Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/57

Click to flip

57 Cards in this Set

  • Front
  • Back
RBC development
What do young cells look like?
nuclear phases:
reticulocyte
: cytoplasm-->blue to red
: as becomes inactive goes condensed and shrunken
: no nucleus but still bluish
Normal values (male/female)
RBC count
Hemoglobin
Hematocrit
reticuloctye
: 4.4-6 / 4.2-5.5
: 14-18 / 12-16
: 40-54% / 37-47%
: .6-1.9 (% of blood) & .025-.105
Formulas:
MCV=
MCHC=
MCH=
: HCT x 10/RBC ct (81-100)
: Hg/HCT = 31-36
: Hgx10/RBC
microcytic hypochromic anemia:
macrocytic anemia:
normochromic/normocytic anemia:
: defect in Hgb synthesis (Fe deficient, thal, lead, sideroblastic, chronic disease)
: bad nuclear maturation (B12/folate)
: blood loss, aplastic anemia, hemolytic
megaloblastic anemia
marrow:
smear:
: megaloblasts seen (big cells, less mature nucleus, big WBC
: macro-ovalocytes, hypersegmented neutros, pancytopenia
: premature cel death
Folic acid
: source/storage
: Purpose
: deficiency
: 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
B12:
: source/storage
: purpose
: deficiency
: 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
achlorhydria
lack of gastric acid production by the stomach from pernicious anemia due to B12 deficiency. Diagnostic test
microcytic hypochromic anemia:
Fe absorption and transport:
Total body iron:
: 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
transferrin
Marrow iron:
: takes iron from macros (dgraded by heme oxygenase)-->transferrin to marrow
: in macros and sideroblasts
ringed sideroblasts
TIBC:
fe deficiency
chronic disease
Fe overload
: 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
Fe deficiency anemia;
: smear
: tests
: target cells, anisocytosis, poikilo. Marrow has low Fe
: low serum Fe, high TIBC, low ferritin
Sideroblastic anemia
Serum Fe:
TIBC:
Saturation:
Ferritin:
Marrow:
Hi
normal or high
high
high
increased e
Thalasemia Iron
TIBC
Saturation
Ferritin
Marrow
normal/high
normal/high
normal/hgih
normal/high
incresed
pernicious anemia
deficiency in intrinsic factor
macro-ovalocytes
anemia of chronic disease
RBC production:
Iron & infections:
cytokine mediation:
: 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
reticuloendothelial system
system in spleen of macrophages etc. that takes out old/bad RBC
hemolysis:
intravascular/extravasc
intra/extracorpuscular
: 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
haptoglobin:
Hemosiderin:
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
bilirubin levels:
hemolysis bili:
: 1.2 mg total. <.6 mg indirect
: no greater than 4 mg unless liver problem. direct bili does not increase, all excreted
intravascular hemolysis signs
Pink serum and urine
: decreased unbound habtoglobin
: increased CO produced and excreted by lung
extravasuclar hemolysis signs
increased indirect bili
: increased CO
: Increased urobilinogen in feces and urine.
extracorpuscular causes of hemolysis
Autoimmune:q
: 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
Mechanical extracorpuscular hemolysis

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

: others: Malaria, babesiosis, clostridia (gas gangrene), toxins, altered plsma components
intracorpuscular causes
membrane;
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
intracorpuscular causes hemolysis
: enzyme deficiencies
: other
: 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
HBG info:
chromosomes:
types
Alpha: 16. beta: 11 delta: 11 gamma 11
Hbg C disease:
: characteristics
: blood smear
3% gene frequency in AA
: homozygous gets mild chronic hemolytic anemia.
: HgC crystals seen on peripheral blood smear with target cells:
Thalassemias
general info:
: quantitative decrease in synthesis of one or more globin chain
Beta Thal
: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
Beta Thal major clinical findings
smear:
severe anemia, hepatosplenomegally, extramedullary hematopoeisis, hypercellular marrow, Fe overload, recurrent infection
: hypochromic target cells. howell jolly body
: medullary bone expansion
beta thal blod smear
aniso and pokylo cytosis w/polychromasia and +/- reticulocytes, microcytic hypochromic RBC w/target cells
alpha thal
: 4 genes, barts Hg
: 3 bad genes
: 2 bad genes
: 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
SS disease
epidemiology:
labs
clinical
: 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
burr cells (echinocytes):
Spur cells (acanthocytes):
MCH significance:
: chronic dialysis, shear stress on blood
: irregularily shaped, from free cholesterol (liver failure)
: low in thalassemia
hepcidin:
associated w/anemia of chronic disease. secreted by liver, blocks iron absorption.
: from high levels of IL 6
aplastic anemia
: causes
: signs
: 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
Blood
type, Ag, Ab in plasma
O: none, anti-A,B (universal donor
A: A, anti B
B: B, anti A
AB: A and B, none (universal reciever)
blood donating
increase HCT, HBG
: why give plasma
: one unit = 2-3% Hct inc. 1 gm/dL
: help increase coagulation factors
cryoprecipiatate
: what in it?
: why give?
: Contains factors VIII, XIII, vWF, fibrinogen and fibronectin
: treat bleeding or prep for surgery, DIC can cause these probs
Acute hemolytic transfusion rxn
: etiology
: signs/symptoms
: eval/therapy
: intravascular hemolysis from Ab and complement
: fever (most common), back/chest pain, nausea others
: stop transfusion, administer saline (maintain BP)
Delayed hemolytic transfusion rxn
etiology:
signs:
therapy:
: 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
Febrile, non-hemolytic rxn
etiology:
signs:
evaluation:
: transfusion of pre-formed cytokines, leukoalutinating Ab in recipient
: fever close to transfusion
: R.O hemolytic, anti-pyretic
Uticarial transfusion rxn
: etiology
signs:
evaluation
: 2nd most common rxn
: allergy to donor proteins, does dependent
: stop transfusion, give benadryl
circulatory overload
: signs
: theraputic
acute respiratory distress
: dyspnea, couch, tachycardia, HT, HA
: O2, diuretic, upright posture
vWF
jobs:
TXA2:
collagen: which pathway?
tissue factor:
: secreted by endothelial cells, stabilizes VIII
: adhesion of platlets to vascular injury site
: released by plats, vasoconstrictor
: intrinsic
: subendothelial tissue, extrinsic
clotting made by liver:
Vitamin K role:
ATIII:
: 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
Plasmin:
Protein C/S:
XIII
: regulates fibrin formation
: inhibits VIII and V. C stabilized by S. C also Vit K dependent
: stabilizes fibrin clot
platlet disorders
symptoms:
causes:
: slow bleeds, acquired is common, inherited is rare
: prosthesis and valves, autoimmune, DIC
vWF disease:
Hem A association:
: 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
hemorrhage disease
: most common sign
: different kinds
: joint bleeding
: Vit K deficiency, hemophilias
: severity related to factor activity level. 5-30% mild
thrombosis
causes:
: auto-imune (lupus), prot C deficiency (most common), ATIII deficiency, prothrombin mutation
: all heterozygotes, no homo
: probably need mult mutations
: autosomal dominant
PT:
PTT:
ITP:
DIC: issue
: 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
lose platlet function
why:
normal #'s:
: uremia, liver disease (makes and clears fibrin factors), nsaids, congenital
150,000-400,000. <5000 risk major GI or cerebral hemorrhage
fibriogen mutation: inheritance
: dominant or recessive depending on mutation
DIC:
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
petichiae
hemophilia tx:
: 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