Blood and Anemia Flashcards

1
Q

What are the two main components of blood?

A

Plasma (55%)

Cells (45%)

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2
Q

What cells are in the blood?

A

RBC
WBC
Granulocytes (Neutro., Eosino., Baso., Mono., Lympho.,)

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3
Q

What are the sites of hematopoiesis during different life stages?

A

Fetus: Yolk sac, Bones, liver, spleen

Child: Most bones have red marrow

Adult: Fewer bones have red marrow (Skull, ribcage, sternum, vertebrae, and pelvis)

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4
Q

Where are red marrow sample taken from in adults?

A

The pelvis

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5
Q

What causes progenitor cells to mature into a specific mature cell?

A

Due to a unique mix/set of growth factors

8 major hematopoietic lineages are generated my multi potential stem cells

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6
Q

What causes initiation of the intrinsic pathway?

A

Vessel damage and exposure to vWBF

Factor 12 —> Factor 12a (which stimulates Factor 11—> Factor 11a), This activates Factor 9 —> Factor 9a (which stimulates Factor 10 —> Factor 10a

Factor 9a and 10a are directly inhibited by Warfarin

Xa inhibiting DOACs and Heparin inhibit Factor 10a

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7
Q

What causes the initiation of the extrinsic pathway of clotting?

A

Caused by trauma

This stimulates conversion of Factor 7 into Factor 7a, which in turn activates Factor 10 into Factor 10a.

Following this point, both intrinsic and extrinsic pathways have shared clotting factors

Activated Factor 10 (Xa), activated Factor 2 into Factor 2A, which in turn activates fibrinogen into fibrin. Fibrin is turned into a fibrin clot after interacting with Factor 13a (XIIIa)

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8
Q

What is the mechanism of Warfarin?

A

It blocks the Vitamin K dependent process of producing factors II (prothrombin), VII, IX, and X. INR monitoring is essential

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9
Q

What is the mechanism of action for DOACs?

A

These drugs are Factor 10a (Xa) inhibitors

ex. Apixaban, Edoxaban, and rivaroxaban

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10
Q

What is the mechanism of action for Heparin?

A

It binds to and activates antithrombin, inactivating Factor Xa and IIa

Often used in acute DVT and MI management

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11
Q

What is the mechanism of action of LMWH?

A

Similar to heparin, except they have less anti-factor IIa activity vs. anti-factor Xa

Ex. Enoxaparin

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12
Q

What is different about Dabigatran vs. other DOACs in terms of mechanism of action?

A

Dabigatran is a direct thrombin inhibitor

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13
Q

What is the mechanism of action for Aspirin?

A

It is an anti platelet drug and it prevents platelets from aggregating.

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14
Q

What is the utility in using a PPI in patients on DOACs + antiplatelet coaguation drugs?

A

PPIs can limit stomach acidity, effectively reducing the number and severity of potential GI bleeds

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15
Q

What is the primary function of erythrocytes?

A

They are suited for their primary function (transport of oxygen from the lungs into peripheral tissue

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16
Q

What is anemia?

A

Anemia is a reduction of hemoglobin in the blood to below-normal levels

Usual definition: less than 13g/dL in males and less than 11.5g/dL in females

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17
Q

What is the common clotting factor where the two pathways converge?

A

Activation of Factor 10 (X)

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18
Q

What is teh function of thrombin?

A

Generates fibrin monomers which polymerize to give structural integrity to the clot

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19
Q

How are clots broken down?

A

Healing endothelium releases tPA which activates plasmin. Plasmin lyses the clot

20
Q

Do different people have different affinity for oxygen in their hemoglobin?

A

Yes, namely fetuses and newborns have a type of hemoglobin that has higher affinity to oxygen than adult hemoglobin

21
Q

What are some causes of anemia?

A

Low production

Destruction

Bleeding

22
Q

What is the etiology of anemia?

A

Appearance of abnormal hemoglobin: abnormal hematopoeisis

Reduced number of RBCs: Decreased hematopoiesis

Structural abnormalities of RBCs: Abnormal hematopoiesis

Anemia may also be a consequence of increased loss or destruction of RBCs

23
Q

What can cause decreased hematopoiesis?

A

Aplastic anemia (bone marrow failure)
Myelophthistic anemia secondary to bone marrow replacement with tumour cells
Leukemia
Deficiency disorders (Fe, Viamin B12, proteins)

24
Q

What can cause abnormal hematopoiesis?

