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Iron deficiency stages:

1. depletion of storage iron  - labs may not show anything yet

2. drop in [Hb]  in blood -> RBCs become smaller (microcytic) and paler (hemochromic), with abnormal size variation

3. fully developed anemia, RBC changes as per above, mean corpurcular volume (MCV) down

mean corpuscular Hb (MCH) down

mean corpuscular Hb concentration (MCHC) down



What is serum iron and TIBC?

Serum iron - amount of iron bound to transferrin (iron transport protein in the blood)

 TIBC - total iron binding capacity - maximum amount of iron that could be bound to transferrin

transferrin saturation (%) = serum iron /TIBC = amount currently bound to transferrin / total amount that could be bound = % currently bound to transferrin


What is serum ferritin?

serum ferritin - storage form of iron (up to 4500 molecules covered by proteins)

females naturally have lower ferritin stres

low ferritin is diagnostic of iron deficiency = iron stores depletion

anemias of chronic disease - inflammation, malignancy, and infection prevents release of Fe from macrophages (RE) that "digest" RBCs - ferritin stores go up, but Fe+ within blood cells may be low


Lab findings in iron deficiency?

serum iron : down!

TIBC: up! (iron wants to bind and get transported)

% saturation of transferrin: down

ferritin: down (storage down)

free erythrocyte protorphyrin: up  (protorphyrin ring that misses Fe2+ on the inside)

hemoglobin: down

MCV: down

MCH: down

abnormal peripheral blood smear: image shows hypochromia (central pallor) and size variation)

platelet count: up



Lab findings in hemochromatosis?

serum iron: up

serum transferrin (TIBC): down

% saturation of transferrin: up

ferritin: up

! opposite to iron deficiency !

test genetics, liver biopsy - measure iron content (less used now b/c DNA testing available)


What is free erythrocyte protoporphyrin?

Small number of protoporphyrin molecules bind Zn2+ instead of Fe2+ to produce zinc protoporphyrin, which then circulates in RBCs. A decrease in iron available to RBCs increases formation of Zn protoporphyrin. Usually measured as free erythrocyte protoporphyrin (FEP) = Zn  -> assessment of iron available for Hb production

Both iron deficiency (absolute lack of iron) and chronic disease (impaired utilization of iron stores) will increase FEP.


Outline general lab results for a variety of anemias?

iron deficiency vs chronic disease vs hemochromatosis


More detailed results for anemias?


Outline blood groups, Rh and their associated antibodies and antigens?

Blood group A: A antigen on RBC surface and anti-B antibody in plasma

Blood group B: B antigen on RBC surface and anti-A antibody in plasma

Blood group AB: A and B antigens on RBC surface, no antibodies in plasma - universal donor of plasma, universal recipient of RBCs (remember that plasma and RBCs separated in blood transfusion)

Blood group O: no antigens on RBC surface, anti-A and anti-B antibodies in plasma - universal recipient of plasma, universal donor or RBCs (remember that plasma and RBCs separated in blood transfusion)

Rh - Rh antigen on RBC surface. Rh - mothers exposed to Rh+ blood (ex. delivery) may make anti-Rh IgG (can cross placenta and cause hemolytic disease of the newborn in the next pregnancy that is Rh+

Anti-A antibodies and Anti-B antibodies are IgM and cannot cross placenta; anti-Rh antibody is IgG and CAN cross placenta - give RhoD immune globulin to mom to prevent sensitization = RhoGam - solution of IgG anti-D (anti-RhD) antibodies that take out any fetal RhD-positive erythrocytes which have entered the maternal blood stream from fetal circulation, before maternal immune system can react to them, thus preventing maternal sensitization



What is available for blood transfusions?

Why do we only give to symptomatic/high risk patients?

