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Heme Flashcards

1
Q

What is type II heparin induced thrombocytopenia?

A

Antibody mediated and causes a mild to moderate thrombocytopenia; venous and arterial thrombotic risk is significant
Presentation: suspected w/ heparin exposure >5d + any of the following:
platelet count reduction >50% from baseline, arterial or venous thrombosis, necrotic skin lesions at heparin injection sites, acute systemic (anaphylactoid) reactions after heparin
Creates a prothrombotic state
Dx: serotonin release assay (gold standard confirmatory test), start treatment in suspected cases prior to confirmatory test
Tx: stop ALL heparin products, start a direct thrombin inhibitor (eg argatroban) or fondaparinux (synthetic pentasaccharide)
Once platelet count is >150,000, most pt can be switched safely to warfarin

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2
Q

What is methemoglobinemia?

A

It results from the oxidization of iron in hemoglobin, which is most commonly due to topical anesthetic agents (benzocaine), dapsone, and nitrates (infants)
Large O2 sat gap = Pulse ox commonly is 85% regardless of true O2 sat, blood gas analysis returns falsely elevated O2 sat as it provides an estimate based only on PaO2, not effective hemoglobin-O2 binding
Presentation: hypoxia (20% methemoglobin), cyanosis (10%), 50% - altered mental status, seizures, respiratory depression
Tx: discontinuing causative agent, administering methylene blue, which helps reduce iron to normal state

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3
Q

What is vitamin K deficiency?

A

The body obtains vit. K exogenously from intestinal absorption of dietary vit K and endogenously from bacterial production of vitamin K in the intestine
Usually due to inadequate dietary intake, intestinal malabsorption, or hepatocellular disease
An acutely ill pt with underlying liver disease can become vit. K deficient in 7-10d
Deficiency decreases plasma levels of factors 2, 7, 9, 10 and protein C and S
Labs: prolonged prothrombin time, followed by prolonged partial thromboplastin time

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4
Q

What are burr cells?

buried in the liver and kidneys

A

Also known as echinocytes; spiculated appearing RBCs w/ serrated edges
Can be seen in liver disease and ESRD

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5
Q

What is cancer-related anorexia/cachexia syndrome?

A

Hypercatabolic state assoc. w/ wt loss, anorexia, and excessive reduction in skeletal msucle
Tx: progesterone analogues (megestrol acetate) or corticosteroids to increase appetite, cause wt gain, and improve well-being
In pt w/ longer life expectancies, progesterone analogues are preferred over corticosteroids due to their decreased incidence of side effects

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6
Q

What is pica?

A

An appetite for items other than food such as paper, clay, or dirt; occasionally develops in Fe deficiency anemia
Pagophagia is pica for ICE and is specific for Fe deficiency
Tx: Fe supplementation

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7
Q

What is hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome)?

A

AD
Presentation: diffuse telangiectasias (eg ruby-colored papules that blanch with pressure), recurrent epistaxis, and widespread arteriovenous malformation (AVMs)
AVMs in lung shunt blood from R to L side of heart causing chronic hypoxemia, digital clubbing, and reactive polycythemia
Pulmonary AVMs can present as massive, fatal hemoptysis

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8
Q

What is idiopathic thrombocytopenic purpura?

A

Isolated thrombocytopenia with no other cause.
Pts should be tested for hepatitis C and HIV, as thrombocytopenia may be initial presentation of HIV infection
Pts w/ chronic ITP have platelets <100K; splenectomy is an option for those w/ persistent bleeding and thrombocytopenia despite repeated pharmacologic interventions (eg glucocorticoids, anti-D, IV Ig)

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9
Q

EPO

A

Up to 30% of pts on erythropoietin therapy develop new or worsening HTN.

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10
Q

What is acute graft versus host disease?

A

Arises when donor T cells (cytotoxic T cells) identify antigens (host major and minor HLA antigens) on host epithelial cells as foreign and generate a strong inflammatory response.
Up to 50% of pts w/ BMT from matched siblings develop the disease
Target organs: skin (maculopapular rash involving palms, soles, face), intestine (blood positive diarrhea), liver (abnormal LFTs and jaundice)
Sxs develop w/in 100d: maculopapular rash, profuse watery diarrhea, liver inflammation w/ damage to biliary tract epithelium
Tx: glucocorticoids

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11
Q

What are common complications of sickle cell trait?

