Class 3-cellular regulation- anemia Flashcards
0
Q
Definition of anemia
A
-anemia is an abnormally low number of circulating red blood cells (RBC’s), low hemoglobin concentration, or both
- common finding in clients, especially women, can be asymptomatic
- routine testing of RBC’s count is usually first indication of anemia unless its severe enough for symptoms
- decrease can be from inadequate RBC production, or increased RBC destruction
- insufficient or defective hemoglobin w/in RBCs contributes to anemia as well, insufficient quantities of iron limit hemoglobin production, in turn affecting the production of RBCs
1
Q
Etiology of anemia
A
-
2
Q
Pathophysiology of anemia
A
-RBC’s are needed to carry oxygen throughout the body, every type of anemia, no matter what the cause is, reduce oxygen carrying capacity of the blood
-anemia results in less oxygen reaching the cells and tissues (tissue hypoxia)
-when anemia develops gradually & RBC production is moderate, the body’s compensatory mechanisms may prevent or mask the appearance of symptoms except during times when oxygen needs of body increase b/c of exercise/infection
-symptoms develop after RBC’s & hemoglobin levels are further reduced
-pallor of skin, mucous membranes, conjunctiva, and nail beds develop as a result of blood redistribution to vital organs & lack of hemoglobin
-heart rate & RR increase in attempt to increase CO & tissue perfusion
-tissue hypoxia=angina, fatigue, dyspnea on execration, & night cramps
-
3
Q
Etiology of anemia
A
- iron deficiency is most common form of anemia
- excessive iron loss as a result of chronic bleeding is usual cause of iron deficiency in anemia in adults, menstrual for women
- can result from inadequate dietary intake ( <1mg/day), malabsorption syndromes, or increased iron requirements (pregnancy & lactation)
- common in older adults & women of child-bearing ages
- can result from chronic, occult (hidden) blood loss caused by slow bleeding peptic ulcers, GI inflammation, hemorrhoids, & cancer
- iron deficiency anemia is most common nutritional deficency in children
- affects 3% of children under 2
- 6-18% of toddlers
- 9-11% of adolescent girls
- les than 1% of adolescent boys
- lead poisoning is associated w/anemia and can worsen those w/anemia b/c lead absorption increase in the anemic state
4
Q
Causes of Iron deficiency anemia (box 3-2, p. 97)
A
- Dietary deficiencies
- vegetarian diet
- inadequate protein intake
- Decreased absorption
- partial or total gastrectomy
- chronic diarrhea
- malabsorption syndromes
- Increased metabolic requirements
- pregnancy
- lactation
- Blood loss
- GI bleed (ulcer disease, chronic use of aspirin)
- Menstrual losses
- Chronic hemoglobinuria
5
Q
Risk factors of anemia
A
- people who don’t eat a well-balanced diet rich in fresh fruits & vegetables, have an increased risk
- during child-bearing years, women lose blood during menstration, inadequate intake of iron can result in reduced RBC production, increasing risk of anemia
6
Q
Clinical Manifestations of Anemia: Blood Loss Anemia
A
- when anemia results from acute/chronic bleeding, RBCs & other blood components (iron) are lost from the body
- w/acute blood loss, circulating volume decreases, cardiac output falls
- compensatory mechanisms are activated to maintain CO:
- HR increases
- peripheral blood vessels constrict
- vessels in the liver, a blood storage organ constrict as well, causing increase in circulating volume
- fluid shifts from interstitial spaces into vascular component to maintain blood volume, diluting the cellular components of the blood & reducing its viscosity
- acute blood loss: circulating RBC’s are of normal size & shape (normocytic)
- early in hemorrhage, everything may be normal,
- but when the fluid shifts from interstitial spaces into vascular space to maintain circulating volume, the Hct & Hgb, & RBC fall
- if enough iron is avail., circulating RBCs & Hgb return to normal w/in 3-4 weeks of each other
-Chronic blood loss: depletes iron stores as RBC production attempts to maintain RBC supply, resulting in small (microcytic) and pale (hypochromic) RBCs
7
Q
Clinical Manifestations of Anemia: Nutritional Anemias: Iron Deficiency Anemia
A
- develops when supply of iron is inadequate for optimal RBC formation
- body cant synthesize hemoglobin w/o iron
- in normal conditions, the body recycles & stores iron, reusing much of the iron contained in RBCs that are removed from circulation b/c of age or damage
- however, small amounts of iron are continually lost in the feces; adequate iron intake is necessary for normal Hgb synthesis & RBC production
- it results in fewer numbers of RBCs, microcytic & hypochromic RB, and malformed RBCs(poikilocytosis)
- chronic iron deficiency= brittle, spoon-shaped nails; cheilosis (cracks at the corners of mouth); smooth, sore tongue; pica
8
Q
Clinical Manifestations of Anemia: Nutritional Deficiencies: Vitamin B 12
A
- vitamin B12 is needed for DNA synthesis, found in foods from animals
- occurs when inadequate B12 is consumed or when it is poorly absorbed from the GI tract
- deficiency impairs cell division and maturation of the cell nucleus,especially in rapidly proliferating RBCs
- -macrocytic (large) , misshapen (oval instead of concave) RBCs w/thin membranes are produced
- these immature RBCs enter circulation; they are fragile, incapable of carrying adequate amounts of oxygen; shortened life span
- Pernicious anemia: failure to absorb vit. b12
- develops from lack of intrinsic factor (secreted by gastric mucosa)
