Sample Write-up ‘Name: School: Date: (RR. Topic: Anemia CHIEF COMPLAINT: Generalized weakness x I day HISTORY OF PRESENT ILLNESS: 73 yo Italian female brought in by the ambulance fo the emergency room en 3/29/07 with c/o of weakness x 1 day. Yesterday, the patient woke up and felt weak, She felt so weak that she could barely stand up. Despite staying in bed, the patient’s weakness lasted the whole day with associated symptoms of lightheadedness, headaches, SOB, and chest discomfort. Moreover, the patient had associated digestive problems such as nausea, vomiting (at night of the same day, with no blood), and reflux. The patient did eat last night, she ate a cookie with milk. Digestive problems were not associated with what she ate as she had these before eating. The patient's last bowel movement was reported to be loose and dark (no blood noticed by the patient). The patient has regular but poor appetite. She has been losing weight (20 Ibs since January 2007). Patient and patient’s daughter denies that the patient had a change in mental status, loss of consciousness, chest pain, palpitations, chills and fever. The patient has been battling with these episodes of weakness and digestive problems since February 3, 2007 which by then she was diagnosed with arteriovenous malformation in the jejunum and AML (Acute Myclogenous Leukemia). The patient has, therefore, been in and out of Methodist hospital numerous times and hhas been receiving multiple blood transfusions for repeated decrease in the patient’s hemoglobin levels Note: You MUST indicate how Jong the patient has had each illness PAST MEDICAL HISTORY: Adult Illnesses: AV malformation in jejunum and AML (February 3, 2007); DM (7-8 yrs duration); Depression (February 2007); GERD (February 2007) ‘Trauma: Wrist fracture (15 yrs ago) Operations/Hospitalizations: frequent hospitalizations due to decreasing hemoglobin in Methodist Hospital (Feb 2007); Hysterectomy (44 yo) Transfusions: numerous Drug sensitivities/Allergies: Sulfur MEDICATIONS? List each medication including dose, Metformin 500 mg po Q12 (every 12 hrs) route of administration, and frequency Glybride 2.5 mg po Q12 eee ‘Nexium 40 mg po daily Megace 40 mg/ml soln 2 tsp daily Ondansetron 4 mg po Q8 Mirtazapine 15 mg po dailyInclude ALL family member) (mother, father, siblings) ages | and related illnesses or cause of death, FAMILY HISTORY: Mother 86 yo deceased (DM) Father 82 yo deceased (unknown) Sister 70 yo alive (Rheumatoid Arthritis) Brother 46 yo deceased (DM complications) SOCIAL HISTORY: Occupation: currently retired, previously sales clerk since Jan 2007 Denies serving in the military Lives in House alone Level of activity: Sedentary since February 2007 (before Patient was working) Level of activity: Patient uses a walker Eats Regularly, Poor Appetite Past smoker: Ippd for 50 yrs, quit just a month ago Denies alcohol use presently and in the past. Denies recreational drug use presently and in the past Be sure to include at least THREE (3) symptoms for each review of systems. REVIEW OF SYSTEMS: General Ficalth: 73 yo Italian female who feels overall progressively ill after her first episode of weakness and digestive problems in February 3, 2007. Patient sees her primary care provider, Dr. __. forher general health maintenance. She also sees a Hem-One physician for her AML. Patient denies polyuria, urgency and polydipsia. No reported heat/cold intolerance. Denies snoring or sleep apnea, but she does have problems sleeping at times. Patient has been losing weight (20 Ibs since january 2007). Skin, Hair, Nails: Denies any rashes, itching, lesions, lumps, bruises. Head, Neck: Denies vertigo and loss of consciousness. Reports lightheadedness and intermittent headaches. Eyes: Patient wears glasses (everyday use). Denies tearing, itching, redness, diplopia, blurry vision Ears: Denies bilateral hearing loss. Denies earache or discharge. ‘Nose: Denies discharge, stuffiness, epistaxis, sneezing. Mouth, Teeth: Denies denture use, bleeding gums, ulcers, dental problems. ‘Throat: Denies hoarseness, dysphagia, sore throat. Chest: