anemia Flashcards

(116 cards)

1
Q
A

-2 ways to get Iron. Iron ingested or breakdown from older erythrocytes

-Iron travels to the stomach and HCL + Vit C changes it from Ferric 3+ to ferrous 2+

-Absorption of FE 2+ occurs in the duodenum and upper Jejunum by the enterocytes

-Fe 2 goes into enterocytes

-Next it goes through Ferroportin (door) changes back to F 3+ goes into blood stream bound to Transferrin

-Iron gets transported on Transferrin
1 Goes to Bone marrow to Makes RBC
2 Gets stored the the live as ferritin

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2
Q
A

-30-40mg of iron to make RBCs
-most is absorbed in GI -> transferrin -> stored in liver
-macrophages store iron

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3
Q
A

How to turn off Iron absorption
Hepcidin is a regulatorinhibator

1.Shut door on Ferroportin : close
2. Stops macrophages do not release Iron

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4
Q

iron tests

A

-Serum iron blood test -> how much iron inside body
-Ferritin test -> how much iron is stored inside cells
-TIBC test (total iron-binding capacity) -> all proteins needed to link iron including transferrin (means the total transferring available).
-UIBC test (unsaturated iron-binding capacity) -> how much iron for saturation of transferrin.
-Transferrin saturation- a percentage to tell how much transferrin is full with iron.

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5
Q

iron facts

A

-Morning iron is higher than the rest of the day’s iron levels by 30%.
-67% of the body’s iron is inside hemoglobin in red blood cells, other iron is bound to transferrin in blood or ferritin in bone marrow, or stored in more body tissues.
-3.5% of the total iron in the body is inside Muscles as myoglobin.
-27% of all iron inside cells are stored in Ferritin & hemosiderin

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6
Q

iron deficiency anemia labs

A
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7
Q
A

transferrin - protein that carries the iron
-TIBC- high

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8
Q

iron deficiency anemia

A

-MC type of anemia.
-body doesn’t have enough iron
-body needs iron to make hemoglobin
-body can’t get amount of oxygen it needs.
-many people don’t know they have iron-deficiency anemia -> possible to experience sx for years w/o knowing cause.

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9
Q

causes of iron deficiency anemia

A

-kids who drink a lot of milk and not hungry otherwise

-women and in people who have a diet that is low in iron
-highest risk:
-Women who menstruate, particularly if menstrual periods are heavy
-Women who are !pregnant or breastfeeding or those who have recently given birth!
-major surgery or physical trauma
-GI diseases such as celiac disease (sprue), inflammatory bowel diseases such as UC, or Crohn disease
-People with PUD
-bariatric procedures, especially gastric bypass operations
-Vegetarians, vegans, and other people whose diets do not include iron-rich foods (Iron from vegetables, even those that are iron-rich, is not absorbed as well as iron from meat, poultry, and fish.)
-Children who drink more than 16-24 ounces a day of cow’s milk (Cow’s milk not only contains little iron, but it can also decrease absorption of iron and irritate the intestinal lining causing chronic blood loss.)

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10
Q

less common causes of iron deficiency

A

-Blood loss from the gastrointestinal tract due to gastritis (inflammation of the stomach), esophagitis (inflammation of the esophagus), ulcers in the stomach or bowel, hemorrhoids, angiodysplasia (leaky blood vessels similar to varicose veins in the gastrointestinal tract), infections such as diverticulitis, or tumors in the esophagus, stomach, small bowel, or colon
-Blood loss from chronic nosebleeds
-Blood loss from the kidneys or bladder
-Frequent blood donations
-Intravascular hemolysis -> RBC break down in the bloodstream, releasing iron that is then lost in the urine. This sometimes occurs in people who engage in vigorous exercise!, particularly jogging. This can cause trauma to small blood vessels in the feet, so called “march hematuria.” Intravascular hemolysis can also be seen in other conditions including damaged heart valves or rare disorders such as thrombotic thrombocytopenia purpura (TTP) or diffuse intravascular hemolysis (DIC).

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11
Q

signs and symptoms of iron deficiency anemia

A

-fatigue
-pallor
-poor concentration
-presyncope/syncope
-weakness
-dyspnea
-cant get up the stairs
-smooth tongue
-craving ice

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12
Q
A

koilonychia

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13
Q

dx and tx of iron deficiency anemia

A

-iron sat is low

-normo -> micro -> micro hypochromic

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14
Q

stages in development of IDA

A
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15
Q

complications of IDA

A

-Mild usually doesn’t cause complications
-if left untreated -> can become severe and lead to health problems, including the following:

-Heart problems
-rapid or irregular heartbeat
-heart must pump more blood to compensate for the lack of oxygen carried in your blood when you’re anemic -> enlarged heart or heart failure

