Anemias

Front 1

RBC development
What do young cells look like?
nuclear phases:
reticulocyte

Back 1

: cytoplasm-->blue to red
: as becomes inactive goes condensed and shrunken
: no nucleus but still bluish

Front 2

Normal values (male/female)
RBC count
Hemoglobin
Hematocrit
reticuloctye

Back 2

: 4.4-6 / 4.2-5.5
: 14-18 / 12-16
: 40-54% / 37-47%
: .6-1.9 (% of blood) & .025-.105

Front 3

Formulas:
MCV=
MCHC=
MCH=

Back 3

: HCT x 10/RBC ct (81-100)
: Hg/HCT = 31-36
: Hgx10/RBC

Front 4

microcytic hypochromic anemia:
macrocytic anemia:
normochromic/normocytic anemia:

Back 4

: defect in Hgb synthesis (Fe deficient, thal, lead, sideroblastic, chronic disease)
: bad nuclear maturation (B12/folate)
: blood loss, aplastic anemia, hemolytic

Front 5

megaloblastic anemia
marrow:
smear:

Back 5

: megaloblasts seen (big cells, less mature nucleus, big WBC
: macro-ovalocytes, hypersegmented neutros, pancytopenia
: premature cel death

Front 6

Folic acid
: source/storage
: Purpose
: deficiency

Back 6

: liver, kidney, liver, veggies
need 50microg daily. 5month storage, absorbed in SI
: carbon transfer in DNA synth
: anemia, glositis, intestinal mucosal changes
: drugs: methotrexate, dilatin, anticonvulsants, antimicrobials

Front 7

B12:
: source/storage
: purpose
: deficiency

Back 7

: from meat,dairy. co-factor. transcobalamin I&II transport. several years to deplete. absorbed in terminal ilium
: Needed for DNA synthesis, myelin synthesis
: no intrinsic factor, bad ileal absorption, tapeworm, blind loop syndrome, diverticulosis

Front 8

achlorhydria

Back 8

lack of gastric acid production by the stomach from pernicious anemia due to B12 deficiency. Diagnostic test

Front 9

microcytic hypochromic anemia:
Fe absorption and transport:
Total body iron:

Back 9

: decrease in Hg synthesis
: Fe 3-->Fe2-->into mucosa-->Fe2 -->some bound in mucosal cells as ferritin-->some into plasma with transferrin
: 500-1000 mg male and 200-400 mg/kg fe

Front 10

transferrin
Marrow iron:

Back 10

: takes iron from macros (dgraded by heme oxygenase)-->transferrin to marrow
: in macros and sideroblasts

Front 11

ringed sideroblasts
TIBC:
fe deficiency
chronic disease
Fe overload

Back 11

: rings of iron in mitochon. of developing RBC.
: normally 30% transferrin saturated. Fe deficiency <10%
chronic diseas: TIBC low, Fe low, ferritin high, marrow lots Fe
: transferrin normal but all saturated

Front 12

Fe deficiency anemia;
: smear
: tests

Back 12

: target cells, anisocytosis, poikilo. Marrow has low Fe
: low serum Fe, high TIBC, low ferritin

Front 13

Sideroblastic anemia
Serum Fe:
TIBC:
Saturation:
Ferritin:
Marrow:

Back 13

Hi
normal or high
high
high
increased e

Front 14

Thalasemia Iron
TIBC
Saturation
Ferritin
Marrow

Back 14

normal/high
normal/high
normal/hgih
normal/high
incresed

Front 15

pernicious anemia

Back 15

deficiency in intrinsic factor
macro-ovalocytes

Front 16

anemia of chronic disease
RBC production:
Iron & infections:
cytokine mediation:

Back 16

: decreased b/c less Fe available and less EPO
: Fe needed for microorg to divide. defend by inc. iron binding
: cytokines start processes that hide Fe from orgs, also hides from RBC

Front 17

reticuloendothelial system

Back 17

system in spleen of macrophages etc. that takes out old/bad RBC

Front 18

hemolysis:
intravascular/extravasc
intra/extracorpuscular

Back 18

: w/in circulation (complement, toxins, mechanical trauma) v. outside RBC (usually macros in spleen and liver)
: abnormal RBC/factor w/in plasma leading to hemolysis

Front 19

haptoglobin:
Hemosiderin:

Back 19

binds free Hbg in serum when RBC are lysed
: when Hbg secreted in urine some is taken up by tube cells, when cells slough see hemosiderin

Front 20

bilirubin levels:
hemolysis bili:

Back 20

: 1.2 mg total. <.6 mg indirect
: no greater than 4 mg unless liver problem. direct bili does not increase, all excreted

Front 21

intravascular hemolysis signs

Back 21

Pink serum and urine
: decreased unbound habtoglobin
: increased CO produced and excreted by lung

Front 22

extravasuclar hemolysis signs

Back 22

increased indirect bili
: increased CO
: Increased urobilinogen in feces and urine.

