Hematology / Oncology Flashcards
Transfusion targets in sickle cell disease
Hgb < 50 unless heart failure, dyspnea, hypotension
Hgb ~ 100 in acute chest syndrome
3 causes of acute drop in hemoglobin in sickle cell disease
Splenic Sequestration
Aplastic Crisis - First test is RETICS (Low in aplastic)
Hemolysis / MAHA
Causes of sickle cell disease
HgbS + HgbS
HgbS + Hgb BThal
HgbS + HgbC
- Usual first presentation of dactylitis
Acute Chest Syndrome Diagnosis and Mgmt
Rehydration
Analgesia
Incentive spirometry
02 > 92%
Empiric antibiotics -
Consider exchange transfusion
treatment of vaso-occlusive crisis
Can be triggered by cold, humidity, stress, EtOH
+++ Pain meds. i.e 1 Dilaudid IV Q15 mins
O2 and IV fluids PRN
Hydroxyurea can prevent reduce incidence.
CLL Diagnosis
Lymphocytes > 5 on repeat test without underlying illness
Blast Crisis definition / mgmt
Hyperviscocity syndrome
- WBC > 100, blasts > 20
- Mucosal bleeding
- Headaches and ataxia
- Visual changes
Tx: Dilute: hydration, oxygen and supportive care. Hematology consult
- Phlebotomy: withdraw 2U of blood.
TTP Presentation and treatment and Mimics
Fever (rare)
Anemia
Thrombocytopenia
Renal failure
Neurologic Sx
Mgmt: Supportive care, Plex, FFP as a temporization
Mimics:
SLE - APLA
Vasculitis
Malignant Hypertension
Compliment mediated HUS
DIC
Pre-eclampsia / HELLP
Disseminated Malignancy
ITP
Look for “wet puppura” in oral mucosa
Usually do ok - low rates of bleeding
Plts < 30, call heme
If > 30, observe ensure f/u
Tx: steroid, IVIG, rituximab (down the road), consult heme
If severe bleed: IVIG 1g/kg. Methylpred 1g IV,, TXA 1g over 15 plus 1g over 8 hrs, call heme, transfuse
Platelet transfusion threshold
Chemotherapy: < 10
Chemo + Fever: < 20
ITP: 30 with bleeding
DIC with bleeding: 50
Life threating bleeding: 50
ICH: 100
LP: 50
Paracentesis: Doesn’t matter
Central Venous: <20
Transfusion fever dx and management
Stop transfusion
- Acute hemoltyic
- Sepsis
- Febrile, non-hemolytic transfusion reaction
- TRALI (resp distress, usually several hours later)
Stop
Full set vitals
RE-check: Call transfusion medicine - clerical check
Hemolytic workup
If mild: give acetaminophen and continue
Transfusion fever dx and management
Stop transfusion
- Acute hemoltyic
- Sepsis
- Febrile, non-hemolytic transfusion reaction
- TRALI (resp distress, usually several hours later)
Stop
Full set vitals
RE-check: Call transfusion medicine - clerical check
Hemolytic workup
If mild: give acetaminophen and continue
Hemolytic Anemia Diagnosis and DDx
Diagnosis:
- CBC, smear, retics, haptoglobin, LDH, bili (total and direct), DAT, fibrinogen
DDx:
-Hereditary: Sickle, G6PD, Spherocytosis
-Acquired: Autoimmune warm / cold (IgG, bind at body temp, usually a malignancy caused / EBV or Mycoplasma pneumonia, lymphoma or Waldenstroms), Alloimmune (newborn, transfuse), drug induced (cephalosproins, sulfa, levodopa, penicillin..)
-Framentation:
DIC - sepsis, meningococcemia, bacteremia, trauma, etc. - Supportive mgmt
TTP - Congenital or acquired ADAMSTS13 deficiency. Bicytopenia, ALTERED MENTAL STATUS, renal failure, neuro issues). Treatment: PLEX +/- steroids
HUS - Post β hemolytic (Shiga toxin producing) E.coli.