Denies chest pain and tightness, palpitations, pinpoint tenderness, masses. Reports chest discomfort. Respiratory: Denies wheezing, hemoptysis, night sweats. Reports SOB Cardiae: Denies CP, palpitations, orthopnea, dyspnea or syncope. Reports chest discomfort. Vascular: Denies cyanosis and spasms, leg swelling, claudication GI: Reports nausea, vomiting, and regurgitation. Denies diarrhea, dyspepsia, acidic taste in ‘mouth, and abdominal pain. GU: Denies urgency, frequency, dysuria, hematuria, genital sores, and discharge. Neurological: Denies loss of consciousness, tremors, shaking spells, ticks, incoordination, paresthesias, aphasia, numbness, tingling of hand or feet, falls, Musculoskeletal: Reports generalized muscle weakness. Denies muscle cramps, decreased ROM, joint swelling, erythema, heat, joint pain in elbows Hematological, Lymphatic: Denies petechiae, purpura, and bruises. Reports hx of anemia 7Endocrine: Denies polyuria, polydipsia, polyphagia, night sweats, heat/cold intolerance, chills. Psychiatrie: Denies unusval perceptions. »ightmares, hallucinations, mood disturbance, poor memory, poor judgment, ill affect, suicidal/ homicidal ideation. Reports depression since first episode of weakness (February 3, 2007) Vital Signs: BP: 137/66 in left arm, Radial pulse: 137bpm, regular bilaterally and symmetrically while sitting upright. Respiration 22 normal breaths per minute. Temperature: 97.7F degrees. Height $°3 and weight 55 kg. General Appearance: Pleasant 73 yo Italian female, awake, alert, and oriented to time, place, and person. She appears weak, pale and ill. Patient is cooperative. Skin, Hair, Nails: Skin is warm and moist. No lesions, ecchymosis, jaundice. rash, Fingemails and toenails appear healthy Head: Normocephalic, no deformities, no lumps on the scalp were felt. Eyes: Pupils are equal and round, reactive to light. Accommodation bilaterally was not noted No signs of jaundice. No funduscopic exam performed. Conjunctiva pale pink, anicteric, no nystagmus. Normal extemal ocular structures and normal papillary reflex were present. No lid lag or strabismus was notes. Ears: Symmetric. Tragus, antitragus, pina free of abnormalities, canal patent drums intact, and no signs of inflammation or effusion. Hearing grossly intact bilaterally. Nose: Smell intact, turbinates pale pink, no polyps. lesions, epistaxis, or discharge. The septum is in the midline and free of erosions or excoriations. No frontal or maxillary sinus tenderness. Mouth, Teeth: Tongue and lips are dry, non-irritated gums, no sores or ulcers. Good dentition, Throat: No exudates, no erythema no swelling. Neck: supple, full range of motion, no bruits, no asymmetry. Trachea is in the midline. No palpable lymph nodes. Swallowing mechanism is intact. Carotid pulses are normoreactive and without bruits Lymphaties: no palpable lymph nodes. Breast/Chest: Chest is symmetrical free of deformities with normal expansion and contraction ‘on deep breathing. Breathing was abdomino-thoracal without the use of any accessory muscles. There is no palpable tenderness or masses, normal tactile fremitus, no dullness to percussion and descent of the diaphragm posteriorly is normal. Breast exam was not performed. ‘Lungs: Normal, clear, resonant sounds were heard in all lung fields bilaterally. Rales, wheezes, stridor absent in both anterior and posterior lung fields. Heart: No visible precordial impulses, thrills, apical heave, RV lift or parasternal heave. Normal SI and $2 are heard. S3 and $4 are not heard. Heart rate is fast but of normal rhythm. No splitting or loud P2. No murmurs, rubs, heaves, or gallops heard. “Abdomen: +BS, sofi, non-tender, Relaxed when recumbent. Normal contour. Auscultation reveals normoreactive bowel sounds in all four quadrants, no bruits. There are no masses or organomegaly to palpation. Percussion reveals no organomegaly or masses. Reetal: 3/29/07 FOBT + Genitourinary: normal hair distribution, extemal genitalia normal appearance, no lesions, excoriations, erythema of the skin, no deformities, non-tender, free of masses. Groin no masses or