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Patho > Anemia > Flashcards

Anemia Flashcards

1
Q

Anemia’s are classified in two ways, what are they?

A

1) Morphology (cell size and hemoglobin content)

2) Etiology (impaired synthesis, destruction, or blood loss)

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2
Q

How does our body compensate for anemia?

A

1) Increased CO and ventilation
2) Redistributes blood flow
3) Makes more erythropoiesis

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3
Q

How does the boy increase cardiac output and ventilation?

A

Chemoreceptors are stimulated in the medulla. These cause increased HR to transport more oxygen and RR to improve oxygen content in blood

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4
Q

What are two ways the body redistributes blood flow when someone’s anemic?

A

1) Dilates to critical areas like brain, heart, lungs, and muscles to increase blood flow to that area.
2) Constricts blood flow to nonvital organs - kidneys, skin, GI tract.

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5
Q

Name some symptoms of anemia

A

fatigue, weakness, dyspnea, angina, headache, faintness, dim vision, pallor, increased HR, RR, murmur if blood is viscous, ventricular hypertrophy (not really a symptom). Increased bili in hemolytic anemia, petechia and purpura in aplastic anemia.

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6
Q

How does the body make more red blood cells?

A

Kidneys - EPO release - bone marrow - red cells. Hypoxia stimulates EPO from kidneys that causes RBC to be produced in bone barrow and this is accelerated (when possible) to increase O2 carrying capacity of the blood.

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7
Q

What’s an acronym to remember Erythropoesis?

A

He Probably Eats Nectarines, Radishes and Eggplants.

1) Hemocytoblast (stem cell)
2) Proerythroblast (erythropoetin stimulates between these 2 steps, between P&E)
3) Erythroblast (Early and Late)
4) Normoblast (drops the nucleus)
5) Reticulocyte (No nucleus)
6) Erythrocyte (RBC)

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8
Q

What type of cell is the first to enter the blood?

A

Reticulocytes enter the blood after a couple days of maturation.

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9
Q

Where is erythropoietin made?

A

90% is made in the kidneys, 10% in the liver.

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10
Q

What does erythropoietin do?

A

It’s a hormone that stimulates RBC production. It does this by sensing decreased oxygen content from chemoreceptors. Kidneys then pump out EPO hormone which binds onto RBC precursors (stem cells) in bone marrow and accelerates EPOesis.

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11
Q

Ribosomes are made in what type of RBC? cell?

A

Early Erythroblast. Ribosomes are important because they make hemoglobin.

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12
Q

Hemoglobin accumulates in what type of RBC?

A

Late Erythroblast

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13
Q

When does the RBC lose it’s nucleus?

A

When it becomes a reticulocyte.

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14
Q

When a RBC gets old, where does it get broken down?

A

Spleen, Liver, and bone.

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15
Q

How does a RBC get broken down?

A

Macrophages eat it up.

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16
Q

When the RBC gets broken down, a lot of hemoglobin needs to get broken down too. What do they get broken down into?

A

Heme and Globin. Globin becomes amino acids. Heme becomes iron and bilirubin.

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17
Q

How does iron make it back to the bone marrow for erythropoesis?

A

Transferrin takes it to the bone marrow.

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18
Q

How does bilirubin leave the body?

A

It’s excreted in feces or reabsorbed and excreted in urine.

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19
Q

What are three terms to describe the size of a red blood cell (Mean cell volume, AKA MCV.)

A

Normocytic, microcytic, macrocytic

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20
Q

What are 3 ways to describe hemoglobin content in blood or Mean Cell Hemoglobin Concentration (MCHC)

A

Normochromic, hypochromic,

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21
Q

What does MCHC stand for? What’s it’s significance?

A

Mean Cell Hemoglobin Concentration. How much hemoglobin is in the cell.

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22
Q

What does MCV stand for? What’s it’s significance?

A

Mean Cell Volume.

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23
Q

What does a low hematocrit mean?

A

Less circulating red blood cells.