Pregnancy
Malignant HTN
Malignancies
Anemia causes by MCV
Microcytic < 80
- Thalassemia
- Anemia of chronic disease
- Iron Deficiency
- Lead poisoning
- Sideroblastic
Normocytic 80-100
- Hemolysis (sometimes macro)
- Bleeding (sometimes macro)
- Anemia of chronic disease (sometimes micro)
- Marrow failure (aplastic anemia, myeloproliferative disorders)
- Infectious (EBV)
- Hypothyroid
- Hypoadrenal / Hypopit
- Renal failure
Macrocytic:
- B12
- Folate
- Reticulocytosis
- EtOH
- Hypothyroisd
What is sideroblastic anemia
Disorder of porphyrin leads to iron deposition in mitochondria of RBC precursors
- Genetic in kids
- Acquired in adults: infections, carcinoma, leukemia, RA, EtOH, lead poisoning
Drugs that can trigger hemolysis in G6OD
Aspirin
Antimalarials (Quinine, Plaquenil)
Nitrofurans
Sulfa
FAVA beans
6 Diagnostic lab tests for hemolytic anemia
Peripheral smear
DAT
Haptoglobin
unconjugated bili
LDH
Serum free Hgb
Types of intravascular hemolysis
Intra: MAHA(s), burn, infections, autoimmune, transfusion
Extra: Malignancy, enzyme deficiency, hemoglobin defects, hypersplenism, toxins
Causes of Leukocytosis / Lymphocytosis
Leuko:
- Infection
- Medications - Steroids
- Trauma
- Pregnancy
- Lymphoproliferative (CML, PV)
- hereditary neutrophilia
- Eosinophilia
- DKA
- Thyrotoxicosis
- Seizures
Lymphocytosis:
- Viral (mono, rubeola, rubella, varicella), CLL, graft rejection
Things affecting O2 dissociation curve
Right shift: acidosis, increased CO2, fever/hyperthermai, increased 2,3 BPG
Left Shift: alkalosis, cold,
Hemostasis steps
Endothelial injury
Platelet plug
Activation of cascade
Clot formation
Fibrinolysis
10 causes of thrombocytopenia
Production:
- Aplastic anemia / Marrow failure
- Liver failure
- Drugs: chemo, EtOH, septra, digoxin, ASA
Destruction:
- ITP
- Collagen vascular disease
- Transfusion reactions
- TTP
- HIT
- DIC
- HUS
- Vasculitis
- Massive transfusion
- Infection - Rubeola, Varicella
Sequestration:
- Hypersplenism
6 causes of thrombocytosis
Reactive:
- Infection
- Iron deficiency
- Trauma
- Non heme malignancy
- Post splenectomy
- Rebound from deficiency
PV
Primary
HIT vs ITP
HIT:
- Usually 5-7 days post exposure
- Present with bleeding and thrombocytopenia or thrombosis
- Isolated thrombocytopenia
ITP:
Acute: usually in age 2-6.
- Preceded by viral prodrome-
- Self limited
- Can use IVIG, steroids and plamapheresis
- Platelets < 20
Chronic: Women>men, insidious onset
- Plt 30-100 k
TTP vs HUS
TTP: ADAMTS-13
- MAHA
- Typically adults age 10-40 years. F > M
- Mnemonic “FAT-RN” with more neuro involvement
“Fever
Anemia
Thrombocytopenia
Renal impairment
Neurologic impairment”
- Most common onset after quinine or plavix
- Tx: Plasma exchange +/- ritux/steroid/ASA
HUS: Usually post infectious
- Autoimmune abdominal vasculitis
- Typically pediatric patients
- Supportive case
PT vs PTT abnormality
PT:
- Rare genetics. Usually warfarin, Vit K deficiency or liver disease
PTT:
- More common, hemophilia A and B
- Factor 8, 9, 11
For PTT inherited disorders:
Tx - FFP 15 ml/kg or factor concentrate at 50U /kg
Hemophilia A and B
Factor VIII and IX
Sex linked recessive M 4x F
Severity based on VIII activity assay
Mgmt with factor replacement or FFP if needed.
Demopressin may be helpful
vWF deficiency
Most common inherited coagulopathy
- lack of vwF.
- presents with mucosal bleeding and menorrhagia
- For severe dsiease fiver factor VIII
For mild give demopressin +/- TXA
DIC Coagulopathy Mgmt
Treat underlying cause
Manage the primary issue:
- Bleeding - platelets, FFP, cryoprecipitate
- Clotting IV heparin
Febrile Neutropenia Def’. and Mgmt
ANC < 0.5 or anticipated to drop within 48 hrs with fever > 38.3 or 38 for > 1 hr
Most common infections:
- Pneumonia, UTI, skin, anorectal, pharyngitis
Tx:
Low Risk: Oral cipro or amox clav
High Risk: Pip-tazo +/- vanco if known MRSA, cellulitis, severe sepsis, severe mucositis, Blood culture with gram +ve cocci
Signs of spinal cord compression
Back pain
Leg weakness
Saddle parasthesia
Autonomic dysfunction
Causes of pericardial effusion in malignancy
Malignancy
Hypoalbuminemia
Radiation
Chemotherapy
Hypercalcemia symptoms and management and causes
Bone pain / fractures
Nephrolithiaisis
Abdo pain / constipation
Altered mental status
ECG: short QT
Ca2+ > 3.0 for symptoms
Mgmt:
- IV fluids resus
- Loop Diuretics
- Dialysis
- Bisphosphonate
- Consider calcitonin
Causes:
Paraneoplastic - PTHrP
PTH producing tumor
Bone resorption
Electrolyte abnormalities in TLS and Mgmt
Hyper K+
Hyperphosphatemia
Hyperuricemia
Hypocalcemia
Treatment of TLS
IVF 5-6 L / day (200-250 /hr)
Hyperkalemia mgmt
Hyperuricemia:
- Allopurinol as preventative, not in acute
- Rasburicase
Hypocalcemia: Give calcium only if cardiac or neuro abnormalities
What is leukostasis
Hyperviscosity syndrome 2nd to markedly elevated WBC in hematologic malignancies
Usually WBC > 100
Symptoms primarily in neuro and pulmonary
Conditions associated with hyperviscosity syndrome, symptoms and mgmt
AML/ALL/PV
Multiple myeloma
Waldenstrom’s
Sickle cell
Malaria or babeiosis
Presents with visual changes, AMS and mucosal bleeding
Mgmt: PLEX, phlebotomy and IV fluids replacement
Presentation of SVC syndrome
Red plethoric face or UE caused by compression of the SVC
- +/- CP, dyspnea or cough
JVD and cyanosis of upper trunk
Pemberton’s sign.
Collateral veins often present
Cancers that met to bone
Prostate
Testes
Breast
Lung
Multiple myeloma
Kidney