  • Red blood cells (RBCs) - contains A/B surface antigens, Rh surface antigens
  • platelet pool
  • plasma: frozen plasma (thawed) - contains anti-A/B,.. antibodies, coagulation factors, etc = FP (for frozen plasma - frozen w/i 24 hrs of collection)
  • plasma: cryoprecipitate - FP that is thawed at low temperatures 
  • In Canada, blood products are leukodepleted via filtration immediately after donation (no lymphocytes, monocytes or granulocytes)
  • think of blood being separated into Plasma, Platelets and RBCs
    ex. plasma for SYMPTOMATIC anemia
    platelets - coagulopathy patient who is BLEEDING or at HIGH RISK of BLEEDING 
    don't just give for numbers, must have clinical indication - transfusion has risks
  • transfusion is always a temporary solution - underlying cause must be adressed


What is a good transfusion rate for RBCs?

2-4 hrs , 3 hrs is ideal

transfuse w/i 42 days of collection - RBCs from donors lyse faster, if transfuse late, risk of hyperkalemia (since RBCs lyse, K+ released - terrible for heart)



Indications for RBC transfusions (lecture)?

Lecture notes: 

1. Improved oxygen carrying capacity

2. supression of abnormal hematopoiesis

transfuse if:

  • symptoms of anemia (SOB, fatigue, angina, confusion)
  • acute blood loss
  • current Hb low and chronic anemia 
  • patient history/special situation (volume loss, fever/chills, CAD, etc)

if Hb 100+ almost always inappropriate to transfuse

<80 Hb - transfuse for symptoms of anemia or consider post-surg

<70 Hb - if in ICU (adult or peds) and stable





Indications for RBC transfusions - Toronto Notes?

Hb < 70 g/L -> goal to maintain Hb between 70-100 during active bleed

consider higher Hb in:

CAD/unstable coronary syndromes

uncontrolled bleed

impaired pulmonary function

increased O2 consumption - high with fever/chills, anesthesia



What tests should be ordered before transfusion?

1. Group and screen

Group: determines ABO GROUP = ABO antigens and D (Rh) = RBC surface  => worry about acute hemolytic transfusion reaction 

Think group anything on RBC surface

screen: for minor blood antigens (Duffy, Kidd, etc), allo-antibodies in patients serum=> worry about delayed hemolytic transfusion reactions (delayed because antibodies to these are made first, 10-14 days)

allo-antibodies = antibodies against something foreign (ex. in transfusion or pregnancy)

2. Crossmatch - donor and recipient blood together to see if they agglutinate - if Y = baaad idea



What are allo-antibodies ?

allo-antibodies = antibodies against something foreign RBC antigens (ex. via blood transfusion or pregnancy), they are non-ABO red cell antigens, IgG (cross placenta)

ex. Rh, Kell, Kidd, Duffy, etc


What are components of informed consent?

1. is patient capable

2. risks and benefits of procuedure

3. alternatives

4. opportunity for questions

5. signature of consent or refusal

6. document conversation


Adverse effects of blood transfusion?

minor allergic reaction (hives, etc) 1:100

anaphylaxis 1: 1600 

fever 1:300 (FNHTR)

volume overload 1:700 (TACO)

lung injury 1:10,000

symptomatic bacterial sepsis 1:10,000

wrong blood transfused 1:14,000

wrong ABO group tranfused: 1:40 000

fatal acute hemolytic reaction: 1:600,000

viral: HIV (1:8 M); Hep B (1:2M); Hep C (1:7M), Malaria (1:4M), bacteria (1:2,500)



If blood transfusion is indicated, how much do you give them? Ex. Hb <70,, symptomatic

Minimum effective dose

single unit, reassess symptoms after= 1 unit




What are some acute blood transfusion reactions? (low priority)

acute hemolytic transfusion reaction (AHTR) - ABO incompatability -> intravascular hemolysis, complement activation

fever, chills, hypotension, acute renal failure (b/c of antibodies <3 glomerulus), DIC 

stop transfusion, notify bank and  check for clerical error, maintain BP with a lot of IV fluids, maintain urine with diuretics to avoid fluid overload


febrile nonhemolytic transfusion reaction (FNHTR)

