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Heme Flashcards

1
Q

What does it mean to have a chemotherapeutic agent with 1st order kinetics?

A

Drug will kill a constant PROPORTION of cancer cells (regardless of HL or cell cycles)

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2
Q

Pt got treated w/ high dose folic for anemia and returned w/ bilateral foot numbness and difficulty walking. What happened?

A

Her megaloblastic anemia is actually from B12 (cobalamin) deficiency and not folate deficiency. Folate deficiency doesn’t have neurologic involvement.

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3
Q

Low platelet, leukocytes, RBCs; bone marrow bx show lots of fat. Dx?

A

Aplastic anemia

Key dx finding is ABSENCE of splenomeg

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4
Q

Hemoglobin electropheresis shows pt’s band migrating less and so being farther away from anode (+ electrode) than normal and sickle cell disease patient. What mutation is this?

A

Missense
It’s HbC disease -> glutamate (- charge) replaced by lysine (+ charge), which makes Hb even less negative (and farther away from + electrode) than sickle cell (where negative glutamate is replaced by neutral valine)

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5
Q

Young pt w/ blasts in peripheral blood smear, worsening dysphagia, dyspnea, tachypnea, stridor. What’s the dx?

A

T-ALL

b/c more likely than B-ALL to present w/ mediastinal mass (thus compression of eso and trachea), SVC syndrome

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6
Q

What do you take with cisplatin to prevent ATI?

A

Amifostine (free radical scavenger) and IV normal saline (establishing chloride diuresis keeps cisplatin in unreactive state)

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7
Q

What does basophilic stippling look like?

A

Abnormal aggregation of ribosomes in RBC, so shows up as bluish dots in RBC (in a background of hypochromic, microcytic anemia)

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8
Q

Replaced histidine w/ serine in hemoglobin beta subunit and gets decreased binding to 2,3-BPG. The Hb is now like what kind of Hb?

A

HbF (serine replaces positively charged histidine so can’t bind w/ negatively charged 2,3-BPG as well

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9
Q

What’s the AA replacement in sickle cell?

A

Glutamate (negative) replaced BY valine (neutral)

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10
Q

What’s the AA replacement in HbC?

A

Glutamate (negative) replaced BY lysine (positive)

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11
Q

What enzyme in the heme synthesis pathway is negatively regulated by the final pathway product (heme)?

A 
ALA synthase (rate-limiting step, first step)
So administering heme prep in ppl w/ AIP (deficiency of downstream enzyme makes ALA accumulate) will help them feel better
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12
Q

What are the 2 enzymes that are inhibited by lead poisoning?

A 
ALA dehydratase (cytoplasm)
Ferrochelatase (mitochondrial)
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13
Q

3 risk factors that promote sickling

A
  1. Low O2 level: including high 2,3-DPG and oxygen unloading state, or the organs where blood move slowly (spleen, liver, kidney)
  2. Increased acidity (thus decreased pH) -> does NOT mean proton release, as proton release actually is from deoxyhemoglobin in lungs where the high pO2 favors the release of CO2 and oxygen binding to Hb -> so proton release actually signifies high O2 content
  3. Low blood volume (dehydration)
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14
Q

Bernard-Soulier syndrome vs. Glanzmann thrombasthenia

A

Bernard-Soulier: BS = “Big Sucker” -> see enlarged platelets, thrombocytopenia (even tho it’s a qualitative disorder), adhesion impaired (GPIb deficiency)
Glanzmann thrombasthenia: normal # of platelets, aggregation impaired (GPIIb/IIIa deficiency) -> aggregation w/ ristocetin will be normal, but is decreased w/ addition of ADP

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15
Q

What does uremia disrupt w/ respect to platelet fx?

A

Both adhesion and aggregation

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16
Q

What activates factor VII and initiates extrinsic pathway?

A

Tissue thromboplastin

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17
Q

How do you tell between hemophilia A and coagulation factor inhibitor?

