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150 Cards in this Set

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Anemia is defined as ________________________.
a reduction in circulating RBC mass
Anemia presents with signs and symptoms of __________. Why?
Hypoxia. May show up as headache & light-headedness.

Low RBC mass --> Low Hb --> Low oxygen carrying capacity
Clinical signs of anemia?
(1) Weakness
(2) Fatigue
(3) Dyspnea
(4) Pale conjunctiva & skin
(5) Headache & light headedness
(6) Angina, especially with pre-existing CAD
Instead of measuring RBC mass (which is hard, apparently) in anemia, we use some surrogate ("erstatning") markers that include [...]
(1) Hb
(2) Hct
(3) RBC count
The technical definition of anemia is?
Hb < 13.5 g/dL in males
Hb < 12.5 g/dL in females
Why do we accept a lower Hb in females?
Because they normally lose a little bit of blood during the menstrual cycle and therefore it may be slightly lower in females. They also have lower testosterone.
Based on the size of the RBCs, anemia can be classified as?
(1) Microcytic (MCV < 80 fL)
(2) Normocytic (MCV 80-100 fL)
(3) Macrocytic (MCV > 100 fL)
The precursor to an RBC is the ______________.
What is the fundamental principle behind why we get microcytic cells in microcytic anemias?
Microcytosis occur due to an "extra" division of the cell, making it smaller. One way by which the cells can try to maintain the concentration of Hb inside the cells. It is as if the RBCs are trying to produce a nice, pretty, red, pink cell. If there is not enough Hb, there is not enough "pink" in the cell, so the cell will divide one extra time in order to try to maintain its "color", i.e. concentration. Cells start out big, divide, and become smaller.
What is hemoglobin made of?
Heme + globin peptide chains. The name gives it away.
Heme is composed of _____________.
iron plus protoporphyrin
Show a simplified scheme illuminating the causes of microcytic anemia. List the causes in the context of this scheme.
(1) Low iron --> Low heme --> Low Hb --> Microcytic anemia
(2) Iron present, but cannot be used (iron locked away in macrophages) --> Microcytic anemia
(3) Sideroblastic anemia, where protoporphyrin cannot be produced. 
(4) Thalassemia, decreased produ
(1) Low iron --> Low heme --> Low Hb --> Microcytic anemia
(2) Iron present, but cannot be used (iron locked away in macrophages) --> Microcytic anemia
(3) Sideroblastic anemia, where protoporphyrin cannot be produced.
(4) Thalassemia, decreased production of globin chain(s)
What is the principle underlying anemia of chronic disease?
Chronic inflammatory state makes it so that iron becomes unavailable for used (locked away in macrophages).
List the main microcytic anemias.
(1) Iron deficiency anemia
(2) Anemia of chronic disease
(3) Sideroblastic anemia
(4) Thalassemia
This is the MC type of anemia
Iron deficiency anemia
Lack of ________ is the MC nutritional deficiency in the world.
Plummer-Vinson syndrome is due to ___________________.
Chronic iron deficiency anemia
Iron is consumed in _____ (_____-derived) and ________ (_____-derived) forms.
heme (meat-derived); non-heme (vegetable-derived)
What is more readily absorbed, heme or non-heme form of iron?
Heme form
Absorption of iron occurs in the ________________.
Enterocytes in the duodenum transport iron into blood via ___________.
______________ transports iron and delivers it to ______ and _______ macrophages for storage.
transferrin; liver; bone marrow
Stored intracellular iron is bound to ___________.
The enterocytes poses a question after iron has been absorbed, what is it?
"Should I send iron into the blood or not."
How does the human body get rid of iron in an efficient way?
It doesn't. It can only regulate absorption. Some is lost by shedding if skin.
What laboratory measurements of iron status are there?
(1) Serum iron
(2) Serum ferritin
(3) TIBC
(4) % saturation
Generally speaking, iron is bound to ____ out of _____ molecules of transferrin. What is the normal percentage saturation?

What are we measuring when we measure TIBC?
The number of transferrin molecules in the blood.
What are we calculating when we calculate % saturation?
How many of the transferrin molecules are actually bound by iron.
If you wanna know how much iron is bound in the storage sites, what would you measure?
Serum ferritin
What two common etiologies are there of iron deficiency?
(1) Dietary lack
(2) Blood loss
Consider each individual subset of patients in the context of the two common etiologies of iron deficiency. Include other causes outside of these causes.
Infants - breast feeding
Child - poor diet
Adults - peptic ulcer disease (males), menorrhagia or pregnancy (females)
Elderly - colon polyps/carcinoma (Western world); hookworm (developing world)

Other causes include:
Malabsorption (celiac disease)
Except for poor nutrition in a growing child as a cause of iron deficiency anemia, what else might cause it?
Bleeding, such as from a bleeding Meckels diverticulum.
What is the MCC of iron deficiency anemia in a middle aged male?
Peptic ulcer disease in a male < 50 yo
Two hookworms you should be familiar with.
(1) Necator
(2) Ancylostoma
What is the MCC of iron deficiency anemia in a middle-aged female?
Menorrhagia in a female less than 50 yo.
How does gastrectomy cause iron deficiency?
Because acid normally maintains the Fe2+ state of iron, which is more readily absorbed.
When a patient becomes iron deficient, they go through a series of phases. What are they? What happens to laboratory markers in each phase?
Things that happen in sequential order:

(1) Storage of iron is depleted (bone marrow is using it up). Serum ferritin is low.
(2) Serum iron is going to be consumed. Serum iron is low. % saturation of iron is going down.
(3) Normocytic anemia. (early stage anemia) What happens first is that less of RBCs are made, because the marrow wants to make "perfect, pretty, pink RBCs".
(4) Microcytic, hypochromic anemia. Marrow is now forced to pump out smaller than normal RBCs
Whenever ferritin decreases, TIBC is going to be _____. Explain.
The opposite. If ferritin is low, TIBC is going to be high.

If ferritin is low, this is sensed and the liver is pumping out more transferrin to try to find more iron.
How does hypochromic RBCs look?
The central area of pallor has expanded.
Mention some clinical features of iron deficiency.
(1) Anemia
(2) Koilonychia
(3) Pica
What is pica?
Think of it as a "Psychological drive to get iron from any source possible". They chew on non-food items, e.g. dirt, paper.
What are the laboratory findings in iron deficiency anemia.
(1) Microcytic, hypochromic anemia with increased RDW.
(2) Decreased ferritin, TIBC high
(3) Low serum iron, decreased saturation
(4) Increased FEP
What does RDW measure?
The spectrum of size of the red blood cells.
What is FEP? What is it useful for?
Free Erythrocyte Protoporphyrin.

Used for iron deficiency anemia. Iron is low, so some % protoporphyrin has no bound iron.
What component of a particular white blood cell should represent the normal size of the RBC?
Lymphocyte nucleus
Lymphocyte nucleus
Treatment of iron deficiency anemia.
Ferrous sulfate. However, is there is an underlying cause such as bleeding or colonic carcinoma (e.g., in an older male), you have to treat that as well.
This syndrome includes iron deficiency anemia. What is it? How do they present?
Plummer-Vinson syndrome.

(1) Iron deficiency anemia
(2) Esophageal web
(3) Atrophic glossitis

Presents with anemia, dysphagia, beefy-red tongue.
What is an esophageal web?
Mucosal protrusion.
Mucosal protrusion.
Hemosiderin is a _______________degradation product.
Absorption of iron is enhanced by ______________ and inhibited by ___________.
ascorbic acid; tannates (in tea)
This blood parameter is a common finding in chronic iron deficiency anemia.
Thrombocytosis. It is a reactive phenomenon to increase blood viscosity.
In the fetus, hematopoiesis begins in the _____________ and subsequently moves to the ________ and finally the ________ by the _____ to _____ months of gestation (svangerskapsperioden).
yolk sac; liver; bone marrow; 5th; 6th
What heart disorder can a patient with severe anemia develop? How low does it have to be?
< 5g/dL. High output cardiac failure.
What is the normal serum iron level?
100 microgram/dL.
Normal TIBC is?
~300 microgram/dL
Iron deficiency in adult men and postmenopausal women in the Western world must be attributed to __________ until proven otherwise
GI blood loss
Iron deficiency is the only microcytic anemia with an increased ______.
Anemia of chronic disease is anemia associated (usually) with ________________ or __________.
chronic inflammation; cancer
This is the MC type of anemia in hospitalized patients.
Anemia of chronic disease
Explain anemia of chronic disease.
Any chronic disease that results in chronic inflammation will lead to an increase in acute phase reactants. One of those reactants are hepcidin. It sequesters iron within storage sites. Limits iron transfer from macrophages to erythroid precursors. It suppresses EPO production. The body essentially doesn't know that there might be an underlying autoimmune disease, it thinks it might be bacteria, which require iron for growth.
What laboratory findings are we gonna see in anemia of chronic disease?
(1) Increased ferritin, decreased TIBC
(2) Low serum iron (marrow takes iron from serum since it can't take iron from macrophages), decreased saturation is seen as well
(3) Increased FEP
What is the sequence of events in ACD?
Same as for iron deficiency anemia.
What is the treatment of ACD?
Treatment involves addressing underlying cause.