A

Genetic hemoglobinopathies (sickle cell, thalassemia)

Structural protein defects

25
Q

What can cause increased loss or destruction of RBCs?

A

Bleeding (GI bleeds especially concerning to drug therapy)

Immune hemolytic anemia

Hypersplenism (enlarged spleen + anemia

26
Q

Is RBC shape relevant to function?

A

Yes, due to internal abnormalities the shape of RBCs can be altered. This altered shape usually reduces function

27
Q

What is normocytic, normochromic anemia?

A

Known as “dilutional anemia”

Acute IV infusion increases blood volume rapidly, effectively reducing hemoglobin concentration. This is temporary and is not a sign of RBC dysfunction

28
Q

What is microcytic, hypochromic anemia?

A

These patients have RBCs that are small, pale, and are iron difficient

29
Q

What is macrocytic, normochromic anemia?

A

These RBCs are large, but normal cells. These cells are Vitamin B12 deficient (likely pernicious anemia)

30
Q

What are some examples of anemias characterized by abnormal RBC shapes?

A

Elliptocytosis, spherocytosis, and sickle cell anemia

Most of these are due to genetic diseases

31
Q

What are some notable symptoms of anemia?

A

Pale skin and weakness

Yellow Eyes (seen in hemolytic anemia, causing buildup of bilirubin)

Rapid heart rate (Low hemoglobin O2 carrying capacity, is compensated by pumping more blood)

Fatigue (this symptoms is not exclusive to anemia)

32
Q

Describe Iron Deficiency Anemia

A

It is the most common form of anemia

Fe deficiency is due to the following:

Increased loss of Fe (chronic bleeding)

Inadequate Fe intake or absorption

Increased Fe requirements (Newborns build adult hemoglobin, muscle growth, menstruation, pregnancy)

33
Q

Should everyone take an iron supplement to avoid iron deficiency?

A

No, iron is oxidizing and is toxic at high concentrations

Only those who have a need for supplementation should use iron supplements

34
Q

What is folic acid?

A

Folic acid (Vitmain B9), works with Vitamin B12 and Vitmain C in protein and DNA metabolism, and int the formation of red and white blood cells

35
Q

What are some factors that can cause folate deficiency?

A

Diseases in which folic acid is not well absorbed (Celiac or Crohn’s)

Heavy drinkers

Overcooked food (eliminates nutrients)

Hemolytic anemia or kidney dialysis

36
Q

What does leukocytosis mean?

A

Abnormally high levels of leukocytes

37
Q

What does Neutropenia mean?

A

Not enough WBCs

38
Q

What does lymphocytosis mean?

A

Abnormally high amounts of lymphocytes

39
Q

What is lymphopenia?

A

Not enough lymphocytes

40
Q

What is Neutrophillia?

A

Abnormally high amounts of neutrophils (WBC)

41
Q

When does neutrophillia occur?

A

Increased marrow activity (Bacterial infections, acute systemic inflammation, leukemia)

Release from Marrow Pool (Stress, corticosteroids, endotoxin exposure)

Demmargination into blood (Bacterial infections, hypoxemia, stress, corticosteroids)

42
Q

When does neutropenia occur?

A

Decreased Marrow Activity (Drugs, Radiation exposure, Megaloblastic anemia, marrow replacement by tumour)

Decreased Neutrophil Survival (Sepsis, Viral infection, immune destruction due to drugs)

43
Q

What can cause lymphocytosis?

A

Medium to large, atypical lymphocytes predominant (Viral infections, Active immune response, Toxoplasmosis)

Small, mature lymphocytes predominant (Chronic infections, autoimmune diseases, Metabolic diseases, lymphoma with circulating cells)

44
Q

What drugs and conditions can cause lymphopenia?

A

AIDS
Corticosteroid therapy
Toxic drugs
Cushing syndrome

45
Q

What are some characteristics of macrocytic anemia?

A

Abnormal nuclear maturation or a high fraction of young, large red cells (reticulocytes)

46
Q

What are some characteristics of normocytic anemia?

A

Decreased numbers of red cell precursors in the marrow

LOw levels of erythropoietin (caused by CKD) and can affect availability of iron in the marrow

47
Q

What are some characteristics of microcytic anemia?

A

Abnormalities in hemoglobin production, either in number of hemoglobin molecules per cell or cell type

Can be caused by things like iron deficiency or thalassemias (reduced hemoglobin production due to genetic factors)