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Anatomy and Physiology-DNP > Chpt. 29-Alterations of erythrocyte function > Flashcards

Chpt. 29-Alterations of erythrocyte function Flashcards

1
Q

Polycythemias

A

Too many cells

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2
Q

Anemias

A
  • Too few cells
  • Reduction in total # of erythrocytes in circulating blood or in the quality or quantity of hemoglobin
  • Acute or chronic blood loss, impaired erythrocyte production, increased erythrocyte destruction or combo of all the above
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3
Q

Cytic

A

-Refers to the size

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4
Q

Macrocytic

A

Large cell

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5
Q

Microcytic

A

Small cell

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6
Q

Normocytic

A

Normal cell

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7
Q

Hemoglobin content

A

ends in chromic

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8
Q

Clinical manifestations of anemia

A
  • Reduced O2 carrying capacity (hypoxia)
  • Syncope, angina, compensatory tachycardia, organ dysfunction
  • Classic signs: fatigue, weakness, dyspnea, elevated HR, and pallor
  • Asymptomatic anemia: may only be seen with exertion and develops gradually.
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9
Q

Treatment of anemias

A
  • Transfusions, dietary correction, administration of supplemental vitamins or iron
  • Correcting underlying cause
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10
Q

Other body system dysfunctions of anemia

A
  • CV: Increased preload, HR, and SV, with reduced afterload
  • Respiratory: Dyspnea
  • Nervous system: Myelin degeneration
  • GI: Pain, N/V, anorexia
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11
Q

Cardiovascular function and anemia

A
  • Blood will dilute & flow faster. Increased CO for better O2 delivery.
  • Hemorrhage: decreases # of RBC’s which causes decreased blood volume-fluid from interstitum move to intravascular space to expand plasma volume
  • Systemic arterial dilation which causes decreases VR and afterload (blood out of the heart)
  • Increased HR activated the SNS-need to intervene before HF
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12
Q

Respiratory function and anemia

A
  • increased RR to increase available O2.
  • When interventions fail you’ll see dyspnea, palpitations, dizziness, fatigue. May only see w/ exercise but as anemia progresses, you’ll see symptoms at rest
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13
Q

Nervous system and anemia

A

-Vitamin B12 deficient will see loss of fibers of spinal cord-causing parasthesias, gait disturbance, and weakness

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14
Q

Acute onset of anemia

A

-Blood is diverted from vital organs (esp kidneys) and starts renin-angiotensin response system to increase water and Na in the blood to increase volume

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15
Q

Macrocytic-Normochromic Anemia

A
  • Also termed megaloblastic anemia
  • RBC’s are large
  • DNA synthesis is defective (due to deficiencies in B12 and folate)
  • Labs: LDH and indirect bilil LDH for cell breaksdown-indirect bili for breakdown of heme.
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16
Q

Pernicious Anemia (Macrocytic-normochromic anemia)

A
  • Most common marcrocytic anemia
  • Caused by B12 defiency
  • Lacks intrinsic factor from gastric parietal cells (required for B12 absorption)
  • Congenital or autoimmune
  • Conditions that increase the risk of PA are gastrectomy, HPylori, PPI
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17
Q

Autoimmune PA

A

-Associated with chronic thyroiditis, DM1, Addisons, primary hypoparathyroidism, and Graves

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18
Q

Environmental factors that contribute to PA

A

-ETOH, tea consumption, smoking

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19
Q

PA manifestations

A
  • Weakness, fatigue
  • Parathesias of feet or fingers, difficulty walking
  • loss of appetite, abdominal pains, weight loss
  • sore tongue that’s smooth and beefy red, secondary to atrophic glossitis
  • lemon yellow (sallow) skin as result of a combo of pallor and icterus
  • neuro symptoms from nerve demylenation-not reversible
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20
Q

PA Eval

A
  • methylmalonic acid and homocysteine levels are elevated early on
  • gastric biopsy
  • Blood tests, serologic test, symptoms, schilling test, B12 absorption, B12 present in urine
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21
Q

Treatment of PA

A
  • B12 (lifelong treatment)

