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HemeOnc > Benign > Flashcards

Benign Flashcards

1
Q

Draw out the lineage of hematopoetic system, starting with HSC (stem cell) and ending with mature classes of myeloid, lymphoid cells.

A

see notes

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2
Q

What cells are next in line after the common myeloid progenitor? What do they diff to?

A

Common myeloid –> granulocyte-macrophage progenitor + megakaryocyte-erythroid progenitor.

Each of these progenitor cells forms colony-forming units (CFUs) which then mature, via several stages, into mature cells.

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3
Q

What are the classes of mature cells that we have to know? Give general fxn and indicate if they are of myeloid or lymphoid lineage.

A

Myeloid (from common myeloid progenitor)

  • Granulocytes (G)
    • neutrophils
    • eosinophils
    • basophils
  • Macrophages (M)
  • Erythrocytes (E)
  • Platelets (P)

Lymphoid (from common lymphoid progenitor)

  • Bc
  • Tc
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4
Q

Hematopoetic stem cells (HSC)

  • Division mechanism
  • Key cell surface Ag
A
  • Asymetric division –> daughter cell that diff’s + daughter cell that self-renews
  • CD34+
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5
Q

Hematopoetic progenitor cells

  • Family of cells that diff to
  • Ability for self-renewal
  • Cytokines/GF role
A
  • Prog cells –> CFU (defined by ability to form CFU’s)
  • Cannot self-renew
  • Require and respond to cytokinds/GF’s
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6
Q

What are the two most important myeloid growth factors? Function, release factor, etc?

A
  • Epo: true hormone, secreted by mesangial cells of glom in response to hypoxemia –> Epo release –> ++poeisis in bone marrow –> ++RBCs
  • Tpo (thrombopoetin): Released constant level by liver , stimulates MK to create platelets.
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7
Q

What type of cell surface receptor-messenger system used by myeloid growth factors?

A

Epo/Tpo bind –> dimerization –> activation of JAK2 (tyr. kinase) –> cascade

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8
Q

What are the four terminal cells of the GMP (granulocyte-macrophage progenitor)? Give the lineage from GMP to terminal cell.

A

GMP –> CFU-G –> G

GMP –> CFU-M –> M

Granulocytes

  1. Neutrophils
  2. Eosins
  3. Basos

plus 4. MP’s!

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9
Q

Give brief desciption of each granulocyte (function + histology) to help compare/contrast

A
  1. Neuts: most common, innate, light-staning nuc. w/ polymorphic nuc.
  2. Eosins: red-staining, allergic rxns, acute infx
  3. Basophils: dark-staining (basophilic)

NB: eosins and basos both have prominent granules

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10
Q

Familial cyclic neutropenia

  • Etiology
  • Time needed to create neut from HSC
  • Typical blood result
A
  • INH mut neut elastase
  • 21 days
  • B/c of 21 day cycle, get cyclical rise/fall of neuts.
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11
Q

What is the general blood smear result for reduced prod’n?

A

Low cellular levels with LOW reticulocyte count (high reticulocytes would indicate increased destruction with increased production - body getting immature cells out quicker)

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12
Q

What would a pancytopenia manifest as in blood smear?

A

low counts (anemia - E, leukpenia - Bc, Tc, thrombocytopenia - P) + low retics

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13
Q

Common causes of pancytopenia

A
  1. Aplastic anemia (stem cell failure)
  2. Marrow disorder (leukemia, etc.)
  3. Deficiency (B12, folate)
  4. Infx
  5. Myelodysplastic synd
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14
Q

In cases of pancytopenia what labs/diag’s are done?

A

smear, bone marrow biopsy

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15
Q

Where are BM biopsies done?

A

Posterior iliac crest

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16
Q

What is a major diff b/t BM aspiration/biopsy and core biopsy?

A

aspiration: live cells
core: dead cells

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17
Q

What tests/labs can be done on bone marrow aspiration (mention five)?

A
  • cell morphoogy
  • diff’l count
  • histochem. staining
  • take cells for flow cyto
  • culture

(basically, all the things you can do with LIVE cells)s

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18
Q

What are the two normal values we shoudl know from a myelogram from aspirate?

A

Blasts should be 0-5%

Myel:Eryth ratio shoudl be 2:1-4:1

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19
Q

what are BM core biopsies good for?

A
  1. architecture
  2. staining
  3. cell popns and patterns

remember cells are DEAD so can’t take samples, do cytology, cytometry, etc.

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20
Q

Fanconi anemia

  • Lab diagnosis?
A
  • Dicentric xsomes in karyotype (induced)
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21
Q

What are two drugs that can cause acquired aplastic anemia?

A
  • methotrexate
  • chloramphenicol (antibiotic, most notorious)
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22
Q

Paroxysmal nocturnal hemoglobinuria (PNH)

  • Def
  • Etiology
  • Pathophys
A
  • A type of acquired BM failure + hemolysis –> aplastic anemia, lysis
  • Mutated CD55 & CD59 –> poorly modulated complement
  • Unusual sensitivity to complement leads to lysis and dmg to HSC’s.
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23
Q

What are the two main approaches to Rx of aplastic anemias?

A
  1. Immune suppression (cort’s, cyclosporine)
  2. HSC replacement (xplantation, allogenic)
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24
Q

Anemia lab def

A
  • decreased Hg >2 SD below mean
  • Decrease HCT
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25
Q

Anemia pathopys def.

A

Low RBC’s means inadequate delivery of O2 to tissues.

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26
Q

HCT def

A

% of RBC’s / volume

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27
Q

Reticulocyte

A

youngest normal RBC entering circ. from BM (large purplish cell on smear w RNA remnants visualized on vital stain)

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28
Q

What is the key/standard measure of reticulocytes?

