Flashcards in UWorld Deck (87):
Stacking of RBCs like coins. Finding seen with elevated serum protein (like in MM)
Aplastic anemia bone marrow bx
Bone Marrow Bx often shows hypoplastic, fat-filled marrow.
Causes pancytopenia (not just anemia)
Megaloblastic erythroid hyperplasia
Seen in megaloblastic anemia, usually caused by B12 or folate deficiency.
Protein that binds free hemoglobin to form hemoglobin-haptoglobin complexes that are easily removed by the liver.
Usually low in hemolytic anemias
Pathophys - monoclonal plasma cell proliferation
1) Bone pain, fractures
2) Constitutional symptoms (weight loss, fatigue)
3) Recurrent infections
1) Normocytic anemia*
2) Renal insufficiency
4) Monoclonal paraproteinemia
Rads - Osteolytic lesions/osteopenia (osteoclast activation)
Why are MM patients prone to infection?
Neoplastic infiltration of bone marrow alters and impairs the normal lymphocyte population, resulting in ineffective antibody production and hypogammaglobulinemia.
Respiratory and UTIs are most common infections seen in MM
Common med that can lead to Fe def anemia?
High Fe, High ferritin, High transferrin sat, low TIBC
Fe overload. Maybe hemochromatosis. Patients receiving frequent transfusions for anemia related to hemoglobinopathies may also develop Fe overload.
Helmet cells. They are fragmented RBCs. They occur in microangiopathic hemolytic anemias (DIC, HUS, TTP) and due to RBC destruction by prosthetic cardiac valves
Hemolytic anemias have low haptoglobin and high LDH and bili
decreased serum albumin level
Associated with cirrhosis (low production), nephrotic syndrome, and protein-wasting enteropathy (increased losses)
Bisphosphonates in the treatment of metastatic bone lesions
Zolendronic acid, pamidronate are drugs of choice for stabilizing bony mets to prevent hypercalcemia of malignancy and pathologic fractures
They inhibit osteoclastic activity of bone and stabilize the bony tumors
Note: ASx or mild hyperCa (less than 12) doesn't require urgent intervention but hyperCa of malignancy may worsen over time.
Pain control for metastatic bone pain
Opioids are first line for metastatic bone pain that is not well controlled by tylenol or NSAIDs.
Radiation in treatment of metastatic bone pain
For moderate-severe pain only
Low MCV, Low Fe, High TIBC, Low Ferritin, Low Transferrin saturation (Iron/TIBC)
Very low MCV, High Fe, Low TIBC, High Ferritin, Very high saturation
Normal or low MCV, low Fe, Low TIBC, Normal or high ferritin, normal or low sat
Hairy Cell Leukemia
AKA leukemia reticuloendotheliosis
A type of B-lymphocyte derived chronic leukemia.
Lymphocytes have fine, hair-like irregular projections. Bone marrow may be fibrotic, explaining why bone marrow aspirates are often unsuccessful (dry tap).
Cytochemical feature includes a tartrate-resistant acid phosphatase (TRAP) stain.
Drug of choice is purine analog cladribine*
Cladribine is toxic to bone marrow, and its adverse effects include neuro and kidney damage
Chlorambucil and prednisone
Clinical features of type 2 HIT
Suspected with heparin exposure more than 5 days and any of the following:
1) Platelet count reduction more than 50% from baseline
2) Arterial or venous thrombosis
3) Necrotic skin lesions at heparin injection sites
4) Acute systemic (anaphylactoid) reactions after heparin
1) Serotonin release assay is gold standard confirmatory test
2) Start tx in suspected cases before confirmatory tests
1) Stop all heparin products
2) Start a direct thrombin inhibitor (argatroban) or fondaparinux (synthetic pentasaccharide)
Heparin induces conformational change in a platelet surface protein (PF4) which exposes a neoantigen. HIT antibodies form in response to the neoantigen and bind to the surface of platelets, causing platelet aggregation, thrombocytopenia (or drop in platelets of more than 50 percent of original levels) and a prothrombotic state
For subQ heparin, you may see necrosis at injection sites
1) Factor V Leiden - Most common in those of white ethnicity. Activated protein C resistance
2) Prothrombin mutation - 2nd most common in white people. Increased Prothrombin levels
3) Antithrombin deficiency - Inherited form is rare. Acquired - usually from DIC, cirrhosis, or nephrotic syndrome
4) Protein C or S deficiency - Reduced inactivation of factors V and VIIIa. Warfarin-induced skin necrosis (protein C only)
Most are autosomal dominant with variable penetrance
Young patient (under 45) with first-time unprovoked DVT/PE, patients with recurrent DVT/PE, and patients with unusual sites of thrombi (cerebral, mesentery, portal veins)
Make sure you test these patients for thrombophilias
Spinal cord compression
1) Spinal injury (MVA)
2) Malignancy (lung, breast, prostate, myeloma)
3) Infection (epidural abscess)
Signs and Symptoms
1) Gradually worsening severe local back pain
2) Pain is worse in recumbent position/at night
3) Early signs: Symmetric lower-extremity weakness, hypoactive/absent DTRs
4) Late signs: Bilateral Babinski reflex, decreased rectal sphincter tone, paraparesis/paraplegia with increased DTRs, sensory loss, Bowel and bladder dysfunction.