A

Hematuria
Hyposthenuria (impairment in concentrating ability) - urine is dilute
Renal: Papillary necrosi, UTI’s, renal medullary cancer

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12
Q

What is thrombotic thrombocytopenic purpura?

A

Due to decrease in ADAMTS13, attacked by antibodies
Thrombocytopenia, microangiopathic hemolytic anemia, renal insufficiency, neurologic changes (acting weird), fever
Dx: schistocytes on peripheral blood smear
Tx: plasma exchange, glucocorticoids

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13
Q

Contraindicated in ESRD

A

LMWH (eg enoxaparin)
Rivaroxaban (oral 10a inhibitor)
Fondaparinux (injection 10a inhibitor)
All are metabolized by the kidney

IV unfractionated heparin is NOT contraindicated.

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14
Q

What is mean corpuscular hemoglobin (MCH)?

A

Calculation of avg AMOUNT of hemoglobin inside a single RBC.

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15
Q

What is mean corpuscular hemoglobin concentration (MHCH)?

A

Calculation of the avg CONCENTRATION of hemoglobin inside a single RBC.

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16
Q

Iron deficiency anemia

A

Microcytic anemia, fatigue, pallor, hx of prolonged bleeding (eg heavy menses), poor dietary intake
Elevated RBC distribution width (size variability) due to variable amount of iron available for RBC synthesis throughout the day.
children less than 1y: due to introduction of cow, goat, or soy milk and inadequate consumption of iron-rich food
children, adults: chronic blood loss from GI tract
Reactive thrombocytosis (>400,000) in response to low RBC cout due to megakaryocytes and erythrocytes sharing a common progenitory cell.
Anisocytosis (RBCs of unequal size) = increased RBC distribution width
Low MCV and MCH correlating w/ microcytosis and hypochromia

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17
Q

What is red cell distribution width (RDW)?

A

Calculaton of the variation in size of RBCs.

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18
Q

What is multiple myeloma?

A

Plasma cell neoplasm
Presentation: wt loss, fatigue, bone pain, renal insufficiency
Neoplastic infiltration of bone marrow alters and imapirs normal lymphocyte population resulting in ineffective antibody production and hypogammaglobulinemia
Respiratory (eg strep pneumo) and UTIs are the most common infections seen in MM
Labs: hypercalemia, renal insufficiency, normocytic anemia, protein gap (total protein - albumin >4)
Protein gap indicates elevated nonalbumin protein in serum
Serum protein electrophoresis can determine if protein gap is caused by monoclonal or polyclonal source
SPEP shows monoclonal M spike in MM
Dx: confirmed by BM biopsy (>10% clonal plasma cells)
Peripheral blood smear: rouleaux formation

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19
Q

What is the main side effect of hydroxyurea?

A

Myelosuppression (neutropenia, anemia, thrombocytopenia).

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20
Q

What is alpha thalassemia major?

A

An inherited disorder of absent alpha-globin chain production necessary to form hemoglobin F.
Fetuses w/ alpha-thalassemia major produce hemoglobin Barts (4 gamma chains), which does not release O2 to the tissues.
Results in severe fetal hypoxemia, high output heart failure, hydrops fetalis (skin edema, ascites) and subsequent fetal demise.

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21
Q

Sickle cell pain crisis in children.

A

Episodes typically begin as early as 6mo when production of defective hemoglobin A increases.
Under 6mo, hemoglobin is primarily fetal hemoglobin and pain crises are unlikely.

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22
Q

Lead poisoning treatment.

A

Sensorimotor neuropathy in stocking glove distribution w/ microcytic anemia
Chelation therapy not routinely administered for lead levels <45.
Dimercaptosuccinic acid (succimer) is used when levels are 45-69.
Dimercaprol + calcium disodium edetate (EDTA) used when levels are 70+ or there is acute encephalopathy.

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23
Q

Acute promyelocytic leukemia.