Front 23

extracorpuscular causes of hemolysis
Autoimmune:q

Back 23

: incompatible transfusions
: Antibodies to RBC's
: autoimmunie hemolytic anemia:
IgG, spherocytes on smear
: cold antibody: mycoplasma
pneum, IgM and autoagluttination
: can see nucleated red cell

Front 24

Mechanical extracorpuscular hemolysis

and others

Back 24

: micrangiopathic (DIC), fibrin plugs, heart valves
: smear has fragmented RBCs

: others: Malaria, babesiosis, clostridia (gas gangrene), toxins, altered plsma components

Front 25

intracorpuscular causes
membrane;

Back 25

Membrane defects: hereditary sphero/elliptocytosis: osmotically fragile and poor deformation
PNH: acquired. membranes don't have anti-complement
non-hereditary: from IgG AB to RBC

Front 26

intracorpuscular causes hemolysis
: enzyme deficiencies
: other

Back 26

: G6PD, pyruvate Kinase
-G6PD RBC can't protect Hbg from oxidative damage from drugs or stress (infection). Oxidated Hbg precipitates (heinz bodies).
-RBC lyse w/intravascular hemolysis
Other: Hbg-opathies. thal

Front 27

HBG info:
chromosomes:
types

Back 27

Alpha: 16. beta: 11 delta: 11 gamma 11

Front 28

Hbg C disease:
: characteristics
: blood smear

Back 28

3% gene frequency in AA
: homozygous gets mild chronic hemolytic anemia.
: HgC crystals seen on peripheral blood smear with target cells:

Front 29

Thalassemias
general info:

Back 29

: quantitative decrease in synthesis of one or more globin chain

Front 30

Beta Thal

Back 30

:decreased production of beta chains.
:decreased Hbg in RBC, ineffective RBC production and hypochromic
:excess alpha precipitate and form heinz bodies
: hemolyis and RBC death

Front 31

Beta Thal major clinical findings
smear:

Back 31

severe anemia, hepatosplenomegally, extramedullary hematopoeisis, hypercellular marrow, Fe overload, recurrent infection
: hypochromic target cells. howell jolly body
: medullary bone expansion

Front 32

beta thal blod smear

Back 32

aniso and pokylo cytosis w/polychromasia and +/- reticulocytes, microcytic hypochromic RBC w/target cells

Front 33

alpha thal
: 4 genes, barts Hg
: 3 bad genes
: 2 bad genes

Back 33

: less alpha chains. SE asian pops.
: 4 bad genes = hydrops fetalis, barts Hbg=4 gammas
: 3 bad genes: Hbg H disease. Hg H=4 beta chains.precipitates in RBC (heinz body), lots of targets, hypo/micro. special die looking for HbH precip.
: alpha thal minor. mild anemia or nothing
: 1 gene = silent carrier

Front 34

SS disease
epidemiology:
labs
clinical

Back 34

: 1 in 500 black children
onset: 6 mo-2yrs
: low grade anemia, erythroid hyperplasia, hemolysis
: pain, hypoxic tissue damage, variable course, infection, ACS, CV, stroke, renal probs

Front 35

burr cells (echinocytes):
Spur cells (acanthocytes):
MCH significance:

Back 35

: chronic dialysis, shear stress on blood
: irregularily shaped, from free cholesterol (liver failure)
: low in thalassemia

Front 36

hepcidin:

Back 36

associated w/anemia of chronic disease. secreted by liver, blocks iron absorption.
: from high levels of IL 6

Front 37

aplastic anemia
: causes
: signs

Back 37

: bone marrow replaced by fat.
: inherited or acquired through variety of things. Most likely T cell mediated destruction of hematopoetic cells. can be reversed if caused by drugs
: anemia, infections bleeding

Front 38

Blood
type, Ag, Ab in plasma

Back 38

O: none, anti-A,B (universal donor
A: A, anti B
B: B, anti A
AB: A and B, none (universal reciever)

Front 39

blood donating
increase HCT, HBG
: why give plasma

Back 39

: one unit = 2-3% Hct inc. 1 gm/dL
: help increase coagulation factors

Front 40

cryoprecipiatate
: what in it?
: why give?

