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NUR 326 (Patho 1) > Anemia (Exam 1b) > Flashcards

Anemia (Exam 1b) Flashcards

1
Q

Anemia

A

Lack of RBC’s

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2
Q

Role of Hemoglobin

A

What provides the oxygen carrying capacity in a RBC

Within each chain, there is a heme unit with iron at the center

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3
Q

HgB reversibly binds

A

O2 and CO2 for transport

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4
Q

Functioning hemoglobin is necessary for

A

Oxygen delivery to the tissues

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5
Q

The Bus Analogy

A

RBC = Bus

HgB = The seats

Iron = What seats are made of

O2= Passengers

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6
Q

Anemia can be related to either

A

The quantity or quality of RBC’s

Regardless of the cause all disease of RBC’s mean less o2 is able to be transported to the tissues

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7
Q

Anemia from loss of Iron or Key nutrients

A

Abnormal Hemoglobin = Sickle Cell Diseae

Decrease HgB content = Hypochromic/pale = Loss of iron and Loss of key nutrients

Decreased number of circulation erythrocytes = decreased production and increased destruction and loss

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8
Q
A
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9
Q

One way we can tell what time of Anemia is going on is by looking at the red blood cells

A

Macrocytic - Normochromic

Microcytic - Hypochromic

Normocytic - Nromochromic

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10
Q

Macrocytic - Normochromic

A

-Large, abnormally shaped erythrocytes

-Hemoglobin concentrations normal

-B12 and folate deficiencies

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11
Q

Microcytic - Hypochromic

A

Small, abnormally shaped erythrocytes

Reduced Hgb concentrations

Iron deficeincy

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12
Q

Normocytic - Normochromic

A

-Normal size

-Normal hemoglobin function

-Blood less, sickle cell, aplastic anemia

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13
Q

Iron Deficiency: Cell Morphology

A

-Iron is essential to normal HgB production

-Is. microcytic, hypochromic

-Is considered a microcytic anemia causes rbcs are smaller than normal. Measured through a MCV (mean corpuscular volume) (decreased)

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14
Q

Vit B12 or Folate deficiency

A

-They are needed for DNA synthesis of RBC’s

-Megaloblastic / Macrocytic anemias

-MCV increase (MCV should be on CBC)

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15
Q

The main way determine Anemia

A

HgB levels are the best indicators

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16
Q

Most people do not seek out care or have symptoms until anemia levels…

A

are very low. Our body is good at compensating

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17
Q

Clinical manifestations of ALL anemias: Mild to moderate

A

Fatigue - Weakness - Tachycardia - Dyspnea

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18
Q

Clinical manifestations of ALL anemias: Moderate - Severe

A

Increased HR and RR - Hypotension - Pallor - Faintness - Cardiovascular symptoms

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19
Q

Pathophysiological cause of the clinical manifestation seen with anemia

A

SS and PPS

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20
Q

Iron Deficiency Anemia

A

Small and Pale RBC’s

Microcytic Hypochromic

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21
Q

Etiology: Iron Deficiency Anemia

A

-Most common anemia

-Decreased intake of iron
-Impaired absorption of iron
-Increased demand for iron
-Excessive loss (Gi bleeding or menstruation)

Remember we can’t make hemoglobin without IRON

22
Q

Who is at risk of iron deficiency anemia

A

Elderly

Teenage girls

Women childbearing age

23
Q

Iron deficiency Clinical Manifestations

A

-Smooth tongue / Glossitis / Mouth ulcers / Cheilosis

-Koilonychia “spoon nails”

-PICA - “Craving non-food items”
-Ice chips
-Hard peppermint Candies
-Dirt

24
Q

Anemia from B12 deficiency

A

Megaloblastic

Macrocytic Normochromic

25
Q

What is megaloblastic anemia?

