Conditional Anemias Flashcards
By definition, _____ is present when hematocrit is reduced
anemia
Anemia in Men vs. women
○ Men- Generally below about 39-40%
○ Women- Generally below about 35-36%
For the most part, anemias as either _____ or _____
conditional; inherited
We can also look at anemias according to pathophysiologic basis:
○ Decreased production: Lacking nutrient, bone marrow suppression, etc.
○ Accelerated blood loss: Hemolysis or hemorrhage
○ Red blood cell size (MCV)
Tests to help us differentiate between the types of anemia are the _____
reticulocyte count, the MCV, and the peripheral blood smear
S/S common to most types of anemia
○ Fatigue or weakness
○ Exercise intolerance
○ Tachycardia
○ Palpitations
○ Dyspnea on exertion
○ Pallor, pale palpebral conjunctiva
○ Headache, depression (less common)
_____ – destruction of the cell by physical ripping or bursting
Hemolysis
Hemolysis of RBCs is always occurring at
a slow, steady rate, taken out of
circulation after ~ 120 days. This is called ____
“physiologic hemolysis”
Hemolytic Anemia
pathologic conditions can result in an
accelerated hemolysis, where RBCs are being destroyed faster than the marrow normally produces them
_____ – A group of disorders in which RBC survival is reduced, either episodically or continuously
Hemolytic Anemias
Classifications of hemolytic anemias
○ Intrinsic Defect
■ Defect is within the RBC – problem with the membrane, enzyme systems, or Hgb creation
■ Typically hereditary
○ Extrinsic Defect
■ Defect from outside the RBC – immune mediated, microangiopathic, infection, burns, and hypersplenism
Anemia caused by IgG antibodies
Autoimmune Hemolytic Anemia
The Antiglobulin Coombs Test (Direct) is the basis of diagnosis for _____
Autoimmune Hemolytic Anemia
Treatment of autoimmune hemolytic anemia
Corticosteroids
Diagnostic studies that may suggest hemolytic anemia
○ Reticulocytosis – Bone marrow will respond to most hemolytic
disorders with an increased production of young RBCs
○ Lactate dehydrogenase (LDH) – Levels can be elevated
○ Bilirubin – Levels can be elevated
○ Peripheral blood smear – shows evidence of hemolysis
Look at the supplementary study material for the anemia slides
:)
Anemias from Nutritional
Deficiency
○ Iron deficiency anemia
○ Vitamin B12 deficiency
anemia
○ Folate deficiency anemia
Anemias from Chronic Disease
○ “Anemia of chronic disease”
○ Anemias associated with:
■ Chronic renal disease
■ Chronic liver disease
Other selected anemias
Aplastic anemia
Most common cause of anemia worldwide
Iron Deficiency Anemia
Iron Deficiency Anemia
In the developed world, it is caused by chronic, slow bleeding unless
proven otherwise
Iron deficiency anemia causes
Excessive menstruation, chronic GI blood loss, etc.
○ Pregnancy/Lactation – increased iron utilization/demand
○ Malabsorption – Celiac disease, intestinal worm, gastritis, etc.
○ Infants – most common cause of anemia in infants
○ Inadequate dietary intake – rare in US
○ Idiopathic (up to 5% of cases)
Iron Deficiency Anemia pathophysiology
○ If due to chronic, slow blood loss, an increase in the production of RBCs depletes iron stores slowly
○ Initially H&H remain normal while iron stores are being depleted (iron deficiency without anemia)
○ Once iron stores are depleted, RBCs form at a slower rate, and less Hgb can be made
■ Results in hypochromia, anisocytosis, poikilocytosis
Less Hgb means _____ cells (MCV decreases)
smaller
Iron Deficiency Anemia unique S/S
○ Pica – craving for food (ice chips, etc.) or even dirt
○ Cheilosis – painful cracking at the corners of mouth
○ Glossitis – smooth tongue
○ Brittle nails
○ Koilonychia – spooning of nails
○ Heme-positive stool (if due to a GI bleed)
Iron Deficiency Anemia Management
○ Treat underlying disorder if one is identified (celiac disease, colon cancer, menorrhagia, gastritis/bleeding ulcer, hookworms, etc.)
○ PO Ferrous Sulfate (325 mg 1-3 times daily; 100 mg of elemental iron) Take on an empty stomach to ensure absorption
○ Reticulocyte count should increase by 7 days of treatment and signifies appropriate response to therapy
○ Treatment should be continued for approximately 6 months following normalization of Hgb
○ If patient cannot tolerate PO Ferrous Sulfate, IM or IV Iron can be given, but beware of anaphylaxis.
