March 14 - Heme/onc Flashcards
Haldane effect
O2 affects affinity of hemoglobin for CO2/H+. Serves to increase CO2 delivery to lungs. Increase in PO2 increases CO2 and H+ offloading from Hb.
LMWH compared with UH
Better bioavailability Can give SC Less monitoring Longer half half Less easily reversible
Direct thrombin inhibitors
Argatroban, dabigatran, bivalirudin
Direct factor Xa inhibitors
Apixaban, rivaroxaban. Oral, don’t require monitoing but not as easily reversible.
Fondaparinux
Factor Xa inhibitor
Antiemetics used for chemo-induced vomiting
1) 5-HT3 antagonists: ondansetron and granisetron
2) Dopamine antagonists: metoclopromide, prochlorperazine
3) Neurokinin1 antagonists which prevent substance P release: aprepitant, fosaprepitant
Mutation in polycythemia vera (specifics)
Mutation in JAK2, which is involved in EPO signaling.
Normal pathway: EPO binds receptor. Receptor interacts with JAK2, which is a cytoplasmic tyrosine kinase receptor. Leads to downstream signling and activation of STATs.
Mutated pathway: JAK2 constitutively active resulting in overproduction of red cell.
Labs in sickle cell trait
Normal retic count, HGB, RBC indices and morphology
Integrins
Bind collagen, laminin, and fibronectin in the ECM to facilitate adhesion
Acute intermittent porphyria: presentation, pathophysiology, prevention, treatment of acute attacks
Presentation: episodes of abdominal pain, N/V, peripheral neuropathy, neuropsych derancements, red urine that darkens on exposure to light and air due to exccess PBG
Pathophys: AD defect in porphobilinogen deaminase in heme synthesis pathway. Causes early heme intermediates to accumulate and cause NS damage.
Prevention: avoid alcohol, smoking, and CYP inducing drugs which increase ALA synthase activity
Treatment : dextrose and IV heme which decrease ALA synthase activity
Cutaneous porphyrias
Caused by defect later in pathway than AIP. Photosensitivity
Heme synthesis pathway
Glycine and succinyl coA ALA Porphobiolinogen many steps Porphyrin IX Heme
Osteoblastic vs osteolytic bone mets: which cancers
Osteoblastic: prostate, small cell lung, hodgkin
Osteolytic: multiple myeloma, non-small cell lung, non-hodkin lymphoma, RCC, melanoma
Congenital parvovirus B infection, type of virus
Mom: arthritis
Fetus: hydrops fetalis due to interruption of erythropoiesis in bone marrow
Virus type: ssDNA
Congenital infections causing chorioretinitis
CMV or toxoplasma
Congenital infections causing sensorineural hearing loss
Rubella, CMV
Presentation of follicular lymphoma
Indolent, waxing and waning course. Painles LAD
Auer rods
Indicate myeloid differentation. Stain for peroxidase
RhoGAM: MOA
Anti-Rh(D) IgG pooled from donor plasma (polyclonal antibody). Binds to Rh-pos fetal RBCs that enter maternal circulation to prevent them from interacting with the maternal immune system and being sequestered in the spleen. Amount given is small enough that there is no significant transplacental fetal hemolysis.
IgG is given because that is what is produced against Rh antigens (vs IgM made against ABO)
Stop codons
UAA, UAG, UGA
Sickle cell mutation
Valine sub for glutamic acid
HMP shunt: location, products, key enzymes
In cytoplasm.
Produces ribose 5-phosphate and NADPH
Enzymes: transaldolase and transketolase
Blood cells in EBV infectious mono
Infects B cells by binding CD21 receptor
CD8+ cells clonally expand to kill the virus-infected cells. Appear larger than usual with abundant cytoplasm, eccentrically placed nuclei, membrane that appears to adhere to neighboring cells
Cyanide poisoning: pathophys, presentation, treatment
Pathophysiology: binds iron-containing cytochrome enzymes, inhibiting aerobic metabolism
Presentation: flushing, increased RR and HR, headache
Antidote: nitrites which induce formation of methemoglobin. Methemoglobin has high affinity for cyanide and sequesters it in blood