-Problems during pregnancy
-severe iron deficiency anemia has been linked to premature births and low birth weight babies
-it is preventable in pregnant women who receive iron supplements as part of their prenatal care

-Growth problems
-infants and children -> severe iron deficiency can lead to anemia as well as delayed growth and development
-associated with an increased susceptibility to infection

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16
Q

iron replacement therapy

A

-they should go to GI so you arnt missing a colon cancer

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17
Q

ferrous sulfate

A

-tx for iron deficiency anemia
-dose- 325mg tid, which provides 180mg of iron daily of which 10mg is usually absorbed
-pts who cant tolerate iron on empty stomach should take it with food
-PO
-give with stool softener
-iron causes constipation

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18
Q

lead poisoning

A

-usually made via screening program
-if suspected must obtain detailed history:
-onset of sx
-hx of PICA
-assess of potential sources
-family hx of lead poisoning

-PE:
-pallor and hyperactivity
-burton lines on gums
-decreased stature
-wrist drop, and cognitive dysfunction

-signs of elevated ICP:
-impaired consciousness
-bradycardia
-HTN
-respiratory depression
-papilledema
-coma

-basophilic stippling on the RBC on cytology -> diff from IDA
-old homes in the city, old pipes, water
-children absorb it more

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19
Q

mild cases of lead poisoning

A

-hypochromic microcytic anemia -> dont confuse it with iron deficiency

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20
Q

hereditary hemochromatosis

A

-Serum ferritin: Measures the amount of iron stored in the liver

-Serum iron: Measures the amount of iron in the blood after fasting

-Transferrin saturation: Measures the amount of iron bound to transferrin, a protein that carries iron in the blood

-LFTs: Check for liver inflammation and normal liver function

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21
Q

hemochromatosis triad

A

-set of symptoms that historically identified the condition, but it’s less common today due to earlier diagnosis:
-Hepatomegaly: An enlarged liver, which occurs in 95% of patients with symptoms

-Skin hyperpigmentation: Also known as bronze skin, this is the condition’s namesake