A

Mixing normal plasma w/ pt’s plasma -> PTT corrected in hemophilia B but not in coagulation factor inhibitor (Ab against factor 8)

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18
Q

Mode of transmission in most common vWF disease? What test will show up abnormal?

A

AD w/ variable penetrance -> decreased vWF

Abnormal ristocetin test: no agglutination (ristocetin can’t induce agglutination by causing vWF to bind platelet GPIb)

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19
Q

What parameter is used to follow effect of liver failure on coagulation?

A

PT (even tho liver’s role is in vitamin K gamma carboxylation of factors II, VII, IX, X, C, S)

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20
Q

DIC vs. disorders of fibrinolysis

A

Both present w/ bleeding and prolonged PT/PTT, differences are
DIC: increase in both FDPs (fibrin degradation products - so from fibrin OR fibrinogen) and D-dimers (from fibrin only), low platelet counts
Disorders of fibrinolysis (release of urokinase from radical prostatectomy activates plasmin, and liver cirrhosis reduces production of a2-antiplasmin): increased FDPs w/out D-dimers (no cross-linked fibrin to start w/), normal platelet counts

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21
Q

Thrombomodulin (fx and origin)

A

Redirects thrombin to activate protein C -> inactivates factor V and VIII
Secreted by endothelium

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22
Q

3 causes of endothelial cell damage

A
  1. Atherosclerosis
  2. Vasculitis
  3. High homocysteine (why B12 and folate deficiencies + cystathionine beta synthase predispose you to thrombosis)
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23
Q

Pathogenesis of prothrombin 20210A

A

Inherited point mutation -> increased gene expression -> increased prothrombin -> increased thrombin -> thrombosis risk

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24
Q

PTT doesn’t rise w/ standard heparin dosing. What disease should you suspect?

A

Antithrombin III deficiency (nothing for heparin to bind)

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25
Q

4 conditions you see target cells in

A

“HALT” said the hunter to his target

  • hemoglobin C disease
  • asplenia
  • liver disease
  • thalassemia
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26
Q

Composition of HbF, HbA, HbA2, HbH, Hb Barts

A

HbF: a2g2
HbA: a2b2
HbA2: a2d2
HbH: b4 (seen in a-thalassemia w/ 3 genes deleted)
Hb Bart: g4 (seen in a-thalassemia w/ 4 genes deleted -> very high affinity to O2 -> doesn’t release O2 to tissue -> tissue hypoxia)

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27
Q

Diff between a-thalassemia and b-thalassemia causes?

A

a: gene deletion (chr 16)
b: gene mutation (chr 11)

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28
Q

Crewcut appearance on X-ray & chipmunk facies are seen in? And what creates these appearances?

A

Globin defects/deficiency -> so seen in b-thalassemia major and sickle cell
It’s from massive erythroid hyperplasia -> expansion of hematopoiesis into skull & facial bones -> reactive bone formation

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29
Q

1 conditions where you see macrocytic anemia + megaloblastic change? 3 conditions where you see macrocytic anemia w/out megaloblastic change?

A

W/ megaloblastic change in rapidly dividing epithelial cells: B12 and folate deficiency
W/out megaloblastic change: alcoholism, liver disease, 5-FU drug

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30
Q

What molecule do you look at to distinguish between B12 and folate deficiencies as a cause of megaloblastic anemia?

A

Methylmalonic acid -> normal level in folate deficiency, accumulation in B12 deficiency (leading to subacute combined degeneration of spinal cord -> affects pos. column and lateral corticospinal tract)

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31
Q

What is corrected reticulocyte count used for?

A

Distinguishing between diff causes of normocytic anemia
Reticulocyte = young RBC -> % falsely elevated in anemia b/c of decreased total RBCs
Corrected reticulocyte % calculated by RC in % x Hct/45
If > 3% -> anemia is due to peripheral destruction (good marrow response -> marrow hyperplasia)
If < 3% -> anemia is due to underproduction

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32
Q

What does serum haptoglobin screen for?

A

Intravascular hemolysis -> haptoglobin decreased b/c it binds Hb and gets destroyed in liver w/ Hb

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33
Q

What is osmotic fragility test used for?