A

absolute reticulocyte count: retic % x total red cell #

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29
Q

Define the following lab values:

  • RBC
  • MCV
  • MCH
  • MCHC
  • RDW
A
  • RBC: # RBCs/uL blood
  • MCV: mean corp. vol.
  • MCH: Hg in single cell
  • MCHC: Hg conc in given vol. of RBCs
  • RDW: size distribution of RBCs
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30
Q

S/S of anemia

A
  • fatigue
  • pallor
  • SOB esp exertion
  • Tachy
  • Orthostatic hypoTN
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31
Q

Reticulocyte index

  • Def
  • Expected value in anemic pt who has adequate BM response
A
  • rectic count x (Hct/40)
  • >2
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32
Q

Hypoprolif anemia (def and lab value)

A
  • Anemia caused by not making enuf RBC’s (inadequate BM response to degree of anemia)
  • Low ret index (<2) and/or count

NB: note that although megaloblastic anemias do have poor production, they are not considered classically hypoproliferative b/c the reticulocytes are killed before leaving the BM. So the reticulocyte count can be normal or low.

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33
Q

Hyperprolif anemia (def, lab value)

A
  • Anemia showing robust BM response, as evidenced by….
  • …increased ret index (>2) +/or count
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34
Q

What is the most common anemia ? is it hypo- or hyperprolif? Micro- or macrocytic?

A

Fe def; hypoprolif.; microcytic.

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35
Q

Common macrocytic (hi MCV) anemias (4)

A
  • B12 def.
  • Folate def.
  • EtOH
  • Liver dz
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36
Q

Common etiologies of microcytic anemias (4)

A
  1. Fe def. (most common by far)
  2. Toxins/Pb
  3. Chronic dz (anemia of chronic dz)
  4. Thalassemia
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37
Q

Normocytic anemias are generally a problem of ______

A

Hemolysis (destruction) - either intra- or extra-vascular

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38
Q

In addition to fatigue and pallor, what are three (3) clinical signs of Fe def ?

A
  1. Hair loss
  2. PICA
  3. Spoon-shaped nails
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39
Q

Three common causes of Fe def?

A
  • Blood loss
  • Malabsorption (due to cel. dz, gastric bypass, etc.)
  • Poor diet
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40
Q

Define the following Fe-related proteins

  • Ferritin
  • Ferroportin
  • Hepcidin
  • Hemosiderin
A
  • Ferritin: Water-soluble Fe storage in liver/heart; lo Fe stores = lo ferritin
  • Ferroportin: xports Fe out of basolateral membrane –> circulation.
  • Hepcidin: triggers degradation of ferroportin on the surface of enterocytes and macrophages. This decreases iron absorption from the intestine and inhibits iron release from macrophages, leading to hypoferremia
  • Hemosiderin: water-insoluble Fe storage
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41
Q

What are the distignuishing lab findings (smear, blood assays) of Fe def. anemia (IDA)?

A
  • Smear: Microcytosis, Hypochromia (low MCH), Low RBC count, Low Retic (hypoprolif)
  • Assays; Low ferritin, high TIBC
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42
Q

What does image show?

A

Fe def anemia w/ wide central pallor = hypochromia

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43
Q

What will ferritin levels be in Fe def anemia?

A

Low (depeletion Fe stores)

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44
Q

What lab findings woud you find in anemia of chronic dz?

A
  • A defining feature of ACD = higher than nl Ferritin i(Hepcidin causes Fe sequestration)
  • Decreased TIBC (not sure why, but remember than in Fe-Def anemia, TIBC will be elevated reflecting a true deficiency)
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45
Q

What are the 2 primary causes of Fe overload?

A
  • Hereditary hemochrom. (Fe overload)
  • Tranfusional
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46
Q

How much Fe (in mg) in 1 cc packed RBCs

A

1 mg

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47
Q

Sources of folate? Where absorbed?

A
  • Vitamin found in leafy green veg’s, foritfied foods, some fruits/vegs
  • Jejunum (proximal)
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48
Q

B12

  • Source
  • Absorbtion site
A
  • Most animal (liver, meat, some dairy)
  • Terminal ileum
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49
Q

Pernicious anemia

A

B12 def. caused by lack of intrinsic factor from stomach parietal cells.

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50
Q

Primary cuases of B12 def?

A
  • Malabsorption (gastrectomy, pern. anemia, no intrinsic factor)
  • GI probs
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51
Q

Smear findings in pernicious anemia? Include any special cells you might find.

A

macrocytic cells w/ some teardrop cells

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52
Q

subacute combined degen

A

chronic B12 deficiency-related neuropathy (irreversible if damages spinal cord)

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53
Q
  • Example of two megaloblastic anemias
  • What does this refer to?
A
  • B12 def and folate def anemias = megaloblastic anemias
  • Megaloblastic: Megaloblastic red cell precursors (seem in BM aspiraton) are larger than normal and have more cytoplasm relative to the size of the nucleus. Promegaloblasts show a blue granule-free cytoplasm and a “salt and pepper” granular chromatin that contrasts with the ground-glass texture of its normal counterpart.
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54
Q

Common causes Folate def

A
  • Dietary
  • Malbsorption/GI
  • Drugs (folate antagonists like methotrexate)
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55
Q

Def hyperprolif anemia

A

Anemia w/ increased destruction (hemolysis) of RBCs and increased reiculocyte count/index.

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56
Q

Hereditary spherocytosis

  • Def
  • Etiology
A
  • Hemolytic anemia (most common)
  • Congenital, w/ membrane protein defects
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57
Q

Lab diagnosis of hered. spherocytosis

  • Smear
  • Special test
A
  • Smear:

Increased retic

Increased MCHC (mean corpuscular Hg conc.)

Spherocytes on smear

  • Abnormal osmostic fragil. test
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58
Q

Hereditary elliptocytosis

  • Def
  • How does it comparie to hereditary spherocytosis (HS)?
A
  • Also a membrane disorder of RBC’s –> hemolytic anemia
  • Milder than HS
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59
Q

What is the difference b/t intra- and extravascular hemolysis?

Examples of each?