ymphadenopahty. Extremities, Muscle strength upper and lower extremities are symmetrical. DTRs are reactive and equal upper and lower extremities. No pathological reflexes are noted. No 8heat or deformities of any joints or muscles. Pulses are regular, full, and without bruits. No masses are palpable, No masses or areas of tenderness are palpable. No clubbing. cyanosis or edema, pulses 2+ all 4 extremities, motor 5/5 all extremities. Back, Spine: CVA tendemess was not present. No signs of scoliosis or kyphosis. Spine had normal contour. No deformities, no erythems present. Neurologic, Psychiatrie: AAOx3, CN II-XII grossly intact, no motor or sensory deficit, no iremors. All reflexes are 2+. The patient shows good judgment, orientation, memory, concentration, affect and cognition LABS: cBc: WBC: 79.0HH Neutrophils: 7 Myelocytes 2H HB: 46LL Band Neutrophil: 2 Promonocyte 27 HCT: 14.7LL. Lymphocytes: 3i Nucleated RBC 4H PLT: 69L Monocytes: 1H ‘Amylase 30 MCV: 84.5 Blast: 20H Lipase 17 RDW: 16.3 Myoglobin 24 CHEM. Liver Profile: Ne 141 AST/ALT: 27/14 : STRAW K; 42 ALP: 71 Clear ch 107 GGT: 42 C02: 16L LDH: 1153H pH: 5.0 BUN: 25 Bilirubin Total: 0. Sugar: negative & 1.0 Bilirubin Direct: 0.1 Ketones: 1+ Glucose: 210H Protein: 5.7L. Hb: negative Ca 95 TSH: 2.34 Free T4: 1.09 Bilirubin: negative Mg: 2.2 HeA1C: 6.2H Leukocyte esterase: negative Ph: 6.3H Urobilinogen: 0.2 Protein: trace Pr 15.2H INR 16H PIT: 23.0 BNP: 148.7H. Troponin 0.35H, 1.03H, 0.95H, 0.76H, 0.68H, 0.42H, 0.29H, 0.19 by 4/2/07 CK.CPK 21L ‘ABO type B Rh - Ab- Blood cultures (3/29/07) no growth for 5 days Urine cultures (3/29/07) negative Imaging CXR (3/29): Hyperaeration bilaterally. No acute infiltrates. Atherosclerotic Aorta CXR (4/1): resolving CHP EKG (3/16): Sinus tachycardia at 131 bpm, slopped ST U1, IIl, AVF, V4, VS EKG (4/3): Normal Sinus Rhythm at 70 bpm, T-wave abnormality. Inferior Ischemia Echo (3/31): 58% EF with adequate LV functionDISCUSSION/DIFFERENTIAL DIAGNOS! Assessment 73 yo female with c/o weakness x 1 day Working Diagn GI bleed secondary to arteriovenous malformation (AVM) in jejunum Arteriovenous malformations are congenital lesions composed of a complex tangle of arteries and veins connected by one ot more fistulae. The vascular conglomerate is called the nidus. The nidus has no capillary bed, and the feeding arteries drain directly to the draining veins. The genetic transmission patterns of AVM are unknown. Abnormal connections between the arteries and veins sometimes form in the stomach and in the small and large intestines. These abnormal blood vessels are fragile and are likely to rupture and bleed intermittently, sometimes heavily, especially in older people. Symptoms of GI bleeding include vomiting blood (hematemesis), passing black tarry stools (melena), and passing visible blood from the rectum (hematochezia) People with long-term bleeding that tend to occur in small amounts or intermittently may develop symptoms of anemia, such as tiring easily and looking unnaturally pale. Extremely large |AVMs may present with low platelet count (due to turbulence and trapping of platelets), and ‘occasionally, with laboratory findings of consumptive coagulopathy such as low platelets, elevated prothrombin time (PT) and partial thromboplastin time (PTT), increased bleeding time, and low fibrinogen. The majority of arteriovenous malformations can be managed and controlled medically. Only a few AVMs demonstrate progressive growth and require surgical intervention. The patient being cared for has a previous medical history of AVM in her jejunum which have caused her to be frequently hospitalized in order to receive multiple blood transfusions. The patient's clinical manifestations of weakness and dark stools along wi physical lab findings of low platelets and elevated PT suggest that she is suffering from a GI bleed that is attributed to her AVM You must include AT LEAST seventeen (17) differential diagnoses. Differential Diagnosis: Anemia 1, Iron Deficiency Anemia 2. Anemia of Chronic disease 3. Thalassemia 4, Sideroblastic Anemia 5. Folate deficiency 6. B12 deficiency/Pemicious Anemia 7. 