Anemia and other Hematological alterations

kidneys

Where is erythropoietin produced?

Erythropoeisis

normal, healthy development of RBCs

kidneys

Where is erythropoietin produced?

Erythropoeisis

normal, healthy development of RBCs

1. anemia

2. low pO2

Erythropoietin is secreted in response to: [2]

1. hemoglobin

2. hematocrit

3. MCV (mean corpuscular volume)

4. MCHC (mean corpuscular hbg concentration)

5. reticulocyte count (% of immature RBCs)

CBC measures: [5]

Hemoglobin count (measured by amount of hemoglobin by weight/L of blood)

The total amount of hemoglobin contained in all of the RBC in the body.

120-140g/L

Normal hemoglobin for females

140-180 g/L

Normal hemoglobin for males

Hematocrit

Percentage of total blood volume that is taken up by red blood cells

42-52%

Normal hematocrit (Males)

37-47%

Normal hematocrit (females)

MCV (mean corpscular volume)

Measures cell size/volume

1. normocytic

2. microcytic (small)

3. Macrocytic (large

MCV can be: [3]

1. normochromic

2. hypochromic (less hbg)

3. Hyperchromic (more hbg)

MCHC can be[3]

Anemia

A reduction in the total number of circulating erythrocytes or RBCs, OR

A decrease in the quality or quantity of hbg

1. Altered production of RBCs

2. Blood loss

3. increased destruction of RBCs

4. a combination of any or all three

Anemia results from:[4]

1. Iron deficiency anemia
2. Pernicious (Vitamin B12 deficiency)
anemia
3. Folate deficiency anemia
4. Post-hemorrhagic anemia
5. Others (aplastic anemia, hemolytic
anemia, and anemia of chronic disease)

Types of anemia (discussed in this course)

Blood loss

Etiology of post0hemorrhagic anemia

Altered RBC production

etiology of iron deficiency, b12 deciciency, and folate deficiency anemia

increased anemia

etiology of aplastic anemia, hemlytic anemia

Activates HPA to

1. increase RR

2. increase HR

3. Pallor from shunted blood

4. other HPA symtoms

How does the body compensate for decreased ATP (common symptoms of all anemia) [4]

1. decreased energy overall (Fatigue)

2. Decreased energy/ffunction in the cell (impaired wound healing)

Negative effects of decreased ATP

1. loss of tissue function

2. fatigue

3. dizziness

4. weakness

5. paresthesia

Common symptoms of loss of ATP (symtpoms of all anemia) [5]

mainly in heme of hemoglobin

where is iron mainly stored

1. bone marrow

2. liver

3. spleen

4. ferritin

besides heme, where is iron also stored?

Ferritin

Iron storage protein

1. hbg synthesis

2. as a cofactor in many biochemical reactions

What is iron used for in the body (2)

serum ferritin levels

this blood test is an indicator of iron stores in the body

1. blood loss (chonic small amounts)

2. ulcerative colitis

3. insufficient daily intake

Causes of iron deficiency anemia: [3]

1. heavy period

2. ulcers

3. NSAIDs

4. bowel cancer, et.c

Reasons for chronic small amounts of blood loss

When iron stores deplete, there is insufficient iron in the marrow for hbg snthesis. We get altered RBC development and hemoglobin deficient cells replace normal circulating RBCs

How does iron deficiency anemia develop?

1. Hypochromic (less hbg per cell,low MCHC)

2. microcytic (cells reduce volume to maintain normal Hbg ratio, low MCV)

Small and fever RBCs so low hemoglobin and hematocrit.

Resut of iron deficiency anemia to RBCs

when circulating cells are hypochromic and cicrocytic (malformed cells and fever)

When do s+s of iron deficiency anemia occur?

Iron stores used up, less ferritin bound

why would IDA have low ferritin?

there are small RBCs and fever are formed

Why would IDA cause low hematocrit>

1. britle, concave fingernails

2. sore, red atrophy of papillae on tongue

3. stomatitis

4. headache

other S+S of iron deficiency anemia

Clinical manifestations and blood work (CBC and serum ferritin)

How is iron deficiency anemia diagnosed?

elemental iron 150-200mg per day

iron replacement treatment for IDA:

1. red meat

2. legumes

3. iron fortified foods

diet corrections for iron deficiency anemia [3]

Until ferritin and iron stores are normal

Continue iron replacement until:

converts foic acid to an active form

How does B12 help for DNA synthesis

folic acid is a key compound of nucleotides that make up DNA

how is folic acid required for DNA synthesis

1. decreased dietary intake

2. small bowel disease or loss

3. gastrectomy, gastritis (B12)

4. malapsorption of B12 (intrinsic factor absence: congenital, atrophy of gastric mucosa)

causes of B12 and folate deficiency anemia

There is a disruption of DNA synthesis, so cell division is disruptied. Cells don’t divide as often, so RBCs remain large but there are fewer of them.

how does vitamin B12 / folate deficiency anemia develop?

because RBCs don’t divide as much, they remain large. Cells are macrocytic.

Why would b12/folate deficiency anemia have high MCV?

1. high MCV

2. low hematocrit

3. low hemoglobin

4. low B12 and folate levels

expected lab values for b12/folate deficiency anemia:

non-specific and vague symptoms

Early symptoms of B12 deficiency anemia:

1. common S+S of anemia

2. sore, red, atrophy of pappillae on the tongue

3. paresthesia

4. headache

later S+S of B12 deficiency anemia:

1. same as B12

2. cheilosis

3. stomatitis

4. ulcerations of the tongue

5. dysphagia, flatulence, watery diarrhea

S+S of folate deficiency anemia:

Cheilosis

mouth fissues

clinical manifestations and blood work (CBC, serum b12 and serum folate)

diagnosis of B12/folate deficiency anemia:

1. dietary corrections

2. oral supplements

3. monthly injections of B12/folate

4. high dose PO b12

treatments for b12/folate deficiency anemia:

1. hypovolemia

2. hypoxia/anemia

Clinical manifestations of post-hemorrhagic anemia [2]

Post-hemorrhagic anemia

loss of large amounts of blood and loss of normally developed RBCs

1. low hemoglobin

2. low hematocrit

3. normal MCV

4. normal MCHC

Expected lab values for post-hemorrhagic anemia:

1. replace red blood cells

2. give fluids

3. give iron

treatment for post-hemorrhagic anemia: [3]

Aplastic anemia

Anemia of chronic disease when stem cells are destroyed. Altered iron recycling, decreased RBC lifespan

Hemolytic anemia

Anemia where RBCs are lysed or destroyed

sickle cell anemia

Anemia associated with abnormal hemoglobin synthesis

Leukocytosis

Increased WBC count

Active infectious process

Leukocytosis etiology

Leukocytopenia

Decreased WBCs.

Neutropenia

Decreased neutrohils

Immune deficiency state

Leukocytopenia etiology

Leukemia

Cancer of the leukocytes

Infectious mononucleosis

Epstein barr virus affecting B cell lymphocytes

Lymphoma

Abnormal growth in lymph nodes affecting B and T cells

Thrombocytosis

increased platelets

Thrombocytopenia

Decreased platelets

Hemophilia A

X-linked recessive bleeding disorder

Deficiency of clotting factor VIII

Hemophilia A etiology

Von Willebrand’s Disease

autosomal dominant or
recessive, 4 types

deficiency of von willebrand factor for clotting

Von Willebrand’s Disease etiology

1. blood transfusion reaction

2. cancer

3. infection

4. sepsis

Disseminated Intravascular Coagulation (DIC) etiology [4]

Idiopathic Thrombocytopenic Purpura

hypercoagulability: