Anemia complication
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Anemia complication Presentation Transcript

  • 1. ANEMIA COPLICAITONS  Aymen fathi zemmal (10110068)
  • 2. CONTENTS SOEPEL  introduction  ANEMIA, difinition, types, causes, pathophysiology, clinical features.  Complications.  Investigations and diagnosis.  Management and treatment.  Prognosis.  References. 
  • 3. SOEPEL Saleh ahmed 86 years old mele saudi from oneiza unembloyed, feeling severe pain tightness of chest started since 3 years, every two months come to hospital to transfute 3 to 4 blood units his chest pain sudden not continuous and not radiated ,sharp relieved by blood transfusion.  His past history medical: hypertension, DM2, since 4 years, heart attack, edema due to nephropathy, develop episodes of mild  jaundice. surgical: left eye lazer. medications: all orally for hypertension, DM2, diuretics,
  • 4. No allergies.  Family history: informant is his son 68 years old with DM2  and his dauter and most of family members have DM2 and hypertension. that’s why should we alwaysadvice to avoid mariage from relatives. o social history: 1 packet half of packet 1 cigareete. review of systems: Respiratory: due to his last episode most doctors to make sure of lungs by auscultation. Due to multiple chest pain shortness of breath and hypoxia. GI: little neausea, no vomiting, no loss of wieght, urination is normal. There is change in bowel habit 1 to 2 per day. dark bloody feces with mucus.
  • 5. SOEPEL Hitory taking  GE: vital signs and alarm signs.  Abdominal examination and respiratory examination.   Elaboration:DD: colon polyp, diverticulitis and colorectal carcinoma.  Plan: investigation: CBC, ECG, stool, edonscopy to look for UGI bleeding LGI bleeding. elaboration:blood transfusion, hydroxycarbamide, learning goals: anemia complications.
  • 6. GENERAL ASPECTS  Blood consist of  erythrocytes 120 days. White cells. Platelets 2 days. Plasma.    blood formation where does it occur(hematopoeisis)?  Bone marrow.  Liver. .spleen. Lymph nodes. Thymus. what occur in patient of anemia? Which is affect in function? hemoglobin performs the main function of RBCs by carrying oxygen to tissues and returning CO2 from the tissues to lungs. the convave shape allow the RBCs to uptake O2 and release CO2. Normal value of hemoglobin is ………………….
  • 7. charac teristi cs  Anemia:is present when there is decrease level of hemoglobin in blood depending on the sex and age of the individual. Clinical features: Symptoms: Common is fatigue, headache and faintness. After complication or long term disease:  Breathlessness.  Angina.  Interminet claudication.  Palpitations. Main fraction of body weight Volum e in adult body PH 8% Female:4-5 L. Male: 5-6 L. 7.35- 7.45 hemog Female: 12-16 g/dl. lobin Male:13-18 g/dl.
  • 8. CLINICAL FEATURES
  • 9. CLINICAL FEATURES  Signs       pallor of extremeties, face, conjuctive. Central cyanosis of tongue and lips. Cholinychia (spoon shape of nails). Tachycardia. Systolic flow murmur. Cardiac failure.
  • 10. TYPE AND CAUSES OF ANEMIA  Microcytic anemia: most cause is iron deficiency due to 1- limited ability of body to absorb iron. 2- frequent loss of iron due to hemorrhage. chronic disease ex: infection tuberculosis, chronic inflammatory disease chron’s disease. Sideroblastic anemia: inherited or acquired.  Normocytic anemia: seen in chronic disease such as 1- endocrine disorders( hypopituitarism, hypothyroidism and hypoadranalism) 2- hematological disorders(aplastic anemia wether primary congenital or secondary due to chemical or certain drugs. 3- seen acutely following blood loss.
  • 11.  Macrocystic anemia: 1-megaloblastic anemia: defect in DNA synthesis in bone marrow thereby affecting: B12 metabolism or causeing deficiency leading to perncicious anemia . Folic acid dificiency or abnormal folate metabolism. 2- non-megaloblastic anemia: physiological cause:      Alcohol excess. Liver disease. Hypothyroidism. Hematolological disease. Drugs.
  • 12.  Which type of anemia?
  • 13.  Sickle cell anemia: single base mutation of adenine to thymine. Mostly in african population. Inherited from both parents.
  • 14. COMPLICATIONS OF ANEMIA Long term problems lead to complications:  every organ is involved.  growth and development: children below normal weight > delayed sexueal maturation > hormone therapy.  Bones: hip joint replacement may be required due to vaso-occlusion episodes leading to chrinic infarcts.  Infection: more common in the tissues which vasoocclusion occur ex: bones, lungs and kidney.  Respiratory: shortness of breath, chest pain and hypoxia > death 
  • 15. Leg ulcers.  Cardiac problems: cardiomegaly. arrhythmias and iron overloaded cordiomegaly. myocardial infarction due to thrombotic episodes not secondary to atheroma.  o o o neurological: in 25% of patients. Cholelithiosis: pigment stones occur as a result of chronic hemolysis. Liver: chronic hepatomegaly.
  • 16. COMPLICATIONS o Renal: chronic tubulo-interstitial nephritis Priapism: unwanted painful erection due to vasoocculsion.  Eye: retinopathy > yearly eye check is required.  Pregnancy: impaired placental blood flow causes spontaneous abortion. intrauterine growth retardation. preclampsia and fetal death o
  • 17. INVESTIGATIONS blood counts.  Blood films.  Sickle solubity test  Hb electrophoresis: always needed to confirm the diagnosis. 
  • 18. MANAGEMENT AND TREATMENT  Patient survive longer with better treatment. Blood transfusion should be given only for clear indications. Ex: surgery, heart failure , painful episodes without complications and in cases of complications.  Hydroxycarbamide is first drug for sickle anemia to reduce the episodes of pain.  Bone marrow transplantation. 
  • 19. PROGNOSIS Some patients with Hb SS die in the first few years of life.  There is indivisual variation in the severity of the disease.  Some patients have normal lifespan with few complication. 
  • 20. REFERENCES