Term
| Thalassemia changes in hb, hct, rbc, mcv:rbc |
|
Definition
| Hb/Hct are dec, rbc count is inc, mcv:rbc <13 |
|
|
Term
| Central pallor area is ____ in dec MCHC and ___ in inc MCHC (what condition): |
|
Definition
| increased in dec MCHC (all microcytic anemias due to dec Hgb synth); dec in inc MCHC (SPHERICAL RBCs! => hereditary spherocytosis) |
|
|
Term
| Fucntion of metHb reductase? |
|
Definition
| To reduce Fe3+ to ferrous iron allowing RBCs to bind O2 |
|
|
Term
| Where is ferritin synth and what stimulate its synth? |
|
Definition
| In Bone marrow macrophages and increases synth during inflammation due to IL1 and TNFalpha |
|
|
Term
| What conditions => inc or dec ferritin? |
|
Definition
| And can use hemosiderin an insoluble prod of ferritin degrade as a measure. |
|
|
Term
| What is serum iron bound to? |
|
Definition
| Transferrin prod in the liver. Inc serum iron in overload (sideroblastic, hemochromatosis), dec in ACD or iron deficiency |
|
|
Term
| Abnormal and normal Hb => |
|
Definition
| abnormal is sickle Hb, HbH, Hb Bart; normal is HbA (2a/2b) = 97%, HbA2 (2a/2delta) = 2%, and HbF (2a/2y) – 1% |
|
|
Term
| a-thal trait, b-thal minor, b-thal major, sickle cell trait, SCD… |
|
Definition
|
|
Term
| what kind of iron is reabs in the gut and what helps convert it? |
|
Definition
| A) Only FERROUS (Fe2+) the reduced form, that’s present in MEAT in a heme form, HAPPENS IN THE DUODENUM B) ascorbic acid reduces it in nonheme foods, and gastric acid frees elemental iron from heme/nonheme products – pathology happens w/ achlorhydria |
|
|
Term
| regulation of amt of iron reabs depends on? |
|
Definition
| HFE gene and binding of plasma transferring to its mucosal cell transferring receptor allowing endocytosis of transferring |
|
|
Term
| Findings of Plummer-Vinson syndrome: |
|
Definition
| caused by chronic Fe-Def, esophageal web (dysphagia for solids), achlorhydria, glossitis, koilonychias |
|
|
Term
|
Definition
| liver synth/release of hepcidin which is normally released as an antimicrobial peptide in response to inflammation => enters BM macros and prevents release of iron to transferrin, so ferritin increases and so do iron stores in the BM macros = RETICULOENDOTHELIAL BLCOK |
|
|
Term
| a-thal TRAIT pathogenesis in blacks vs. Asians: |
|
Definition
| gene deletions on both chromosomes in blacks (a/-, a/i) and on only one in Asians => put them at riks of more severe types of a-thal. |
|
|
Term
|
Definition
| 4 beta chains due to combination of 3 gene deletions => severe hemolytic anemia due to macrophage destrx of RBCs due to excess b-chain inclusions. |
|
|
Term
|
Definition
| 4 gene deletions (4 gamma chains) – incompatible with life. |
|
|
Term
| B-thal minor vs. major and pathogenesis of mild vs. severe anemia? |
|
Definition
| Dec b-globin chain synthesis, severe anemia due to nonsense mutation with stop codon vs. mild is due to DNA splicing defects; Minor – protective against falciparum, dec HbA, inc in everything else. Major – alpha chain inclusions => removed by macrophages in spleen => inc in unconj bilirubin and erythropoeisis in BM is not effective, NO HbA and need extramedullary hematopoesis, long-term transfusions. |
|
|
Term
| Pathogenesis of sideroblastic anemia: |
|
Definition
