Anemia Flashcards
definition
Reduction in the total number of circulating erythrocytes
Decrease in quality or quantity of hemoglobin (Hb)
common causes
1 impaired RBC production
2 blood loss
3 inc RBC destruction
4 combination of the above
Measures
CBC to include: RBC count Hematocrit - % RBC in whole blood Hemoglobin concentration WBC count
Classification
By the cause: Nutritional Physical injury Chronic disease Infections Toxins
By the morphology
Morphological anemia includes what
Microcytic Macrocytic Hyperchromic Hypochromic Abnormal cell shape Normocytic Normochromic
Morphological anemia - Microcytic and Macrocytic
Microcytic = abnormally small Macrocytic = abnormally large
Morphological anemia - Hyperchromic and hypochromic
Hyper = inc concentration of hemoglobin Hypo = dec concentration of hemoglobin
Common clinical features - symptoms
Fatigue HA Dizziness SOB Exertional angina Intermittent claudication Palpitations
Common clinical features - signs
Pallor Tachycardia Systolic flow mumur Dec mental status Hypotension (orthostatic too) Weight loss
Pernicious anemia is what
Chronic condition
Malabsorption of B12
Macrocytic, Normochromic anemia
AKA megaloblastic anemia
Pernicious anemia - how common and in who
One of the most common types
Late adulthood
F more than M
Pernicious anemia - common cause assoicated with
lack of intrinsic factor - GI system lacking it so can’t absorb B12 properly
Pernicious anemia - progression
develops slowly
early s/s vague and often ignored (mood swings, GI upset, cardiac and renal upset)
late s/s are more classic s/s of anemia (big one is Hb dec to 7)
Pernicious anemia - s/s are associated with
nervous system demyelination
If not treated will end up with peripheral neuropathy - glove pattern
Pernicious anemia - diagnosis with
blooc count
bone marrow aspiration
schilling test (inject B12 and see if absorb)
Pernicious anemia - prognosis and tx
If untreated is fatal within 1-3 years (cardiac arr)
Replacement therapy is tx - injections of B12 every 3-6 months
Folic acid anemia is what
Folate deficiency - Inadequate intake of folic acid
Macrocytic, Normochromic
Folic acid anemia - epidemiology
Alcoholics
Elderly
Pregnant females
Those in puberty
Folic acid anemia is often what type of issue
supply vs. demand - inadequate leafy greens (inadequate folic acid)
Folic acid anemia s/s
May or may not have neuro issues
Fissuring and ulceration of mouth and oral cavity
Dysphagia and other GI upset
Folic acid anemia - prognosis and tx
Takes 1 to 2 weeks for folate strores to be restored
Iron deficiency anemia
Microcytic, Hypochromic anemia
Iron deficiency anemia - epidemiology
Most common type of anemia worlwide
Females usually with menstruation or with pregnancy
Males is usually secondary to GI bleed
Children during growth spurts
Iron deficiency anemia - causes
dietary lack of Fe
Fe stores are tightly controlled and daily ingestion is needed
F require mroe than M
Bleeding is a common cause - daily loss of 2-4ml/day
Iron deficiency anemia - clinical presentation
Onset is gradual
Most common is fatigue, weak, SOB
Neuro changes - mental status change, paresthesia, weak
Alterations in epithelial tissues - changes in quality of hair, skin, tongue surfaces
Iron deficiency anemia - prognosis and tx
Treat cause
Iron replacement
Rapid improvement
Normocytic and Normochromic anemias includes:
Aplastic Posthemorrhagic Hemolytic Anemia of chronic disease Sickle cell Polycythemia Multiple myeloma Hemochromatosis
Aplastic anemia
related to bone marrow aplasia or hypoplasia
RBC stem cells damaged - leading to dec production
Aplastic anemia - clinical manifestations include
classic anemia s/s as well as bleeding disorders! DIC is common
Aplastic anemia - treatment
depends on cause
- blood transfusions
- bone marrow transplants may be required
Posthemorrhagic anemia
Sudden massive blood loss
leads to cardiovascular complications
Posthemorrhagic anemia - prognosis
it take 4 to 6 wks to restore normal blood counts
6 to 8 wks for normal hemoglobin to be restored
Hemolytic anemia
Premature, accelerated destruction of RBCs
Hemolytic anemia - what will you see with physical exam
increased spleen size
jaundice
bone deformities, bone pain, pathologic fractures
Hemolytic anemia - treatment
depends on cause - splenectomy may be required
Anemia of chronic disease
usually occurs within a coupld of months of active disease onset
Anemia of chronic disease s/s
often mild and in many cases the pt is asymptomatic
usually discovered inadvertently
This is usually the least of the pt problems
Sickle cell anemia
group of disorders characterized by abnormal form of hemoglobin
autosomal recessive disorder
sickle cell anemia - epidemiology
Tends to occur in people with origins in equatorial countries
In US - most common in AA
1 in 400 live births!