- w/o intrinsic factor, it can’t be absorbed by body
- manifestations develop gradually
- pallor, slight jaundice, weakness,
- numbness or tingling
- proprioception of ones space
- CNS manifestations <6 months are reversible
- beefy red tongue
- diarrhea
9
Q
Manifestations: Nutritional Anemias: Folic Acid Anemia
A
- also required for DNA synthesis & normal maturation of RBCs
- characterized by fragile, megaloblastic (large & immature cells)
- it is found in green leafy veggies, fruits, cereal, meats & absorbed from the intestines
- result of inadequate intake, more common in chronically undernourished
- older adults w/alcoholism & drug intake
- higher risk for alcoholism b/c it suppresses folate metabolism, which forms folic acid
- pregnant women (increased intake of folic acid)
- teens & infants, from periods of rapid growth (temporary)
- impaired folic acid & metabolism can cause folic acid deficient anemia
- malabsorption disorders; ex, celiac sprue (GI disorder, inability to metabolize amino acids found in gluten); medications, chemotheraputic agents
- manifestations: develop gradually, as stores are depleted
- diarrhea, cheilosis, glossitis
- s/s: pallor, progressive weakness & fatigue SOB, heart palpations
- this & vit. b12 sometimes coexist
- maternal folic acid deficiency strongly associated w/neuronal tube defects, develops early in process of fetal development
10
Q
Manifestations of Anemia: Hemolytic Aanemias
A
- characterized by premature destruction (lysis) of RBCs
- when RBCs break down, iron and by-products remain in the plasma
- can occur w/in circulatory system or result of phagocytosis by WBCs
- in response to hemolysis, the hematopoietic activity of bone marrow increases, leading to increased reticulocytes (immature RBCs)
- characterized by normocytic & normochromic RBCs
- can be intrinsic
- cell membrane defects, defects in Hgb structure and function, inherited enzyme deficiences
-extrinsic (outside RBCs)
-drugs, bacterial & other toxins, trauma
-
11
Q
Hemolytic Anemia: thalassemia
A
- inherited disorders of hemoglobin synthesis in which either beta or alpha chains of hemoglobin molecule are missing or defective (intrinsic)
- leads to deficient hemoglobin production and fragile hypochromic, microcytic RBCs (bulls eye appearance)
- affects certain populations
- Mediterranean descent (italy and greece) beta-defect
- Asian descent-alpha-defect
- Africans/african american- both beta-alpha decfects
- children w/it rarely reach adulthood,
- often asymptomatic in minor
- maifestations:
- mild to moderate anemia, mild splenomegaly, bronze skin coloring, bone marrow hyperplasia
- major form of disease: severe anemia, HF, liver & spleen enlargement, fractures of long bones, ribs, and vertebrae result from expansion of bone marrow and thinning from hematopoiesis
- jaundice, hepatomegaly, and splenomegaly result from hemolysis
- accumulation of iron in heart, liver, pancreas can cause failure of organs
12
Q
Hemolytic Anemias: Acquired Hemolytic Anemia
A
- caused by hemolysis resulting from factors outside of RBCs (extrinsic)
- causes
- mechanical trauma to RBC produced by heart valves, severe burns, hemodialysis, or radiation
- autoimmune disorders
- bacterial or protozoal infection
- immune-system mediated response (ex: transfusion reaction)
- drugs, toxins, chemical agents, venoms
- manifestations depend on extent of hemolysis:
- mild/moderate as erythropoiesis increases to replace destroyed RBCs
- spleen enlarges as it removes damaged/destroyed RBCs
- if breakdown continues exceeds livers ability to conjugate and excrete bilirubin, jaundice develops
- severe condition: bone marrow expands, bones deformed or pathological fractures
- severity of manifestations tachy and pallor depends on degree of anemia & tissue oxygenation
13
Q
Hemolytic Anemia: Glucose-6-Phosphate Dehydrogenase Anemia
A
- intrinsic
- caused by hereditary defect in RBC metabolism
- common in African & Mediterranean descent
- defective gene is on the X chromosome, affecting more women than men
- it is an enzyme that catalyzes glycolysis, the process which an RBC derives cellular energy
- a defect in the action can cause direct oxidation of hemoglobin, damaging RBCs
- the G6PD impairs necessary compensatory increase in glucose metabolism and causes cellular damage
- damaged RBCs are destroyed over period of 7-12 days
- when client is exposed to a stressor trigger (drugs such as aspirin, sulfonamides or vit, K), symptoms of anemia develop w/in days
- pallor, jaundice, hemoglobinura (hemoglobin in urine), elevated reticulocyte count
- when new RBCs develop, counts return to normal
14
Q
Aplastic Anemia
A
- bone marrow fails to produce all 3 types of blood cells, leading to pancytopenia (deficiency in RBCs &WBCs) it is rare
- normal bone marrow replaced by fat
- underlying cause is unknown
- some cases follow stem cell damage caused by exposure to radiation or certain chemical substances (arsenic, nitrogen mustartd, certain antibiotics, & chemotheraputic drugs)
- may occur w/viral infections (mono, hep. C, HIV)
- number of stem cells in bone marrow is reduced
- anemia develops when bone marrow fails to replace RBCs that have reached end of life span
- remaining RBCs can be normocytic & normochromic, may be large, or w/an increased mean corpuscular volume
- manifestations:
- onset is insidious, but can be sudden
- fatigue, pallor, progressive weakness, exertional dyspnea, HA, tachy, and HF
- platelet deficency leads to bleeding problems
- deficiency of WBCs increases risk of infection(sore throat/fever)