Exogenous EPO is useful in a subset of patients, especially those with cancer.
The anemia in ACD is rarely less than _____.
9 g/dL
Sideroblastic anemia is due to what?
Defect in protoporphyrin synthesis. Decreased protoporphyrin leads to microcytic anemia.
Between what two compartments of the cell is protoporphyrin produced?
Cytosol and mitochondria
What is the first step in hemoglobin biosynthesis?
What is the rate limiting step in the production of protoporphyrin?
Delta-aminolevulinic acid synthase (ALA synthase; ALAS)
The first step in hemoglobin biosynthesis requires which vitamin?
Vitamin B6, pyridoxal phosphate.
What is the second step in the synthesis of hemoglobin? What is important about this step?
Inhibited by lead.
Inhibited by lead.
What are two abbreviations of the enzymes catalyzing the first two steps in hemoglobin biosynthesis?
ALAS and ALAD, in that order.
ALAS and ALAD, in that order.
The joining of protoporphyrin to iron is accomplished by an enzyme called ____________.
The reaction performed by ferrochelatase occurs in the _____________ (cytosol/mitochondria).
The reaction catalyzed by ferrochelatase is inhibited by ______.
While protoporphyrin is being generated in erythroid precursors, ________ is being transferred to them.
If protoporphyrin is deficient, __________ remains trapped in mitochondria. What might happen?

This happens in sideroblastic anemia. As iron is trapped in mitochondria, the iron in the mitochondria that are adjacent to the nucleus, eventually forms a ring-shaped stain around the nucleus.

This happens in sideroblastic anemia. As iron is trapped in mitochondria, the iron in the mitochondria that are adjacent to the nucleus, eventually forms a ring-shaped stain around the nucleus.
The most common cause of sideroblastic anemia is? Mention two other causes.
Chronic alcoholism (because alcohol is a mitochondrial poison, it damages the production of protoporphyrin and inner mitochondrial membrane)

Pyridoxine deficiency, lead poisoning (can denature enzymes, ALAD and ferrochelatase)
What stain would you use to mark iron?
Prussian blue
Congenital sideroblastic anemia MC involves ___________.
ALAS (rate limiting enzyme)
A small child has undergone treatment for tuberculosis for some time. Develops learning disabilities and change in mental status. What might be going on?
Sideroblastic anemia due to isoniazid which can make you vitamin B6 deficient. Delta-ALA damages neurons, demyelinates and increases vessel permeability. Also causes learning disabilities. Growth retardation is seen in sideroblastic anemia due to lead deposits in epiphysis of growing bones.
What are the laboratory findings going to be in a sideroblastic anemia?
Lab findings indicative of iron overloaded state.

(1) Increased ferritin and serum iron (when iron accumulates, it is going to leak out of the cell, getting captured by macrophages).
(2) Low TIBC
(3) % saturation is high (because serum iron is high)
Sideroblastic anemia and _____________ share the same laboratory findings as far as iron state or status is concerned.
What is thalassemia? What is the consequence of thalassemia?
Decreased synthesis of globin chains of Hb. Decreased globin leads to decreased hemoglobin, resulting in a microcytic anemia.
Thalassemia is usually due to _____________.
an inherited mutation
One useful aspect of Thalassemia to the patient is that ____________.
carriers are protected against Plasmodium falciparum malaria
Thalassemia is divided into ________ and _______________.
alpha thalassemia and beta thalassemia
What are HbF, HbA and HbA2 hemoglobins composed of? (These are normal types of hemoglobin)
HbF: α2γ2
HbA: α2β2
HbA2: α2δ2
Normally, there are _____ alpha (chain) alleles and they are present on chromosome ____.
4; 16 (four times four)
Allele 1 Allele 2
_____ _____
---| |----| |---
¨¨¨¨ ¨¨¨¨
Allele 3 Allele 4
_____ _____
---| |----| |---
¨¨¨¨ ¨¨¨¨
α-thalassemia is usually due to ________________.
gene deletion
You do gene studies and find out that a patient has one alpha chain gene on chromosome 16 deleted, how would the patient present?
He would be asymptomatic.
If we knock out two genes in α-thalassemia, what is the clinical presentation in a patient?
Mild anemia with a slightly increased RBC count.
What two types of deletions occur in α-thalassemia with two deleted genes? What is worse and why?
Cis-deletions and trans-deletions.

