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SP 16 - Path Test 2 > Red Blood Cell Disorders > Flashcards

Red Blood Cell Disorders Flashcards

1
Q

What are the mechanisms of Anemia?

A

RBC loss
Decreased RBC Survival
Decreased RBC Production

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2
Q

What can cause RBC loss?

A

Hemorrhage

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3
Q

What can cause Decreased RBC Survival?

A

Hemolysis

RBCs usually survive 120 days, but destroying them earlier can cause anemia

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4
Q

What can cause Decreased RBC production?

A

Nutritional deficiencies
Aplastic anemia
Myelophthistic processes

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5
Q

How much blood loss can a young, healthy individual tolerate with minimal symptoms?

A

Up to 1000mL (1L) of rapid blood loss with minimal symptoms

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6
Q

Rapid loss of 2000mL (2L) of blood can lead to what?

A

Shock

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7
Q

Loss of RBC stimulates what?

A

Erythropoeitin, which leads to increased RBC production

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8
Q

What causes chronic hemorrhage

A

Rate of RBC loss exceeds production

It is typically secondary to GI bleeding or increased menstrual bleeding

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9
Q

What are the two types of Intravascular hemolysis

A

Immune

Non-immune

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10
Q

What causes immune intravascular hemolysis?

A

Transfusion reaction

Not seen much anymore

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11
Q

What causes non-immune intravascular hemolysis?

A

Mechanical trauma - turbulence caused by a bad heart valve

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12
Q

What is a key feature of intravascular hemolysis?

A

A decrease in free haptoglobin - haptoglobin binds to hemoglobin released form lysed RBCs and takes it to the liver to be cleared

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13
Q

What happens if plasma hemoglobin exceeds the amount of available haptoglobin

A

Free hemoglobin is excreted to the kidney

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14
Q

Free hemoglobin effect on the kidney

A

Hemoglobin is toxic to the kidney, and iron that accumulates in the proximal tubular cells
That iron can only get excreted if tubular cells are shed and lost
Can lead to hyperbilirubinemia and jaundice

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15
Q

Extravascular hemolysis

A

Destruction of RBCs in reticuloendothelial system (liver and spleen)
Hemoglobin is broken down intracellularly

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16
Q

What happens to hemoglobin that is broken down intracellularly (via Extravascular hemolysis)

A

Free hemoglobin is not released directly into the blood and urine, but hemoglobin products (bilirubin) are increased (hyperbilirubinemia) and jaundice may result

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17
Q

What are some clinical complications of extravascular hemolysis?

A

Spleen and liver may become enlarged

Chronically elevated levels can promote formation of gallstones

18
Q

Extrinsic defects causing Hemolytic Anemia are what?

A

Immune-related

19
Q

Autoimmune Hemolytic Anemia

A

Pt makes autoantibodies to his/her own RBCs
The antibody-coated cells can be lysed or removed via the reticuloendothelial system
Phagocytosis of antibody-coated RBCs can lead to partial loss of RBC membrane, creating spherocytes

20
Q

Erythroblastosis fetalis

A

Caused by blood group incompatibility between the mother and the fetus
An extrinsic hemolytic anemia

21
Q

Intrinsic defects causing Hemolytic anemia are what?

A

Non-immune related

22
Q

Hereditary Spherocytosis

A

RBC membrane defect leading to hemolytic anemia
Causes a loss of deformability of the RBC
Can be a qualitative or quantitative deficiency of spectrin (structural protein of the cytoskeleton)
Cells can’t squeeze through the splenic sinusoids, so the effected cells are sequestered and destroyed in the spleen

23
Q

Sickle-Cell Anemia cause

A

Single b.p. a.a. substitution at the position 6 of the beta-chain
Defect of the globin chain causing hemoglobin to gel upon deoxygenation

24
Q

Sickle-Cell Anemia mechanism

A

Low oxygen tension induces hemoglobin S polymerization, leading to a sickled shape
The cells are rigid and prone to sequestration
Sickled cells can also be trapped in microcirculation - leading to ischemia

25
Q

Sickle-Cell Anemia Complications

A

Moderate to severe anemia

Autosplenectomy - spleen fibroses because the over-engorement of macrophages

26
Q

If 8% of all African-Americans in the US are heterozygous, why are they not effected?

A

It’s Autosomal Codominant
They’re asymptomatic because less than half the hemoglobin is abnormal, and the concentration of HbS is insufficient to cause sickling

27
Q

Thalassemia

A

Diminished or absent synthesis of the a or B chains of hemoglobin, leading to decreased globin produciton
The ineffective RBC produciton in the bone marrow will cause the bone marrow to grow
Extravascular RBCs are lysed - leads to hemolytic anemia

28
Q

Glucose-6-Phosphate Dehydrogenase Deficiency

A

Red cells are susceptible to oxidant injury by drugs or toxins
Denaturation of oxidized hemoglobin causes hemoglobin to precipitate and attach to the RBC membrane
The RBC becomes less flexible and subject to extravascular hemolysis
RBCs look like Bite Cells (looks like Pacman or a bite was taken out)
Pts are asymptomatic without a trigger

29
Q

Schistocytes

A

RBC fragments
Indicate that there was a hemolysis due to mechanical trauma
They look like a popped balloon

30
Q

What are the settings of Iron Deficiency Anemia

A 
Inadequate Intake (seen in infants)
Increased demands (pregnancy)
Increased loss (due to bleeding)
31
Q

What would the blood make up of a Iron deficient patient look like?

A

Decrease serum iron
Decreased serum ferritin
Increased serum iron-binding capacity
Hypochromatic RBCs

32
Q

What causes Megaloblastic Anemia

A

Vitamin B12 and Folate deficiencies

33
Q

What is the pathology of Megaloblastic Anemia

A

B12 and Folate are responsible for the synthesis of thymidine - a base of DNA
Without thymidine, mitosis is delayed - and the cell grows but can’t divide (hence the name Megaloblastic)

34
Q

Vitamin B12

A

Present in Animal foods
Large body stores
In addition to hematologic abnormalities, deficiency can cause neurologic symptoms
Deficiency can be due to decreased intake (vegans), malabsorption, pernicious anemia

35
Q

Folic Acid

A

In fresh veggies
Body stores are small
Deficiency can be due to increased requirements, decreased dietary intake, malabsorption

36
Q

How can we tell Vitamin B12 deficiency of Folic Acid deficiency apart?

A

They’re indistinguishable clinically, so we have to rely on lab tests

37
Q

Polycythemia

A

An increase in Red Blood Cell mass

38
Q

Relative Polycythemia

A

Occurs with hemoconcentration from dehydration or vomitting

39
Q

What are the types of Absolute Polycythemia?

A

Primary

Secondary

40
Q

Primary Absolute Polycythemia

A

Neoplastic proliferations of RBCs that are unregulated

Treatment is removal of excess RBCs by phlebotomy

41
Q

Secondary Absolute Polycythemia

A 
Increased erythropoeiting production
Can be due to:
-cyanotic heart disease
-pulmonary disease
-living at high altitudes
-erythropoeitin-producing tumors
42
Q

How can you tell if it is primary or secondary polycythemia

A

If there is elevated erythropoeitin, it is secondary

If not, it’s primary

SP 16 - Path Test 2 (5 decks)

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