1) Emergency MRI
2) IV glucocorticoids (right away - even before imaging)
3) Rad-onc and neurosurg consult
Anaphylactic blood transfusion reaction
1) Rapid onset of shock, angioedema/urticaria and respiratory distress
2) Within a few seconds to minutes of transfusion
3) Caused by recipient anti-IgA antibodies
Present with difficulty breathing (wheezing or bronchospasm), angioedema, and hypotension, which can rapidly progress to respiratory failure, LOC and shock
Transfusion must be stopped immediately and IM Epi given.
Histamine blockers and Glucocorticoids should be given as well.
Future transfusions should include IgA-deficient plasma and washed Red Cell products
Transfusion-related acute lung injury
1) Respiratory distress and signs of noncardiogenic pulm edema
2) Within 6h of transfusion
3) Caused by donor anti-leukocyte antibodies
CXR shows bilateral interstitial infiltrates
Rapid onset of respiratory failure and shock are more from anaphylaxis
Primary hypotension reaction (blood transfusion rxn)
1) Transient hypotension often in patients taking ACEI's
2) Within minutes of transfusion
3) Caused by bradykinin in blood products (normally degraded by ACE)
Bacterial sepsis (transfusion rxn)
1) Fever, chills, septic shock and DIC
2) Within minutes to hours of transfusion
Rare, but can still happen due to clerical errors. Can cause acute hemolytic transfusion rxn.
Patients often present with fever, chills, flank pain, and hemoglobinuria within an hour of transfusion
Can progress to renal failure and DIC. Rapid onset of shock and respiratory failure suggest anaphylactic rxn though.
Febrile nonhemolytic transfusion reaction
Most common adverse rxn to transfusion. Occurs within 1-6h of transfusion.
During blood storage, leukocytes release cytokines that, when transfused, cause transient fevers, chills, and malaise
Autoimmune disorder in which body makes anti-intrinsic factor antibodies. It's the number one cause of B12 deficiency.
Leads to B12 def in 2 ways. First, antibodies decrease the amount of functional IF available to facilitate B12 absorption. Second, patients develop a chronic atrophic gastritis with lower production of IF by gastric parietal cells
Atrophic gastritis increases the risk of intestinal-type gastric cancer and gastric carcinoid tumors by 2-3 times.
Patients with pernicious anemia should be monitored for development of gastric cancer (periodic stool testing for presence of blood)
Features of CO poisoning
1) HA (most common), confusion, malaise, dizziness, nausea
1) Seizure, syncope, coma
2) Myocardial ischemia, arrhythmias
1) Smoke inhalation (most common)
2) Defective heating systems
3) Use of fuel-burning appliances or motor vehicles in poorly ventilated areas
1) Carboxyhemoglobin level
2) Check ECG in all patients!!!
3) Measure cardiac enzymes in the elderly and in those with cardiac risk factors or signs of ischemia
1) 100% O2 (non-rebreathing face mask)
Shifts O2-dissociation curve to the left, impairing the ability of heme to unload O2 at the tissue level
This causes tissue hypoxia. Kidney responds by making more EPO. EPO stimulates the bone marrow to differentiate more RBCs. Chronic CO toxicity is a cause of secondary polycythemia
Pulse Ox does not differentiate between carboxyhemoglobin and oxyhemoglobin; it cannot be used in dx of CO poisoning. Dx is made by ABG with cooximetry.
When is it safe for most patients to switch to warfarin after HIT?
Once platelets are above 150k
Driven by abnormal fusion gene BCR-ABL (due to translocation between chromosomes 9 and 22)
This gene causes leukemogenesis due to a perpetually active tyrosine kinase
First line treatment for most CML patients involves tyrosine kinase inhibitors such as imatinib. These drugs often cause long-term remission
Patients may present asymptomatically although fatigue, night sweats, weight loss and abdominal fullness (due to splenomegaly) are not uncommon.