A

This just refers to where the RBC’s are being destroyed. Extravascular refers to the spleen.

Intravascular

  • Burn
  • G-6-PD deficiency
  • Malaria
  • thrombotic thrombocytopenic purpura
  • disseminated intravascular coagulation
  • paroxysmal nocturnal hemoglobinuria (PNH)
  • Immune hemolytic anemia (warm & cold)

NB: all of the microangiopathic hemolytic anemias are intravascular (HUS, TTP, DIC, etc.)

Extravasc.

  • Sickle cell dz
  • Hered. spherocytosis
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60
Q

What are the two kinds of autoimmune hemolytic anemias? What differentiates them immunologically?

A

warm & cold; warm = IgG Ab’s (extravascular hemolysis), cold = IgM (intravascular hemolysis)

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61
Q

What are examples of non-immune acquired hemolytic disorders?

A
  • Infx
  • Burns
  • Liver dz
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62
Q

Warm autoimmune hemolysis

  • Def
  • Mechanism of cell destruction
  • Location of cell destruction
A
  • IgG-mediated autoimmune lysis of RBC’s –> hyperprolif. anemia
  • IgG Abs directed against RBC Ag’s –> hemolysis via complement.
  • extravasc
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63
Q

Coombs test

A
  • To dx immune hemolytic anemia
  • Uses agglutination to test for autoAb’s and/or complement on RBC surface
  • RBCs are incutaed w/ Abs to Ig and C3
  • If agglutination takes place then test is positive and RBC’s presumed to have IgG/C3 bound to surface.
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64
Q

Indirect Coombs test

  • Used for ?
A

Testing for immune hemolysis in newborns and transfusion pts - also an agglutiation test

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65
Q

Clin features of hered. spherocytosis (5)

A
  • Jaundice (increased indirect bilirubin)
  • splenomegaly (EV hemolysis)
  • Hyperhemolytic crises
  • Aplastic crises (Parvo B19 infxn)
  • Pigment gallstones (due to hemolysis)
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66
Q

G6PD Deficiency

  • Def
  • Two common variants
  • Sign in newborn
A
  • hereditary cause of hemolytic anemia
  • African (milder), mediterranean (more severe, all RBCs deficient)
  • Common cause of neonatal jaundice
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67
Q

G6PD Def pathophys

A

Lack/mutated G6PD –> impaired prodn of NADPH which is needed to produce reduced glutathione, the primary superoxide salvager. This leads to hemolysis via oxidative dmg.

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68
Q

What are some signs of G6PD deficiency anemia on periph. smear?

A
  • ghost cells, bite cells on smear
  • Heinz body w/ supravital stain (RNA frag)
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69
Q

What are the types of abnormal cells? What dz is this?

A
  • bite and ghost cells
  • G6PD anemia
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70
Q

what cell?

A

neut: polymorphic nucleus

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71
Q

cell type?

A

eosin

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72
Q

cell type?

A

basophil

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73
Q

cell type?

A

Lc

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74
Q

What would increase the number of neuts and bands?

A

acute bact. infx

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75
Q

What are some conditions that would increase eosin’s?

A

“worms, wheezes and wierd diseases”: allergies, parasites, TB, sarcoid, etc.

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76
Q

What are three causes for increased monocyte count?

Two causes of decreased?

A

Increased

  • Chronic infx eg TB
  • Chronic INF eg Sarcoid
  • Chronic neutropenia

Decreased

  • BM failure
  • Cort’s
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77
Q

What are factors that can decrease neut count via (1) decreased prod’n or (2) increased destruction

A

Dec. production

  • congential
  • acquired via viral, meds, aplastic anemica, malignancy

Increased dest.

  • hypersplenism (sequestration)
  • immunological
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78
Q

def. toxic granulation

A

dark azurophilic granules in neut’s, seen in INF states

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79
Q

What is a relatively common disease that would show more than 5-10% basophils?

A

CML

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80
Q

Pelger-Huet anomlay

  • Cell type & anomaly
  • Causes (2)
A

Bilobed neutrophil nucleus due to benign disorder or myelodysplastic syndrome

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81
Q

What is seen in some of these neutrophils? What are two causes?

A

Pelger-Huet anomaly - caused by “benign” hereditary disorder or myelodysplastic syndrome

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82
Q

What does the image show? What generally causes it?

A

Dohle body: Döhle bodies are discrete, blue-staining nongranular areas found in the periphery of the cytoplasm of the neutrophil in infections and other toxic states. They represent aggregates of rough endoplasmic reticulum.

(The cell is a band, the inclusion is the Dohle body)

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83
Q

When are Dohle bodies often seen? What cell type?

A

In Neuts, during sepsis (chronic INF).

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84
Q

What are the two primary ways that phagocytes kill microbes once they are phagocytosed?

A

Oxygen independent

  • lysosome fusion + enzymes

Oxygen dependent

  • respiratory burst (superoxides)
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85
Q

Def. respiratory burst and give two key enzymes

A

Burst of activity that creates superoxides. Key enzymes are superoxide dismutase (SOD) –> H2O2 + O2

and

myeloperoxidase –> .OCl-

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86
Q

Chediak-Higashi syndrome

  • Genetics
  • Def
  • Clinical picture
A
  • Rare, AR
  • Failure of phagolysosome formation (ineff. lysosomes)
  • recurrent skin and syst. infxs, s. aureus
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87
Q

Chronic granulomatous dz (CGD)

  • Defect
  • Clinical picture
A
  • Defect in resp. burst enzyme complex –> very lo H2O2 prodn
  • Because CGD neut’s cannot scavenge H2O2 from catalase + bacteria, these are much more problematic.
  • Severe skin, sinopulm. infxs, granulomas, sepsis w/ lymphadenopathy, hepatosplenomegaly
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88
Q

Job’s syndrome

  • Defects
  • Clinical picture
A
  • aka hyperimmunoglobulin E–recurrent infection syndrome
  • HyperIgE + defect in chemotaxis… leads to:
  • recurrent skin and sinopulm. infxs
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89
Q

Myeloperoxidase def

  • Def
A
  • most common neutrophil defect
  • AR trait
  • Isolated myeloperoxidase deficiency is not associated with clinically compromised defenses, presumably because other defense systems such as hydrogen peroxide generation are amplified.
  • Microbicidal activity of neutrophils is delayed but not absent. Myeloperoxidase deficiency may make other acquired host defense defects more serious.
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90
Q

Leuk. adhesion defect

  • Genetics
  • Defect
  • Clinical
A
  • Very rare AR
  • Defect in ICAM1, problem w/ phagocytosis
  • Delayed loss umb. cord, poor would healing, bact. infxs
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91
Q

What are two specific tests for CGD? What is result when pt has dz?