A

Dx of hereditary spherocytosis (increased fragility in those cells in hypotonic solution b/c of loss of membrane tethering proteins), sickle cell & thalassemia
Plot a graph of % hemolysis (y) vs. NaCl conc (x) -> graph of HS will shift right from normal (higher % hemolysis for any given NaCl conc) and graph of thalassemia will shift left (have target cells w/ extra room to fill things in), SS will shift left as well (decreased osmotic fragility even tho its mechanical fragility is increased

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34
Q

What’s Howeell-Jolly body and what does it mean to have this floating arond?

A

RBC containing fragments of nuclear material
Means you no longer have functioning spleen to remove cells that should have been removed -> so seen in splenectomy (ie as tx for hereditary spherocytosis), sickle cell anemia (autosplenectomy)

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35
Q

What 2 circumstances do you see increased MCHC?

A

Increased MCHC -> Hb becomes more concentrated in the cells
Hereditary spherocytosis
Autoimmune anemia (cause of acquired spherocytosis)

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36
Q

What is metabisulfite screen used for?

A

Positive in both sickle cell disease and trait -> causes any amount of HbS to sickle

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37
Q

What are sucrose test and acidified serum test used for?

A

These tests activate complement
Sucrose test: screening test for PNH
Acidified serum test: confirmatory test for PNH

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38
Q

2 complications of PNH?

A

Iron deficiency anemia (from chronic loss of Hb in urine)

AML (from likelihood to develop mutations in myeloid cells)

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39
Q

What other condition do you see spherocytes in besides hereditary spherocytosis?

A

Immune hemolytic anemia (both warm and cold agglutinin types)

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40
Q

Wht is it called when pathologic process (like metastatic cancer) replaces bone marrow and creates pancytopenia?

A

Myelophthistic process

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41
Q

What is basophilia classically seen in?

A

CML

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42
Q

The one bacteria that promotes leukocytosis (normally a virus thing) instead of elevated neutrophils?

A

Bordetella pertussis -> lymphocytosis-promoting factor blocks circulating lymphocytes from leaving the blood to enter LN

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43
Q

What is Downey cell? And what is it seen in?

A

Atypical T lymphocyte -> reactive CD8+ T cells from EBV infection (even tho EBV actually infects and lays dormant in B cells, T cells are the ones reactive)

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44
Q

What are heterophile antibodies

A

IgM that cross reacts w/ horse or sheep RBC -> detects EBV (monospot test)
Infectious mononucleosis w/ negative monospot -> consider CMV

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45
Q

What 2 things are you not supposed to do after having infectious mononucleosis?

A 
Contact sports (splenomegaly makes capsule prone to rupture)
Take ampicillin -> maculopapular rash
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46
Q

Large cell w/ punched out nucleoli & positive nuclear staining for TdT

A

Lymphoblasts

TdT = DNA polymerase

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47
Q

Large cell w/ punched out nucleoli, Auer rods & positive cytoplasmic staining for MPO

A

Myeloblasts

Auer rods = crystal aggregates of MPO

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48
Q

2 subsets of AML that lack MPO?

A

Acute monocytic leukemia (gum infiltration)

Acute megakaryoblastic leukemia (Down kids before age 5)

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49
Q

What do you call the disease where you have cytopenias + blasts < 20%

A

Myelodysplastic syndrome (not high enough blasts to be called AML) -> from prior exposure to alkylating agents or radiotherapy

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50
Q

Richter transformation?

A

CLL -> diffuse large B-cell lymphoma

See enlarging LN or spleen

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51
Q

Dx for proliferation of cells that co-express CD5 and CD20/CD19?