-Diabetes: A type of diabetes mellitus

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22
Q

genes for hemachromatosis

A

-C282Y
-every 3-4 months get blood removed

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23
Q

dx of hemochromatosis

A

-ferritin goes up with any inflammation
-look at the saturation

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24
Q

approach to macrocytic anemia

A
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25
macrocytic with neutrophils >5 lobes
megaloblastic
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macrocytic anemia: megaloblastic vs non-megaloblastic
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causes of macrocytic megaloblastic anemia
-neurological symptoms for b12
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vitamin b12 deficiency
-can be taken by mouth, shot, or inhaling through nose -neurological symptoms! -mimics elderly sx -> check them -absorption of b12 in the terminal ileum -bypass surgery is deficient -you need intrinsic factor -B12 transformed in the liver and stored
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neurological changes in b12 deficiency!
30
folic acid deficiency anemia
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low folate in pregnancy
-causes neural tube defects -fetus needs folate -can be low in the pregnancy -> you NEED IT
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macrocytic megaloblastic anemia causes
-dont need to know all the drugs -methotrexate for RA
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macrocytic non-megaloblastic anemia causes
high MVC in heavy alcohol use
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congenital hemolytic anemia
-Genetic conditions of RBC Membrane -Hereditary spherocytosis -Hereditary elliptocytosis -Genetic conditions of RBC metabolism (enzyme defects). This group is sometimes called congenital nonspherocytic (hemolytic) anemia, which is a term for a congenital hemolytic anemia without spherocytosis, and usually excluding hemoglobin abnormalities as well, but rather encompassing defects of glycolysis in the erythrocyte.[2] -Glucose-6-phosphate dehydrogenase deficiency (G6PD or favism) -Pyruvate kinase deficiency -Aldolase A deficiency -Hemoglobinopathies[3]/genetic conditions of hemoglobin -Sickle cell anemia -Congenital dyserythropoietic anemia -Thalassemia
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hemolytic anemia labs
-reticulocytes HIGH -MCV HIGH -bilirubin very HIGH -haptoglobin LOW -plasma hemoglobin HIGH -urinary hemoglobin N or HIGH -LDH HIGH
36
symptoms of hereditary spherocytosis
-inherited blood disorder of RBC -RBC are round rather than donut shape -destroyed in the spleen at increased rate bc of abnormal shape -anemia, jaundice, enlarged spleen -symptoms of anemia- pale skin (pallor) compared to your child’s normal colour, low energy (fatigue), irritability -lifelong condition -can be managed and treated -some benefit from having a portion or all of spleen removed -discuss options with doctor
37
red blood cell membrane structure: spherocytosis
-problem with ankyrin and spectrin
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hereditary spherocytosis labs
MCHC
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dx of spherocytosis
-osmotic fragility! (PANCE)
40
osmotic fragility
test of choice for spherocytosis -Osmotic fragility is a blood test to detect whether red blood cells are more likely to break down.
41
spherocytosis with viral illnesses: aplastic crisis
-does not usually affect your child’s blood counts -BUT in some viral illnesses can worsen anemia and increase jaundice -This condition is called an aplastic crisis -Parvovirus is a common virus associated with an aplastic crisis in HS and may cause the following symptoms: -Significant change in pallor or jaundice -Lethargy (lack of energy) -New onset headache (along with other symptoms listed here) -Light-headed or dizzy -Shortness of breath with activity
42
spherocytosis tx
-Phototherapy -Jaundice can be a problem in the newborn period if the bilirubin levels are too high and may require treatment, such as phototherapy. Phototherapy involves exposing the skin to a special blue light that changes bilirubin to a form that can be passed out of the body more easily. -Blood transfusion -In some cases, a blood transfusion is required for severe anemia. This is most common in the first year of life but may be ongoing if the anemia is severe. Most children with HS do not need blood transfusions on a regular basis. -Splenectomy- this treats -Cholecystectomy- might need to get it out bc of gallstones -> doesnt treat
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hereditary elliptocytosis labs
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hereditary elliptocytosis
due to various defects in skeletal proteins, spectrin and protein 4.1 -results increased membrane rigidity and decreased cellular deformability -autosomal-dominant mode of inheritance -elliptocytes varies from 50-90% -osmotic fragility normal and increase (not as helpful) -tx- transfusions, splenectomy, prophylactic folic acid
46
folic acid
-1mg daily -HE and HS tx
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G6PD deficiency
-africa -south america
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types of G6PD deficiency
severe* -most of the time they have intermittent hemolysis
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function of G6PD
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G6PD risk factors
-legumes -infections -certain chemicals
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drugs that trigger G6PD hemolysis
-henna
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labs found with G6PD
-severe anemia with Hb 4-6g/dl PCV and RBC count are decreased -WBC increased in many cases
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blood film of a H6PD deficient pt with acute hemolytic anemia
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thalassemia
-worlds MC genetic disease -autosomal recessive inheritance -millions of carriers and 100s of 1000s of pts worldwide
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thalassemia: a quantitative defect
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world incidence of alpha thalassemia
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world incidence of beta-thalassemia
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alpha-thalassemia
-4 is normal number of alpha-globin genes -if 1 or 2 genes are missing- alpha thalassemia trait, causing mild microcytosis with or without anemia -if 3 genes are missing- alpha thalassemia (HbH disease)
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alpha thalassemia
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alpha thalassemia dx
-HbH inclusion bodies -severe hypochromia -results in an excess of beta globins, which leads to the formation of beta globin tetramers (β4) called hemoglobin H. These tetramers are more stable and soluble, but under special circumstances can lead to hemolysis, generally shortening the life span of the red cell.
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beta-thalassemia
-chromosome 11 problem
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beta thalassemia: thalassemia minor
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electrophoresis testt
-hemoglobin A2 is how you dx -> HIGH
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beta thalassemia: thalassemia major
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peripheral blood smear: beta thalassemia
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thalassemia pathophysiology
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clinical features of thalassemia
-RBC is high -microcytic anemia
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skeletal changes: thalassemia
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thalassemia tx
