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Practice topics Exam 1 > Anemia > Flashcards

Anemia Flashcards

1
Q

definition

A

Reduction in the total number of circulating erythrocytes

Decrease in quality or quantity of hemoglobin (Hb)

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2
Q

common causes

A

1 impaired RBC production
2 blood loss
3 inc RBC destruction
4 combination of the above

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3
Q

Measures

A 
CBC to include:
RBC count
Hematocrit - % RBC in whole blood 
Hemoglobin concentration
WBC count
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4
Q

Classification

A 
By the cause:
Nutritional
Physical injury
Chronic disease
Infections
Toxins

By the morphology

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5
Q

Morphological anemia includes what

A 
Microcytic
Macrocytic
Hyperchromic 
Hypochromic
Abnormal cell shape
Normocytic
Normochromic
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6
Q

Morphological anemia - Microcytic and Macrocytic

A 
Microcytic = abnormally small
Macrocytic = abnormally large
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7
Q

Morphological anemia - Hyperchromic and hypochromic

A 
Hyper = inc concentration of hemoglobin
Hypo = dec concentration of hemoglobin
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8
Q

Common clinical features - symptoms

A 
Fatigue
HA
Dizziness
SOB
Exertional angina
Intermittent claudication
Palpitations
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9
Q

Common clinical features - signs

A 
Pallor
Tachycardia
Systolic flow mumur
Dec mental status
Hypotension (orthostatic too)
Weight loss
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10
Q

Pernicious anemia is what

A

Chronic condition
Malabsorption of B12
Macrocytic, Normochromic anemia
AKA megaloblastic anemia

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11
Q

Pernicious anemia - how common and in who

A

One of the most common types
Late adulthood
F more than M

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12
Q

Pernicious anemia - common cause assoicated with

A

lack of intrinsic factor - GI system lacking it so can’t absorb B12 properly

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13
Q

Pernicious anemia - progression

A

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)

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14
Q

Pernicious anemia - s/s are associated with

A

nervous system demyelination

If not treated will end up with peripheral neuropathy - glove pattern

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15
Q

Pernicious anemia - diagnosis with

A

blooc count
bone marrow aspiration
schilling test (inject B12 and see if absorb)

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16
Q

Pernicious anemia - prognosis and tx

A

If untreated is fatal within 1-3 years (cardiac arr)

Replacement therapy is tx - injections of B12 every 3-6 months

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17
Q

Folic acid anemia is what

A

Folate deficiency - Inadequate intake of folic acid

Macrocytic, Normochromic

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18
Q

Folic acid anemia - epidemiology

A

Alcoholics
Elderly
Pregnant females
Those in puberty

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19
Q

Folic acid anemia is often what type of issue

A

supply vs. demand - inadequate leafy greens (inadequate folic acid)

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20
Q

Folic acid anemia s/s

A

May or may not have neuro issues
Fissuring and ulceration of mouth and oral cavity
Dysphagia and other GI upset

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21
Q

Folic acid anemia - prognosis and tx

A

Takes 1 to 2 weeks for folate strores to be restored

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22
Q

Iron deficiency anemia

A

Microcytic, Hypochromic anemia

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23
Q

Iron deficiency anemia - epidemiology

A

Most common type of anemia worlwide
Females usually with menstruation or with pregnancy
Males is usually secondary to GI bleed
Children during growth spurts

24
Q

Iron deficiency anemia - causes

A

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

25
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
26
Iron deficiency anemia - prognosis and tx
Treat cause Iron replacement Rapid improvement
27
Normocytic and Normochromic anemias includes:
``` Aplastic Posthemorrhagic Hemolytic Anemia of chronic disease Sickle cell Polycythemia Multiple myeloma Hemochromatosis ```
28
Aplastic anemia
related to bone marrow aplasia or hypoplasia | RBC stem cells damaged - leading to dec production
29
Aplastic anemia - clinical manifestations include
classic anemia s/s as well as bleeding disorders! DIC is common
30
Aplastic anemia - treatment
depends on cause - blood transfusions - bone marrow transplants may be required
31
Posthemorrhagic anemia
Sudden massive blood loss | leads to cardiovascular complications
32
Posthemorrhagic anemia - prognosis
it take 4 to 6 wks to restore normal blood counts | 6 to 8 wks for normal hemoglobin to be restored
33
Hemolytic anemia
Premature, accelerated destruction of RBCs
34
Hemolytic anemia - what will you see with physical exam
increased spleen size jaundice bone deformities, bone pain, pathologic fractures
35
Hemolytic anemia - treatment
depends on cause - splenectomy may be required
36
Anemia of chronic disease
usually occurs within a coupld of months of active disease onset
37
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
38
Sickle cell anemia
group of disorders characterized by abnormal form of hemoglobin autosomal recessive disorder
39
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!
40
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
41
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
42
Sickle cell anemia - x and prognosis
Treatment includes prevention of infections and elimination of triggers Genetic counseling and psychological support may be needed
43
Polycythemia
Excessive RBC number | Can be relative or absolute
44
Relative polycythemia
Hemoconcentration due to dec in plasma volume as seen with dehydration Usually this relative type is not as big of a deal
45
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
46
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
47
POlycythemia - treatemnt
dec blood volume
48
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
49
Multiple myeloma - common bones affected
vertebrae, ribs, skull, pelvis, femur, clavicle, scapula
50
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
51
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 ```
52
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
53
Hemochromatosis
Iron absorption disorder autosomal recessive gene has been identified
54
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)
55
Hemochromatosis - ss
often asymptomatic until an overload occurs
56
Hemochromatosis - diagnosis
primarily via measurement of trasnferrin or genetic testing | liver biopsy for definitive diagnosis migh tbe needed
57
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

Practice topics Exam 1 (15 decks)

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