examination Blood examination Macrocytic anemia Leukopenia Thrombocytopenia Decreased reticulocyte count Bone marrow examination It reveals hypercellular changes, abnormal large megaloblasts with nuclear cytoplasmic asynchrony. Schilling Test : a medical investigation used to evaluate vitamin B12 absorption. Usually result will be positive for this type of anemia .

TREATMENT : Increasing dietary cobalamin will not correct anemia , if any impaired absorption is there in Ileum. However, patient is instructed on adequate dietary intake to maintain good nutrition. Parenteral administration of cobalamin ( Cyanocobalamin ) is the treatment of choice. Dosage & frequency may vary. A typical treatment schedule consists of 1000mg of cobalamin (IM) daily for 2 weeks, then weekly once until hematocrit is normal and then monthly once for lifetime. A nasal gel is also available ( Nascobal ). As long as supplemental cobalamin is used, anemia can be reversed.

FOLIC ACID DEFICIENCY ANEMIA Folic acid is needed for DNA synthesis leading to RBC formation & maturation. Food supply folic acid : Spinach, Asparagus, Brocolli , Beans, Peanuts, Liver, Aquatic foods, sunflower seeds, etc. Banana rich in folate can meet daily needs when they are combined with other folic acid foods. It is absorbed in Duodenum of small intestine.

ETIOLOGY : Poor nutrition / Inadequate intake : green leafy vegetables, citrus fruits, Yeast, dreid beans, nuts & grains Malabsorption syndromes : small intestine disorders. Alcohol abuse / Excessive alcoholism Medications that affect absorption of Folic Acid : Methotrexate, Oral contraceptives, Anti seizure drugs. Hemodialysis Pregnancy & Lactation and during Infancy. Malignancy

CLINICAL MANIFESTATIONS : Clinical features during Folic acid deficiency are similar to those of cobalamin deficiency except neurologic problems. GI disturbance include dyspepsia & smooth beefy red tongue.

DIAGNOSTIC STUDIES : History collection & Physical Examination Decreased Hemoglobin level Decreased Serum Folate level Gastric analysis : positive for HCl .

TREATMENT : Encourage the patients to consume foods rich in Folic acid. Replacement therapy : oral dose is 1mg / day & in malabsorption upto 5mg can be administered. The duration of treatment depends on cause.

APLASTIC ANEMIA A rare condition in which body fails to produce sufficient new blood cells. It is a syndrome of bone marrow failure characterized by peripheral pancytopenia & bone marrow hypoplasia. It is a severe, non cancerous, hematologic condition in which body fails to make enough blood cells.

ETIOLOGY : The causative factors can be divided into two major groups. Congenital : chromosomal alterations. Fanconi syndrome (A disease of proximal renal tubule in which glucose, uric acid & amino acids are not absorbed properly. Congenital Dyskeratosis Amegakaryocytic thrombocytopenia Acquired : it results from Exposure to Ionizing Radiation, chemical agents (Benzene) Viral & Bacterial infections (Hepatitis) Medications (Antimetabolites, Alkylating agents, Antiseizure drugs) Idiopathic (more than 70% cases)

Clinical Manifestations : General : Fatigue, Dyspnea , weight loss Neurologic : Headache, Vertigo, Irritability, Depression Cardiovascular : Tachycardia, Neutropenia, Cardiac murmur Susceptible to infection, Febrile Thrombocytopenia can lead to Petechiae , Ecchymosis, Epistaxis

Diagnostic Studies : History collection & Physical Examination Decreased Hemoglobin , WBC & platelets Low Reticulocyte count Prolonged Bleeding time Elevated serum iron & Total Iron Binding capacity (TIBC) Bone marrow examination : dry tap – marrow is hypocellular with increased yellow marrow (fat content).

Treatment : Prognosis of untreated anemia is very poor (75% fatal ). It is based on identifying & removing the causative agent and providing the supportive care. Bone marrow transplantation. Immunosuppressive therapy with Anti Thymocyte Globulin (ATG) & Cyclosporine. ATG is a horse serum that contains polyclonal antibodies against human T Cells. This therapy is partially beneficial & avoids transfusion.

SICKLE CELL DISEASE Sickle Cell Disease is a group of inherited, autosomal recessive disease characterized by the presence of abnormal form of Hemoglobin in the Erythrocyte. It is a group of disorder that cause red blood cells to become mishappen and break down. It is a genetic disorder in which red blood cells bend out into a sickle shape.