A

Medical emergency due to high risk of pulmonary/cerebrovascular hemorrhage from tumor-induced consumptive coagulopathy.
APL promotes bleeding diathesis via activation of tissue factor (DIC) + increased generation of plasmin (primary hyperfibrinolysis)
Tx: all-transretinoic acid promotes differentiation of the atypical promyelocyte

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24
Q

What is intravascular hemolysis?

A

Due to significant RBC structural damage resulting in RBC destruction w/in the intravascular space (paroxysmal nocturnal hemoglobinuria, DIC)
Low haptoglobin, elevated UCB, elevated LDH (released from RBCs)

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25
Q

What is extravascular hemolysis?

A

RBCs are predominantly destroyed by phagocytes in the reticuloendothelial system (eg LN, spleen)
Can be due to antibody-mediated RBC destruction (most cases of AIHA) or intrinsic RBC enzyme (G6PD deficiency) or membrane (eg hereditary spherocytosis) defects
Normal to slightly low haptoglobin, slightly elevated LDH, elevated indirect bilirubin
AIHA - negative fhx, positive coombs test
Hereditary spherocytosis - positive fhx, negative coombs test

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26
Q

Mgmt of acute DVT or PE.

A

Oral direct 10a inhibitors (rivaroxaban, apixaban)
Rapid onset of action, no requirement for lab (INR) monitoring, no requirement for overlap therapy w/ heparin; do not increase risk of bleeding complications
Contraindications: impaired renal function or DVT/PE secondary to malignancy

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27
Q

Thrombolytic tx + PE.

A

Typically reserved for hemodynamically unstable (hypotension, tachycardia) pts w/ PE.
Less commonly used for massive proximal DVT assoc. w/ significant sx swelling and/or limb ischemia.

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28
Q

What is pernicious anemia?

A

Most common cause of vit. B12 deficiency (macrocytic anemia, glossitis, peripheral neuropathy)
Due to: anti-intrinsic factor antibodies, or development of chronic atrophic gastritis w/ decreased production of IF by gastric parietal cells
Assoc. w/ at least double the risk of gastri cancer compared to general population.

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29
Q

What is hodgkins lymphoma?

A

15-35, >60yo
Fever, fatigue, painless cervical and supraclavicular LAD, pruritis (a paraneoplastic process classically assoc. w/ HL and likely due to cytokine and interleukin release)
Mediastinal LAD can compress adjacent structures and lead to cough, SOB, and retrosternal chest pain
Alcohol may exacerbate pain
Usually arises in a single LN and disseminates to contiguous nodes via lymphatic and thoracic ducts
Labs: normocytic anemia, eosinophila (tumor cells secrete cytokines that generate eosinophils), lymphopenia, elevated LDH (assoc. w/ high tumor burden)
Dx: exicisonal lymph node biopsy (reed sternberg cells are diagnostic)

30
Q

EBV

A

Fever, fatigue, peripheral LAD, sore throat; resolves in a month
tender LAD
splenomegaly

31
Q

Hemophilia

A

Pts present w/ joint pain and swelling following little or no trauma due to spontaneous bleeding into a joint (hemarthrosis).
Recurrent hemarthrosis can result in long-term complications such as hemophilic arthropathy, joint damage caused by intra-articular bleeding.
Hemosiderin deposition w/in jt triggers synovial inflammation, which leads to fibrosis and destruction of cartilage and bone.
Visible on XR, MRI allows for earlier detection and characterization of degree of jt damage
Early prophylaxis w/ factor concentrates can significantly reduce risk of developing arthropathy
BM evaluation is contraindicated in severe hemophilia due to bleeding risk.

32
Q

OSA + hypoxemia

A

Presentation: obesity, snoring, daytime somnolence
Short periods of hypopnea and apnea reduce blood O2 levels.
Kidneys respond to hypoxemia by increasing erythropoietin. EPO stimulates BM to differentiate mor RBCs.
Therefore, it is quite common for pts w/ OSA to have elevated hematocrite (polycthemia).

33
Q

Relative polycythemia.

A

Due to reduced plasma volume.

34
Q

Absolute polycthemia.