A
  • Nitroble-trarazolium (NBT) test (measures activity of resp. burst pathway) negative in CGD
  • Measured level of superoxides & H2O2 s/p stimulus.
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92
Q

To what types of microbes are CGD patients especially susc to?

A

catalase +

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93
Q

What characterizes leukemoid reaction?

A
  • Increased neuts, bands and other young leukocytes…

…reflecting heightened BM response.

94
Q

What is a “left shift” on smear?

A

Increase in bands on perip. blood smear, a normal resp. to infx or hemorrhage.

95
Q

Draw out the factors in the intrinsic pathway. What is the relationship b/t these factors?

A

The factors become activated factors for the next in the cascade:

Factor XII –> XI –> IX –> VIII (VIII helps to activated IX which feeds into cmoon pathway)

96
Q

What is the instrinc pathway?

A

Factor VII (VIIa feeds into the common pathway by helping to form Xa)

97
Q

Sketch out the common pathway

A

Factor X is activated by IXa (instrinsic) and VIIa (extrinsic). Xa activates thrombin from prothrombin.

fibrinogen —(thrombin)—> fibrin –> crosslinked fibrin

98
Q

How does quiescent endothelium act to prevent clots? Mention four mediators and their fxn.

A
  • Prostacyclin prevents platelet activation
  • Antrithrombin III lowers thrombin
  • tPA increases fibrinolysis
  • NO reduces adherence, etc.
99
Q

How does activated endothelium create a procoagulatory milieu?

A
  • Upregulation of adhesion
  • Opsonization –> neut. recruit
  • Upreg. of thrombin
  • Upreg of endothelin (vasoconst)
100
Q

F XIII

A

XIII: activated by thrombin, crosslinks fibrin monomers

101
Q

What is characteristic of FXIII def? Why?

A
  • Late/delayed bleeding b/c it’s a late step in clotting cascade.
  • Not reflected in screening assays.
102
Q

Vit K role in clotting, and med that counteracts

A
  • Needed for synth of F’s 2,7,9 and 10
  • warfarin inhibits K-dependent pathway
103
Q

PTT

  • What part of pathway does it test?
A

The partial thromboplastin time (PTT) tests the instrinsic system.

104
Q

vWF function (2)

A

Released in resp to vessel injury, it

  • Leukocyte adhesion (binds collagen, then binds platelet via Gp Ib)
  • Interacts positively w/ f8
105
Q

PT - what part of pathway does it test?

A

extrinsic

106
Q

TT (thrombin time) - what does it measure? what part of pathway?

A

measures time for conversion of fibrinogen to fibrin clot (late steps). Part of common pathway.

107
Q

What are two importnat coag. mediators NOT reflected in PTT or PT?

A

vWF & f13

108
Q

Describe the key parts of the fibrinolytic pathway

A

endothel. release of tPA

Plasminogen –(tPA)—>plasmin

fibrin —(plasmin)—> fibrin degradation products

109
Q

What are some things that could slow down clotting NOT in TT, PT or PTT (6)?

A
  • vWF
  • fXIII
  • platelet problem
  • bleeding
  • DIC
  • vit K
110
Q

How does a fXII def usually present?

A

Longer PTT but no abnormal bleeding

111
Q

What is the general pattern for coagulation tests (PT, PTT, TT) for vit K def?

A
  • Prolonged PT, PTT
  • Normal TT
112
Q

HbF (fetal Hb)

A

2 alpha, 2 gamma (begins to decline at 6 mos.)

113
Q

HbA

A

2 alpha, 2 beta

114
Q

HbA2

A

2 alpha, 2 delta

115
Q

Def. thalassema

A

a quantitative disorder of Hb synth –> S/S

116
Q

def. Beta thal & alpha thal

A
  • B-thal: decreased or absent B chain synth
  • A-thal: decreased/abset A chain synth
117
Q

Alpha thalassemia minor

  • Genetics
  • Clinical
A
  • deletion of 2 alpha globin genes (cis or trans)
  • mild anemia
118
Q

Pathophys of alpha thal’s?

A
  • Def in alpha chains leads to…
  • …B tetramers
  • These precipitate causing hemolysis.
119
Q

Hydrops fetalis

  • Genetics
  • Outcome
A
  • 4 alpha chain deletions
  • incompat. w/ life
120
Q

HbH dz

  • def
  • genetic abnormality
  • abnormal Hb?
  • phenotype
A
  • type of alpha thal
  • deletion of 3 alpha globin genes
  • HbH: these become common in HbH - they are beta tetramers.
  • can be severe
121
Q

alpha thal trait

  • def
  • clinical
A
  • deletion of 1 alpha gene
  • no anemia
122
Q

Hb Constant Spring

  • Describe the abnormal Hb - which globin locus is affected - alpha or beta?
  • What type of mutation is this?
  • Describe the clinical picture of hetero- and homozygous.
A
  • A substition in the a2 termination codon leads to abnormal a2 Hb (a non-deletional alpha thal, much less common)
  • As above - non-deletional in alpha chain
  • Hetero: No abnormality
  • Homo: mild thalassemic changes with normal-size red cells. The hemoglobin consists of approximately 5 to 6 percent hemoglobin Constant Spring, normal hemoglobin A2 levels, and trace amounts of hemoglobin Bart’s. The remainder is hemoglobin A.
123
Q

Alpha thal’s are caused mostly by _______ whereas B thal mutations are often ______.