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24
Q

Someone is described as having normochromic normocytic anemia. What does that mean?

A

They have normal sized RBC, they have a normal concentration of hemoglobin but they might have less RBC (a low Hematocrit). Example: Hemolytic anemia (sickle cell, transfusion reaction), Acute hemorrhage, Aplastic Anemia (stem cells are destroyed to can’t make a lot of RBC’s)

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25
Q

Someone is described as having hypochromic microcytic anemia. What does that mean?

A

Low MCV, Low MCHC. (Small RBC’s, and low concentration of hemoglobin). Example: Iron deficiency anemia, and thalassemia.

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26
Q

Someone is described as having normochromic macrocytic anemia. What does that mean?

A

They have large sized RBC’s, and normal concentration of hemoglobin. Examples: vitamin b12 deficiency, pernicious anemia, folate deficiency.

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27
Q

Anemia is caused by three etiologies. They are…

A

1) Impaired Synthesis
2) Increased RBC destruction
3) Blood loss

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28
Q

The etiology of leukemia is…

A

Bone marrow is affected, so impaired synthesis

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29
Q

The etiology of sickle cell anemia…

A

Destruction

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30
Q

The etiology of chemotherapy anemia…

A

Impaired Synthesis (killing rapidly dividing cells)

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31
Q

The etiology of prosthetic heart valve…

A

Destruction

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32
Q

The etiology of menorrhagia…

A

Blood loss

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33
Q

The etiology of hypersplenism…

A

Destruction. RBC’s get broken down in spleen so this makes it bigger when there’s a lot of RBC destruction

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34
Q

The etiology of iron deficiency anemia….

A

Synthesis

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35
Q

The etiology of blood transfusion reaction…

A

Destruction

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36
Q

The etiology of renal failure anemia

A

Synthesis - Kidneys can’t detect the decreased O2 content and doesn’t secrete erythropoetin.

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37
Q

Someone has a low hct, low hgb, low MCV, and low MCHC. What type of anemia do they have?

A

Hypochromic microcytic.

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38
Q

What’s thalassemia?

A

A genetic condition that causes defective synthesis of alpha and beta globin chains. Too few globins chains are produced which causes less hemoglobin to be made. Cells become hypochromic (not enough hemoglobin) and microcytic (small)

39
Q

What are two ways we classify thalassemia?

A

Alpha and Beta Thalassemia

40
Q

Explain the pathogenesis of Thalassemia

A

Not enough alpha or beta globin chains are made. The converse globin chain continues to be produced. The accumulation of the other globin (For example, beta in alpha thalassemia) and this damages the RBC. The RBC’s that are destroyed in the bone marrow before the RBC’s are released or in the spleen (hemolytic anemia). This RBC destruction causes a decreased RBC count.

41
Q

Who is prone to getting Beta Thalassemia?

A

People with mediterranean heritage who have thallasemia in their genetics.

42
Q

What does it mean when someone has Beta thalassemia “minor”

A

They have one defective beta chain gene.

43
Q

What does it mean when someone has Beta Thalassemia “major”

A

They have two defective beta chain genes.

44
Q

Why do people with beta thalassemia minor have less symptoms of anemia?

A

It’s a heterozygous autosommal recessive gene. The other gene is enough to carry some oxygen so they don’t have as many symptoms.

45
Q

When do symptoms of beta thalassemia major start?

A

6 months after birth. They don’t start earlier than that because the infant has stores of RBC’s in their liver and spleen. They stop producing RBC’s here after, and run out of these stores.

46
Q

What are S+S of beta thalassemia major?

A

Jaundice, fatigue, delayed growth, splenomagaly, hepatomegaly, babies have trouble feeding (fatigue)

47
Q

What treatments does someone with thalassemia need?

A

1) Chelation to get rid of excess iron from multiple blood transfusions.
2) Lots and lots of blood transfusions - every 3-4 weeks.

48
Q

Sickle Cell disease and Thalassemia are both hemoglobinopathies. How are they different?

