HEME 2 Flashcards
How do you manage a Hydatiform Mole?
- SUCTION CURATAGE
- OCP + Weekly B-HCG until undetectable.
- -> If B-HCG starts increasing = Trophoblastic neoplasia - After B-HCG if undetectable, Cont OCP + Montly B-HCG X 6 months
- -> If B-HCG starts increasing = Trophoblastic Neoplasia
For a Hydatiform Mole…
How do you get a COMPLETE MOLE?
How do you get an INCOMPLETE MOLE?
COMPLETE MOLE:
- 1 sperm + Egg w/out DNA (46 chromosomes)
- 2 sperm + Egg w/out DNA (46 chromosomes)
INCOMPLETE MOLE:
- 2 sperm + 1 egg (69 chromosomes)
What cancer are individuals with Hydatiform Moles at increase risk of?
Gestational Trophoblastic Neoplasia
What is the pathophysiology of PERNICIOUS ANEMIA
Autoimmune destruction of Parietal cells, which secrete Intrinsic Factor, which binds B12 and helps it’s absorption in terminal ilium. –> b12 deficiency.
Pernicious anemia is associated with what type of Gastritis? (HIGH YIELD)
What are the 3 main features of this type of Gastritis?
AUTOIMMUNE METAPLASTIC ATROPHIC GASTRITIS (AMAG)
- Glandular atrophy = loss of rugae in body/fundus
- Intestinal metaplasia of Gastric cells into villous cells intestinal cells
- Inflammation
What is the test of choice if you suspect Pernicious Anemia?
Anti-IF Ab testing (superior to Schillings which is not really done)
What three drugs classically cause Megaloblastic Anemia due to interference with FOLATE metabolism?
- MTX
- Trimethoprim
- Phenytoin
What is the TRX of MTX induced megaloblastic Anemia?
FOLONIC ACID (LEUKOVORIN) - Bypasses the inhibition of MTX on Folic Acid metabolism
Multiple Myeloma is a malignancy of what type of cells?
What age does MM typical present?
What are is the common clinical presentation?
Monoclonal proliferation of Plasma cells , producing significant amounts of monoclonal Abs.
Age > 65 yo.
Presentation:
- Pathologic fractures
- Fatigue
- Frequent infection
- END ORGAN damage (Renal insuff, hyper Ca, normocytic anemia, Lytic Bone lesions)
How do you dx Multiple Myeloma?
DX:
First –> SPEP and UPEP.
Confirm –> Bone marrow Bx showing > 10% clonal plasma cells.
In an individual with MM who acutely presents with bleeding gums/mucosa, blurred vision, HA, dizziness, and heart failure….what should you consider on differential?
TRX?
Hyperviscosity Syndrome
TRX: Plasmapheresis
Treatment of a SUPRATHERAPEUTIC INR depends on the INR level and if there is active bleeding…
What is the treatment for the following situations?
- INR <5 + no/min bleed?
- INR 5-9 + no/min bleed?
- INR > 9 + no/min bleed?
- Any INR + Serious bleed?
- INR <5 + NO/MIN BLEED:
- Hold warfarin dose for 1-2 days, then decrease dose. - INR 5-9 + NO/MIN BLEED:
- Hold Warfarin until INR is therapeutic then resume at lower dose.
OR
- Low dose oral Vit K (1-2.5 mg) if concern for risk of bleed) - INR > 9 + NO/MIN BLEED:
- Hold Warfarin
- Give High dose oral K (2.5-5mg) - ANY INR + SERIOUS BLEED:
- Hold Warfarin
- Give 10 mg IM K + (Fresh Frozen plasma or prothrombin complex concentrate)
Oral K and IV K have similar effectiveness in decreasing INR over 24 hour period…so as long as you don’t have a major bleed, you should use oral K. Additionally IV K has the risk of what?
Anaphylaxis.
What is the trx for Vaso-occlusive pain crisis of Sickle Cell Disease?
- Analgesics (NSAID, OPIOIDS)
- IV hydration
- RBC transfusion for:
- Priapism
- Stroke
- MI
- Acute Chest (if criteria met)
Acute Chest Syndrome is a potentially life threatening Pulmonary complication of Sickle Cell Disease..
What is the diagnostic Criteria?
What is the TRX?
- New pulmonary Infiltrate on CXR + 1 of the following
- Increase work of breathing/tachypnea
- Fever
- Hypoxemia
- CP
TRX:
- Ceftriaxone or Azithromycin (bc infection is most common cause)
- IVF + Pain control
- Blood transfusion if:
- SpO2 < 92
- Significant anemia
- Worsening dyspnea despite above trx.