A

A condition in which the bone marrow produces unusually large immature RBC’s (megaloblasts)

Leading cause is B12 and folic acid deficiency

Most common in elderly

26
Q

Causes of Deficiency of V B12 Anemia

A

-Atrophic Gastritis - The stomach lining has thinned (body is not producing intrinsic factor)

-Conditions that affect the small intestine, such as Crohn’s disease, celiac disease, bacterial growth, or parasite

-Autoimmune system disorder - Pernicious Anemia (very common cause)

27
Q

Clinical Manifestations Specific to B12 deficiency

A

-S and S of anemia plus

-Neuropathy

-Ataxia (gait problems)

-Glossitis

-Dementia

28
Q

Anemia related to Folate Deficiency

A

Folate is B9 vitamin that is needed for RBC formation

Folate needs increase greatly during pregnancy. Low folate more likely to have babies with low birth weight and neural defects

Not a problem with absorption, but with decreased intake (alc-diet-cirrhosis)

29
Q

What anemia is most common is malnourished population

A

Folate Anemia because it is a problem with intake not absorption

30
Q

Anemia of Chronic Kidney Disease

A

Impaired erythropoietin production. This tells bone marrow to make RBC’s so when this is broke bone marrow doesn’t make new RBC’s

Hgb/Hct correspond with the DEGREE of kidney insufficiency

31
Q

Clinical manifestations of chronic kidney disease anemia

A

General s/s anemia

32
Q

Aplastic Anemia

A

Primary condition of BONE marrow stem failure

Rare

Autoimmune most common cause -blood cells in the bone marrow attacked

33
Q

Classification of aplastic anemia

A

-Congenital

-Acquired

34
Q

Aplastic Anemia is characterized by

A

Pancytopenia

Lack of erythrocytes, leukocytes, and platelets

35
Q

Aplastic Anemia: Treatment

A

Whole blood transfusions

Bone marrow transplant

Immunosuppressants

Corticosteroids

Drugs to stimulate erythropoiesis (bold)

36
Q

Causes of Aplastic Anemia

A

Idiopathic = don’t know

High dose of exposure to toxic agents: Radiations and chemical/toxins (Bone marrow cancer) (Insecticides)

Autoimmune mechanism: complication of infection

37
Q

Increased Destruction of RBC’s

A

Abnormal hemoglobin

Acquired hemolytic anemia

Sickle Cell Anemia (decrease life span)

Thalassemia

38
Q

Acquired Hemolytic Anemia

A

Premature destruction of RBC’s caused by some external agent

39
Q

What are common causes of acquired hemolytic anemia

A

-Autoimmune attack

-Blood incompatibilities (give wrong blood type)

-Drug reactions

-Severe Burn or Microangiopahties

40
Q

Hemolytic Anemia: What happens?

A

-Formation of IMMUNE COMPLEXEs

-These complexes kill normal RBC’s

41
Q

Hemolytic Anemia: What do you look for?

A

-Low hemoglobin

-Increase Reticulocyte count (immature red blood cell) (Body starts making more and releasing them young)

-Mild Jaundice

42
Q

Anemia Abnormal Hemoglobin

A

Sickle Cell Disease

Thalassemia

43
Q

Sickle Cell Anemia

A

-Genetic disorder

-Inability to bind hemoglobin

-Hemoglobin S sitors shape, especially when O2 is low. Fragile sickle shaped cells deliver less O2 to tissues

-Clog blood vessels and break into pieces that disrupt blood flow leading to ischemia and necrosis

44
Q

Sickle Cell Anemia: Clinical manifestations

A

Swelling of hands and feet with fever

Painful episodes / crisis from ischemia and necrosis from clogged vessels

45
Q

Sickle Cell Crisis Triggers

A

-Dehydration
-Stress
-High altitudes
-Fever
-Extreme temperatures

46
Q

Sickle Cell Anemia: Treatment

A

O2 therapy
Hydration
Pain management

Hydroxyurea

Blood transfusions and CRISPR and Bone marrow transplants

Treat pain and increase oxygenations

47
Q

Thalassemia Anemia: Patho

A

Genetic disorder occurring mostly in person of mediterranean descent

Severe cases lead to death in childhood from heart failure

Moderate cases with treatment live to 30

48
Q

Thalassemia: Characterized by

A

Abnormal hemoglobin
Lack of one of two proteins that make up hemoglobin - alpha and beta globin

49
Q

Thalassemia: Treatment

A

Blood Transfusion (weekly)
Bone marrow transplant
Splenectomy

50
Q

thalassemia: Clinical maifestations

A

Delayed growth
Fatigue
Dyspnea
Jaundice
Bone deformities
Hepatomegaly
Splenomegaly

51
Q

Acute blood loss: Anemia

A

Hemorrhage

Manifestations depends on speed of blood loss

Result from gross or occult

Rate of blood loss is important

Can not compensate with acute and rapid blood loss vs slow

NUR 326 (Patho 1) (27 decks)

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