Patients may experience weight loss and early satiety from splenomegaly. Peripheral blood smear reveals dramatic leukocytosis (often over 100k) with absolute basophilia and a shift toward very early neutrophil precursors (promyelocytes, myelocytes)
Acute promyelocytic leukemia. (M3 AML). Use all-trans retinoic acid.
APML often presents with complications due to pancytopenia.
Tumor Lysis Syndrome
Tumors with high cell turnovers (poorly differentiated lymphomas and leukemias) are the frequent culprits. Allopurinol may greatly reduce the possibility of acute urate nephropathy
Burkitts and leukemias (esp ALL, sometimes AML)
The released phosphate binds Ca and causes the hypoCa.
HypoCa also due to release of intracellular products by cell lysis.
TLS may lead to fatal arrhythmias, ARF, and even sudden death. Correct the metabolic issues!
May be asymptomatic if it's below 12. May see fatigue, CONSTIPATION and depression
Treatment given in addition to standard therapy.
Ex/patient given radiation at same time as radical prostatectomy
Typically given after induction therapy with multidrug regimens to further reduce tumor burden.
Ex/ Multidrug therapy after induction therapy for acute leukemia
Initial dose of treatment to rapidly kill tumor cells and sent the patient into remission (less than 5% tumor burden).
Ex/ Induction chemo for acute leukemia
Usually given after induction and consolidation therapies (or initial standard therapy) to kill any residual tumor cells and keep the patient in remission.
Ex/ Daily antiandrogen therapy for prostate cancer
Treatment given before the standard therapy for a particular disease.
Ex/ RT before radical prostatectomy
Tx for a disease when standard therapy fails
Ex/ RT for PSA recurrence after radical prostatectomy for prostate cancer
Condition where obstruction of the SVC impedes venous return from the head, neck and arms to the heart
Dyspnea, venous congestion, and swelling of the head, neck and arms.
Malignancy is most common cause (Lung, non-Hodgkin), account for over 60%.
CXR can ID the cause of SVCS in more than 80% of cases
Abnormal CXR warrants follow-up Chest CT and Histo
Clinical features of PNH
1) Hemolysis leading to fatigue
2) Cytopenias (impaired hematopoiesis)
3) Venous thrombosis (intraabdominal, cerebral veins)
1) CBC (hypoplastic/aplastic anemia, thrombocytopenia, leukopenia)
2) Elevated LDH and low hapto
3) Indirect hyperbilirubinemia
4) UA (hemoglobinuria)
5) Flow cytometry (absence of CD55 and CD59)
1) Iron and folate supplementation
2) Eculizumab (inhibits complement activation)
Usually in 4th decade of life!
Genetic defect in PNH
It's acquired. Lack of glycosylphosphatidyllinositol anchor, which connects proteins like CD55 and CD59 to the cell surface. These proteins normally inhibit the activation of complement on RBCs, but their absence allows the complement MAC to form and results in hemolysis
Normally, people have two functional copies of the B-hemoglobin gene. In B-thalassemia, there is a point mutation in 1 or both of these genes. This results in reduced hemoglobin synthesis and eventually produces a hypochromic microcytic anemia due to poor hemoglobinization of RBCs
Two severities. Minor results from defect of 1 gene. Modest anemia with hematocrits btw 28 and 40. MCV typically ranges from 55-75.
Major is 2 gene mutation. Severe anemia and transfusion dependence at early age.
Look for mediterranean descent
Common causes of macrocytic anemia (8) and some common features
1) Folate def
2) B12 def
3) Myelodysplastic syndrome
5) Drug-induced (hydroxyurea, zidovudine, chemo agents)
6) Liver disease
7) Alcohol abuse
Low retic count, macrovalocyte RBCs, hypersegmented neutrophils (mean lobes more than 5), anisocytosis, poikilocytosis.
Ribosomal precipitates that form varying sizes of blue granules in the RBC cytoplasm.
Nonspecific - Lead poisoning, Thalassemia, B12/Folate, alcoholism
Definition of microcytic anemia
MCV below 80
Auto dominant characterized by diffuse telangiectasias, AVMs tend to occur in the mucous membranes, skin and GI tract, but may also be present in liver, brain and lung.