A

Thalassemia is a problem with the quality of hemoglobin.

49
Q

How does someone get sickle cell disease?

A

You need to inherit 2 defective genes. One from your mother, one from your father.

50
Q

How do genetic mutations causing sickle cell anemia affect the RBC?

A

The homozygote gene HbS causes the hemoglobin to be made into a chain shape which causes the hemoglobin to bend into a sickle shape in low oxygen states like high altitudes, respiratory infections, and exercise.

51
Q

What’s the problem with having sickled cells?

A

1) They rupture or are destroyed in the spleen (hemolytic anemia)
2) They clump together and block blood flow causing pain, organ damage and strokes

52
Q

What’s iron deficiency anemia? (IDA)

A

Not enough iron content in the body causing impaired Hb synthesis. Normal amount of RBC’s, but hypochromic and microcytic. It’s the most common form of anemia.

53
Q

Where is iron absorbed?

A

Duodenum and jejunum

54
Q

How do we lose iron?

A

Skin and GI epithelium cells slough off, and menstruation.

55
Q

If we eat a bunch of iron one day a week, is that enough?

A

No, we need a daily supply

56
Q

Where is iron stored?

A

Iron gets stored in GI epithelial cells.

57
Q

How does your body compensate for low iron stores?

A

It speeds up the absorption of iron.

58
Q

What’s the difference between Fe2+ and Fe3+

A

We need Fe3+ to be converted in order for it to enter and leave the cell.

59
Q

How do we get heme iron?

A

Think blood iron. Red meat, fish, poultry. We eat it, and we break it down and that releases iron. Only about 10-20% is actually absorbed. You get hemoglobin and myoglobin from these sources.

60
Q

How do we get non-heme iron? Fe2+ and Fe3+

A

Vegetables - spinach and broccoli, beans, tofu, nuts, seeds (pumpkin seeds), and fortified cereals. Also is absorbed in intestinal cells. 1-10% gets absorbed

61
Q

Why does non heme iron not absorb as well as heme iron?

A

Their positively charged cations cause all these complexes to form with anions and that impairs absorption.

62
Q

How do we enhance non heme absorption?

A

Vitamin C and stomach acids.

63
Q

How does non heme iron become inhibited from absorbing?

A

Caffeine, calcium (it competes for absorption) and fibre (bran).

64
Q

Normally, transferrin is only 20-45% saturated with iron.

A

We keep excessive transferrin to protect us in case we need it because excess iron causes damage to cells.

65
Q

What’s hemochromatosis?

A

An autosomal recessive disorder that causes increased absorption of iron and systemic iron overload.

66
Q

Where is iron stored in someone who has hemochromatosis?

A

Liver, pancreas, heart, joints, brain, and pituitary gland.

67
Q

What are the symptoms of hemochromatosis?

A

Vertigo, hair loss, memory loss, arrhythmias, cardiomyopathy, bronze skin, arthritis, hepatomegaly, elevated liver enzymes, cirrhosis, diabetes mellitus, testicular atrophy, decreased FSH/LH secretion

68
Q

What two cells does hepcidin act on to decrease iron release into the blood?

A

Macrophages and intestinal cells.

69
Q

What protein is mutated in hemochromatosis? What is it’s impact?

A

Hemojuvelin. There’s 8 different proteins that regulate hepcidin release and in hemochromatosis hemojuvelin is malfunctioning.

70
Q

What are four causes of Iron Deficiency Anemia?

A

1) Increased loss of iron (menstruation)
2) Inadequate intake (vegetarians)
3) Impaired absorption (celiac disease)
4) Increased iron requirements (pregnancy)

71
Q

Iron gets depleted from these parts of the body and in what order…

A

Iron stores get used up, then iron in plasma gets used up, and then iron in RBC’s

72
Q

What are some S+S of iron deficiency anemia?

A

Sore tongue (glossitis), brittle nails and hair, and painful cracking lips, pica.

73
Q

What would someone’s MCV and MCHC be with IDA?