| in alcoholics (it’s a mitochondrial toxin), pyridoxine (B6 deficiency – in INH therapy for TB since it complexes with pyridoxine that’s needed for S-aminolevulinic acid synthase, the rate limiting reaction of heme synth), Pb poisoning, X-linked recessive inheritance; defect in heme synth in mitoch => ringed sideroblasts. |
|
|
Term
|
Definition
| Denatures ferrochelatase (impaired iron binding with protophoryin to form heme, increase in upstream FEP), ALA dehydrase (increased proximal delta-ALA), ribonuclease (lack of ribosome degradation => basophilic stippling) |
|
|
Term
| Clinical findings in Pb toxicity: |
|
Definition
| abdominal colic, encephalopathy, growth retardation (Pb deposits in epiphysis of growing bone), peripheral neuropathy, urine levels are diagnostic, renal toxicity, Pb lines in gums, treatment = CHELATION with succimer, dimercaprol, EDTA |
|
|
Term
| Macrocytic Anemias – name them: megaloblastic (folate, b12 def), and nonmegaloblastic (macrocytosis due to alcohol intoxication) |
|
Definition
|
|
Term
|
Definition
| HCl from parietal cells => activates pepsin to free B12 from proteins, free B12 binds to R-binders from saliv glands, which are cleaved off by panc enzymes in the duodenum and B12 binds to IF to form a complex => reabs in the terminal ileum, B12 binds to transcobalamin II => plasma |
|
|
Term
|
Definition
| veganism, dec IF/gastric acid, dec reabs due to surgery, crohn’s, or celiac dz, or in pregnancy/lactation w/ inc utilization |
|
|
Term
|
Definition
| in veggies/proteins as a polyglutamate => conv to monoglutamate by intestinal conjugase (inhibited by phenytoin) => reabsorbed monoglutamates in the JEJUNUM => MTHF. EtOH/OCPs block abs of monoglutamates. |
|
|
Term
| Pathogenesis of macrocytic anemia in B12/folate def: |
|
Definition
| 1) imp DNA synth => delayed nuc maturation => enlarged nucleated hematopoetic cells (megaloblasts) due to blocked cell division, fx all rapidly dividing cells!, cellular RNA and protein synth continue unabated so inc volume, megaloblastic precursors outside BM sinusoids are phagocytosed by macros. 2) ineffective erythropoiesis – megaloblastic precursors outside BM sinusoids are phagocytosed and undergo apoptosis => anemia, neutropenia, TCP |
|
|
Term
| Big marker of folate deficiency? |
|
Definition
| Inc homocysteine levels due to methylB12 inability to transfer the methyl group to homocysteine to make it methionine. Homocystein also elevated in B12 def. |
|
|
Term
|
Definition
| Irreversibly inhib thymidylate synthase that converts dUMP to dTMP… |
|
|
Term
| What drugs inhibit DHFreductase that converts dihydrofolate to FH4? |
|
Definition
|
|
Term
|
Definition
| inc in propionyl and methylmalonyl CoA => propionyl replaces acetyl CoA in neuronal membranes => demyelination! The pathway is propionyl => mmCoA => (B12/mutase) succinylCoA… |
|
|
Term
| Pernicious anemia findings: |
|
Definition
| more in blood group A, achlorhydria due to parietal cell destrx, TII hypersensitivity antibodies against the proton pump in parietal cells, or b12/IF binding to each other or to ileal receptors…antibodies destroying parietal cells => atrophic gastritis and gastric adenocarcinoma! |
|
|
Term
|
Definition
| peripheral neuropathy, subacute combined degen of spinal cord (posterior column => dec vibratory and proprioception), lateral corticospinal -> spasticity, dorsal spinocerebellar => ataxia, dementia |
|
|
Term
| Alcohol’s effect on RBCs? |
|
Definition
| Round macrocytes (TARGET CELL!), due to excess RBC membrane from inc membrane cholesterol (from liver disease), NO anemia due to normal lifespan, vacuolization of RBC precursors in BM, reversed by abstinence. |