A

CLL (mature B cell leukemia)

CD5 normally on T cells, CD20/CD19 normally on B cells, but these cells are naive B cells

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52
Q

Dx for B cells positive for TRAP + expansion of splenic red pulp + dry tap on bone marrow aspirate

A

Hairy cell leukemia

TRAP = tartrate-resistant acid phosphatase

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53
Q

Dx for punched-out bone lesions w/ generalized LAD + rash

A

Adult T-cell leukemia/lymphoma (assc. w/ HTLV-1 which is a Retroviridae esp in southern Japan)
If NO rash -> think MM

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54
Q

Dx for Pautrier microabscesses + lymphocyte w. cerebriform nuclei

A

Mycosis fungoides -> chronic leukemia of mature CD4+ T cells
Pautrier microabscesses: aggregates of neoplastic cells in epidermis
Sezary cells: lymphocyte w. cerebriform nuclei

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55
Q

What can CML transform into?

A

AML (2/3) or ALL (1/3) b/c mutation is in pluripotent stem cell

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56
Q

Distinguish CML from leukemoid rxn?

A

In CML, see negative LAP (leukocyte alkaline phosphatase) stain or reduced LAP level & increased basophils

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57
Q

One condition where you can see tear-drop RBC (dacrocytes)?

A

Myelofibrosis (myeloproliferative disorder - “atypical megakaryocytic hyperplasia”) -> RBC stretched out to leave bone marrow (which is fibrosed from excess PDGF produced by excess megakaryocytes)

58
Q

3 regions of hyperplasia in LAD and their assc.

A
  1. follicular hyperplasia (B-cell area): RF, early stage of HIV (follicular dendritic cells are CD4+)
  2. paracortex hyperplasia (T-cell area): viral infection
  3. sinus histiocyte hyperplasia: cancer
59
Q

What’s tingible body and what does it mean if you don’t see this in LN?

A

Macrophage containing debris
If don’t see this in LN follicles -> disruption of normal LN architecture -> probably follicular lymphoma
Normal follicular hyperplasia will have tingible bodies

60
Q

Reed-Sternberg cells + Owl-eyed nulei

A

Hodgkin lymphoma

61
Q

Dx of CD15 and CD30 (no CD20 even tho it’s B cells)

A

Hodgkin lymphoma

62
Q

Lytic bone lesion + M pike + hypercalcemia + AL amyloid + rouleaux formation of RBC

A

MM

63
Q

M spike + retinal hemorrhage or stroke + bleeding

A

Waldenstrom macroglobulinemia
similar features to MM but NO lytic bone lesion
M spike composed of IgM (instead of IgG and IgA like MM)

64
Q

Cells that are CD1a+ and S100+?

A

Langerhans cell

65
Q

Lytic skull defects + DI + exophthalmos in a child

A

Hand-Schuller-Christian disease (one of langerhans cell histiocytosis)
Also can see scalp rash

66
Q

How does the chance of hemolytic disease of newborn and erythroblastosis differ w/ maternal blood type?

A

Maternal blood type A and B: mom has IgM Ab so doesn’t cross placenta -> no hemolysis
Maternal blood type O: mom has IgG Ab so does cross placenta -> see cases of hemolysis
Unlike Rh, ABO disease can occur w/ first pregnancy

67
Q

What are smudge cells seen in?

A

CLL

68
Q

AIDs-related lymphomas?

A

Non-hodgkins, esp those assc w/ EBV -> Burkitt’s, diffuse large cell
Primary CNS lymphoma (universally assc w/ EBV)

69
Q

What virus is assc. w/ adult T cell leukemia and lymphoma?

A

HTLV-1

70
Q

Most common cause of aplastic crisis in sickle cell pts & other chronic hemolytic disease pts?

A

Parvovirus B19 -> infects erythrocyte precursor cells

71
Q

Pathogenesis and 3 causes of pure red cell aplasia (PRCA)

A

Pathogenesis: IgG autoAb or CD8+ T cells target erythropoietic precursors
Causes: thymoma (so should do chest CT in PRCA), lymphocytic leukemia, parvovirus B19 (detects anti-B19 IgM)

72
Q

3 tumors that can produce EPO

A

Renal cell carcinoma
Cerebellar hemangioma
Uterine fibroids

73
Q

Timeline of Hb types from conception to the time you switch to HbA?