A

deletions; point mutations

124
Q

Clinical picture of B thal major (5)

A
  • severe anemia w/ hemolysis
  • bone deformities (chipmunk facies, crewcut appearance on head x-ray due to expansion of marrow compartment)
  • splenomegaly
  • Fe overload (why?)
  • Hi output heart failure (secondary to chronic anemia)
125
Q

Rx for B thal major

A
  • RBC xfusion (birth –> life-long)
  • Fe chelation
  • BM xplant
126
Q

What will be typical labs in Thal’s?

A
  • Low Hb, HCT
  • Microcytosis (abs. requirement)
  • High RBC disproportionate w/ Hb value
  • NORMAL Fe studies
127
Q

How will Fe studies look in Thal?

A

Normal

128
Q

Typical periph blood smear, thal?

A
  • microcytic
  • hemolytic
  • variable shapes (poikilocytosis)
  • target cells
  • hi retic
129
Q

Gel results for the following

  • Alpha thal trait
  • HbH
  • Beta thal
A
  • Normal, w/ HbA only
  • fast migrating band formed by B tetramers
  • Increased HbA2 & HbF levels
130
Q

How can HPLC pick up Thal? Which one?

A

Can detect B thal by reliably quantifying HbA2 & HbF fractions in B thal.

131
Q

HbE

  • Def
  • Features
A
  • Variant Hb
  • Mutation causes reduced synth of Beta chain and a mild B-thal phenotype.
132
Q

Pathophys of SS dz

A
  • HbS easily polymerized in deoxy conformation
  • Dec. solubiity –> precipitates –> aggregation –> membrane distortion –> sickling
  • Sickle cells cause occlusion –> ischemia, pain
  • Precipitation –> hemolysis
133
Q

SS dz genetics (HbSS)

A

AR mutatation in B globin allele; 2 abnormal Beta alleles = Sickle dz; HbS = Alpha2,Bs2

134
Q

Genotype of sickle trait; what is the mix of Hb’s?

A

HbAS (heterozygous); gives a mix of A2/Bs2 (HbS) and HbA (so the name sort of reflects this mix of Hb’s) … however, in sickle trait, generally have <50% HbS.

135
Q

Diagnosis of Sickle dz

  • Smear
  • Gel electrophoresis
  • HPLC
  • Specific test for Sickle
A
  • anemia w/ hi retic, normal MCV unless sickle thal, sickled RBCs
  • Gel: distinctive migration pattern
  • HPLC: HbS has distinctive retention time, can quantify HbS proportion (SS will be 100%)
  • Sickle solubility: Positive if pt has any HbS.
136
Q

Explain four (4) types of crises in Sickle cell

A
  1. Vasooclusive crisis: acute pain epidose w/ hypoxia (most common)
  2. Hemolytic
  3. Aplastic: erythroid aplasia due to Parvo B19 infx
  4. Sequestration: pooling in spleen –> splenomeg + shock-like state (more common children)
137
Q

What are some of the organ manifestations of SS dz?

A
  1. Blood: Chronic hemolytic anemia + chronic pain (vasooclusion)
  2. Skin: Chronic leg ulcers
  3. Endo: growth retardation, hypogonadism
  4. Ocular: sickle retinopathy
138
Q

Selected complications of SS dz (5)

A
  • Heart failure
  • Pulm. HTN
  • Stroke
  • Renal failure
  • Infections
139
Q

Acute chest syndrome def.

A

fat embolus from marrow infarction (or other etiology) causing lung necrosis, pulmonary hypertension/infiltrate, cor pulmonale, pleuritic pain; risk death; treat supportively for symptoms.

140
Q

Two primary indications for RBC transfusion in SS dz

A
  1. Acute chest
  2. Stroke prophylaxis
141
Q

Two primary complications of RBC xfusion in SS dz

A
  1. Ab’s to RBC Ag’s
  2. Fe overload
142
Q

How is it believed that hydroxyurea helps pts w/ SS dz?

A
  • Increased HbF which leads to….
  • …improvement in S/S.
143
Q

Mixing study

  • def
  • interpretation/results
A
  • In pt w/ prolonged PT and/or PTT, mix blood 1:1 w/ pooled plasma, then repeat PT/PTT at 2 hours.
  • Correction = clotting factor def.
  • Failure = INH protein
144
Q

vWD S/S (2)

A
  • Mild mucosal & skin bleeding
  • Epistaxis
145
Q

2 major fxns of vWF

A
  • Mediates platelet adhesion
  • Stabilizes factor VIII in circulation
146
Q

Type I vWD

A
  • Most common
  • Mild
  • Deficient vWF
147
Q

Type 2 vWD

A
  • Qualitative defect in vWF
  • Similar to others… low f8 etc
148
Q

Type 3 vWD

A
  • Severe def/absence of vWF w/ lo levels FVIII (cannot stabilized FVIII –> lo levels)
  • AR, very rare
149
Q

Etiologies (3) of acquired vWD

A
  1. Autoimmune: Ab’s bind to vWF
  2. Hypothyr: lo synth
  3. Cardiac: destruction of vWF (Ao stenosis, cong. heart dz, etc.)
150
Q

Lab evaluation for vWD

  • PTT/PT
  • Bleeding time
  • Special test?
A
  • Increased PTT (vWF stabilizes f8) but overall secondary hemostasis works pretty well
  • Increased bleeding time
  • Ristocetin test will be abnormal, hwoing deficiency of vWF
151
Q

What dz can be treated w/ DDAVP (desmopressin)?

How does it work?

A

vWD

  • promotes release of stroed vWF ffrom endoth. cells.
152
Q

Rx of type 2 & 3 vWD often requires ?