alloantibodies to WBC, platelets, etc -> release of cytokines

0-6 hrs post ransfusion

fever, rigors, facial flushing, headache, myalgia, etc

rule out hemolytic reactions or infection

if T< 38C - continue transfusion but decrease rate and give antipyretics

if T>38C - stop transfusion, give antipyretics and anti-histomaines


Transfusion-Related Acute Lung Injury (TRALI)

new-onset acute lung injury during transfusion or w/i 6 hrs of transfusion

severe hypoxemia, pulmonary edema on CXR, etc - > pathogenesis uncertain

resolves in 24-72 hrs, do supportive therapy (oxygen)


bacterial infection


Transfusion Associated Circulatory Overload (TACO)

impaired cardiac function and excessive rapid transfussion

transfuse at lower rate, give diuretics and oxygen



due to increased K+ release from stored RBCs (shorter life cycle -> lyse and release K+


Dilutional Coagulopathy

with massive transfusions (>10 units) : RBCs don't contain clotting factors, fibrinogen, platelets etc - give FP (plasma), platelets and cryoprecipitate




What are Delayed Blood Transfusion Reactions?

Delayed Hemolytic Reactions

alloantibodies to minor antigens such as Rh, Kell, Duffy

at transfusion time antibodies low, but level increases once in recipient body

anemia and mild jaundice (increased bili from RBC lysis)

no treatment, but important for future transfusion

5-7 daus


Transfusion Associated Graft Vs Host Disease

transfused T-lymphoctes recognize and react against host

4-30 days post transfusion

usually if immune system already severely impaired

can give irradiated blood products with no T-cells


Iron overload 

since adding more Hb (with Fe2+) in RBCs


Viral infection riks (HBV, HCV, HIV, EBV, CMV, etc)



What do you do if patient has fever during or post-tranfusion?


* RN will collect blood sample and send ot lab - they will run all the necessary tests automatically

* watch for signs of acute transfusion reactions: hives/itching, fever, hypotension, pain, red urine (AHTR - acute hemolytic transfusion response), shortness of breath or hypoxia (TRALI = transfusion related acute lung injury), ...

after transfusion, group and screen is outdated - have to order a new one!


What is RDW?

Red cell distribution width (RDW) is a parameter that measures variation in red blood cell size or red blood cell volume. RDW is elevated in accordance with variation in red cell size (anisocytosis), ie, when elevated RDW is reported on complete blood count, marked anisocytosis (increased variation in red cell size) is expected on peripheral blood smear review.


What is the name for RBC size variation ?


(think anise and how it can have different pods)


What is the name for variation in RBC size?


think poi = small; kilo - 10000 => small and big!

poikilocyte - abnormally shaped RBC - sickle, target, etc


What disease are bite cells (image) and blister cells (answer image) characteristic of?

Bite and blister cells suggest hemolysis, in particular oxidative injury to the RBCs.  Both are present in glucose-6-phosphate dehydrogenase deficiency (G6PD deficiency)

G6PD is an enzyme in cytoplasm of RBCs, whose job is to help reduce hemoglobin which has become chemically oxidised (lost electrons). If G6PD is impaired, Hgb becomes more oxidized until it precipiates wihtin the RBC. The spleen is able to "fix" some of these cells by "pitting out" the lump of precipitated Hgb - leaves RBC looking like it was bitten (bite cell) or as if it had a blister with an empty area underneath (blister cell). RBCs too damaged to survive, and may lyse within spleen or circulation. 


what does elevated d-dimer test mean?

D-dimer is a breakdown product of formed blood clot (thrombus). If your patient has elevated D-dimer, this means the patient has clotted somewhere in the body


What are schistocytes?

Schistocytes are fragmented RBCs, similar to schizophrenia ("split" mind). Usually get schistocytes due to membrane damage as RBCs pass narrowed vessels. Vessels can be narrowed either by clot (fibrin strands stretching and occluding lumen) or shearing b/c of abnormal turbulent flow like atherosclerosis. 


What is polychromasia on blood smear?

polychromasia = "bluish-purple" discoloration of immature RBCs due to their immaturity (remember basophilic erythrocyte -> polychromatic erythrocyte (greyish purple cytoplasm) -> normocyte ->reticulocyte (pink cytoplasm)

sign of immature RBC b/c cytoplasm not quite pink, meaning some organelle material left over ie. cell not fully developed and organelles not fully extruded


What do target cells on blood smear mean?