Back 40

: Contains factors VIII, XIII, vWF, fibrinogen and fibronectin
: treat bleeding or prep for surgery, DIC can cause these probs

Front 41

Acute hemolytic transfusion rxn
: etiology
: signs/symptoms
: eval/therapy

Back 41

: intravascular hemolysis from Ab and complement
: fever (most common), back/chest pain, nausea others
: stop transfusion, administer saline (maintain BP)

Front 42

Delayed hemolytic transfusion rxn
etiology:
signs:
therapy:

Back 42

: extravascular via Ab coating and spleen
: fever, fall in hgb/hct, jaund
: bank finds new Ab
: can also happen in newborns when fetal blood stimulates mom IgG response

Front 43

Febrile, non-hemolytic rxn
etiology:
signs:
evaluation:

Back 43

: transfusion of pre-formed cytokines, leukoalutinating Ab in recipient
: fever close to transfusion
: R.O hemolytic, anti-pyretic

Front 44

Uticarial transfusion rxn
: etiology
signs:
evaluation

Back 44

: 2nd most common rxn
: allergy to donor proteins, does dependent
: stop transfusion, give benadryl

Front 45

circulatory overload
: signs
: theraputic

Back 45

acute respiratory distress
: dyspnea, couch, tachycardia, HT, HA
: O2, diuretic, upright posture

Front 46

vWF
jobs:
TXA2:
collagen: which pathway?
tissue factor:

Back 46

: secreted by endothelial cells, stabilizes VIII
: adhesion of platlets to vascular injury site
: released by plats, vasoconstrictor
: intrinsic
: subendothelial tissue, extrinsic

Front 47

clotting made by liver:
Vitamin K role:
ATIII:

Back 47

: VII,IX,X,II
: COO- added by Vit K mediated enzyme in liver, COO binds Ca. coumadin inhibits
: anti-thrombin: inhibits IX, X, II. potentiated by heparin

Front 48

Plasmin:
Protein C/S:
XIII

Back 48

: regulates fibrin formation
: inhibits VIII and V. C stabilized by S. C also Vit K dependent
: stabilizes fibrin clot

Front 49

platlet disorders
symptoms:
causes:

Back 49

: slow bleeds, acquired is common, inherited is rare
: prosthesis and valves, autoimmune, DIC

Front 50

vWF disease:
Hem A association:

Back 50

: most common congenital bleeding disorder, decreased plat adhesion
:can act as autosomal dominant b/c consumed
: keeps VIII from being consumed by proteases in serum
: can look like VIII deficiency b/c w/out vWF VIII is probably down

Front 51

hemorrhage disease
: most common sign
: different kinds

Back 51

: joint bleeding
: Vit K deficiency, hemophilias
: severity related to factor activity level. 5-30% mild

Front 52

thrombosis
causes:

Back 52

: auto-imune (lupus), prot C deficiency (most common), ATIII deficiency, prothrombin mutation
: all heterozygotes, no homo
: probably need mult mutations
: autosomal dominant

Front 53

PT:
PTT:
ITP:
DIC: issue

Back 53

: extrinsic path. 10-12 s
: intrinsic. 22-33 sec
: immune thrombocytopenia. chronic (bad) or acute (usually ok). immunosuppresion or splenectomy. no splenomegally. usually in kids remission, chronic in adults
: increased consumption of clotting factors

Front 54

lose platlet function
why:
normal #'s:

Back 54

: uremia, liver disease (makes and clears fibrin factors), nsaids, congenital
150,000-400,000. <5000 risk major GI or cerebral hemorrhage

Front 55

fibriogen mutation: inheritance

Back 55

: dominant or recessive depending on mutation

Front 56

DIC:

Back 56

generalized IV clotting and fibrinolysis. Clotting in small vessels and hemorrhage from consumption of factors.low plats, factros, fibrinogen
: hypoxic and hem damage in renal, skin, brain, mucous, GI

Front 57

petichiae
hemophilia tx:

Back 57

: non-blanching lesion, push on it and doesn't go away
: transfusions, fibrinolysis inhibitors, give VIII. Cryprecipitate not good for hem B, doesn't have IX in it