Cis is worse. Associated with an increased risk of severe thalassemia in offspring.
Cis-deletion α-thalassemia is more commonly seen in which ethnic group?
Seen in Asians
Trans-deletions α-thalassemia are more common in _________.
Patients who have three genes deleted in α-thalassemia get a ___________ (moderate/severe) anemia.
A fetus has 3 α-globin chain genes deleted. How does it progress?
One α-chain is sufficient for the fetus to avoid any problems. When the fetus is born and hemoglobin A and hemoglobin A2 is produced, that is going to pose a risk for forming tetramers of beta-chains. These damage RBCs.

A tetramer of beta chains (β2β2) is called?
Hemoglobin H (HbH)
HbH could be seen with what laboratory technique ________________.
Four alpha-globin chain deletions is ______________ in utero. What happens?
lethal. HbF is affected now.

Tetramers of gamma form, called Hb Barts that damage RBCs.
What is a hemoglobin composed of tetramers of gamma called?
Hb Barts
Hb Barts can be seen on ______________.
Beta-thalassemia is due to ______________.
gene mutations
Two beta genes are present on chromosome ____.
Mutations of beta chain genes result in what?
beta null = absent chains
beta + = diminished production
What is the mildest form of beta thalassemia? How does it present?

Usually asymptomatic with elevated RBCs.
Microcytic, hypochromic RBCs and target cells on smear.
What are target cells?
Normal HbA2 is ____%.
Normal HbF is ____%.
What would be seen on labs in beta thalassemia minor?
(1) Slightly decreased HbA
(2) Increased HbA2 to 5% (normal 2.5%)
(3) Increased HbF to 2% (normal 1%)
What is the most severe type of beta-thalassemia? How does it present? How does the damage occur?
beta-thalassemia major (beta0/beta0)

Presents with severe anemia a few months after birth because HbF (alpha2gamma2) at birth is temporarily protective.

No beta chains allows alpha-tetramers to aggregate and damage RBCs.
The damage that occurs in beta thalassemia major results in something called _______________. What happens after RBCs leave the marrow?
ineffective erythropoiesis (precipitated alpha chains damage the RBCs as they are being made). If they leave, the spleen will recognize the RBCs and destroy them (extravascular hemolysis).
What happens to the marrow in patients with beta thalassemia major? How do the patients present what is the result?
Because of the severe anemia they get massive erythroid hyperplasia. Expansion of hematopoiesis into marrow of skull and facial bones (crew cut appearance on x-ray and chip-munk face). Extramedullary hematopoiesis occurs with hepatosplenomegaly.
A complication seen in patients with beta thalassemia major. Why are they susceptible to this?
Risk of aplastic crisis with parvovirus B19. It infects erythroid precursors and shuts them down. It's a problem because they are dependent on every single RBC being made. For a normal person, it wouldn't be a problem to shut it down for a week or two, we have a tremendous reserve.
What is this indicative of?
What is this indicative of?
Massive expansion of hematopoiesis into regions where hematopoiesis normally don't occur in the bone.
It's not uncommon for beta-thalassemia major patients to be dependent on _______________ (treatment). What are they are risk for due to this+
chronic transfusions (often necessary)

At risk for secondary hemochromatosis (bag of blood = bag of iron)
On blood smear of patients with beta thalassemia major, what do we see?
Microcytic, hypochromic target cells and nucleated RBCs
What are seen on electrophoresis in a patient with beta thalassemia major?
(1) Little or no HbA
(2) Increased HbA2 and HbF (no need for beta in these)
In macrocytic anemia, the patient develops an anemia with RBCs that have a size of?
> 100 MCV
Anemia with an MCV of >100 is usually due to?
MC due to folate or vitamin B12 deficiency (megaloblastic anemia). In macrocytic anemia one less division occurs, leaving cells bigger (disruption in necessary precursors for DNA synthesis)
Folic acid is ingested in a polyglutamate form. Polyglutamates are converted into monoglutamates in the jejunum by intestinal __________.
Folic acid is stored in the liver, providing a ___ to ___ month supply.
Folate absorption occurs in the __________.
Folate monoglutamate absorption is blocked by _________ and ____________, leading to folate deficiency.
alcohol; OCP
What cells in the body are affected in folate/B12 deficiency?
Not just RBCs but cells that are rapidly dividing. That's why it's called a megaloblastic anemia.