A

Earliest Hb in fetus (yolk sac): zeta2epsilon2 (Hb Gower) -> then Hb Portland -> then Hb Gower 2
10-12 wks of gestation (liver now): HbF
FIRST 6 MOs of life (bone marrow): HbA gradually replaces HbF

74
Q

How to differentiate bet. absolute and relative polycythemia and what are common causes of each? How do you tell bet. primary and secondary polycythemia?

A

Absolute polycythemia: increase in RBC mass -> from polycythemia vera or 2ndary erythrocytosis (to increased EPO, such as in hypoxia) -> tell apart from the fact that 2ndary polycythemia will only have increased RBC and nothing else, whereas there’s elevation in all cell types in primary polycythemia vera
Relative polycythemia: normal RBC mass -> from dehydration, excessive diuresis (so think of this in pt who was recently treated for HF exacerbation!)

75
Q

How low does O2 have to go to cause secondary polycythemia?

A

SaO2 < 92% (PaO2 < 65 mmHg)

76
Q

What are 4 conditions assc. w/ autoimmune hemolytic anemia?

A

SLE & other autoimmune diseases
Hodgkin & non-Hodgkin lymphoma
Mycoplasma infection (cold agglutinins)
Infectious mononucleosis

77
Q

Pt w/ hx of motor vehicle accent died of Strep pneumo despite being initiated on broad spectrum antibiotics. What process is impaired?

A

Bacterial clearance
Probably had spleen removed after that accident -> no clearance by splenic opsonizing Ab -> overwhelming postsplenectomy infection -> susceptible to encapsulated bac like Strep pneumo, H. influenzae, N. meningitidis

78
Q

What anticoagulant should you use in acute coronary syndrome?

A 
Unfractionated heparin -> has both anti-factorXa and anti-thrombin effects -> will treat existing clot + prevent propagation
The LMWH (Enoxaparin) and Fondaparinux only inhibit factor Xa -> no effect against thrombin
79
Q

What happens to bleeding time, TT, PT, and PTT in dysfibrinogenemias?

A

Abnormalities in fibrinogen molecules -> excessive bleeding
Bleeding time is unaffected
TT, PT, and PTT are prolonged

80
Q

What does factor XIII do? What happens to bleeding time, PT, and PTT in the deficiency state? What’s the sx?

A

Factor XIII is a transglutaminase that cross-links fibrin polymers -> stabilizes clots
Deficiency: does NOT prolong bleeding time, PT, or PTT (altho might see delayed bleeding)
Sx: hemophilia-like bleeding (deep tissue)

81
Q

Infant w/ anemia, jaundice, edema, nucleated erythrocytes, extramedullary hematopoiesis. What should you suspect?

A

Hemolytic disease of the newborn (esp Rh-related)
Don’t think about infant immune system having anything to do w/ it -> their humoral defence first 6 mos come from maternal circulating IgG (placental) and mucosal IgA (breastfeed)

82
Q

Why do defects in early steps of heme synthesis not cause photosensitivity but late steps do?

A

Photosensitivity is induced by formation of porphyrin-mediated superoxide free radicals from O2 upon exposure to sunlight
So if no porphyrin -> no photosensitivity (why it’s not a component of AIP)

83
Q

What is the difference bet. FFP and cryoprecipitate?

A

FFP: all coagulation factors (so give in warfarin toxicity)
Cryoprecipitate: only cold-soluble proteins -> factor VIII, XIII, vWF, fibrinogen, vitronectin

84
Q

What do you give in rodenticide poisoning before sx shows? After sx shows?

A

Before sx shows: give syrup of ipecac to induce vomiting
After sx shows (bleeding stuff): rodenticide contains derivative of 4-hydroxycoumarin -> so sx are from depleted vit K-dependent clotting factors -> give FFP + Vit K1

85
Q

What is “nuclear maturation defect due to defective DNA synthesis” a pathophysiologic mechanism of?

A

Megaloblastic anemia

86
Q

Menorrhagia since menarche and frequent nosebleeds as a child. Most likely dx?