- While on treatment should see increase in reticulocytes and then normalization of blood counts

22
Q

Folate deficiency (Macrocytic-normochromic anemias)

A
  • Folate is essential for RNA and DNA synthesis
  • Absorption of folate occurs in upper small intestine
  • Common in alcoholics and chronic malnourishment
  • Folate is stored in the liver
  • This is more common than PA-esp in ETOH
23
Q

Folate Deficiency-Manifestations

A
  • Severe cheilosis-scales and fissures of lips and corners of mouth
  • stomatitis-mouth inflammation
  • painful ulcerations of the buccal mucosa and tongue
  • Dysphagia, watery diarrhea
  • Neuro symptoms not seen
24
Q

Treatment for Folate def

A
  • Life long is not necessary

- Oral doses of 1mg/day or ETOH may need up to 5mg/day-See improved symptoms within 1-2 wks.

25
Q

Microcytic Hypochromic anemia

A
  • Small RBC’s and reduced amounts of hgb

- Causes: iron metabolism, disorders of porphyrin and heme synthesis, disorders of globin synthesis

26
Q

Iron deficiency anemia

A
  • Most common anemia worldwide
  • highest risk-older adults, women, infants and those in poverty
  • Associated with cognitive impairment in children
  • From inadequate dietary intake, blood loss, chronic parasite infections, metabolic or functional iron deficiency, menorrhagia, meds that cause GI bleeding (NSAIDS, ASA), surgeries that decreases absorption of iron, as well as eating disorders (PICA)
27
Q

Patho of iron

A
  • Iron is in demand for erythropoiesis. Found in hgb and in storage. Releases from damaged or dead RBCs-thus iron recycling cycle
  • When iron is deficient then hgb synthesis decreases and so does the delivery to bone marrow.
  • body iron stores are depleted-still can have normal RBC’s
28
Q

Iron deficiency manifestations

A
  • fatigue, weakness, SOB
  • Pale earlobes, palms and conjuctivae
  • Brittle, thin, coarsely ridged and spoon shaped (convave) nails
  • red, sore, or painful tongue
  • Angular stomatitis: dryness and soreness in corners of mouth
29
Q

Iron deficiency eval and treatment

A
  • Eval-serum ferritin, CBC, transferrin saturations and TIBC
  • Tx: eliminate blood loss, oral iron (iron dextran), sodium ferric gluconate complex in sucrose (ferrlecit) and iron sucrose injection (venofer)
  • Therapy is usually 6-12 months after bleeding has stopped but may continue for as long as 24 months
30
Q

Sideroblastic anemia (Microcytic hypochromic anemia)

A
  • makes up a group of disorders characterized by anemia
  • caused by a defect in mitochondrial heme synthesis (causes ineffective iron uptake, and results in dysfunctional hgb synthesis)
  • ringed sideroblastic in the bone marrow are dx
31
Q

Sideroblastic anemia

A
  • Acquired vs hereditary
  • reversible is associated with alcoholism
  • Myelodysplastic syndrome
  • Manifestations: iron overload (hemochromatosis), enlarged spleen and liver
  • Eval: bone marrow examination, dimorphism
32
Q

Sideroblastic anemia

A

Treatment-Identify cause (drugs or toxins)

  • Transfusion, iron depletion therapy
  • phlebotomy
  • prolonged administration of erythropoietin
  • Hereditary: pyridoxine therapy; life-long maintenance therapy
  • congenital: stem cell transplantation
33
Q

Normocytic-normochromic anemias

A
  • RBC’s that are normal in size and hgb content but insufficient in number
  • no common cause, pathologic mechanism or morphologic characteristics exist
  • Less frequent
34
Q

Aplastic Anemia (normocytic-normochromic anemias)

A
  • pancytopenia: reduction or absence of all three types of bloods cells
  • most aplastic anemias are autoimmune disorders; some are due to chemical exposure (benzene, arsenic, chemotherapy drugs)
35
Q