What happens with sickle cell anemia
RBCs change in shape as they deoxygenate, causing complications
There are triggers to the sickling (and usually pt will knoe their trigger)
Once re-oxygenated, the cell can return back to normal shape
Sickle cell anemia - clinical manifestations
Most result from vascular occlusions which can lead to visceral infection
Includes typical anemia s/s
May present with anaplastic anemia too
Sickle cell anemia - x and prognosis
Treatment includes prevention of infections and elimination of triggers
Genetic counseling and psychological support may be needed
Polycythemia
Excessive RBC number
Can be relative or absolute
Relative polycythemia
Hemoconcentration due to dec in plasma volume as seen with dehydration
Usually this relative type is not as big of a deal
Absolute polycythemia
Primary - uncommon, seen in white male 40-60yr)
Secndary - physiologic response to the hypoxia, might been seen in those living at high altitudes, smokers, pt with CHF or COPD - non physiological response can be seen with renal disease
Clinical presentation for polycythemia
Plethora - ruddy, red colored face, hands, feet, ears, mucous membranes
Liver and spleen enlargement
Severe pruritis
Thrombosis and inc blood viscosity s/s
POlycythemia - treatemnt
dec blood volume
Multiple myeloma
Neoplasia of plasma cells
Characterized by multiple malignment masses of plasma cells scattered throughotu the skeletal system
Progresssive destruction of corticol bone (flat ones)
Humeral suppression occurs
Multiple myeloma - common bones affected
vertebrae, ribs, skull, pelvis, femur, clavicle, scapula
Multiple myeloma - epidemiology
Incidence 3x greater than all other bone cancers
M more than F
AA more than C 2 to 1 ratio
Tyical age of diagnosis is over 40, mean age is 62
Multiple myeloma clinical presentation
Bone pain (t60%) severe! Anemia and renal insufficiency (25%) Osteomyelitits Chronic and recurrent infections Pathologic fractures Mental status changes, lethargy Nerve root impingement is possible
Multiple myelima - treatment and prgnosisn
Without treatment 6 to 12 month survival after bone lesions
With treatment is 2-5 yrs
10 year survival is 3%
Chemotherapy and prevention o complications
Exercise and ambulation are important to keep pt active and dec complications
Hemochromatosis
Iron absorption disorder
autosomal recessive
gene has been identified
Hemochromatotis - fundamental problem is
excessive loevels of iron in the blood, secondary to increased absorption
Excessive Fe is depositied in various cells
Liver, pancreas, heart, skin, joints (synovium - gets crystals)
Hemochromatosis - ss
often asymptomatic until an overload occurs
Hemochromatosis - diagnosis
primarily via measurement of trasnferrin or genetic testing
liver biopsy for definitive diagnosis migh tbe needed
Hemochromatosis - traeatment and prognosis
Phlebotomy on weekly basis until iron is normal
Chelation migh tbe used if phleb has complications
Normal lifespan if Fe can be maintained at normal levels and no organ damage has occured
Arthropathies tend to worsen and will always be there even with controlled iron levels