Cells affected could be in the intestine (enlargement of epithelial cells in the gut)
Folate and vitamin B12 are necessary for synthesis of _______________.
DNA precursors
What characteristic change in a WBC happens in folate/B12 deficiency?
Hypersegmented neutrophil
How many neutrophil lobes are considered abnormal?
Anything greater than 5
Anything greater than 5
If you have a macrocytic anemia due to other than B12 or folate deficiency, we call that not a _____________ but a __________.
megaloblastic anemia; macrocytic anemia
What are causes of macrocytic anemia?
(1) Alcohol
(2) Liver disease
(3) Drugs (e.g., 5-FU)
A distinction between megaloblastic anemia and macrocytic anemia?
Macrocytic anemias doesn't show hypersegmented neutrophils or megaloblastic change in other rapidly dividing cells.
Folate is obtained from ____________ and some ________.
green vegetables; fruits
Folate deficiency usually develops within ___________.
Folate deficiency is the MCC of macrocytic anemia. Causes include?
(1) Poor diet (alcoholics, elderly)
(2) Increased demand (pregnancy, cancer, hemolytic anemia)
(3) Folate antagonists (methotrexate)
When a patient becomes folate deficiency, what laboratory findings can we observe?
(1) Macrocytic RBCs and hypersegmented neutrophils
(2) Glossitis (cells not turning over)
(3) Decreased serum folate
(4) Increased serum homocysteine
(5) Normal methylmalonic acid
(1) Macrocytic RBCs and hypersegmented neutrophils
(2) Glossitis (cells not turning over)
(3) Decreased serum folate
(4) Increased serum homocysteine
(5) Normal methylmalonic acid
You differential diagnosis is folate or b12 deficiency. What laboratory finding, excluding direct measurement of b12 could clue you in to the fact that this might be a folate deficiency?
Methylmalonyl levels, which would be normal.
Dietary vitamin B12 is complexed to ___________________.
animal derived proteins
How is B12 absorbed from the intestine?
Vitamin B12 deficiency is ________ (less/more) common than folate deficiency. Why?

Because it takes years to develop due to large hepatic stores of vitamin B12.
What is the MCC of vitamin B12 deficiency? What is it due to?
Pernicious anemia. It is due to an autoimmune destruction of parietal cells (body of stomach) leads to intrinsic factor.
How does a parietal cell look like in a light microscope?
Large, round or pyramid shaped cells. Eosinophilic. Basal located nucleus.

P for Pink. Chief cells look more blue.
Large, round or pyramid shaped cells. Eosinophilic. Basal located nucleus.

P for Pink. Chief cells look more blue.
Parietal cells are also known as ____________ cells.
There is an increased incidence of pernicious anemia in individuals with blood type ___.
Antibody destruction of parietal cells causes __________ of the body and fundus. There is an increased incidence of what?
chronic atrophic gastritis.

gastric adenocarcinoma
List causes of B12 deficiency other than pernicious anemia.
(1) Pure vegan diet
(2) Chronic pancreatitis: cannot cleave off R factor
(3) Bacterial overgrowth: vitamin B12-IF complex is destroyed
(4) Fish tapeworm (Diphyllobothrium latum)
(5) Terminal ileal disease (e.g., Crohn's disease)
Pure vegans must take ____ to prevent anemia in their babies.
B12. Dietary deficiency is rare except in vegans.
What are the clinical and lab findings in vitamin B12 deficiency?
(1) Macrocytic anemia with hypersegmented neutrophils
(2) Glossitis
(3) Subacute combined degeneration of spinal cord
(1) Macrocytic anemia with hypersegmented neutrophils
(2) Glossitis
(3) Subacute combined degeneration of spinal cord
Why subacute combined degeneration of spinal cord.
Methylmalonic acid builds up in myelin in particular, in spinal cord. Cause degeneration of certain regions.
Methylmalonic acid builds up in myelin in particular, in spinal cord. Cause degeneration of certain regions.
Neurologic findings are seen with ________ (B12/folate) deficiency and not with _______ (B12/folate).
B12; folate
What lab findings do we see in B12 deficiency?
(1) Decreased serum B12
(2) Increased serum homocysteine
(3) Increased methylmalonic acid