A

VWF-containing factor VIII concentrate

153
Q

How to Rx acquired vWD?

A

Most important - Rx underlying condition & use immunosupression

154
Q

Hemophilia

  • Genetics of A & B types
  • Etiology of A & B
A
  • both x-linked recessive
  • A: F VIII def; B: F IX def.
155
Q

Classic S/S of hemophilia

A
  1. hemarthroses, often spontaneous
  2. Other bleeds
156
Q

What level factor measured in severe hemophlia A/B?

A

<1%

157
Q

Three (3) lab studies that would correspond to hemophilia diagnosis.

A
  • Prolonged PTT
  • Correction w/ mixing study
  • Factor assay (VIII or IX) w/ low result.
158
Q

Rx hemophilia

  • 1st line
  • adjunctive
A
  • Plasma derived (rare) or recombinant factor.
  • Adjuntive: Ortopedic, RICE, narcotics (pain - avoid NSAIDS), DDAVP (mucosal bleeds)
159
Q

Acquired hemophilia

  • Etiology
  • Clinical
  • Rx
A
  • AutoAb to FVIII
  • Severe soft tissue bleeds
  • Immunosupp., FVIII conc.
160
Q

DIC

  • Def
  • Etiology
  • Pathophys
  • Labs
  • Rx
A
  • Bleeding disorder caused by pathological activation of coag. cascade
  • Generally secondary to sepsis, obstetric complication, venom. These cause a consumptive coagulopathy –> hemorrhage, thrombosis
  • Labs: lo platelets, prolonged PT/PTT, lo coag factors, low fibrinogen, hi d-dimer, schistocytes (microangiopathic hemolysis).
  • Rx: platelet xfusion, factor replacement, correct underlying cause
161
Q

How can liver failure –> bleeding disorder?

A
  • impaired synth of clotting factors –> coagulopathy
  • vitK deficiency (due to lo bile) –> clotting problems
162
Q

Alpha granules in platelets contain substances that act in aggregation/adhesion, coagulation, and late stage healing. Give examples from each category.

A
  • Aggregation & adhesion factors
  • ADP (released on activation, induces Pt to express Gp IIb/IIIa which binds fibrinogen b/t two receptors to help Pt’s aggregate)
  • TXA2 (pro-aggregation also by upregulating expression of IIb/IIIa)
  • Coagulation
  • Factor V (released by alpha granules but also in circulation)
  • Healing
  • PDGF
  • P-selectin (adhesion of activated platelets to phagocytes; also released from Weibel-Palade bodies of endothelial cells which also contain vWF)
163
Q

Content of dense granules (3), w/ functions

A
  • ATP, ADP: platelet activation & recruitment
  • 5-HT (serotonin): vascoconst.
  • Ca: cofactor for forming fibrin clot
164
Q

Discuss the function of the following receptors on the platelet cell membrane:

  • Gp 1b
  • Gp 1a/2b
  • Gp 2b/3a
A
  • ** ** Gp 1b: Binds vWF which is bound to collagen in damaged endothelium, adhesion.
  • Gp 1a/2b: Can bind collagen directly, adhesion.
  • ** Gp 2b/3a:** Binds fibrinogen, forming bridge b/t platelets, aggregation.
165
Q

What is the role of thrombin WRT platelets?

A

Binds to receptor on platelets and and activates them.

166
Q

Along w/ thrombin, what is another potent platelet activator? How is it synthesized?

A

TXA2: ptent activator, binds to platelet receptor. ARA derivative formed via COX.

167
Q

Name the primary mediators for these activities of platelets:

  • Adhesion
  • Activation
  • Aggregation
  • Clot retraction/healing
A
  • Adhesion: vWF, collagen (bind to receptors on platelet)
  • Activation: TXA2, thrombin
  • Aggregation: fibrinogen (via Gp IIb/IIIa)
  • Clot retraction/healing: PDGF
168
Q

Explain the following tests for platelet disorders:

  • Bleeding time
  • Platelet aggregation
  • PFA-100
A
  • Bleeding time: not as commonly done, increased time could indicate platelet dys.
  • Platelet aggregation: self-explanatory
  • PFA-100: tests adhesion & aggregation, EZ screening w/ small amount whole blood
169
Q

Make note of the image and learn it!

A
170
Q

Bernard-Soulier Dz

  • Def
  • What receptor affected
  • Results in?
A
  • Congenital platelet disorder (cytopathy)
  • Gp Ib (vWF receptor - vWF bound to collagen)
  • Results in poor adhesion –> prolonged bleeding time.
171
Q

Glanzmann’s thombasthenia

  • Def
  • Receptor affected
  • Results in ?
A
  • Congenital thrombocytopathy
  • Gp IIb/IIIa (fibrinogen receptor)
  • Abnormal aggreg., PFA 100 and bleeding time
172
Q

What is the most common acquired thrombocytopathy? What is the etiology?

A
  • ASA/NSAID induced
  • COX inhibition –> deficiency in TXA2 which is needed to activate platelets.
173
Q

DIC

  • Def
  • Etiology
  • Most common causes
A

DIC

  • Consumptive coagulopathy w/ cytopenia - over-coagulation leads to depletion of platelets.
  • Most commonly cuased by release of tissue factor from…
  • …inflammed tissues (commonly due to endotoxin/sepsis, tissue injury, infections)
174
Q

ITP

  • Def
  • Etiology of primary ITP
  • Common conditions that can present w/ secondary ITP
A
  • common acquired autoimmune disorder defined by a low platelet count
  • autoimmune: Ab’s against platelets –> removal/destruction
  • SLE, pregnancy
175
Q

What are some acquired conditions/stimuli that can lead to decreated prod’n of platelets (4)?

A
  • Malignicancy
  • Infectious (Parvo)
  • Drugs
  • Radiation
176
Q

What are some acquired causes of increased dest. of platelets?