8. 9 Sickle cell disease Hereditary spherocytosis Paroxysmal nocturnal hemoglobinuria 10. Glucose-6-Phosphate Dehydrogenase Deficiency (G6PD) 11. Autoimmune hemolytic anemia 12, Microangiopathic hemolytic anemia 13, Chronic Renal Failure 14, Alcoholic Liver disease 15, Malaria 16, Aplastic anemia 17. Acute/Chronic Blood Loss 18, Acute Myeloid Leukemia 101) R/O Iron Deficiency Anemia Iron deficiency anemia is the most common form of anemia, and the most common cause of microcytic anemia. Iron deficiency anemia occurs when the dietary intake or absorption of iron is insufficient, and hemoglobin, which contains iron, cannot be formed. Anemia develops slowly afer the normal stores of iron have been denleted in the body and in the bone marrow The principal cause of iron deficiency anemia in premenopausal women is blood lost during menses. In men and postmenopausal women, anemia is usually caused by gastrointestinal blood loss associated with ulcers, the use of aspirin or NSAIDS, or certain types of cancer (esophageal, stomach, colon). Iron deficiency anemia is characterized by pallor, fatigue and weakness. Because it tends to develop slowly, adaptation occurs and the disease often goes unrecognized for some time. In severe cases, dyspnea can occur. Unusual obsessive food cravings, known as pica, may develop. iron levels were not monitored in the patient at hand, but it is possible that the patient can be suffering from iron deficiency due to her GI bleed. Nevertheless, the patient's MCY levels are not low enough 10 qualify as microcytie anemia. Write 1-2 summary statements explaining why each differential diagnosis can be ruled out. 2) R/O Anemia of Chronic disease Chronic disease often leads to anemia, especially in older adults. Conditions such as infections, inflammation, and cancer particularly suppress production of red blood cells in the bone marrow. Since the suppression is usually not severe, anemia develops slowly and is evident only after time. Because the bone marrow is unable to use stored iron in the developing red blood cells, this type of anemia is often referred to as iron-reutilization anemia. Because this type of anemia develops slowly and is generally mild, it usually produces few or no symptoms. When symptoms do occur, they usually result from the disease causing the anemia rather than the anemia itself. There are no specific laboratory tests, so the diagnosis is typically made by excluding other causes. Because no specific treatment exists for this type of anemia, physicians usually treat the underlying cause. Taking iron supplements or vitamins generally does not help. (On the rare occasion that the anemia becomes severe, transfusions may help. The patient being cared for has been recently diagnosed with two major chronic illnesses (AVM and AML). This differential is therefore possible in this patient. On the other hand, the patient's MCV levels are not low enough to qualify as microcytic anemia. 3) R/O Thalassemia Thalassemia is a recessive trait inherited disease of the red blood cells. In thalassemia, the genetic defect results in reduced rate of synthesis of normal globin chains. The thalassemias are Classified according to which chain of the globin molecule is affected: in alpha (a) thalassemia, the production of « globin is deficient, while in beta (B) thalassemia the production of B globin is defective. Alpha thalassemia is a decrease in a-globin chain synthesis on chromosome 16 due to gene deletions. Beta thalassemia syndromes are characterized by a genetic deficiency in the synthesis of B -globin chains, In the homozygous state, beta thalassemia (thalassernia major) causes a severe, transfusion-dependent anemia in which both beta chains are mutated. In the heterozygous state, the beta thalassernia trait (thalassemia minor) causes mild-to-moderate microcytic anemia in which one beta chain is mutated. Both major and minor lead to an imbalance of alpha to beta globin chains, leading to ineffective erythropoiesis and even severe microcytic hypochromic anemia, The excess alpha chains aggregate