|
|
Term
| Acute blood loss, early Fe-Def or ACD = reticulocyte response: |
|
Definition
| reticulocytes takes 5-7 days for acute loss, you see normocytic anemia BEFORE microcytic in fe-def/acd (need serum ferritin to distinguish) |
|
|
Term
|
Definition
| drugs most common (alkylating agents, chloramphenicol), most idiopathic, infections, radiation, thymoma, or PNH |
|
|
Term
| Aplastic anemia pathogenesis: |
|
Definition
| antigenic alteration of myeloid stem cells (T-cell activation and release of cytokines to suppress myeloid stem cells), defective myeloid stem cells |
|
|
Term
| Triad of clinical and lab findings in AA: |
|
Definition
| fever bleeding fatigue…lab findings are pancytopenia, reticulocytopenia, hypocellular bone marrow with lots of adipose cells! |
|
|
Term
|
Definition
| bs abx to prevent infx, transfusions with irradiated blood, immunosuppressive therapy, BM transplantation |
|
|
Term
| Anemia of chronic renal failure: |
|
Definition
|
|
Term
| Malignancy => anemia…causes? |
|
Definition
| ACD, gastrointestinal bleeding, bone marrow metastases (myelophthisic anemia with marrow hematopo cells or leukoerythroblastic smear with nucleated rbcs/immature myeloids), immune hemolytic anemia (IHA) |
|
|
Term
| Normocytic anemias with corrected reticulocyte >3%: |
|
Definition
| intrinsic (prob w/ RBC such as membrane defect, abnormal hgb, enzyme def) or extrinsic (immune destruction or valve) |
|
|
Term
| Extravascular hemolysis causes: |
|
Definition
| rbc phagocytosis by macros in spleen/liver, due to coating with IgG +/- C3b, or abnormally shaped RBCs (spherocytes/sickles) |
|
|
Term
| Tests of extravasc hemolysis: |
|
Definition
| inc in unconj bilirubin, inc LDH from hemolyzed rbcs |
|
|
Term
| Intravasc hemolysis causes: |
|
Definition
| enzyme deficiency (G6PD), complement destruction (IgM), mechanical damage from calcified valve. |
|
|
Term
| Tests of intravasc hemolysis: |
|
Definition
| plasma/urine hgb inc, hemosiderinuria, dec serum haptoglobin (acute phase reactant that combines with hgb to form a complex that is phagocytosed and degraded by macros), not enough Hb in these complexes to => jaundices |
|
|
Term
| Hereditary spherocytosis pathogenesis: |
|
Definition
| AD, extravascular hemolysis due to membrane protein defect from mutation in ankyrin, band 2, spectrin, band 3, inc permeability of membrane to Na+ (so increase RBC osmotic fragility => will rupture in mildly hypotonic solution) |
|
|
Term
|
Definition
| jaundice, inc Ca bilirubinate gallstones (from inc conj bilirubin), splenomegaly, post-viral aplastic crisis |
|
|
Term
|
Definition
| splenectomy so the spherocytes end up remaining in the peripheral blood… |
|
|
Term
| Hereditary elliptocytosis pathogenesis: |
|
Definition
| AD, defective spectrin and band 4.1 |
|
|
Term
|
Definition
| no anemia or mild hemolytic anemia, splenomegaly, >25% elliptocytes in blood, inc osmotic fragility and tx w/ splenectomy in symptomatic px. |
|
|
Term
| Paroxysmal nocturnal hemoglobinuria path: |
|
Definition
| acquired membrane defect in myeloid stem cells => mutation causes loss of the anchor for decay accelerating factor (DAF) key to preventing the activation of membrane attack complex and lysis (from C3/C5 convertase adhering to RBCs, platelets, neutrophils). |
|
|
Term