A

Erythrocytosis. Due to increased RBC mass and can be primary (polycthemia vera) or secondary (due to chornic hypoxia or EPO producing tumors).

35
Q

What is carbon monoxide poisoning?

A

Increases carboxyhemoglobin levels.
This shifts the O2 dissociation curve to the left, resulting in tissue hypoxia.
Kidneys respond by increasing EPO, which may cause erythrocytosis.
Pts w/ CO poisoning typically present w/ dizziness, headaches, nausea, and confusion.
Severe: seizures
Pulse ox is unreliable and may appear normal b/c it cannot differentiate carboxyhemoglobin from oxyhemoglobin.
Tx: 100% O2 via nonrebreather facemask
Hyperbaric O2 used in severe cases that are unresponse to facemask administered O2

36
Q

What is acute intermittent porphyria?

A

Abdominal pain + neuropsych issues (psychosis, neuropathy)
Occurs early in porphyrin synthesis
Caused by partial deficiency of porphobilinogen deaminase, an enzyme involved in heme synthesis
Patchy sensorimotor neuropathy and autonomic dsyfunction

37
Q

What is salvage therapy?

A

A form of treatment for a diseae when a standard treatment fails.

38
Q

What is adjuvant therapy?

A

Treatment given in addition to standard therapy.

-radiation therapy given at the same time as radical prostatectomy

39
Q

What is induction therapy?

A

An initial dose of treatment to rapidly kill tumor cells and send the patient into remission (<5% tumor burden)
-induction therapy for acute leukemia

40
Q

What is consolidation therapy?

A

Typically given after induction therapy w/ multidrug regimens to further reduce tumor burden.
-multidrug therapy after induction therapy for acute leukemia

41
Q

What is maintenance therapy?

A

Usually given after induction and consolidation therapies (or initial standard therapy) to kill any residual tumor cells and keep pt in remission.
-daily antiandrogen therapy for prostate cancer

42
Q

What is neoadjuvant therapy?

A

Treatment given before the standard of therapy for a particular disease.
-radiation therapy given before radical prostatectomy was done

43
Q

What is acute lymphoblastic leukemia?

A

Most common childhood cancer
Bone pain (caused by leukemic infiltration of BM)
LAD and hepatosplenomegaly due to extramedullary leukemic spread.
Labs: low platelets, anemia
Dx: bone marrow biopsy w/ 25% lymphoblasts
Tx: multidrug chemo

44
Q

Sickle cell disease

A

Fever, splenomegaly, bone pain
No assoc. w/ lymphadenopathy
Most common cause of pediatric stroke, dx confirmed by hemoglobin electrophoresis.

45
Q

Antiphospholipid antibody syndrome

A

Pts w/ antiphospholipid antibodies (lupus anticoagulant) generally have prolonged PTT b/c antiphospholipid antibodies bind the phopholipids used in most testing assays and prevent them from inducing coagulation.

46
Q

What is Diamond Blackfan anemia?

A

Pure red cell aplasia w/ reticulocytopenia and normal platelet and WBC counts
Caused by congenital (inherited or sporadic) defect of erythroid progenitor cells, which leads to increased apoptosis of RBCs
Macrocytic anemia, craniofacial anomalies, triphalangeal thumbs, short stature, cleft palate, webbed neck
Tx: corticosteroids or transfusion therapy in refractory cases

47
Q

What is Fanconi anemia?

A

Autosomal recessive
Pancytopenic bone marrow failure
Most common cuase of congenital bone marrow failure due to defective DNA repair
In addition to pancytopenia, characteristic features include short stature, hypoplastic thumb, polydactyly or a flat thenar eminence, and abnormal skin pigmentation
Dx: made by demonstrating chromosomal breakage following DNA exposure to interstrand crosslinking agents
Tx: definitive - hematopoietic stem cell transplantation

48
Q

What is von willebrand disease?