Target cells = RBCs with "bull's eye", caused by relative excess of membrane to cytoplasm. The excess membrane piles up in the centre of the RBC on the glass slide (since there is indent in the middle) and causes target appearance. Target cells can be seen in conditions with too much membrane - ex. liver disease, or too little cytoplasm - thalassemias (low content inside, low cytoplasm)


What do elliptocytes on peripheral blood smear mean?

eliptocytes ar eelongated "pencil shaped" RBCs, commonly seen in iron deficiency and hereditary RBC syndromes (like hereditary elliptocytosis).



Cause of hypersegmented neutrophils?

 hypersegmented neutrophil is a clinical laboratory finding. Normal 3-5 lobes, hypersegmented 6+ lobes.

Hypersegmented neutrophils have classically been thought to be pathognomonic of the class of anemias called megaloblastic anemias (anemias caused by failure of bone marrow blood-forming cells to make DNA, often caused by vitamin B12 or folate deficiencies, or DNA-replication poisons).


What is a mixing study? why use it?

ex. abnormal PT or PPT

Mixing studies are tests performed on blood plasma used to distinguish factor deficiencies from factor inhibitors, such as lupus anticoagulant, or specific factor inhibitors, such as antibodies directed against factor VIII. Mixing studies take advantage of the fact that factor levels that are 50 percent of normal should give a normal Prothrombin time (PT) or Partial thromboplastin time (PTT) result.

"Mixing studies are very helpful, and very simple. In a mixing study, normal plasma with normal amounts of factors (i.e. by definition 100% factor activity is considered normal) is added to patient plasma in a 50-50 mix. If the patient’s plasma has a factor deficiency, the normal plasma will supply enough of that factor to give you a final factor percentage of at least 50%. Since you only need 40-50% of any factor to have a normal PTT, the mix will “correct”: i.e. it will give you a normal PTT."


What does lupus anticoagulant do in mixing tests and in body?

Lupus anticoagulant is a condition characterized by the presence of antibodies to phospholipids.  These antibodies interfere with intrinsic coagulation cascade in vitro, in the laboratory test tube, and cause the PTT to be prolonged. Mr. White’s lab test results are perfectly compatible with a lupus anticoagulant. But his history is completely wrong for lupus anticoagulant: in vivo (that is to say, in the patient) lupus anticoagulant antibodies actually produce a pro-coagulant state leading to vascular thromboses, e.g. DVT, stroke, etc. In pregnant patients they can cause pregnancy loss by producing vascular occlusion in the placenta. The name “lupus anticoagulant” is very confusing because it is NOT an anticoagulant in the patient, and most patients do NOT have lupus (although many patients with lupus do have a lupus anticoagulant). 


What does positive D-dimer test indicate?

D-dimer is a molecule which is formed when the body begins to break down fibrin clot. The formation of thrombus is always faster than the destruction of thrombus, so it’s not as if the thrombus will be broken down before it has plugged whatever vascular hole required it in the first place. But to prevent the thrombus from growing too big, the body begins breaking it down as soon as it has formed. The enzymes responsible for fibrinolysis, such as plasmin, act like scissors cutting the fibrin clot into pieces. One of the pieces that plasmin cuts off the fibrin clot is called D-dimer (which, unsurprisingly, is a dimer of the D domain of fibrin). If a patient has an elevated D-dimer level, this is proof that the patient has clotted somewhere in his or her body... because you have to form clot before your plasmin enzymes can cut D-dimers off it. As you will appreciate, there are physiologic clots (e.g. a vascular wound that generates a thrombus) and pathologic clots (e.g. a DVT), and D-dimer does not tell us which is which. An elevated D-dimer may be a “good” thing or a “bad” thing, depending on whether we want the patient to clot somewhere or not. All we can say with an elevated D-dimer is that clotting has taken place, somewhere in the patient.