| Why does PNH result in COMPLEMENT mediated destruction at night? |
|
Definition
| b/c respiratory acidosis enhances complement attachment |
|
|
Term
| PNH increases risk of what? |
|
Definition
| AML and vessel thrombosis (due to aggregating agents released from platelet destruction) |
|
|
Term
|
Definition
| normocytic anemia with pancytopenia, leukocyte alkaline phosphatase decreased, decreased haptoglobin, and inc Hgb in serum/urine. |
|
|
Term
|
Definition
| screen with sucrose hemolysis test (inc complement destrx), confirm with acidified serum test! |
|
|
Term
| Sickle Cell pathogenesis: |
|
Definition
| AR! Missense point mutation => subs of Val for Glutamic acid at 6th pos of B-globin chain => aggreg/polymerization of HbS molec. |
|
|
Term
| What makes sickling more likely to occur? |
|
Definition
| sickling in >60% conc of HbS and when you have increased deoxyhb (i.e. dec O2 saturation) |
|
|
Term
| Why no sickling in first 6mos? |
|
Definition
|
|
Term
| Clinical findings in HBSS? |
|
Definition
| Dactylitis (painful swelling of hand/foot due to bone infarcts in 6-9mo kids), acute chest syndrome -> common cause of death, aseptic necrosis of the femoral head, autosplenectomy (dysfunctional spleen by 2yo) => Howell-Jolly bodies in RBCs, and inc risk of infx (sepsis, or osteomyelitis from salmonella) |
|
|
Term
|
Definition
| transfusions, infx tx, pain relief; hydroxyurea to inc HbF, routine immunizations |
|
|
Term
| G6PD deficiency pathogenesis: |
|
Definition
| X-L recessive, most common enz deficiency => hemolysis, intrinsic defect => intravasc hemolysis mostly…due to dec synth of reduced NADPH (that becomes oxidized glutathione (GSSG) => GSH) and glutathione (GSH) in the pentose phosphate pathway. |
|
|
Term
| GSH’s role in this and lab finding: |
|
Definition
| GSH neturalizes H2O2 but in this G6PD-D, peroxide oxidizes Hb => precipitates as HEINZ BODY! This damages the rbc membranes/removed from RBC membranes by splenic macrophages and produces BITE cells! |
|
|
Term
| Lack of NADPH also causes what? |
|
Definition
Impaired neutrophils and monocyte killing of bacteria by the O2 dependent myeloperoxidase MPO system that requires NADPH as a cofactor for NADPH oxidase.
Drugs that would normally be taken care of by GSH but now cause oxidative stress: infection, primaquine, dapsone, sulfonamides, fava beans |
|
|
Term
|
Definition
| sudden onset of back pain with hgburia 2-3 days post an oxidative stress |
|
|
Term
|
Definition
| Heinz bodies IDd with supravital stain, enzyme test after hemolysis has subsided, BITE cells in peripheral blood |
|
|
Term
| Pyruvate Kinase deficiency pathogenesis: |
|
Definition
| AR, PK normally converts PEP to pyruvate to generate 2 ATP! The defect => lack of ATP and membrane damage, basically dehydration of the cells => EXTRAVASCULAR HEMOLYSIS! |
|
|
Term
| Clinical findings in PK-def: |
|
Definition
| jaundiced at birth, inc in 2,3 bph synthesis upstream (can off-set initial clinical effects due to right-shifted OBC) |
|
|
Term
|
Definition
| echinocytes – thorny projections from RBC membranes (so cell looks like one of those spiky baby balls), normocytic anemia, enzyme assay is best confirmatory test. |
|
|
Term
| Immune mediated hemolytic anemias: |
|
Definition
| AIHA, Drug-induced, alloimmune… |
|
|
Term
|
Definition
| warm is IgG, cold IgM (post-infectious with mono, mycoplasma), chronic lymphocytic leukemia is BOTH |
|
|
Term
|
Definition