A

Due to quantitaive or qualitative vonWF deficiency
Presentation: mucocutaneous bleeding (epistaxis, gingival bleeding, postpartum hemorrhage)
Factor 8 is more rapidly degraded when unbound leading to prolong aPTT
However pts can have normal aPTT: mild to moderate deficiency w/ adequate factor 8, vWF and F8 are acute phase reactants (stress + inflammation can acutely raise levels), vWF synthesis is increased by estrogen and TH (pregnancy, ocps, TH replacement can raise vWF and normalize aPTT)
Plt count and PT are normal
Impaired plt function = prolonged bleedint time
Dx: vWF antigen level, vWF activity (ristocetin cofactor activity), F8 levels
Tx: desmopressin potentiates release of vWF from endothelial cells and can be used in mgmt of acute bleeding or for prophylaxis

49
Q

What is Waldenstrom macroglobulinemia?

A

A B cell neoplasm assoc. w/ elevated monoclonal IgM
High levels of IgM may cause hyperviscosity syndrome (visual changes, HA, vertigo, dizziness, ataxia), peripheral neuropathy, cryoglobulinemia, and/or renal insufficiency
Dx: serum protein electrophoresis and bone marrow biopsy

50
Q

Chronic lymphocytic leukemia

A

Significant leukocytosis (often >100,000)
LAD
B symptoms

51
Q

Hairy cell leukemia

A

Hepatomegaly, LAD, + B sxs are UNCOMMON

52
Q

Folate deficiency

A

Alcohol abuse is the most common cuase of nutritional folic acid deficiency in the US
Deficiency occurs quickly (5-6w) due to naturally low stores.
Normal methylmalonic acid levels.
No neurologic manifestations.

53
Q

B12 (cobalamin) deficiency

A

Common after a total of partial gastrectomy.
Necessary cofactor in purine synthesis, and its deficiency causes defective DNA synthesis, which results in ineffective erythropoiesis, presenting as megaloblastic anemia
Glossitis, pale palmar crease
Takes years (not months) to develop.
HIGH methylmalonic acid levels.

54
Q

What is hereditary spherocytosis?

A

Autosomal dominant
Hemolytic anemia, jaundice, splenomegaly
High MCHC (due to membrane loss and RBC dehydration)
Negative coombs test, increased reticulocytes in response to RBC destruction
Spherocytes on peripheral sphere
Due to their shape, these abnormal RBCs get trapped and destroyed in the spleen
Tx: supportive care, transfusions; splenectomy for severe hemolysis

55
Q

What is glucose 6 phosphate dehydrogenase (G6PD) deficiency?

A

X linked recessive
Jaundice, splenomegaly
Elevated reticulocytes, negative coombs test, LOW MCHC
Heinz bodies leading to bite cells
Tx: avoidance of hemolytic triggers rather than splenectomy

56
Q

What is thalassemia minor?

A

Typically presents w/ microcytic anemia and normal RDW.

An elevated reticulocyte count reflects a compensatory bone marrow response to the anemia.

57
Q

What is Factor V Leiden?

A

Most commonly inherited hypercoaguable disorder in the white population, leading to increased risk of thrombosis.
Testing should be considered for an unprovoked 1st time thrombus in young (<45) pts or those w/ an unsual site of thrombus.

58
Q

Porphyria cutanea tarda

A

Most common porphyria
Due to abnormalities in later steps of heme synthesis
Photosensitivity due to accumulation of porphyrinogens that react w/ O2 on excitation by UV light
Due to deficiency of UROporphyrinogen decarboxylase
Blisters that heal w/ scarring, hyperpigmentation, triggered by estrogens, common in pts w/ hep C
Dx: elevated plasma or urinary porphyrin levels
Tx: phlebotomy or hydroxychloroquine may provide relief, as can tx for hep C

59
Q

Polycthemia vera

A

Classic thrombotic complication: Budd-chiari syndrome, a disorder marked by hepatic venous outflow obstruction (usually due to hepatic vein thrombosis)
-progressive discomfort, ascites, hepatosplenomegaly

60
Q

Paroxysmal nocturnal hemoglobinuria

A

Pts w/ autoimmune hemolytic anemia have tendency for venous thromboembolism, but those with PNH are at particular risk esp. w/in intraaabdominal or cerebral veins.
Should be suspected in pts who have a combination of hemolytic anemia, cytopenias, and hypercoaguable sate (intraabdominal or cerebral venous thrombosis)
Flow cytometry tests are used to confirm the diagnosis by assessing for absence of the CD55 and CD59 proteins on the surface of RBCs.