AVMs in lung can shunt blood from R to L side of heart, causing chronic hypoxemia and a reactive polycythemia***
Pulm AVMs can also present as massive, sometimes fatal hemoptysis
Look for recurrent nose bleeds and oral lesions too
1) Reduced ADAMTS13 activity leading to large vWF multimers and resulting in diffuse microvascular platelet-rich thrombi
2) Acquired (autoantibody) or hereditary
1) Hemolytic anemia with schistocytes
2) Thrombocytopenia (increased bleeding time, normal PT/PTT)
3) Renal failure
4) Neuro manifestations (HA, confusion, coma, stroke)
Tx - plasma exchange emergently (90% mortality without) - this replenishes ADAMTS13
Giant Cell tumor of bone
Benign and locally aggressive skeletal neoplasm seen in young adults. Patients usually present with pain, swelling, and decreased range of joint motion at involved site.
Nearly 10-35% experience pathologic fractures due to thinning of the bone cortex in weight bearing areas
Typically presents on XR of the epiphyseal regions of the long bones, usually the distal femur and proximal tibia around knee joint. Soap bubble appearance (expansile and eccentric lytic area).
MR can show the tumor containing both cystic and hemorrhagic regions.
Path shows sheets of interspersed large osteoclast giant cells that appear as round to oval polygonal or elongated mononuclear cells.
Tx - surgery (intralesional curettage with or without bone grafting)
Clinical features of Baker's (Popliteal) Cyst
1) Trauma (meniscal tear)
2) Underlying knee joint disease (OA, RA)
1) Can be ASx
2) Posterior knee pain, swelling, or stiffness
3) Posterior knee swelling increased with patient standing and knee extended
4) Swelling usually decreases with knee flexion to 45 degrees (Fouchers sign)
1) Cyst enlargement with dissection into calf - can present with redness, distal edema, positive Homan sign
2) Cyst enlargement into popliteal space - can compress adjacent vein and cause leg/ankle swelling
3) Cyst rupture with severe calf pain, warmth, tenderness, erythema - can also have ecchymoses from posterior calf to ankle
Osgood Schlatter Disease
Overuse injury caused by repetitive strain. It is typically seen in young kids and teens who have recently undergone a rapid growth spurt
XR of knee shows avulsion of the apophysis of the tibial tubercle.
Osteoitis Fibrosa Cystica (von Recklinghausen disease of bone)
Rare condition most commonly due to hyperparathyroidism from parathyroid carcinoma
Osteoclastic resorption of bone leads to replacement of with fibrous tissue (brown tumors) and causes bone pain.
Imaging shows subperiosteal bone resorption on the radial aspect of the middle phalanges, distal clavicular tapering, "salt and pepper" appearance of the skull, bone cysts, and brown tumors of the long bones
Sclerotic, cortical lesion on imaging with central nidus of lucency
Typically causes pain that is worse at night and unrelated to activity.
Pain quickly relieved by NSAIDs
Common causes of thrombocytopenia
Decreased platelet production
1) Viral infections (EBV, Hep C, HIV)***
1A) THROMBOCYTOPENIA CAN BE PRESENTING SYMPTOM IN 5-10% OF CHRONIC HIV INFECTIONS. ALL PATIENTS WITH PRESUMED ITP SHOULD BE TESTED FOR HIV AND HEP C!!!!
3) Myelodysplasia (esp if older than 60)
4) Alcohol use
5) Congenital (Fanconi syndrome)
6) B12 or folate deficiency
Increased platelet destruction
2) Meds (heparin)
3) ITP, DIC, TTP-HUS
4) Antiphospholipid syndrome
1) Dilutional due to massive red blood cell transfusion
2) Splenic sequestration
Classical findings in chronic HIV infection
1) Oral candidiasis or hairy leukoplakia
2) Aggressive seborrheic dermatitis
3) Peripheral neuropathy
4) Unexplained weight loss
5) Generalized LAD
6) Fever of unknown origin
7) Disseminated herpes zoster
8) Opportunistic infections
9) Kaposi's sarcoma
10) B Cell lymphoma
11) Unexplained cytopenias***
Side effects of EPO therapy
1) Worsening of HTN - seen in 30% of patients. Tx is fluid removal (dialysis) and use of anti-hypertensive drugs (B-Blockers and vasodilators preferred). Prevention involves slowly raising the hematocrit, with goal of 30-35%
2) HA - 15% of patients
3) Flu-like symptoms - 5%. Responsive to NSAIDs. Not seen as much with subQ EPO
4) Red cell aplasia
Major cause of anemia in patients with ESRD
Deficiency of EPO. The anemia is normochromic and normocytic.