| PNC -> IgG ab directed against drug attached to rbc membrane, quinidine (drug-IgM immunocomplex deposits), methyldopa (autoantibody induction, drug alters Rh ag on RBCs => synth of autoantibodies) |
|
|
Term
|
Definition
| C5-C9 coating RBCs, or IgM |
|
|
Term
|
Definition
| IgG (splenic macros), IgG +C3b (liver and splenic macros, as in SLE), C3b (liver macros) |
|
|
Term
|
Definition
| DAT coomb’s – detects rbcs sensitized with igG and or C3b; indirect just detects antibodies in the serum; unconj hyperbilirubinemia if extravasc hemolysis is present. Hgburia => dec serum haptoglobin (in INTRAVASC hemolysis). Spherocytosis if damage to RBC membrane. |
|
|
Term
|
Definition
|
|
Term
|
Definition
| enhance ATIII activity and neutralize activated serine protease coagulation factors (XII, XI, X, IX, thrombin) |
|
|
Term
|
Definition
| synth by endoth cells, conv by prostacyclin synthase to PGI2 => inhibits platelet aggreg and vasodilates. Not inhibited by ASA |
|
|
Term
|
Definition
| inhibits V/VIII and enhances fibrinolysis. |
|
|
Term
|
Definition
| synth by endothelial cells, activates plasminogen to release plasmin and plasmin degrades coag factors and lyses fibrin clot. |
|
|
Term
| Prothrombus formation due to? |
|
Definition
| TXA2 (platelet aggregation, vasoconstrictor) and vWF (platelet adhesion, complexes with VIII) |
|
|
Term
|
Definition
| Irreversibly inhibits platelet COX that prevents formation of PGH2 (the precursor to TXA2). |
|
|
Term
|
Definition
| It’s from endothelial cells/megakaryocytes, 1) binds platelets to exposed collagen using the GpIB receptor, 2) complexes with VIIIc in the circulation prevents degradation until VIIIc is activated by thrombin |
|
|
Term
|
Definition
| It’s factor III that is released from injured tissue and activates VII in the extrinsic coag system. |
|
|
Term
| Diff between GPIb and IIb/IIIa? |
|
Definition
| Ib receptor is for vWF and IIb/IIIa is for fibrinogen (ADP induced expression of IIb/IIIa is inhibited by clopidogrel, direct antibody against the receptor = abciximab) |
|
|
Term
| What activates the kininogen system? |
|
Definition
| Factor XIIa, which also activates plasminogen |
|
|
Term
| Final common pathway has what? |
|
Definition
X, V, II, I with the complex being Xa, V, PF3, and Ca2+
Factors consumed in a fibrin clot: I, V, VIII, II so if you spin a tube of blood down…the serum supranate is missing these!!! |
|
|
Term
|
Definition
| alteplase => activation of plasmin from plasminogen => FIBRINOLYSIS! |
|
|
Term
| Plasminogen is also activated by: |
|
Definition
| streptokinase, factor XIIa, urokinase |
|
|
Term
|
Definition
| blocks plasminogen activation and inhibits fibrinolysis |
|
|
Term
| Fibrin(ogen) degradation products: |
|
Definition
| result from plasmin and are insoluble fibrin monomers/fibrinogen. D-dimers are cross linked insol fibrin monomers. |
|
|
Term
|
Definition
| V, VIII, and fibrinogen and a2-antiplasmin (from the liver) inactivates plasmin |
|
|
Term
| VWD vs. Bernard soulier syndrome: |
|
Definition
| they both increase Bleeding time, but BS is ARec and due to abset GpIB platelet receptors for vWF => platelet adhesion defect; vWD is ADom and due to absent or defective vWF => decreased VIIIc |
|
|
Term
|
Definition
| test of platelet fxn to formation of temporary plug only. |
|
|
Term
| What does ristocetin cofactor assay measure? |
|
Definition
| vWF function => so abnormal in vWD and BS and do vWF antigen assay to distinguish… |