A
  • HIT (heparin)
  • hypersplenism
  • ITP
  • HUS
  • APLA (antiphospholipid Ab synd)
177
Q

HELLP syndrome

A

Hemolysis, ELevated liver enzymes, Low Platelets; a complication of pregnancy. The hemolysis is secondary to formation of thromboses which shear the RBCs and consume Pt’s.

178
Q

Rx for ITP?

A
  • Immunomodulation: steroids, IVIG, rituximab.
  • adjunctive: control bleeding, anti-fibrinolytics, FVIIa
179
Q

Explain how vessel injury can create a pro-thrombotic state

A

Vessel injury –> platelet activation via vWF & collagen

Vessel injury –> release of tissue factor –> activaton of coagulation cascade

180
Q

Explain how quiescent endothelium is normally antithrobmotic

A
  • Prostacyclin INH platelets
  • Thrombomodulin & antithrombin III downregulate thrombin
  • tPA upregulates fibrinolysis
  • NO reduced adherence overall
181
Q

Virchow’s Triad

A
  • stasis
  • thrombophilia
  • vessel injury…

…lead to thrombosis.

182
Q

What are four (4) key inhibotorsy of thrombosis (bloodborne factors)?

A
  • TFPI: neutralizes factors Xa and VIIa
  • Proteins C and S: INH fV and fVIII
  • Antithrombin III: binds/INH’s thrombin
183
Q

Clinical features assoc. w/ thrombosis (and the disease/condition that causes it)

A
  • acute chest pain (PE)
  • swelling of extremeties (DVT)
  • SOB (PE)
  • Ill pt. w/ skin necrosis (DIC)
  • Stroke (DVT/ other thrombosis)
  • Frequent miscarriages/fetal loss (placental thrombosis)
184
Q

What are some key acquired prothrombotic states (3)

A
  1. age
  2. surg
  3. estrogens (OCPs)
185
Q

Factor V Leiden

  • Def
  • Etiology/pathophys
A
  • Most common inherited hypercoag
  • Mutant Factor V resistant to deg. by Protein C
186
Q

Prothrombin gene mutation

  • Def
  • Pathophys
A
  • Inh. hypercoag.
  • Mutation –> increased prod’n of prothrombin –> increased plasma levels and venous clots
187
Q

Antithrombin def.

  • Def
  • Pathophys
A
  • Inherited hypercoag.
  • Lack of antithrombin
188
Q

Protein C or S def.

  • Def
  • What factors affected?
A
  • Hypercoag., inherited
  • Proteins C and S inhibit V and VIII
189
Q

Antiphospholipid Ab Syndrome

  • Def
  • Pathophys
  • Epidem.
  • Clinical (4)
A
  • Acquired hypercoag.
  • Immune-mediated, with IgX against proteins on endothel. & platelet membranes.
  • F>M
  • thrombosis (venous or arterial), recurrent fetal loss, livido reticularis, thombocytopenia
190
Q

What does this show? Whas is a hypercoag. syndrome assoc. with it?

A

Livido reticularis - assoc. w/ antiphospholipid Ab syndrome (acquired hypercoag.)

191
Q

Antithrombin III

  • Function
  • What it inhibits
  • Drug that potentiates
A
  • Inhibits coag via…
  • …inh of thrombin (IIa), Xa
  • Heparin potentiates ATIII 1000x
192
Q

Unfractionated heparin

  • Administration
  • t1/2
  • Activity (2)
A
  • IV
  • Very short (1-2 h.)
  • Augments anthithrombin inhibition of thormbin, Xa
  • Impairs platelet fxn
193
Q

What are the two major complications of heparin?

A
  • Bleeding
  • Hep. induced thrombocytopenia (HIT): body develops Ab’s to heparin —> T-penia.
194
Q

HIT (hep induced cytopenia)

  • Pathophys
  • Overall concern in HIT
  • What type of heparin has 10x greater incidence of HIT?
A
  • Immune-mediated (Ab against heparin)
  • Altho platelets LOW, major concern is thrombosis because of endothelial cell activation
  • 10x greater w/ unfractionated heparin (vs. LMWH)
195
Q

Rx for HIT?

A
  • Stop heparin
  • Thrombin inh’s
  • Bridge to warfarin when platelets nl
196
Q

what is a key advantage of low mol weight heparin (LMWH) over unfractionated hep?

A

Less incidence of HIT

197
Q

Warfarin

  • Use
  • Route admin.
  • t1/2
  • MOA
A
  • Anticoag.
  • Oral
  • 36 h.
  • INH’s Vit. K formation (Vit K reductase) –> lower amounts of fII, VII, IX, X b/c the active form of Vit K not able to gamma-carobxylate them to active forms.
198
Q

Key complications of warfarin therapy (2)

A
  • bleeding
  • avoid in pregnancy - teratogenic
199
Q

What are the most common thrombolytic agents? Where do they affect thrombosis?

A

tPA derivs

tPA activates plasminogen which converts to plasmin. Plansim breaks down fibrin to subunits/deriv’s.

200
Q

Indications for thrombolytic (tPA) therapy

A

In general, a life or limb threatening situation

  • Acute MI (alternative is stenting)
  • PE
  • DVT
  • Thrombotic stroke
201
Q

Some key contraIND’s of tPA (4)

A
  • Major bleeding past 6 mos.
  • s/p surgery 10 days
  • HTN >200 SYS
  • Bleeding disorder
202
Q

Discuss the MOA of these three anti-platelet drugs:

  • ASA
  • Clopidrogel
  • Abciximab
A
  • ASA: COX INH (INH formation of TXA2 which is pro-aggregator)
  • Clop: ADP-R antagonist (INH activation)
  • Abciximab: Antibody to GpIIb/IIIa receptor (INH’s aggregation)
203
Q

Thymoma

A

Type of lymphoid malignancy (T cell tumor) - a cause of acquired aplastic anemia.

204
Q

What methods are used to remove Lc’s from blood products? Why?

A

Irradiation & Lc depletion; done to avoid graft vs. host dz (GVH)

205
Q

What is a compatible transfusion?