A

vW disease -> diff from ITP b/c in ITPbleeding is episodic (not chronic and unrelenting since childhood)

87
Q

What does protein C deficiency predisposes to?

A

Recurrent DVT

88
Q

What does wVF bind to on its two ends?

A

One end binds to GpIb (platelet glycoprotein)

Another end binds to exposed collagen underneath damaged endothelium

89
Q

What areas does diffuse large cell lymphoma commonly involve?

A 
Waldeyer ring (oropharyngeal lymphoid tissue)
GI tract
90
Q

What should you suspect in “waxing and waning” LAD?

A

Follicular lymphoma - most common indolent non-Hodgkin lymphoma in adults

91
Q

What deficiency are you thinking about when alcoholics present w/ megaloblastic anemia?

A

Folate more common than B12 in alcoholics

92
Q

What is hepcidin and how does it work?

A

Central regulator f iron homeostasis, secreted by liver -> it binds ferroportin and induces its degradation -> so get decreased intestinal iron absorption and decreased release from macrophages
If too much iron or inflammatory condition -> increased hepcidin to sequester iron
If hypoxia, more EPO, and anything that would make you wanna make more RBCs -> decreased hepcidin to release iron

93
Q

Iron channels on enterocytes on the gut lumen side and blood side?

A 
Gut lumen (apical): DMT-1
Blood side (basolateral): ferroportin (also on macrophages)
94
Q

What makes RBCs blue w/ increased bone marrow erythropoeisis (such as after administering iron in iron deficiency anemia)

A

Reticulocytes -> blue on Wright-Giemsa stain is from reticular precipitates of residual ribosomal RNA

95
Q

Dx of “diffuse medium-sized lymphocytes and proliferation fraction (Ki-67 fraction) of > 99%”?

A

Burkitt lymphoma

High proliferation/high mitotic index is represented by Ki-67 fraction

96
Q

Dx of lymphoma w/ “large cells, big nuclei, and prominent nucleoli” assc w/ HHV-8?

A

Primary effusion lymphoma

97
Q

What’s the difference bet. anemia caused by glycolytic defects vs. by HMP shunt defects?

A

Glycolytic defects: chronic hemolytic anemia

HMP shunt defects: episodic hemolytic anemia

98
Q

What kind of abnormal RBCs do you see in abetalipoproteinemia?

A

Acanthocytes

99
Q

Dx of “diffuse sheets of large lymphocyttes w/ nuclei at least 5x the size of small lymphocytes”?

A

Large B-cell lymphoma

100
Q

2 other names for leucovorin? For what drug can be used for prevention of myelosuppression?

A

Leucovorin = folinic acid = N5-formyl-tetrahydrofolate
Reverse toxicity of methotrexate but NOT 5-FU
Leucovorin bypasses the DHF reductase step (which is a step inhibited by methotrexate) so can be used to rescue it. But 5-FU blocks a different step (thymidylate synthetase)

101
Q

Why can you use leucovorin to potentiate toxicity off fluoropyrimidines (like fluorouracil)?

A

Leucovorin strengthens the assc. of the drug w/ thymidylate synthase

102
Q

What is defective in beta thalassemia?

A

transcription, processing, and translation of mRNA

NOTHING TO DO w/ DNA synthesis!

103
Q

When to use heparin or aspirin as prophylaxis?

A

Heparin: prevents DVT/PE in high risk situations (post. hip surgery, etc)
Aspirin: prevents recurrent coronary thrombosis and ischemic strokes

104
Q

What’s the defect in bare lymphocyte syndrome?

A

Expression of HLA II Ag on surfaces of Ag-presenting cells

105
Q

What happens to Ig production in CLL? What happens to RBC?

A

Depressed Ig production

Normochromic, normocytic anemia

106
Q

What should you be thinking w/ eosinophilic casts in renal tubules + low Hb + back pain?