○ Because IDA is rarely life-threatening, the most important part of treatment is identification and correction of blood loss
Iron deficiency demands a search for ____
chronic blood loss, especially
if menorrhagia and frequent blood donations are not the cause
The most common cause of B12 deficiency in the US is _____
Pernicious Anemia
Those at risk for B12 deficiency due to inadequate dietary intake include the following groups:
○ Strict vegetarians and vegans
○ Those who have had a gastrectomy (low
production of intrinsic factor)
○ Those with disease of the ileum (as commonly
seen with Crohn’s disease)
_____ – autoimmune destruction of gastric parietal cells
resulting in insufficient intrinsic factor
Atrophic Gastritis
The impairment of DNA synthesis by B12 deficiency slows _____, but not
_____
nuclear maturation; cytoplasmic maturation
B12 deficiency anemia results in _____
Megaloblastic anemia
Macro-ovalocytes (megaloblastic RBCs,
macrocytic), and may show characteristic
Hypersegmented Neutrophils
Vit B12 Deficiency Anemia Unique S/S
○ Glossitis
○ Paresthesias – in the extremities (characteristic)
○ In severe disease, the posterior columns of the spinal cord become impaired, and cerebellar function may be altered as well
■ Diminished vibratory or position sense
■ Positive Romberg Test
■ Irreversible ataxia
____ is very characteristic of a B12 deficiency
Paresthesias
Clinical Management for vitamin B12 deficiency anemia
○ Parenteral administration of Vitamin B12, IM or SC injections of 100 mcg per dose
○ PO Vitamin B12 may be administered after repletion, but not always successful
it is recommended that you also prescribe
simultaneous folic acid replacement (1 mg daily) with _____ because ____
Vit B12 Deficiency Anemia; Some patients are concurrently folic acid deficient from intestinal mucosal atrophy
Highest risk populations for folate deficiency anemia
alcoholics, anorexic patients, those who do not eat fresh fruits and vegetables or overcook their food
Medications that interfere with folate absorption
Phenytoin, methotrexate, TMP/SMX, etc.
Sometimes seen in scenarios of increased requirement
Pregnancy, hyperthyroidism, or malignancy
Folic acid (B9) is present in _____
fruits and vegetables, especially citrus fruits
and green leafy vegetables
Folate Deficiency Anemia pathophysiology
○ Like Vitamin B12, Folate is necessary for adequate DNA synthesis
(affects all bone marrow precursors)
■ The impairment of DNA synthesis slows nuclear maturation, but
not cytoplasmic maturation
● Cells do not progress from the G2 growth stage into mitosis,
so they do not divide (stay large/flimsy)
● Megaloblastic anemia (sound familiar?)
Folic Acid deficiency in pregnancy can result in ____
neural tube defects!
Prenatal folic acid is important
Basically, folate deficiency anemia is clinically identical to _____
Vitamin B12 deficiency anemia
If there is isolated folate deficiency, deficiency, the patient does not
develop the _____
neurologic symptoms
Important lab findings of folate deficiency anemia
Hypersegmented neutrophils. Just like with Vitamin B12 deficiency. Decreased serum folate level. Decreased RBC folate level
Clinical management of folate deficiency anemia
○ Folate replacement is the key to treatment
○ Monitor response to therapy by watching for increased reticulocyte count after 5-7 days
○ Do not treat without confirming Vitamin B12 levels are normal!
Common causes of anemia of chronic inflammation:
Rheumatoid arthritis, HIV/AIDS, TB, lupus, inflammatory bowel disease, malignancy
Pathophysiology of Anemia of Chronic Disease
○ Chronic inflammatory diseases seem to trigger increased storage and protection of iron stores (saving for later?)
○ Hepcidin is a protein hormone that normally impairs release of iron from storage
■ In chronic disease states, inflammatory cytokines trigger increased production of hepcidin, which results in iron being locked away in storage
■ Referred to as “iron-restricted erythropoiesis”
Chronic kidney disease and anemia
Erythropoietin levels are
decreased, resulting in anemia
Chronic liver disease and anemia
Portal hypertension leads to hypersplenism (increased RBC phagocytosis), resulting in anemia
Signs and Symptoms of Anemia of Chronic Disease
Clinical presentation is generally consistent with the underlying condition
Anemia of Chronic Disease clinical management
Treat the underlying disease process
■ The anemia often improves when the underlying condition is
adequately treated (if possible)
A condition of bone marrow failure that arises from suppression or
injury to the hematopoietic stem cell
Aplastic Anemia
Aplastic anemia is considered idiopathic about ___% of the time
50
Pathophysiology of aplastic anemia
○ Most cell lines are affected, so it usually includes low WBC and platelet
counts in addition to anemia
■ The hallmark of aplastic anemia is pancytopenia due to bone marrow
hypocellularity
○ That being said, early in the evolution of aplastic anemia, only one or two
cell lines may be reduced
Thrombocytopenia can result in
Gingival bleeding, epistaxis, other bleeding, and maybe bruising
can cause vulnerability to bacterial and fungal infections
Neutropenia
Clinical Management of Aplastic Anemia - Mild cases
■ Supportive care, including erythro or myeloid growth factors
■ Transfusions and antibiotics are often needed
Clinical Management of Aplastic Anemia - Severe cases
■ Isolation precautions and bone marrow transplantation (BMT)
● If BMT is not possible due to lack of a donor match, immunosuppression with certain strong medications is attempted
○ Severe cases are fatal without treatment
■ Prognosis is better for those who get a BMT
All cases of Aplastic Anemia need to be referred to and managed by a ____
Hematologist, usually urgently