A

Decreased MCV and MCHC (small amount of hemoglobin and small cells; microcytic hypochromic)

74
Q

What would someone’s ferritin level be if they had IDA?

A

Low

75
Q

What would someone’s Hct be if they had IDA?

A

Low

76
Q

What is megaloblastic anemia caused by?

A

deficiency in vitamine b12 or folate

77
Q

Why do we need vitamin b12 and folate?

A

They’re needed for DNA synthesis.

78
Q

Why does decreased vitamin b12 and folate levels make someone anemic?

A

Without these vitamins we can’t properly make DNA which erythroblasts need to replicate their DNA and make more RBC’s.

79
Q

Does Vitamin B12 and folate levels affect RNA and protein synthesis?

A

No. Vitamin B12 and folate deficiencies do not affect RNA or protein synthesis

80
Q

What do cells with megaloblastic anemia look like and why do they look like this?

A

The RNA and protein synthesis doesn’t get affected, so the cells grow really big but they don’t divide. This affects any rapidly dividing cell (GI cells, epithelial cells, platelets, WBC’s.).

81
Q

Where are megaloblasts found?

A

They’re found in the bone marrow, they can be destroyed in the bone marrow before their release, or they can lose their nucleus and get released into circulation.

82
Q

If someone had megaloblastic anemia, what would their MCV and MCHC look like?

A

The MCV (cell size) would be increased. The MCHC (mean cell hemoglobin [ ] ) would be normal. They would therefore be categorized as macrocytic normochromic.

83
Q

Why does megalobastic cells cause anemia?

A

The cell wall is very fragile, and the shape of the cel is abnormal. These cells tend to have short life spans and because they die so quickly, you have less circulating RBC’s.

84
Q

What would the hematocrit be of someone with megaloblastic anemia?

A

Low because the cells would be destroyed.

85
Q

What would the platelet count be for someone with megaloblastic anemia?

A

Low, because vitamin b12 and folate affects all fast growing cells and makes them weaker so platelets would also get destroyed. That’s why you get patechia, and other signs of bleeding.

86
Q

What would the WBC count be like for someone with megaloblastic anemia?

A

Low WBC, making someone prone to infections

87
Q

Why would someone with magloblastic anemia be jaundiced?

A

RBC’s bursting all the time, and you’d get breakdown of macrocytes in the spleen

88
Q

How do we metabolize vitamin b12?

A

1) You eat a food containing vitamin b12 - milk, eggs, meat, etc.
2) The animal protein gets bound to an intrinsic factor (a protein secreted by gastric parietal cells)
3) This vitamin b12/intrinsic factor complex prevents the vit b12 from being digested by intestinal enzymes.
4) This complex travels to the ilium, and it binds to epithelial cells.
5) Vitamin b12 and intrinsic factors split when it hits an intrinsic factor receptor
6) Vitamin b12 is then brought into the storage and tissue sites through transobalamin II (a carrier protein)

89
Q

What enzyme helps vitamin b12 get metabolized?

A

Pepsin

90
Q

What sort of cell releases intrinsic factor?

A

Parietal cells in the gastric glands. Intrinsic factor binds to vitamin b12 so that it doesn’t get digested by the stomach acids

91
Q

What are some causes of vitamin b12 deficiency due to dietary deficiency?

A

Vegan or vegetarian diet

92
Q

What’s pernicious anemia?

A

It’s an autoimmune disease that causes gastric atrophy and loss of parietal cells. The body makes antibodies that inhibit intrinsic factor from binding to vitamin b12. So vitamin b12 isn’t protected from gastric acids and can’t be metabolized.

93
Q

What would inhibit vitamin b12 from being absorbed?

A

Gastrectomy, ilial resection, inflammation or neoplasms in the terminal ilium, malabsorption syndromes - celiac disease.

94
Q

What’s signs and symptoms are different in vitamin b12 deficiency compared with folate deficiency?

A

Vitamin B12 can cause neuro changes whereas folate deficiency does not cause neuro changes.

Patho (12 decks)

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