and form precipitates that damage red cell membranes, leading to intravascular hemolysis. Premature destruction of erythroid precursors results in intramedullary death and ineffective erythropoiesis. The severe ulanemia is generally associated with erythroid hyperplasia and extramedullary hematopoiesis. The patient at hand hes ne know family history of thalassemia. Moverover, the patient's MCV is not low enough to qualify as a microcytic anemia. Thvs, thalassemia is an unlikely cause of the patient's anemia 4) R/O Sideroblastic Anemia The three causes of Sideroblastic anemia that are most known are lead poisoning (the most common), aleohol, and vitamin B6 deficiency. The symptoms of lead poisoning include neurological problems, such as reduced IQ, nausea, abdominal pain, irritability, insomnia, excess lethargy, hyperactivity, headache, foot/wrist drop. or in extreme cases seizures and/or coma. There are also Gl problems associated with lead poisoning, including constipation, diarrhea, abdominal pain, vomiting, poor appetite and weight loss. Lead toxicity can also cause “Burton’s line,” which is a bluish line along the gums. Microscopically, red blood cell stippling is evident, as well as microcytosis and hypochromia. It is unlikely that this patient is suffering from sideroblastic anemia as she has no risk factors/exposures as well as no significant past medical history that would suggest this differential. Moreover, the patient does not demonstrate neurological problems present in this differential. 5) R/O Folate deficiency Folate deficiency results from a deficiency of folic acid in the diet. Many plant and ‘animal tissues contain folic acid, especially green leafy vegetables, yeast, liver, and mushrooms. If overcooked, however, then these are not good sources of folate. Alcohol interferes with folic acid’s intermediate metabolism and absorption. Folic acid deficiency may develop in long-term anticonvulsant therapy or with use of oral contraceptives. Folate deficiency leads to macroeytic anemia and megaloblastic anemia. It is indistinguishable from vitamin B12 deficiency in peripheral blood and bone marrow findings. However, the neurological lesions seen in B12 deficiency are not characteristic of folate deficiency. This is not a possible differential in this patient who has a normal MCV. 6) R/O B12 deficiency/Pernicious Anemia The most common cause of B12 deficiency is pemicious anemia, which is a chronic illness caused by impaired absorption of B12 due to the absence of intrinsic factor (IF) in gastric secretions. Pemicious anemia is associated with gastric atrophy and a subsequent loss of IF production. It can also occur in a congenital autosomal recessive form in which IF production is lacking, but without gastric atrophy. Other disorders that interfere with the absorption and metabolism of B12 can produce cobalamin deficiency, leading to a macrocytic anemia that is associated with neurological complications—these include demyelination and irreversible nerve cell death, Symptoms include numbness or tingling of the extremities and an ataxic gait, a syndrome known as subacute combined degeneration of the cord. Although the patient's B12 levels were not checked, the patient’s MCV levels were not elevated. 7) RIO Sickle cell disease Sickle cell disease is a general term for a group of genetic disorders caused by sickle hemoglobin (Hgb S or Hb S). In many forms of the disease, the red blood cells change shape, upon deoxygenation because of polymerization of the abnormal sickle hemoglobin. ‘Ihis process damages the red blood cell membrane, and can cause the cells to become stuck in blood vessels. This deprives the downstream tissues of oxygen and causes ischemia and infarction. The disease ‘hronic and lifelong. Individuals are most often well, but their lives are punctuated by periodic painful attacks. In addition to periodic pain, there may be damage of internal organs, such as 12stroke. Lifespan is often shortened with sufferers living to an average of 40 years. Sickle-cell disease occurs more commonly in people (or their