Treatment is recombinant EPO started when Hb gets below 10 (or Hct less than 30)
Clinical manifestations of hereditary hemochromatosis
1) Skin - hyperpigmentation
2) MSK - arthralgia, arthropathy, chondrocalcinosis
3) GI - Elevated hepatic enzymes with hepatomegaly (early), cirrhosis (later) and increased risk of HCC (20 fold increase)
4) Endocrine - Diabetes, secondary hypogonadism, hypothyroidism
5) Cardiac - restrictive or dilated cardiomyopathy and conduction abnormalities
6) Infections - Increased susceptibility to Listeria, Vibrio vulnificus, and Yersinia enterocolitica
Diagnostic criteria for antiphospholipid antibody syndrome
1 clinical and 1 lab criterion MUST be met
A) Vascular thrombosis
1) Arterial/venous thrombosis
B) Pregnancy morbidity
1) 3 or more consecutive unexplained fetal losses before 10th week
2) 1 or more fetal loss after w10
3) 1 or more premature birth of normal neonate before w34 due to preeclampsia, eclampsia, placental insufficiency
1) Lupus anticoagulant
2) Anticardiolipin antibody (IgG/IgM - medium or high titer)
3) Anti-b2GP1 antibody (IgG/IgM - high titer)
Heme manifestations of SLE
Anemia (1-4 common, 5-8 uncommon mechanisms)
2) Renal insufficiency from SLE nephritis
3) Fe def anemia (GI loss)
7) Microangiopathic hemolytic anemia
8) Aplastic anemia
Leukopenia (1 is common, 2-4 not so much)
1) Autoimmune mediated destruction
4) Bone marrow dysfunction
Thrombocytopenia (1 is common, 2-3 not so much)
1) Immune mediated destruction
3) Increased consumption due to thrombotic microangiopathy (TTP)
Promotes coagulation in vivo. In vitro, it prolongs the partial thromboplastin time (PTT) as it binds the phospholipids used in most assays
This is a lab artifact and does not correlate with bleeding in vivo.
PT may also be prolonged. PTT will not correct if mixed in 1:1 dilution with normal plasma. Prolonged PTT is indirect indicator for the presence of LA and highly suggestive in certain clinical settings.
Specific tests are diluted Russell Viper venom test and kaolin clotting time!! (For APLS)
inherited def of ankyrin and spectrin (proteins that provide scaffolding for RBCs)
Sphere-shaped RBCs are not flexible and get trapped in the fenestrations of the spleen's red pulp.
Highly variable presentation. Usually increased MCHC, hemolytic anemia, jaundice and splenomegaly in a patient of northern european descent.
Short life span of spherocytes and chronic hemolysis cause high Hbg turnover and excess bilirubin that overwhelm conjugation and elimination from the body
Resulting hyperbili manifests as jaundice, dark urine, and pigment (calcium bilirubinate) gallstones. Look for signs of acute cholecystitis
Patients with acute gallbladder inflammation need cholecystectomy. Patients also need folate supplements since chronic hemolysis consumes folate. Many patients require splenectomy to minimize hemolysis
Warfarin induced skin necrosis
Typically occurs within the first few days of warfarin therapy. It is caused by a rapid decline in protein C levels, usually in patients with underlying hereditary protein C deficiency
Tx - warfarin cessation and administration of protein C concentrate
Hemophilia A and B
Inheritance - X
1) Delayed/prolonged bleeding after mild trauma or procedure - hemarthrosis, hemophilic arthropathy, IM hematomas, GI or GU tract bleeding
1) Prolonged activated PTT
2) Normal platelet count, bleeding time and PT
3) Decreased or absent factor 8 (A) or 9 (B) activity
1) Administration of factor 8 or 9
2) Desmopressin for mild hemophilia A
Leukemoid rxn vs CML
1) Leukocytes above 50k
2) Caused by severe infection
3) High LAP score
4) More mature neutrophil precursors (metamyelocytes greater than myelocytes)
5) Absolute basophilia NOT present
1) Leukocytes often above 100k
2) Caused by BCR-ABL fusion
3) Low LAP score
4) Less mature neutrophil precursors (metamyelocytes less then myelocytes)
5) Absolute basophilia present
Leukocyte alkaline phosphatase score
Can help differentiate leukemoid rxn from CML. It is a marker for neutrophil activity. Low is CML. High is LR
Most common source of symptomatic PE
Proximal deep leg veins (Ext Iliac, Common Femoral, Deep femoral, Femoral, Popliteal).