In this condition, the abnormal hemoglobin ( HbS ) causes the erythrocyte to stiffen & elongate taking on a sickle shape. It results from substitution of Valine for glutamic acid on β globin chain of Hemoglobin on Chromosome 11. Sickle cell disease is identified during infancy or early childhood. It is an incurable disease. It is commonly seen in African americans , 1 in 350 to 500 live births.

Types of Sickle Cell Disease : Sickle cell Anemia Sickle cell – Thalassemia Sickle cell – HbC disease Sickle Cell Trait

1. Sickle Cell Anemia It is the most severe form. It occurs when a person is Homozygous for Hemoglobin S, The person has inherited HbS from both parents. 2 & 3. Sickle cell – Thalassemia & Sickle cell – HbC disease It occurs when a person inherits Hb S from one parent & another type of abnormal Hemoglobin (such as Thalassemia or Hb C) from another parent. Both the above forms are not common & are less severe.

4. Sickle Cell Trait It occurs when a person is Heterozygous for Hemoglobin S, the person has inherited Hemoglobin S from one parent & normal Hemoglobin from the other parent. It is typically a very mild to asymptomatic condition.

Clinical Manifestations : Pallor Decreased activity tolerance Jaundice Primary symptom is pain, which is severe and affects back, chest, extremities and abdomen. Damaged vision : the sickled blood cells affect the blood vessels that connect to retina, causing optimal damage. Limited Growth : the scarcity of oxygen caused by sickled cell anemia is detrimental to healthy human growth.

Diagnostic Studies : History collection & Physical examination Peripheral blood smear Sickling test Electrophoresis X – Ray (preferably long bones) Doppler studies MRI

Complications : SYSTEM DISEASE CONDITIONS Respiratory system Pneumonia, Pulmonary Hypertension, Acute Chest syndrome Cardio Vascular system Myocardial Infarction, Congestive Heart failure, corpulmonale Opthalmic Retinal Hemorrhage , scarring & detachment, blindness, Musculo – Skeletal system Osteoporosis, Osteosclerosis Neurologic Cerebro vascular accident Others Renal failure, chronic leg ulcers, Priapism

MANAGEMENT : No specific treatment for this disease. Treatment mainly focuses on alleviating the symptoms & minimizing the end stage organ damage. Instruct to avoid high altitude, maintain adequate fluid intake and treat infections promptly. If leg ulcers are present, treat them with adequate bed rest, antibiotics, warm saline soak, mechanical debridement and grafting. Acute chest syndrome treated with broad spectrum antibiotics, oxygen administration & fluid therapy. Continued ……………….

MANAGEMENT : Oxygen therapy Fluid therapy / administration Transfusion therapy Pain management Anti Sickling agents ( Hydroxy urea)

ANEMIA DUE TO BLOOD LOSS : It can be occurred due to Acute blood loss Chronic blood loss Etiology : Trauma Complications of Surgery Conditions or diseases that disrupt vascular integrity

CLINICAL MANIFESTATIONS : Volume lost 10% : No identified features or display of symptoms. Volume lost 20% : No detectable signs or symptoms at rest. Tachycardia with exercise & mild postural hypotension. Volume lost 30% : Postural hypotension & Tachycardia at exercise. Volume lost 40% : Blood pressure, Central venous pressure & cardiac output below normal at rest, Rapid thready pulse, cold & calmy skin. Volume lost 50% & above : potential shock & death. Internal hemorrhage causes pain in abdomen.

MANAGEMENT : IV Fluids : Dextran, Albumin, Hetastarch and Crystalloid electrolyte solutions like Ringer’s Lactate, etc.. Blood Transfusion (packed RBC) may be needed, if the blood loss is significant. If the bleeding is related to platelet or clotting disorder, replacement of the deficiency is addressed. Supplemental Iron is prescribed on regular basis.

NURSING MANAGEMENT : Impaired tissue perfusion related to decreased cellular components required for the delivery of Oxygen to the cells. Activity intolerance related to weakness, imbalance between oxygen supply and demand. Imbalanced nutrition, less than body requirement related to poor nutritional intake, failure to digest or absorb food necessary for the formation of blood cells . Hypoxemia related to decreased hemoglobin . High risk for infection related to inadequate secondary defence (Leukopenia). Ineffective therapeutic regimen management related to lack of knowledge, exposure & inadequate interpretation of information.

THANK YOU