A

Match of ABO + Rh matched.

206
Q

What can result from incompatible transfusion?

A

Risk of fulminant hemolytic reaction

207
Q

Hemolytic dz of newborn (HDN)

  • Mechanism
  • Rx
A
  • Rh- mom exposed to Rh Ag ==> generation of anti-Rh Ab’s –> cross placenta –> cause ** fetal EV hemolysis**
  • Rx: RhoGam - hi-dose anti-Rh Ab’s –> bind/sequester Rh Ag’s.
208
Q

Neonatal immune thrombocytopenia (NAIT)

  • Def
A

maternal anti-Pt Ab’s cross placenta

209
Q

ABO mismatch can cause _______ while Rh mismatch can cause ________.

A

IV hemolysis; EV hemolysis;

210
Q

What characterizes a delayed transfuions rxn? Test used?

A

Jaundice and anemia 7-10 days s/p xfusion; test: will be Coomb’s + at time of reaction.

211
Q

TRALI

  • Def
A

Transfusion-related acute lung injury

  • Allergens in Lc’s of transfused blood –> allergic rxn w/ hives & pulm. edema.
  • Non-hemolytic
212
Q

Febrile transfusion reaction

A
  • Rxn b/t Lc’s (host) and Lc’s (xfusion) –> fever (non-hemolytic)
213
Q

three most common hazards of xfusion? Give brief explanation of each.

A
  • Fe overload (can lead to hemochromatosis)
  • Infection: small chance for viral infx (HIV, hep)
  • Allo-immunization: sensitization to certain Ag’s on RBC’s can lead to hemolytic anemias.
214
Q

Where is Fe absorbed?

A

Duodenum

215
Q

Microangiopathic hemolytic anemia

  • Def
  • Characteristic lab result (smear)
  • Etiologies (6)
A
  • Hemolytic anemia, normocytic, intravascular, caused by shear stress often caused by thrombi, or other things.
  • Smear: schistocytes aka “helmet cells”
  • Etiologies:

TTP

HUS

DIC

HELPP syndrome

Ao stenosis

Prosthetic valves

216
Q

Type III vWD can resemble _________. How to Rx?

A

Hemophilia A…. b/c can also present w/ deep bleeding including joint bleeding. If DDAVP not sufficient Rx w/ f8 concentrate that has vWF.

217
Q

TTP

  • Pathophysiology/etiology of the congenital form
A
  • Decrease in Adam TS13 enzyme leads to thrombosis which then results in microangiopathic hemolytic anemia & consumptive thrombocytopenia.
  • AdamsTS13 is a thrombolytic protein.
218
Q

Two ligands that help to identify a HSC, and one that is not present, which also helps to ID.

A
  • CD34+
  • c-Kit + (CD 117)
  • Lin -
219
Q

What blood product imparts highest risk of bact. infxs? Why?

A

Pt’s b/c they are stored close to room temp.

220
Q

c-kit/CD 117

A

c-kit is an important HSC marker. it is the receptor for stem cell factor and is also referred to as CD 117.

221
Q

What are three thrombin INH’s to know?

What is a use for them (think heparin)?

A
  • *Lepirudin
    *Argatroban
    *Dabigatran
  • Can use to Rx heparin-induced TCpenia (HIT)
222
Q

What are two LMWH’s

A

enoxaparin, dalteparin

223
Q

Rivaroxaban

  • Def
  • MOA
  • Uses
A
  • an anticoagulant drug
  • f10a INH
  • Venous thrombosis
224
Q

Prasugrel

  • Type
  • MOA
  • Indications (2)
A

Prasugrel

  • Antiplatelet drug inhibiting primary hemostasis
  • ADP receptor blocker (like clopidrogel)
  • Indications: treatment of ACS and established peripheral artery disease, as well as for secondary prevention of myocardial infarction and ischemic stroke
225
Q

Abciximab

  • Drug type
  • MOA
A

Abciximab

  • Drug type: Antiplatelet (anticoagulant)
  • MOA: Mab drug that directly binds Gp 2a/3b (fibrinogen receptor) –> poor aggregation of Pt’s.
226
Q

Fondaparinux

  • Drug type
  • MOA
A

Fondaparinux

  • Drug type: A heparin derivative anticoagulant medication.
  • MOA: Factor Xa inhibition (Heparin INH’s Xa & thrombin)
227
Q

Aminocaproic Acid

  • Type/uses (3)
  • MOA
A

Aminocaproic Acid

  • Type/use: Procoagulant drug used often (1) post-surgically in cases of heavy bleeding, (2) in situations w/ excess fibrinolysis and (3) as antidote to tPA overdose.
  • MOA: Inhibits plasmin.
228
Q

Romiplostim, Eltrombopag (in devt?)

  • Indication
  • MOA
A
  • To treat refractory ITP.
  • Tpo analog.
229
Q

Cryoprecipitate

  • What active substances does it have?
  • Can be used for which disorders?
A
  • fibrinogen, f8, and vWF.
  • f8: hemophilia A, esp. if recomb. f8 not available.
  • vWF to patients with dysfunctional (type II) or absent (type III) vWD
230
Q

Fresh frozen plasma

  • Major components (4)
  • Indications (3)
A

Fresh-Frozen Plasma

  • FFP contains stable coagulation factors (II, V, VII, IX, X, and XI) and plasma proteins: fibrinogen, antithrombin, proteins C and S.

Indications (3)

  • correction of coagulopathies (can be used in place of specifc factors if they are not available not that f8/wVF are from cryoprecipitate not FFP)
  • rapid reversal of warfarin
  • supplying deficient plasma proteins
  • treatment of thrombotic thrombocytopenic purpura
231
Q

RhoGAM

  • Indication
  • MOA
A
  • To prevent hemolytic dz of the newborn
  • Anti-RH-antibody: binds Anti-Rh Ab’s from mom to prevent above condition.

HemeOnc (2 decks)

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