Hemato-onco Flashcards
Very large nucleated cells (blasts) with purple-red inclusions (Auer rots) is a hallmark of
It’s most common in
Acute myeloid leukemia
65 year old patients
Hallmarks of Hodgkin lymphoma
-Reed-stenberg cells
-B sts + presents with mass
Hypersegmented neutrophils with6 or more lobules should always make you suspect
Megaloblastic anemia
Hallmarks of B12 deficiency
Neurological disfx: usually start affecting proprioception (recurrent falls) and vibration
-MVC > 110 (also in Folic acid def)
-Hypersegmented neutros (“ “)
How and why does an Acute hemolytic transfusion rx present?
Fever, chills, dyspnea, chest or back pain and hemoglobinuria within min to hours of transfusion.
Usually due to ABO incompatibility (Type ll hypersensitivity rx - mainly IgM)
Possible triggers of DIC
Sepsis
Malignancy
Trauma
Obstetric complications
Pancytopenia in the settings of sepsis most likely indicates
DIC
What’s the mec of DIC due to sepsis ?
Endotoxins activate coagulation cascade which leads to widespread fibrin deposition, shearing of RBC = schistocytes
Atypical lymphocytes are usually seen in
Infections, specially Mononucleosis
Howell-Jolly bodies are round, dark, purple-red inclusions in RBC seen in
Splenectomy, spleen disfx, sickle cell disease.
Howell-Jolly bodies are round, dark, purple-red inclusions in RBC seen in
Splenectomy, spleen disfx, sickle cell disease.
Which type of donor is most appropriate for Congenital diseases that require bone marrow transplants?
Matched unrelated donor (can have near perfect HLA matching)
Why aren’t Autologous and syngenetic donor a good option for congenital genetic disorders?
Autologous = Cells harvested from patients (eg umbilical cord) will have the same problem.
Syngenetic = cells from identical twin will have exact HLA match and not be rejected but will have same congenital mutation
Pathophysiology Chronic myeloid leukemia ?
Translocation of genes between chromosomes 9 and 22 with the resulting fusion of genes BCR-ABL
Sickle cell disease hallmarks
-hemolysis
-vasoocclusion
-Infections
*small and firm spleen
Pathophisiology of sickle cell disease
Beta globin Mut (Glu for Val) Polymerization of HbS lead to sickle shaped RBCs which cause small vessel occlusion and hemolysis
Numerous plasma cells (>10%) in BM aspirate is characteristic of
Multiple myeloma
Features of multiple myeloma
-Monoclonal ig spike
-Normo-normo anemia
-hypercalcemia and bone lesions
-Light-chain cast nephropathy/renal insuf
-Amyloidosis
Main difference between sickle cell anemia and sickle cell disease
No HbC present in SC anemia
Pathophysiology of Homozygous sickle cell anemia
Mut in both beta globin genes (change of glutamate for valine) = forms beta sickle globins = unable of producing HbA (has beta globin) but can produce HbF and HbA2 (don’t have beta globin)
Acute intermittent porphyria presents as
Recurrent abdominal pain
Neurological symptoms
Port-wine colored urine
Pathophysiology of Acute intermittent porphyria and tto
Failure to produce heme. Accumulation of perphyrin precursors in blood and urine due to enzyme deficiency (porphobilinogen deaminase.
tto is hemin infusion (downreg aminolevilinate synthase)
A mutation in beta globin gene (beta thalassemia) affects which cellular process?
Initiation of translation bc mutation occurs before methionine start codon (AUG) needed for the Kozak consensus seq to initiate protein translation
Blood smear Findings in Beta thalassemia:
-microcytosis
-increased central pallor (hypochromia)
-target cells
-anisopoikilocytosis (different shape,sizes)
-basopholic stippling
Hereditary spherocytosis is caused and characterized by
RBC membrane cytoskeleton defect.
Hyperchromia. Defects in spectrin, ankyrin.
Difference between iron deficiency anemia and thalassemia’s anemia
There’s usually iron overload in thalassemia
Sickle cell anemia occurs due to
A to T Mutations in beta globin gene that make glutamate be replaced by valine
Which anticoagulant is most appropriate during pregnancy
Heparins bc they do not cross the placenta
Difference in use between LMWH and Unfractioned ?
LMWH: long-term life. Does not req lab monitoring. Renal clearance (can’t use if GFR<30). It’s usually preferred. (Ex enoxaparin, dalteparin)
Unfractioned: used in severe renal insufficiency and at term pregnancy (37 weeks)
Difference in use between LMWH and Unfractioned ?
LMWH: long-term life. Does not req lab monitoring. Renal clearance (can’t use if GFR<30). It’s usually preferred. (Ex enoxaparin, dalteparin)
Unfractioned: used in severe renal insufficiency and at term pregnancy (37 weeks)
Direct thrombin inhibitors (factor IIa)
-batran
-gatran
-troban
Which factors are targeted by heparins
Xa
IIa (thrombin)
Which factors are targeted by heparins
Xa
IIa (thrombin)
Werfarin must-knows
-Vit k antagonist: inhibits factors Vll, IX, X, ll
-Monitored with PT and INR
-Can cause skin necrosis (Prot C reduction befor affection of other factors) -> Req Heparin bridge (before Werfarin)
-Teratogenic toxicity
PT, PTT and BT are used to monitor
-Werfarin and extrinsic pathway disease
-LMWH and intrinsic “
-Platelets function
Which drugs are most commonly rel to drug induced immune mediated hemolysis?