Blood transfusions: You may need frequent blood transfusions (as much as every two weeks) with beta thalassemia major. During the procedure, you receive blood from a donor. The influx of blood from a transfusion supplies red blood cells needed to carry oxygen to tissues throughout your body. Iron chelation therapy: Iron is an important part of the hemoglobin protein allowing it to carry oxygen. Too much iron, however, can be harmful. Iron chelation therapy can help prevent iron overload. Folic acid supplements: Folic acid can help boost your body’s ability to make red blood cells. Your doctor may recommend supplements if you have beta thalassemia minor. You may also take folic acid in addition to receiving regular blood transfusions if your condition is more severe. Luspatercept: If you have severe thalassemia, you may receive an injection (shot) of luspatercept every three weeks to help your body make more red blood cells. Luspatercept improves anemia in people diagnosed with beta thalassemia who are receiving blood transfusions. Bone marrow and stem cell transplant: You may receive bone marrow stem cells from a donor. Bone marrow stem cells eventually mature into red blood cells. Replacing your bone marrow stem cells with the stem cells of a healthy donor can cure beta thalassemia. Unfortunately, finding a compatible donor can be a challenge. Also, this type of transplant is considered a high-risk procedure.
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thalassemia is preventable
in cyprus and in Greece, extensive screening -public health education have led to a nearly complete disappearance of thalassemic births
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sickle cell anemia: RBC membrane changes
-shape of it causes it be be clogged -> pain
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sickle cell: gene
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how is sickle cell caused
glutamine changes to valine
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sickle cell anemia: sickling episodes
-infection -dehydration -hypoxia -renal circulation (mild)
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sickle cell anemia morbidity
-MCC of morbidity is vaso-occlusion -reticulocytes and sickled cells adhere to endothelium of small and large vessels, leading to tissue infarction and organ damage
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sickle cell anemia: organs involved
-MC: -skin (ulcers) -bones (painful crises, infections) -respiratory system (acute chest syndrome) -brain (infarction) -eyes (retinopathy)
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sickle cell anemia: dx
-peripheral smear -reticulocyte count -high MCV (secondary folic acid deficiency is common) -Hb electrophoresis -howell-jolly body
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clinical features of sickle
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sickle cell anemia crisis tx
-hydration -analgesia -steroids -antibiotics -ventilatory support -do NOT give transfusions -> hyperviscosity
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sickle cell anemia: exchange transfusion
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sickle cell anemia: chronic tx
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hydroxyurea
-new mainstay of tx -for life -know this -immunosuppressant -takes 6 months to work -change it very slowly
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transfusion: sickle cell
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advantages and disadvantages of simple vs exchange transfusions
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clinical presentation of sickle cell
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hemoglobin c
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2-Hb C disease
-target cells -hemoglobin C crystals
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hemolytic anemias
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classification of hemolysis
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intra vs extravascular hemolysis
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acquired hemolytic anemia: immune vs non immune
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lab findings in hemolysis
schistocytes
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extravascular vs intravascular hemolysis
-symptoms are about the same -extravascular- enlarged spleen
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warm auotimmune hemolytic anemia causes
-antiviotics optimally active at 37 degrees -IgG -causes: -idiopathic -secondary: -SLE -CLL -lymphomas -drugs- methyl dopa
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warm autoimmune hemolytic anemia pathogenesis
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warm autoimmune hemolytic anemia clinical features and investigations
-schistocytes -helmet cells
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direct coombs test
+ -warm autoimmune hemolytic -sphyllis -mono
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warm autoimmune hemolytic anemia treatment
-corticosteroids -splenectomy -immunosuppresive - Azathioprine -folic acid -tx underlying cause
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cold agglutinin disease
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cold autoimmune hemolytic anemia investigations
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cold autoimmune hemolytic anemia clinical features
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cold autoimmune hemolytic anemia tx
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autoimmune hemolytic anemia
look at the antibody
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pre splenectomy / post splenectomy
-PRE SPLENECTOMY -pneumococcal vaccination, both types of meningococcal (MenACWY and MenB) vaccination, and Hib vaccination should all be completed at least 2 weeks before a scheduled splenectomy!!!!!!!!!!!!!! -POST SPLENECTOMY -Patients who have had a splenectomy following trauma should continue antibiotic prophylaxis for a minimum of two years after surgery -Howell–Jolly bodies!! are found in patients who have had splenectomies or are hyposplenic (e.g., sickle cell anemia) and rarely in megaloblastic anemias -spherocytosis -warm antibody -sickle cell (autorejects)
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paroxysmal cold hemoglobinuria
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hemolytic anemia resulting from infections with microorganisms
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babesia
-tics -hemolytic -flu like
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what dx increases likelihood of IDA
PUD
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-MCV much lower -> really small -thalassemia -follow up with electrophoresis
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iron deficiency
112
A 14 year-old female has sickle cell anemia. Which factors below can increase the patient's risk for developing sickle cell crisis? Select all that apply:*
a. Shellfish B. Infection!! C. Dehydration!! -> more get stuck D. Hypoxia!! E. Low altitudes -> it would be high F. Hemorrhage!! G. Strenuous exercise!!- stress in body
113
You're providing education to a patient with sickle cell anemia who is taking Hydroxyurea. You will make it priority to tell the patient to?*
a. Consume foods high in calcium and potassium B. Avoid sick people and maintain strict hand hygiene C. Take this medication with at least 8 oz of water D. Monitor your blood glucose level daily
114
A mother brings in her 8 month-old child to the ER. The mother reports the baby has recently started being extremely fussy, has a fever, and swelling in the hands and feet. The child is diagnosed with sickle cell disease. As the nurse you know that the swelling in the hands and feet in the infant is termed?*
A. Dactylitis!!!! B. Erythromelaglia C. Dyshidrotia D. Phalitis
115
What is the primary risk to thalassemia major patients who receive frequent and multiple blood transfusions?
A. Iron overload!!!! B. Citrate toxicity C. Polycythemia D. Hyperviscosity
116
Hemoglobin H!!! disease is characterized by the deletion of........................................?
a) One alpha gene b) Two alpha gene c) Three alpha gene !!!!! d) Four alpha gene- do not live