|
|
Term
|
Definition
| extrinsic system down to the formation of the fibrin clot (VII, X, V, II, I) – normal is 11-15 seconds and only when a factor is 30-40% of normal does it get prolonged. |
|
|
Term
|
Definition
| We use it in monitoring warfarin patients (std INR = 2-3), detect VII deficiency, or see if liver synthetic dysfunction (severe dz) |
|
|
Term
| Partial Thromboplastin Time |
|
Definition
| use it for intrinsic system down to formation of fibrin clot (XII, XI, IX, VIII, X, V II, I), normal is 25-40 seconds. |
|
|
Term
|
Definition
| monitor heparin (that enhances ATIII), not required for enoxaparin; detect factor deficiencies. |
|
|
Term
| REVIEW THE GOLJAN 257 Table: HUS, TTP, ITP, chronic ITP, Heparin-TCP, Neonatal Alloimmune TCP, Post-transfusion purpura. |
|
Definition
|
|
Term
| Primary thrombocytosis vs. secondary: |
|
Definition
| ET, PV is primary, secondary from chronic fe-def, malignancy, infection, or splenectomy! |
|
|
Term
| Hemophilia A pathogenesis: |
|
Definition
| X-linked recessive, dec synth of VIIIc (of the intrinsic system) => excessive bleeding after cutting umbilical cord or circumcision. |
|
|
Term
| Hemophilia A pathogenesis: |
|
Definition
| X-linked recessive, dec synth of VIIIc (of the intrinsic system) => excessive bleeding after cutting umbilical cord or circumcision. |
|
|
Term
| Hemophilia A pathogenesis: |
|
Definition
| X-linked recessive, dec synth of VIIIc (of the intrinsic system) => excessive bleeding after cutting umbilical cord or circumcision. |
|
|
Term
| Hemophilia lab findings => |
|
Definition
| INC PTT, normal PT!!! dec VIIIc activity and DNA techniques most sensitive for female carriers |
|
|
Term
| Treatment of hemophilia A: |
|
Definition
| mild cases (5-25% normal viiic) can treat w/ desmopressin acetate that inc viiic release from storage; severe must get infusion of recomb viii |
|
|
Term
| Blood is irradiated to kill what and why? |
|
Definition
| To kill donor lymphocytes to prevent the patient from developing GVH reaction or disseminated CMV!!! Esp the case for newborns or those w/ T-cell deficiencies. |
|
|
Term
| IgA deficient px MUST have blood given to them that is IgA deficient b/c they can develop a severe anaphylactic reaction. |
|
Definition
|
|
Term
| Someone w/ anti-HLA who gets leukocytes with HLA => fever TII hypersensitivity |
|
Definition
|
|
Term
| Cryoprecipitate vs. packed RBCs vs. platelets vs. FFP? |
|
Definition
| CPP for tx of coag factor deficiencies involving fibrinogen and VIII (such as DIC), RBCs for anemia with each unit raising 1 hgb and 3% hct, platelets for TCP, FPP for tx of multiple coag deficiencies or tx of warfarin overdose. |
|
|
Term
| Acute hemolytic transfusion reactions IV vs. EV hemolysis: |
|
Definition
| IV – abo incompatibility with anti-a-igm attaching to A positive donor RBCs => TII hypersens; EV – ab reacts with foreign antigen on rbcs so => splenic macro destruction (TII hs)…resulting in jaundice. |
|
|
Term
| Hemolytic Disease of the Newborn 2 causes: |
|
Definition
| ABO incompability (mother is O and sends her antiA/antiB IgG antibodies to the baby who is AB => fetal spleen destroys RBCs); RhHDN (Mother is Rh negative, fetus is Rh +) |
|
|
Term
| Signs and treatment of ABO HDN: |
|
Definition
| jaundice within 24 hrs, lower risk of kernicterus than Rh, positive DAT on fetal cord blood and you see spherocytes due to RBC membrane damage. |