A

MM!
Eosinophilic casts are NOT the same as eosinophil cell cast
They’re Bence Jones proteins (light chains)

107
Q

What happens to kidney in chronic lead intoxication?

A

Chronic tubulointerstitial nephritis

108
Q

Electrolyte complications after blood transfusion?

A

Hypocalemia & hypomagnesemia (esp if receive a lot of blood): citrate added to stored blood chelates Ca2+ and Mg2+

109
Q

What happens to PT, PTT, platelet count & bleeding time in pts who bleed around catheter sites who’s also happen to have ESRD?

A

ESRD -> think uremic platelet dysfx! -> so everything else is normal (incl. platelet count) but bleeding time is prolonged b/c it’s a qualitative platelet disorder

110
Q

Triad characteristics of PNH?

A

Hemolytic anemia
Hypercoagulability (eg Budd chiari)
Pancytopenia

111
Q

What should you assc. low CD55 and CD59 w/?

A

PNH!
CD55 = DAF
CD59 = MAC inhibitory protein

112
Q

What does thrombin time evaluate? What 2 conditions prolong thrombin time?

A

Evaluates rate of conversion of fibrinogen to fibrin

Prolonged by heparin and dysfibrinogenemia

113
Q

Dx of 5-yo who had fever + abd pain + diarrhea mixed w/ small amount of blood who later develop pallor and oliguria?

A

Recognize this as a two out of HUS triad! = acute renal failure & microangiopathic hemolytic anemia
So should expect thrombocytopenia (last part of triad) -> prolonged bleeding time

114
Q

What do you see on spleen histology in young vs. old sickle cell pts?

A

Younger pts: congestion from splenic sequestration (can be emergency - rapidly enlarging spleen and hypovolemic shock)
Early adulthood ohward: probably will see scarring, fibrosis, and atrophy of spleen (autosplenectomy completed)

115
Q

What kind of anemia is assc. w/ sickle cell disease and other hemolytic anemias?

A

Folic acid deficiency from increased erythrocyte turnover -> macrocytic anemia

116
Q

What drugs are assc. w/ microangiopathic hemolytic anemia?

A

Cisplatin, cyclophosphamide

117
Q

A girl w/ Hb abnormality that shifts O2 dissociation curve to the left. What’s the sequelae of this?

A

Erythrocytosis 2ndary to EPO release
Don’t even think of HbF generated from sickle cell in this scenario -> the MAIN defect is this weird Hb that shifts the curve left; in SC the main defect is HbS which actually shifts the curve right

118
Q

What do you find in antiphospholipid Ab syndrome besides hypercoagulability?

A

Paradoxical PTT prolongation + spontaneous abortions

119
Q

What’s really wrong w/ HbS?

A

There’s altered hydrophobic part of beta chain that fits into a complementary site on alpha chain of another Hb -> allows hydrophobic interaction among Hb molecs

120
Q

What is Hb M disease?

A

Mutation in heme binding pocket (either alpha or beta) -> histidine replaced w/ tyrosine -> iron phenolate complex resists reduction of iron to ferrous state -> methemoglobin

121
Q

What 4 things should you think about w/ burr cells?

A

Traumatic hemolysis from mechanical damage (like prosthetic valve)
Microangiopathic hemolytic anemia -> will have thrombcytopenia too
Uremia
Pyruvate kinase deficiency

122
Q

Who else besides Down are at an increased risk of developing acute leukemia?

A 
Ataxia-telangiectasia
NF1
Patau
Bloom syndrome
Fanconi anemia
123
Q

What are Pappenheimer bodies and in what condition do you see them?

A

Iron inclusions

Seen in sideroblastic anemia

124
Q

What kind of anemia does B6 deficiency cause?

A 
Sideroblastic anemia (remember that it's involved in the first ALA synthase step of heme synthesis)
Hypochromic, microcytic
125
Q

What does intravascular hemolysis do to serum LDH?

A

Increases it

126
Q

Recurrent otitis media/sinusitis/bronchitis/pneumonia + anaphylactic rxn following blood transfusion even when it’s O-. Dx?