Anti-inflam, penicillins and cephalosporins. The last two cause extravasc hemolysis by IgG binding to surface of RBC
Which drugs are most commonly rel to drug induced immune mediated hemolysis?
Anti-inflam, penicillins and cephalosporins. The last two cause extravasc hemolysis by IgG binding to surface of RBC
Hemolysis is characterized by
Symptomatic anemia
Indirect hyperbilirubinemia
Retycolocytosis
Low haptoglobin (binds to Hb)
Confirmed by direct Coombs test
Anemia of chronic disease is caused by
Cytokine mediated iron desreg
Iron deficiency anemia is characterized by:
-Microcytosis
-Hypochromia
-Poikilocytosis (several shapes) if severe
-common in young women (menstruation)
- high EPO but reduced RBC and reticulocytes
-high transferrin (increased iron scavage) but low saturated transferrin
-hepcidin is low (no inflam related)
Chronic disease anemia
Normo-normo
Mediated by hepcidin
Inflam: High hepcidin, High serum cytokins, PCR
Low serum iron
Transferrin normal or decreased and transferrin sat low
EPO is variable
High bone marrow iron (due to sequestration by macrophages)
Severe chronic hemolysis is associated with
Presence of erythroid precursors in liver and spleen (increased size). Extramedullary hematopoiesis (driven by increased EPO)
Causes can be beta thalassemia or sickle cell disease
Burr and helmet cells are associated to
Traumatic hemolysis
Paroxysmal nocturnal hemoglobiuria
Complement mediated
Pancytopenia
Hallmarks of B-lymphoblastic Leukemia
Expression of TdT
markers CD > or same as 10
Lack of MPO
Target cells are seen in
Def hemoglobin level synthesis = thalassemia, iron deficiency
Obstructive liver disease, splenectomy
The following are associated to:
1.Pappenheimer bodies
2.Howell-jolly bodies
3.Heinz babies
4.Sphirocytosis
5. Basophilic stippling
1.sideroblastys anemia (dark blue)
2.hyposplenia asplenia (dark purple, blue inclusions
3.G6PD def, thalassemia
4. Hemolysis and hereditary spherocytosis
5. Thalassemia, heavy OH use, lead/metal poisoning
Which heparin is most effective inactivating Thrombin?
-Unfractioned H: Thrombin = Xa
-LMWH: Xa > thrombin (less antithrombin activity)
Rasburicase is given prior or during chemo to
Protect organs by converting Uric acid into soluble metabolites
Tumor lysis sd causes
HyperK
HyperPHO4
Hyperuricemia -> AKI
How do you treat Tumor lysis sd after chemo Adm
Aggressive intravenous to flush phosphorus and uric acid out of kidneys
Rasburicase: adds urate oxidase to increase allontin (more soluble)
Allopurinol: competitive inhibition of xanthine oxidase to produce less uric acid
Mesna is used to prevent
Hemorrhagic cystitis’s by Cyclophosphamide or ifosfamide
Leucorovin prevents
Methrotrexate adverse side effects
Hepcidin’s mec in chronic anemia
Binds to ferroportin on enterocytes and reduces iron absorption in gut
Heparin’s mec
Binds to antithrombin lll which neutralizes clotting factors Xa and lla (indirect effect)
Vincristine’s mec and effect
Microtubule formarion inhibitor by binding to beta tubulin and inhibiting proliferation.
Microtubules are critical for axonal transport ~> peripheral neuropathy
Vincristine’s mec and effect
Microtubule formarion inhibitor by binding to beta tubulin and inhibiting proliferation.
Microtubules are critical for axonal transport ~> peripheral neuropathy
Anthracycline’s main adverse effect
Cardiotoxicoty
What’s aspirin’s mec? And lifespan?
Blocks Cox1 primarily and it’s irreversible
Cox1 can’t produce Troboxane A2 -> no increase glucoprot llb, lllA -> no platelet aggregation/activation
Lifespan: 3-7 days
How many days prior to sx should aspirin be suspended?
Minimum 5 days prior to
Principal site of uric acid precipitation
Distal tubules and collection ducks (where pH is lowest, key for its precipitation)
Tumor lysis management
Alkalinization and Hydration
Allopurinol (xanthine oxidase inhibitor) reduces uric acid production
What can Exclusive breastfeeding cause ? Why?
Iron deficiency anemia due to loss through shedding of epithelium which depletes the low reserves of babies
Iron deficiency stages
1.Reduced storage: low ferritin level only
2.Iron limited erythropoiesis: transferrin increases and transferrin sat decreases
3. Iron deficiency anemia: low MVC and MCHC. Reduce reticulocytes
Iron deficiency stages
1.Reduced storage: low ferritin level only
2.Iron limited erythropoiesis: transferrin increases and transferrin sat decreases
3. Iron deficiency anemia: low MVC and MCHC. Reduce reticulocytes
Francisella tularensis causes ___ and risk factor
Single papiloulcerative lesion
Contact with wild animals
