Based on smear morphology and the red blood cell indices (mean cell volume [MCV], mean cell hemoglobin [MCH], mean corpuscular hemoglobin concentration [MCHC]), the patient has a severe microcytic, hypochromic anemia most likely caused by iron deficiency (see Chapter 5). This was confirmed by iron studies showing: Serum iron – I 0 Jlg/dl,TIBC – 460 Jlg/dl, % saturation – 2% Serum ferritin – 3 Jlg/L The history of repeated epistaxis and the positive test for blood in the stool strongly suggest chronic blood loss as the etiology of the iron deficiency. This obviously will require a careful workup of the gastrointestinal (GI) tract for a bleeding site and any correctable anatomic lesion. At the same time, a search for a coagulation defect is in order. Therefore, additional screening….
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The patient's history and physical examination (telangiectasia involving the lips, tongue, and palms) are consistent with a diagnosis of hereditary hemorrhagic telangiectasia (HHT). Three diagnostic criteria are met: multiple telangiectases, recurrent epistaxis, and a positive family history (father's history of epistaxis and a brain abscess, which can occur in 5%-10% of patients with H HT). The diagnosis of HHT can be confirmed by screening for mutations in the endoglin and AL.K. / genes, which are present in more than 80% of patients fulfilling HHT clinical criteria. As for the evaluation of the patient's ongoing blood loss, upper endoscopy revealed multiple telangiectases in the mucosa of the stomach and duodenum, while colonoscopy was unremarkable. Because of the marked dyspnea, she was also screened for the presence of arteriovenous malformations….
As this patient with HHT grows older, her bleeding tendency will likely become progressively more difficult to manage. If she were premenopausal, oral contraceptives would be an option, but in this patient, she may respond instead to tamoxifen. She must also be carefully followed for any symptoms of arteriovenous malformations, which need to be immediately treated by catheter-directed embolization.
The management of this patient's iron deficiency will also become a significant problem. She should receive maximum oral iron therapy in combination with repeated doses of parenteral iron (see Chapter S). lf this regimen fails to correct her anemia, she will eventually require increasingly frequent red cell transfusions to maintain a stable hematocrit around 30%.
A 56-year-old man presents with a complaint of rash and bleeding from the nose and mouth for the past week. His history is notable for non-Hodgkin lymphoma (NHL;follicular center cell) treated with chemotherapy and radiation therapy I 0 years prior. He has been taking cholesterol lowering medication for 3 years; no new drugs have been prescribed. Examination is notable for a petechial rash, which is prominent on the feet and shins, and multiple blood blisters in the mouth. The remainder of the examination is benign. CBC: Hemoglobin/hematocrit – 12 g/dU36% MCV – 84 fL WBC count – 7,500/tL Platelet count – I 0,000/-tL • SMEAR MORPHOLOGY Normocytic, normochromic; no abnormal red cell morphology. White blood cells are normal. There are very few platelets; giant platelets are noted.
Based on the CBC and smear morphology, the patient has an isolated thrombocytopenia, which is
almost certainly the cause of the petechial lesions noted on examination. The history of NHL is important; recurrent disease involving the bone marrow may interfere with platelet production. NHL is also associated with autoimmune thrombocytopenia. The absence of splenomegaly and any evidence of organ damage (TTP) make increased platelet sequestration or organ-based consumption unlikely. To evaluate platelet production, a bone marrow aspirate and biopsy are performed, revealing a normocellular marrow with no evidence of lymphomatous infiltration, but a clear increase in the number of megakaryocytes and the percentage of hyper lobulated megakaryocytes. This finding supports the diagnosis of a destructive thrombocytopenia, most likely an immune thrombocytopenia. A reticulated platelet count of 42% (normal….
The patient's history, physical examination, and smear/ marrow studies are consistent with a diagnosis of autoimmune idiopathic thrombocytopen ic purpu ra (AITP). ITP secondary to a relapse of his lymphoprol iferative disorder needs to be ru led out by additional studies, including thoracic and abdominal scans for lymphadenopathy and flow cytometry of blood and marrow to detect re-emergence of clonal disease (see Chapter 22).Assays for anti-platelet or platelet glycoprotein-specific antibodies are not routinely recommended to confirm AITP, due to their poor sensitivity and specificity. The diagnosis is primarily made by exclusion of other causes of thrombocytopenia and response to immunosuppressive therapies. Because of the patient's very low platelet count, he was hospital ized and started on IV methylprednisolone, I g/d x 3 days. By day 4, the platelet….
A 76-year-old man presents with a complaint of headache, which began several hours after a fall and has steadily worsened. His history is notable for hypertension and coronary artery disease, status post-bypass grafting 4 years prior. He denies any history of bleeding or thrombosis other than his previous coronary symptoms. Medications include a cholesterol-lowering agent, beta-blocker; and a daily aspirin. Examination is notable for a tender bruise over the left occipital region. The remainder of the examination is benign. CBC: Hemoglobin/hematocrit – 13 g/dU39% MCV – 94 fL MCH – 31 pg MCHC – 32 g/dL RDW-CV – I I% White blood cell count – 8,500/-tL Platelet count – 3 I 0,000/-tL
BLOOD SMEAR MORPHOLOGY
Normocytic, normochromic with no aniso- or poikilocytosis or polychromasia. White blood cells are….
The platelet count, prothrombin time (PT), and partial thromboplastin time (PTT) are all normal, ruling out thrombocytopenia or a factor deficiency, but this is not surprising given the patient's age and lack of bleeding history or liver disease. Neither cholesterol-lowering agents nor betablockers are strong inhibitors of platelet function, but daily aspirin use can significantly inhibit platelet function through its blockade of cyclooxygenase-dependent activation. Furthermore, von Wille brand disease, a common inherited platelet functional defect, must be considered in any patient with uncontrolled bleeding after trauma or with surgery. To look at these possibilities, a PFA screening test is ordered, the results of which are as follows: PFA collagen/ADP closure time = 95 seconds (80-1 20 seconds} PFA collagen/epinephrine closure time (I I 0- 1 80 seconds) 245….
The prolonged collagen/epinephrine PFA closure time, together with a normal collagen/ADP PFA closure time, is indicative of a platelet-based coagulopathy, namely inhibition by aspirin. However, concurrent type I von Willebrand disease, worsened by aspirin therapy, cannot be fully excluded given the setting of acute trauma causing an acute phase reaction. A diagnostic workup for vWD (including ristocetin cofactor activity, vWF antigen, and factor VI II activity) must wait until the patient is fully convalescent. Since aspirin irreversibly blocks platelet cyclooxygenase function, and the patient has been taking aspirin on a daily basis, nearly all of the platelets in circulation can be assumed to be affected. Depending on the severity of the defect in platelet function, this can lead to excessive bleeding with surgery or trauma and may have….
A 66-year-old man presents with a complaint of bruising and severe pain in the right arm and forearm after painting a wall yesterday. His history is notable for osteoarthritis, hypertension, and non-insulin-dependent diabetes mellitus; he denies any prior history of bleeding. His medications include hydrochlorothiazide and glyburide (a sulfonylurea), and he took ibuprofen for the pain last night. Examination is notable for large ecchymoses over the right shoulder and triceps, with swelling and tenderness of the right forearm and wrist. The remainder of the examination is benign. CBC: Hemoglobin/hematocrit – 13 g/dU39% MCV – 94 fL MCH – 29 pg MCHC – 28 g/dl RDW-CV – I I% WBC count – 1 3,500/Jll Differential: Neutrophils – 45% Lymphocytes – 50% Monocytes – 5% Platelet count – 300,000/Jll Questions….