A

IgA deficiency -> blood products contain small amount of IgA and ppl w/ IgA deficiency often have IgG Ab against IgA
So DON’T use gamma-globulin prep for tx of these pts!

127
Q

Pt w/ obvious sign of hemophilia (deep tissue bleeding and such). Administer what molec would make them clot?

A

Things that are downstream from what they lack -> so thrombin
Don’t be distracted by choices like factor XII thinking maybe that’s what they lack -> if sx look like hemophilia, it’s prob hemophilia, and those are either VIII or IX -> so XII would be upstream of that and won’t clot

128
Q

What 2 parasites cause microcytic anemia? How do you get them and how do you tx them?

A

Ancylostoma and Necator (hookworms)
Larvae penetrate skin
Tx: bendazoles or pyrantel pamoate if pregnant

129
Q

What is a sure finding in ppl w/ sickle cell TRAITS?

A

They’re protected from plasmodium falciparum
They do NOT have abnormal peripheral smears, elevated reticulocyte count, increased MCHC (only seen in homozygous), or painful crises -> they’re generally asymptomatic besides hematuria

130
Q

Fever and chills, hypotension, dyspnea, chest/back pain, hemoglobinuria after blood transfusion. What HSR?

A

Acute hemolytic transfusion -> type II HSR (Ab-mediated) -> but cell lysis is complement mediated!! (after IgM bind Ag and lead to complement activation)
Don’t think of complement mediation as being exclusively type III HSR

131
Q

Drugs that inhibit ADP in platelet aggregation? PDE? IIb/IIIa?

A

ADP: ticlodipine and clopidogrel
PDE: dipyridamole and cilostazol
IIb/IIIa: abciximab, eptifibatide, tirofiban

132
Q

Dx of B cell tumor w/ predominantly small cleaved cells (centrocytes) and few large noncleaved cells (centroblasts)?

A

Follicular lymphoma

133
Q

How does sickle cell disease usually present in young children?

A

Dactylitis (painful swelling of hands and feet) from vasoocclusion

134
Q

Fever and sweating that occur every 48 hrs. What malaria species?

A

P. vivax and P. ovale -> erythrocyte lysis is what causes relapsing fever and sweating
Don’t forget to use primaquine on top of chloroquine to eliminate latent hepatic infection (hypnozoites)!

135
Q

Graph of blood level (y) vs. time (x) in pt w/ pernicious anemia who’s being given IM B12. What parameter increases steadily as time passes and what parameter rises to peak then falls?

A

Rises steadily: Hb

Peaks then falls: reticulocyte count

136
Q

What is chronic lymphedema a risk factor of?

A

Chronic lymphedema is classically from radical mastectomy

Risk factor of cutaneous angiosarcoma (infiltration of dermis w/ slit-like abnormal vascular spaces)

137
Q

Diff in features of HUS and TTP? How do you treat them?

A

Both present w/ triad of fever + thrombocytopenia + microangiopathic hemolytic anemia
TTP: usually adults w/ predominant neurological sx
HUS: usually children w/ renal involvement
Tx both w/ emergent plasmapheresis

138
Q

A particular phospholipid causes bronchoconstriction, vasoconstriction, platelet aggregation w/ microthrombus formation. What’s the substance and what’s the effector?

A

PAF -> acts thru Gq and PLC pathway (Ca2+)

139
Q

What are sx of iron deficiency anemia that might not seem super obvious?

A

Dry mouth, atrophy of tongue papillae, alopacia, glossal pain, pagophagia

140
Q

32-yo w/ fatigue&pallor + white patches on gingival and buccal mucosa + retinal hemorrhage. What’s the dx?

A

Don’t think of HIV
Think of acute leukemia -> sx are from pancytopenia -> fatigue and pallor from anemia, oral thrush from leukopenia, and retinal hemorrhage from low platelets

141
Q

How do you know it’s ITP when you have low platelets?

A

Increased # of megakaryocytes (so might say something like “anikopoikilocytosis” which means RBCs of varying shapes and sizes)

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