Other less common sources of emboli include calf veins, renal veins, pelvic veins, upper extremity veins, and right heart.
Distal deep veins of leg are anterior tibial, posterior tibial.
Management of bone pain in patients with prostate cancer who have undergone orchiectomy
Type 1 vs Type 2 HIT
Type 1 - Due to nonimmune direct effect of heparin on platelet activation and usually presents within first 2 days of heparin exposure. The platelet count then normalizes with continued heparin therapy and there are no clinical consequences
Type 2 - We know the deal
Unfractionated heparin has more risk of HIT. Enoxaprin also will not prolong aPTT.
Which marker is specific for hairy cell leukemia?
CD11c. TRAP positive.
Typical presentation of hairy cell leukemia
Pancytopenia and splenomegaly. 10-20% present with leukocytosis.
Patient presents with fever, sore throat, malaise, jaundice and mild HSM.
2) Sore throat
3) Toxic symptoms
4) symmetrical LAD involving posterior cervical chain of LNs more often than anterior chain. Inguinal and axillary LAD can also be present.
7) Tonsillar exudates
8) Mild petechiae on palate, but this is non-specific and can also be seen in strep pharyngitis
9) Tonsillar enlargement can cause airway compression
10) Hepatitis and jaundice are present in minority of cases
1) Confirmed by presence of atypical lymphocytosis and anti-heterophile antibodies (monospot), which typically indicate EBV.
Heme complications - due to cross-reactivity of EBV-induced antibodies against RBCs and platelets. The antibodies are IgM cold-agglutinin known as anti-i-antibodies. They lead to complement mediated destruction of RBCs (usually Coombs positive). Onset of AIHA is 2-3w after onset of symptoms, even though initial labs may be normal.
Splenic infarct in patients with IM
DOESNT happen. They are at risk for splenic RUPTURE (usually from trauma) not infarct.
What kinds of LNs are always suspicious for cancer?
Hard, unilateral, non-tender LNs. Must be evaluated immediately
Vast majority of head and neck cancers?
SCC. In a patient with smoking history and submandibular, cervical LNs get a prompt biopsy.
What do you give to prevent chemo-induced nausea and vomiting?
Serotonin (5HT) antagonists that block 5HT3 receptors. This includes odansetron. Low side-effect profile and are highly efficacious. Can be used to manage acute emesis but are also useful as ppx, sometimes in combo with corticosteroids.
Patient suffering from an acute hemolytic crisis, with bite cells and Heinz bodies seen on smear.
G6PD is enzyme involved in creating NADPH, a cofactor required to create glutathione and prevent the oxidation of hemoglobin. Without G6PD, Hgb becomes oxidized and denatures into Heinz bodies (RBC inclusions seen after crystal violet staining). The denatured Hgb disrupts RBC membranes and causes hemolysis.
Rxn typically occurs in response to oxidant drugs (antimalarials, sulfas) and infection. Fava beans too.
It is X linked and more in black men.
Vit K def
usually due to inadequate dietary intake, intestinal malabsorption, or hepatocellular disease. An acutely ill patient with underlying liver disease can become Vit K deficient in 7-10 days.
Labs show prolonged PT followed by prolonged PTT
Liver can normally store 30 days worth.
Also look out for recent ABX use.
Administration of vit K rapidly replenishes stores in 8-10h and FFP can be given for management of acute hemorrhage in interim
Hematological manifestations of alcohol abuse
Folate deficiency, iron deficiency from chronic blood loss (microcytic), ACD (normo or micro), thrombocytopenia, and macrocytosis (may appear even before development of anemia)
Alcohol abuse is most common cause of nutritional folate deficiency in USA
B12 deficiency treatment
B12 def causes neuro symptoms like loss of proprioception and vibration mostly in lower extremities due to defect in myelin in dorsal column. May also see memory problems, irritability, dementia.
Replenishing folic acid without B12 supplementation corrects the megaloblastosis but leads to worsening neuro symptoms.
Risks of splenectomy
Immediate risks are hemorrhage, postop infection, injury to nearby organs
Long term, the biggest risk is overwhelming sepsis with encapsulated bacteria, namely strep pneumo
The risk for pneumo sepsis is present up to 30 years following the procedure. To lower risk, anti-pneumococcal, Haemophilus, and meningococcal vaccines should be given several weeks before the operation. Daily oral penicillin ppx for 3-5 years following splenectomy or until adulthood (for peds patients)
ABx can also be made available at home for immediate treatment of any significant fever.