Beruflich Dokumente
Kultur Dokumente
OBJECTIVES
To be able to do a proper history taking and physical examination on a patient presenting with anemia To be able to give a differential diagnoses to arrive at a primary diagnosis To be able to present the proper work up and management for anemia
OUTLINE
I. CASE PRESENTATION II. DISCUSSION OF ANEMIA
ANEMIA CASE
General Data R.E. is a 51 year old, Roman Catholic, married male, residing at San Pedro, Laguna who came in with a chief complaint of weakness.
Chief complaint
weakness
Family History
Father Unkown Mother Hypertension, DM, Cancer
ROS
General: (+) significant weight loss (documented,lost 50 lbs since December, 2011), (+) weakness, (+) fatigability, no fever. Skin: (+) pale hands and feet, no flushed skin, no rashes, no lumps Head: no headache, no dizziness, no head injury, no lightheadedness Eyes: no pain, no redness, no excessive tearing no blurring of vision,
ROS
Ears: no hearing problems, no tinnitus, no vertigo, no earaches Nose: (+) colds, no discharge, no epistaxis Throat: no sore throat, no hoarseness Respiratory: no cough, no shortness of breath Cardiovascular: no chest pain, no palpitations, no pnds Gastrointestinal: no changes in stool caliber
ROS
Genitourinary: no nocturia, no polyuria, no dribbling Musculoskeletal: no pain, no stiffness, no arthritis, no gout Nervous System: no loss of consciousness, no paralysis
Physical Examination
General: awake, conscious, coherent, not in cardiorespiratory distress, and cooperative. Vital Signs:
sitting BP-120/80 HR- 76 supine 130/80 HR-80
Ht.- 56
BMI- 23 - Normal
Physical Examination
Skin- (+) pale, (-) petechiae, no lesions, no rashes and cold to touch on both hands and feet, (+) pale nail beds HEENT- (+) pale palpebral conjunctivae, anicteric sclerae, no hearing disabilities, no discharge, no septal deviation, no obstruction, no sinus tenderness, no lump ,no mass no mass, Neck veins not distended, JVP at 7cm at 45deg, no cervical lymphadenopathy
Physical Examination
Chest- No scars, No lesions, symmetrical chest expansion, No retractions, equal tactile fremitus, Both lung fields resonant to percussion, clear breath sounds, (-)crackles, all lung fields, (-) wheezing, (-) ronchi Heart- adynamic precordium, normal rate, regular rhythm, S1>S2 at the apex, S1<S2 at the base, PMI heard at 5th ICS MCL, no heaves, no thrills, no murmurs
Physical Examination
Blood Vessel- full, equal pulses Abdomen- flat, normoactive bowel sounds, no bruit, tympanitic on all quadrants, no shifting dullness, no fluid wave, Traubes space not obliterated, Liver span at 8cm, (+) direct epigastric tenderness, Liver edge smooth, No mass palpated. Extremities- Full and equal pulses, no cyanosis, no clubbing, no edema Neurological- CN intact
Subjective 54 year old Male From Surigao Body weakness epigastric pain sudden in onset characterized as humihilab occuring any time of the day unaffected by food intake pain scale of 10/10 radiating to the whole abdomen continuous unrelieved by medication (+) DM Type II, Controlled (+) weight loss of >10%, fatigue, night sweats (+) changes in bowel movement 4days PTA (-) bleeding, fever, diarrhea, changes in stool caliber,
Objective VS: BP- sitting 120/80, SALIENT FEATURES HR 76 supine 130/80, HR 80 RR-20 temp- 36 Wt- 60kg Ht.- 56 BMI- 23 - Normal PE: (+) Pale palpebral conjunctivae, Pale nailbeds (+) Direct epigastric tenderness (-)cyanosis, no clubbing, Lymphadenopathy, Splenomegaly,Petechiae
(+) NSAID Use for 20 years, epigastric pain, pale skin color, shortness of breath and weakness,
INITIAL IMPRESSION
ANEMIA SECONDARY TO GI BLEEDING
FINAL DIAGNOSIS
ANEMIA SECONDARY TO GI BLEEDING
Reticulocyte Count
ANEMIA
The physiologic response to anemia varies according to acuity and the type of insult. compensatory mechanisms to take place In the medullasympathetic outflow is enhanced, while parasympathetic activity is diminished. Increased sympathetic outflow norepinephrine release from sympathetic nerve endings and discharge of epinephrine and norepinephrine from the adrenal medulla.