descendants) fcom paris of the world such as sub-Saharan Africa, where malaria is or was common, but it also occurs in people of other ethnicities. Sickle cell anemia can lead to various complications such as acute chest syndrome, which is a life-threatening condition characterized by chest pain, shortness of breath, fever, hypoxemia and pulmonary infiltrates on chest X-ray. It can be triggered by pain crisis, respiratory infection, bone-marrow embolization, or possibly by atelectasis, such as can be caused by opiate administration, or surgery. The patient at hand, however, does not have a history of sickle cell disease and this is therefore of very low suspicion 8) R/O Hereditary spherocytosis Hereditary spherocytosis is a genetically-transmitted form of spherocytosis, an auto-hemolytic anemia characterized by the production of red blood cells that are sphere-shaped rather than donut-shaped, and therefore more prone to hemolysis. The hallmark is the microspherocyte, which is caused by loss of membrane surface arca, and an abnormal osmotic fragility in vitro. ‘The abnormal membrane (caused by mutated membrane proteins) causes the body to constantly attack and clear these RBC’s, Major complications include aplastic or megaloblastic crisis, hemolytic erisis, cholecystitis and cholelithiasis, and severe neonatal hemolysis. The patient did not have a peripheral blood smear during her stay in the hospital to consider this differential. Nevertheless, she has no organomegaly (specifically, splenomegaly) to highly suggest this differential 9) R/O Paroxysmal nocturnal hemoglobinuria Paroxysmal nocturnal hemoglobinuria (PNH) is a rare, acquired, potentially life- threatening disease of the blood characterised by hemolytic anemia, thrombosis and red urine due to breakdown of red blood cells. PNH is the only hemolytic anemia caused by an acquired intrinsic defect in the cell membrane. A common finding in PNH is the presence of breakdown products of RBC» (hemoglobin and hemosiderin) in the urine. An inconsistent, but potentially life-threatening, complication of PNH is the development of clot in the veins (venous thrombosis). These clots are often found in the hepatic (causing Budd-Chiari syndrome), portal (causing portal vein thrombosis), and cerebral veins (causing cerebral venous thrombosis). The patient at hand does not present with physical findings of red urine and venous thrombosis which would make one highly suspect this differential. 10) R/O Glucose-6-Phosphate Dehydrogenase Deficiency (G6PD) GOPD deficiency is the most common disease-producing enzymopathy in humans. Glucose-6- phosphate dehydrogenase (G6PD) deficiency is an X-linked recessive hereditary disease featuring nonimmune hemolytic anemia in response to a number of causes. The classic reaction to consumption of broad beans has led to the commonly used term favism. It confers protection against malaria, which may account for its high gene frequency. This enzyme is crucial in forming NADPH, which is a required cofactor for maintaining glutathione in its reduced form. The highest prevalence of this deficiency is among African, Asian, or Mediterranean descent ‘Most patients are asymptomatic. Some patients present with a history of neonatal jaundice, often requiring exchange transfusion, A history of infection or drug-induced hemolysis is also common. Gallstones may be a prominent feature, as well as splenomegaly. This differential cannot entirely be ruled out because GOPD levels were not ordered. However, the patient's lack of associated symptoms, such as gallstones and splenomegaly, makes this unlikely:11) P/O Autoimmune hem Autoimmune hemolytic anemia is a type of hemolytic anemia where the body's immune system attacks its own red blood cells (RBCs), leading to their destruction (hemolysis) Antibodies and associated complement system components become fixed onto the RBC surface. These antibodies can be detected with the direct antiglobulin test, also known as the direct Coombs test. Subtypes include warm antibody autoimmune hemolytic anemia (idiopathic, systemic lupus erythematosus, chronic