|
|
Term
|
Definition
| more duing last trimester or during childbirth when she gets exposed to Rh+ blood from kid => develops antiD-IgG antibodies, NO spherocytes detected…b/c macros phagocytosed the entire RBC. |
|
|
Term
|
Definition
| severe anemia due to fetal spleen destroying RBCs, high output cardiac failure => hydrops fetalis (L/R combined HF with ascites, edema), much more unconj bilirubin => kernicterus bilirubin into brain and deposition in the basal ganglia |
|
|
Term
| Why can ABO incompatibility be a good thing? |
|
Definition
| It can prevent a O mother from developing Rh sensitization b/c any A+ fetal RBCs entering her system would be destroyed by anti-A-IgM antibodies. |
|
|
Term
|
Definition
| In mothers without anti-D, give Rh immune globulin (anti-D globulin) during the 28th week of pregnancy…this doesn’t cross the placentaand protects mom from sensitization, lasts 3 months in mothers blood, give more to mom after delivery if infant is Rh+ |
|
|
Term
| Following anti-D+ women in subsequent pregnancy: |
|
Definition
| do amniocentesis and look for OD450 spike indicating bilirubin and severity of hemolysis. Treat newborn jaundice with blue fluorescent light => unconj bilirubin=> dipyrrole (lumirubin that’s exc in bile/urine) |
|
|
Term
| Immune mediated hemolytic anemias: AIHA, Drug-induced, alloimmune… |
|
Definition
|
|
Term
|
Definition
| warm is IgG, cold IgM (post-infectious with mono, mycoplasma), chronic lymphocytic leukemia is BOTH |
|
|
Term
|
Definition
| PNC -> IgG ab directed against drug attached to rbc membrane, quinidine (drug-IgM immunocomplex deposits), methyldopa (autoantibody induction, drug alters Rh ag on RBCs => synth of autoantibodies) |
|
|
Term
|
Definition
| C5-C9 coating RBCs, or IgM |
|
|
Term
|
Definition
| IgG (splenic macros), IgG +C3b (liver and splenic macros, as in SLE), C3b (liver macros) |
|
|
Term
|
Definition
| DAT coomb’s – detects rbcs sensitized with igG and or C3b; indirect just detects antibodies in the serum; unconj hyperbilirubinemia if extravasc hemolysis is present. Hgburia => dec serum haptoglobin (in INTRAVASC hemolysis). Spherocytosis if damage to RBC membrane. |
|
|
Term
|
Definition
| IVIg to coat the macro receptors, splenectomy, immunosupp, ccs, discontinue offending drug |
|
|
Term
| Micro/macroangiopathic hemolytic anemias – name them: |
|
Definition
| Microangiopathic (Platelet thrombi – HUS, TTP; Fibrin thrombi – DIC, HELLP), Macro (aortic stenosis, prosthetic heart valves). You get schistocytes in MHA!!! And this is INTRAVASC hemolysis |
|
|
Term
|
Definition
| dec serum haptoglobin, hgburia, schidstocytes, normocytic anemia. |
|
|
Term
|
Definition
| plasmodium inside erythros => IV hemolysis that correlates w/ fever spikes |
|
|
Term
| P vivax vs. P falciparum vs. P malariae: |
|
Definition
| vivax is mst common and binds to duffy Fy TBC antigen which is often absent in blacks and is protective, fever spikes ever 48 hrs (tertian); falciparum is most lethal -> daily fever spikes w/ no pattern (quotidian), malariae (72 hrs and a/w nephrotic syndrome) |
|
|
Term
|
Definition
| chloroquine (safe during preg, gametocidal to all malaria except falciparum); for falciparum use atovaquone-proguanil or mefloquine |
|
|
Term
| Treatment of vivax/ovale vs. falciparum: |
|
Definition
| V/O – chloroquine + primaquine, falciparum: quinine sulfate + doxycycline if chloroquine resistant… |
|
|