AA patho

A

-hypocellular bone marrow that’s been replaced w/ fat

36
Q

AA Manifestations

A
  • hypoxemia, pallow (occasionally w/ brownish pigmentation of the skin)
  • weakness along w/ fever and dyspnea w/ rapidly developing signs of hemorrhaging if platelets are affected
  • Eval: bone marrow biopsy
37
Q

AA treatment

A
  • bone marrow transplant
  • peripheral blood stem cell transplant (may receive radiation or chemo before procedure)
  • immunosuppression (antihymocyte globulin w/ cyclosporin, corticosteroidal meds)
  • Identify high risk individuals
38
Q

Posthemorrhagic anemia (normocytic-normochromic anemia)

A
  • Acute blood loss from vascular space
  • Manifestations: depends on the severity of the blood loss
  • Treatment: IV administration of saline, dextran, albumin, or plasma, fresh whole blood
39
Q

Hemolytic anemia (normocytic-normochromic anemia)

A
  • accelerated destruction of RBC’s
  • Congenital vs. acquired
  • Intravascular versus extravascular hemolysis
  • paroxysmal nocturnal hemoglobinuria
  • Autoimmune hemolytic anemias
40
Q

Autoimmune hemolytic anemias

A
  • Warm reactive antibody type
  • Cold agglutinin type
  • Cold hemolysin type
  • Based on the optimal temperature at which the antibody binds to erytrhocytes
41
Q

Drug induced hemolytic anemia

A
  • form of immune hemolytic anemia that’s usually the result of an allergic reaction against foreign antigens
  • Called hapten model
  • Penicillin, cephalosporins, hydrocortisone
42
Q

Hemolytic anemia manifestations and eval

A
  • May be asymptomatic, jaundice, splenomegaly
  • Eval: bone marrow: abnormally increased numbers of erythrocyte stem cells (erythroid hyperplasia)
  • Labs: haptoglobin,, peripheral smear, lactate, dehydrodenase
43
Q

Hemolytic anemia treatment

A
  • acquired removal of the cause or treatment of the underlying disorder
  • First line: corticosteroids
  • Second line: splenectomy and rituximab (monoclonal antibody)
  • Paroxysmal nocturnal hemoglobinuria: eculizumab
44
Q

Anemia of chronic disease

A

-mild to moderate anemia from decreased erythropoiesis-AIDS, malaria, RA, lupus erythematosus, hepatitis, renal failure, and malignancies

45
Q

Anemia of chronic disease

A
  • Competitive iron binding from increased lactoferrin and apoferrin
  • Failure to increase erythropoiesis in response to decreased numbers of erythrocytes
  • Kidney damage, affecting erythripoetin (hormone for production of erythrocytes)
46
Q

Apoferritin

A

protein capable of storing iron in bodily cells, especially of the liver by combining with iron to form ferritin
-During inflammation neutrophils release lactoferrin to bind iron and to reduce its availability for bacteria

47
Q

Polycythemia (Myeloproliferative RBC disorders)

A

-Overproduction of RBC’s occurs

48
Q

Relative polycythemia

A
  • Overproduction of RBC’s occurs.
  • Is a result of dehydration
  • Fluid loss results in relative increases of RBC counts and hgb and hct values
  • Resolves w/ fluid intake
49
Q

Polycythemia Vera

A
  • Chronic neoplastic, nonmalignant condition
  • Overproduction of RBC’s (frequently increased levels of WBC’s-leukocytosis & platelets-thrombocytosis)
  • Splenomegaly
  • Disease can convert to AML
  • an acquired mutation in Janus Kinase 2
50
Q

Polycythemia Vera Treatment

A

-Phlebotomy, low dose asa, interferon a, hydroxyurea, radioactive phosphorus

51
Q

Virchow triad

A
  • Three factors that can cause thrombus formation
  • 1: Vessel wall injury
  • 2: Blow flow abnormalities
  • 3: altered blood constituents leading to hypercoaguability
52
Q

DIC

A
  • Cycle of bleeding and active bleeding
  • can result due to sepsis
  • Treatment: focused on removing the cause, nonstandardized, and complex.
  • Increase in fibrin, and thrombin activity (ptt, platelet count, d-dimer-elevated, fibrinogen-elevated)

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