lymphocytic leukemia, methyldopa) and cold antibody autoimmune hemolytic anemia (idiopathic cold hemagglutinin syndrome, infectious ‘mononucleosis, paroxysmal cold hemoglobinuria, lymphoma). Clinical presentation depends on whether the onset of hemolysis is gradual or abrupt and on the severity of erythrocyte destruction. A patient with mild hemolysis may be asymptomatic, In more serious cases, the anemia may be life threatening. Patients can present with angina and cardiopulmonary decompensation. Clinical presentation also reflects the underlying cause for hemolysis. The patient's red blood cells were not being hemolyzed. Therefore, autoimmune hemolytic anemia can be ruled out. 12) R/O Microangiopathic hemolytic anemia Microangiopathic hemolytic anemia is a subgroup of hemolytic anemia caused by several factors in the small blood vessels. The most important causes are thrombotic thrombocytopenic purpura (ITP), hemolytic uremic syndrome (HUS), disseminated intravascular coagulation (DIC), HELLP syndrome and eclampsia, heparin-induced thrombocytopenia (HIT), and severe glomerulonephritis. ‘This differential is identified by the finding of anemia and shistocytes (bite cells) on microscopy of the blood film, Hemolysis is the final event triggered by a large number of hereditary and acquired disorders such as intrinsic membrane defects, abnormal hemoglobins, erythrocyte enzymatic defects, immune destruction of erythrocytes, mechanical injury, and hype-splenisin, As explained previously, the patient's red blood cells were not being hemolyzed. This differential can be ruled ou. 13) R/O Chronic Renal Failure Chronic renal failure is a slowly progressive loss of renal function over a period of months or years and defined as an abnormally low glomerular filtration rate, which is usually determined indirectly by the creatinine level in blood serum. CRF that leads to severe illness and requires some form of renal replacement therapy (such as dialysis) is called end-stage renal disease (ESRD). As the kidney function decreases: blood pressure is increased due to fluid overload and production of vasoactive hormones leading to hypertension and congestive heart failure, urea accumulates, leading to azotemia and ultimately uremia (symptoms ranging from lethargy to pericarditis and encephalopathy), potassium accumulates in the blood (with symptoms ranging from malaise to fatal cardiac arrhythmias), erythropoietin synthesis is decreased (leading to anemia causing fatigue), fluid volume overload - symptoms may range from mild edema to life- threatening pulmonary edema, hyperphosphatemia - due to reduced phosphate exeretion, associated with hypocalcemia (due to vitamin D3 deficiency), later this progresses to tertiary hyperparathyroidism, with hypercalcaemia, renal osteodystrophy and vascular caleification, and metabolic acidosis, due to decreased generation of bicarbonate by the kidney, leads to uncomfortable breathing and further worsening of bone health. The patient does not have CRF as her creatinine levels are within normal limits.14) R/O Alcoholic Liver disease Alcoholic liver disease involves an acute or chronic inflammation of the liver induced by alcohol abuse. Alcohol is a bone marrow suppressant that ultimately causes pancytopenia. Tt also directly interferes with erythropoiesis and blocks the response to folate in subjects who are folate deficient, Changes start within the liver as inflammation (hepatitis) and progress to fatty liver and cirthosis. Cirrhosis is the final phase of alcoholic liver disease. Symptoms may not be present until the disease is relatively advanced. Malnutrition develops as a result of empty calories from alcohol, reduced appetite, and malabsorption. The patient being cared for does not use alcohol presently or in the past, She therefore does not have risk factors that would suggest this differential. Moreover, her liver enzymes are within normal levels 15) R/O Malaria Malaria is a vector-borne infectious disease that is widespread in tropical and subtropical regions. The disease is caused by protozoan parasites of