61
Q

What is anemia of chronic disease?

A

A disorder of iron utilization that most commonly occurs in setting of chronic inflammation.
Characterized by normocytic anemia
Low FE, low TIBC, low iron saturation
Normal/elevated serum ferritin (keeping Fe stored away)
Treating underlyling inflammatory disorder improves anemia

62
Q

Hemolytic uremic syndrome

A

Most commonly occurs 5-10d after an acute, often bloody, diarrheal illness caused by shiga-toxin producing strain of e. coli
Presentation: edema, bruising, bloody diarrhea, jaundice
Labs: anemia, thrombocytopenia, elevated cr
Smear: schistocytes
Treatment of prodromal diarrhea w/ antibiotics or antimotility agents (eg loperamide) can increase risk of developing HUS and is not recommended.

63
Q

Prostate cancer

A

May initially present w/ symptoms related to metastatic disease.
Spread to axial skeleton is common and manifestation typically include slowly progressive lower back pain or functional impairment (eg motor weakness, incontinence)
Prostate cancer usuallly causes osteoblastic bone lesions w/ normal or low ca, elevated ALP, and XR evidence of focal, sclerotic lesions.

64
Q

What is the leukemoid reaction?

A

Occurs as a response to severe infection, which mobilize mature and immature leukocytes, and is marked by leukocyte counts >50,000.
Compared to chronic myeloid leukemia, LR is characterized by the presence of a high alkaline phosphatase score, a greater proportion of late neurtorphil precursors (metamyelocytes, bands) rather than early (promyelocytes, myelocytes), and a lack of absolute basophilia.

65
Q

Thymoma

A

Often causes an anterior mediastinal mass
Growth can compress adjacent stuctures.
No eosinophilia, pain does not worsen w/ alcohol

66
Q

Germ cell tumor + mediastinum

A

Can cause anterior mediastinal mass and can compress adjacent structures (leading to sxs)
However, most cases arise in 20-40yo not 65yo
Eosinophilia is not common, pain does not worsen w/ alcohol

67
Q

What is beta thalassemia major?

A

Characterized by increased HbA2 and HbF on electrophoresis due to absent beta globin expression.
Since HbF predominates first few months of life until HbA is synthesized, beta thalassemia major is generally asymptomatic in newborn period. Around 6-12mo, pts develop fatigue and pallor due to microcytic anemia
Splenic hemolysis of RBCs: jaundice, dark urine, splenomegaly
If left untreated pt can develop skeletal abnormalities due to extramedullary hematopoiesis
Pts are transfusion-dependent and at risk for iron overload.
Therfore, chelation therapy is required to improve survival.

68
Q

Venous thromboembolism

A

The proximal deep leg veins (femoral*, iliac, popliteal) are the most common source of symptomatic PE - 90% due to their large caliber and proximitiy to the lungs
Other less common sources of emboli include the calf veins, renal veins, pelvic veins, upper extremity veins, and right heart - less likely to embolize and more likely to spontaneously resolve.

69
Q

DVT + IVC filters

A

Pts w/ a DVT/PE who have a contraindication to or complicatoin from anticoagulation (eg significant active bleeding, recent surgery, acute hemorrhagic stroke) should have an IVC filter placed.
Another indiciation for placement includes if anticoagulaton fails (eg the pt develops a new or recurrent proximal DVT while on therpeutic anticoagulation)
In a pt w/ life-threatening GI bleed (w/ a therapeutic INR and a normat plt countt), therapeutic anticoag (ie warfarin, heparins, rivaroxaban) is contraindicated

70
Q

Lymphoproliferative disorders

A

Anemia can be due to decreased RBC production, increased RBC destruction, and frank blood loss.
The anemia of lymphoproliferative disorders is due to bone marrow infiltration w/ cancerous cells.

71
Q

What are spur cells (acanthocytes)?

A

RBCs w/ irregularly sized and spaced projections that are most commonly seen in liver disease.

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