ANEMIA
Sympathetic connection to the hypothalamic nuclei increases antidiuretic hormone (ADH) secretion from the pituitary gland. ADH increases free water reabsorption in the distal collecting tubules. In response to decreased renal perfusion, juxtaglomerular cells in the afferent arterioles release renin into the renal circulation, leading to increased angiotensin I, which is converted by angiotensin-converting enzyme (ACE) to
ANEMIA
strictly defined as a decrease in red blood cell (RBC) mass. accomplished by using hemoglobin (Hb), a tetramer protein composed of heme and globin. impairs the bodys ability for gas exchange by decreasing the number of RBCs transporting oxygen and carbon dioxide
ANEMIA
a symptom that requires investigation to determine the underlying etiology. Often, practicing physicians overlook mild anemia. quantified by measurement of the RBC count, Hb concentration, and hematocrit (Hct)
ANEMIA
Signs
General pallor (pale skin, mucosal linings andnail beds) koilonychia (in iron deficiency), jaundice bone deformities leg ulcers
Signs
severe anemia tachycardia bounding pulse cardiac ventricular hypertrophy signs of heart failure
Classification of Anemia
I. Etiologic Classification 1. Impaired RBC production 2. Excessive destruction 3. Blood loss II. Morphologic Classification 1. Macrocytic anemia 2. Microcytic hypochromic anemia 3. Normochromic normocytic anemia
1. Abnormal bone marrow 1.1 Aplastic anemia 1.2 Myelophthisis : Myelofibrosis, Leukemia, Cancer metastasis 2. Essential factors deficiency 2.1 Deficiency anemia : Fe, Vit. B12, Folic acid, etc 2.2 Anemia in renal disease : Erythropoietin 3. Stimulation factor deficiency 3.1 Anemia in chronic disease 3.2 Anemia in hypopituitarism 3.3 Anemia in hypothyroidism
3. Blood Loss
1. Acute blood loss : Accident, GI bleeding 2. Chronic blood loss : Hypermenorrhea Parasitic infestation
MCV > 94 MCHC > 31 1. Megaloblastic dyspoiesis 1.1 Vit. B12 deficiency : Pernicious anemia 1.2 Folic acid deficiency : Nutritional megaloblastic anemia, Sprue, Other malabsorption 1.3 Inborn errors of metabolism : Orotic aciduria, etc. 1.4 Abnormal DNA synthesis : Chemotherapy, Anticonvulsant, Oral contraceptives
1.
2.
3.
4.
MCV < 80 MCHC < 31 Fe deficiency anemia : Chronic blood loss, Inadequate diet, Malabsorption, Increased demand, etc. Abnormal globin synthesis : Thalassemia with or without Hemoglobinopathies Abnormal porphyrin and heme synthesis : Pyridoxine responsive anemia, etc. Other abnormal Fe metabolism :
6.
7.
Treatments
depend on severity and cause. Iron deficiency from nutritional causes is rare in men and postmenopausal women. diagnosis of iron deficiency mandates a search for potential sources of loss, such as gastrointestinal bleeding from ulcers or colon cancer. Mild to moderate iron-deficiency anemia is treated by oral iron supplementation with ferrous sulfate, ferrous fumarate, or ferrous gluconate.
Treatments
Vitamin supplements given orally (folic acid) or intramuscularly (vitamin B12) will replace specific deficiencies. In anemias of chronic disease, associated with chemotherapy, or associated with renal disease, some clinicians prescribe recombinant erythropoietin or epoetin alfa, to stimulate RBC production. In severe cases of anemia, or with ongoing blood loss, a blood transfusion may be necessary.
Treatments
Blood transfusions
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