the genus Plasmodium. The most serious forms of the disease are caused by Plasmodium falciparum and Plasmodium vivax, but other related species (Plasmodium ovale, Plasmodium malariae, and sometimes Plasmodium knowlesi) can also infect humans. Malaria parasites are transmitted by female Anopheles mosquitoes. The parasites multiply within red blood cells, causing symptoms that include symptoms of anemia (light headedness, shortness of breath, tachycardia ete.), as well as other general symptoms such as fever, chills, nausea, flu-like illness, and in severe cases, coma and death The patient has no recent history of travel to places where she would have been exposed to this differential. Moreover, she has no associated symptoms of fever and flu-like illness that wou! suggest that the patient’s condition is of infec 16) R/O Aplastic anemia ‘Aplastic anemia is a condition where the bone marrow does not produce sufficient new culls to replenish blcod cells. Typically, anemia refers to low red blood cell counts, but aplastic ‘anemia patients have lower counts of all three blood cell types: red blood cells, white blood cells, and platelets. In many cases, the etiology is impossible to determine, but aplastic anemia is sometimes associated with exposure to substances such as benzene, radiation, or to the use of certain drugs, including chloramphenicol, carbamazepine, phenytoin, quinine, and phenylbutazone. The patient at hand does not have low white blood cells as she is suffering from AML. This differential is therefore unlikely in this patient 17) R/O Acute/Chronic Blood Loss The less blood in the body, the more reduced the oxygen-carrying capacity. Both acute and chronic blood loss leads to a decreased intravascular volume. This is followed by hypoxia and hypovolemia. In states of hypovolemic hypoxia, increased sympathetic discharge leads to increased venous tone, leading to the vasodilator effects of hypoxia. The patient does present with a history of intermittent blcod loss which continue to contribute and worsen the patient's anemia. 18) R/O Acute Myeloid Leuker AML is a cancer of the myeloid line of white blood cells, characterized by the rapid proliferation of abnormal cells which accumulate in the bone marrow and interfere with the production of normal blood cells. AML is the most common acute leukemia affecting adults, and its incidence increases with age. The symptoms of AML are caused by replacement of normal bone marrow with leukemic cells, resulting in a drop in red blood cells, platelets, and normal white blood cells, These symptoms include fatigue, shortness of breath, easy bruising and bleeding, and 15increased risk of infection, While a number of risk factors for AML have been elucidated, the specific cause of AML remains unclear. As an acute leukemia, AML progresses rapidly and is typically fatal in weeks to months if left untreated. The patient at hand is diagnosed with this differential but it was not the cause of her GI bleed that has been an on-going problem for her. In any case, AML further complicates the patient's health condition. Assessment/Plan 73 yo female admitted 3/29/07 with c/o generalized weakness x 1 day 1. GI bleed/AV malformation in jejunum/Nausea/Differential diagnosis -2L nasal cannula 02 -0.9 Normal Saline 100m! bolus/0.9 NS 125 mL/hr -Reglan 10 mg IVPB Q6 PRN -Carafate 1 g po Q8 -s/p multiple transfusions: 3/29 > 2 units RBC, 2 units FFP 3/30 > 2 units RBC, 2 units FFP 3/31 > 1 unit RBC, 6 units of platelets “flu CBC 2. ACS/ CHF resolving -Lasix 40 mg IVPB single orders -Lopressor 12.5 mg po QI2 -Serial troponins, Serial EKG, CXR, Echo performed 3. AML Patient and family refuse chemotherapy Physician, patient and family agree on supportive hospice care 4. DM -Lantus 10 units SC Q24 5. Anaerobic infections - Flagyl 200 mg IVPB Q8 References used: Ayala, Carlos and Spellberg, Brad. Boards and Wards, 3 edition. New York: Lippincott Williams & Wilkins, 2007. Braunwald, Eugene, Fauci, Anthony, etal. Harrison's Principles of Internal Medicine, 16" edition. New York: McGraw-Hill, 2005, huip://www.emedicine.com