Term
| Macrocytic-Normochromic Anemias |
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Definition
result of ineffective DNA synthesis
Pernicious (B12) anemia
Folate Anemia |
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Term
| Normochromic-Normocytic Anemias |
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Definition
Aplastic Anemia (reduction or absence)
Post-hemorrhagic anemia
Anemia of Chronic disease
Hemolytic anemia |
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Term
| Microcytic-Hypochromic Anemia |
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Definition
Iron deficiency Anemia (most common)
Sideroblastic Anemia (Ineffective iron uptake and dysfunctional heme synthesis) |
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Term
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Definition
caused by autosomal recessive inheritance causing loss of parietal cells which causes absence of Instrinsic factor that transports B12 or caused by destruction of parietal cells by gastric diseases
Most common macrocytic caused by B12
mostly seen in older women
20-30% of relatives will have it (1st degress female relatvies have gastric antibodys)
R/t: hasimotos, Type 1 dM, Addisons, primary hypothyroidsim, graves, MG
Excessive alcohol intake, hot tea, smoking; H.pylori and gastrectomy
2-3% develop carcinoma |
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Term
| Clinical Manefestations and Diagnostics for Pernicious Anemia: |
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Definition
Sx: Early:infection, mood swings, GI, cardiac, & kidney ailments
Hgb 7-8: weakness, fatigue, paresthesias of feet and fingers, difficulty walking, loss of appetite, abdominal pain, weight loss, tongue sore smooth and beefy red, SALLOW skin tone, liver & spleen enlargement, R side HF may occur
Diagnostics: CBC with indices, low/normal serum cobalamine (B12), serum folate, elevated serum homocysteine, increased methyl. acid, MCV above 100fL, normal MCHC, macrocytes seen on smear |
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Term
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Definition
more common than cobalamine
Folate is req. for RNA & DNA synthesis in the RBC
absorbed in SI and stored in Liver
Seen more in alcoholics and chronic malnourished people
Increased risk for neuronal defects in newborns and heart disease and colon cancer in adults
Sx: severe cheilosis (scales & fissure of lips and corners), stomatitis, painful ulcers in mouth & on tongue; weakness, fatigue, intermittent abdominal pain; dysphagia, gas, diarrhea, changes in GI tract suggestive of Sprue; NO NEURO SX UNLESS thiamine efficiency seen
Diagnositcs: CBC with indices, elevated homocysteine, methyl acid normal |
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Term
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Definition
most common anemia world wide
Chronic poor women of childbearing age and children are most at risk
Children infected with parasites causes iron loss
Occurs in lead poisoning
9% of kids iron deficient 3% anemic
Highest risk are black females in urban poverty
Most common causes in developed countries: pregnancy and chronic blood loss
Other causes: meds like NSAIDs, surgerical procedures that decrease stomach acidity, intestinal transit time, and absorption; insufficient dietary intake of iron; eating disorders
Pathogens need iron for survival (therefore may be bodys response to infection)
Patho; nutritional iron defeciency is from low dietary intake or excessive blood loss causing depletion of iron stores and reduces Hgb synthesis
May be functional (ineffective iron delivery or impaired use within bone marrow) or metabolic
Stage1: stores depleted 2:transportation to bone marrow diminished 3: small Hgb deficient cells enter circulation in sufficient #s to replace normal erythrocytes that have been removed from circulation (Sx appear here) |
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Term
| IDA clinical manifestations and diagnostics |
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Definition
most Sx not severe or dont need attention until Hgb is 7-8
Early: weakness, fatigue, SOB, pale earlobes, palms and conjunctivae
Progressive: mails brittle, thin, coarsely riged, speen shapped or concave (KOILONYCHIAS); tongue is sore red and painful; angular stomatitis; difficulty swallowing; hyposalivation
Gastritis, neuromuscular irritability, headache, numbness, tingling, vasomotor disturbances
mental confusion, memory loss, and disorientation common in elderly
Diagnostics: CBC with indices, decreased seruym ferritin (iron stores), increased total iron binding capacity (TIBC), decreased serum iron, transferrin saturation |
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Term
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Definition
ineffective iron uptake leaving iron in tissues and dysfunctional heme synthesis
ringed sideroblasts in bone marrow indicative of SA
blood contains hypochromic erythrocytes (micro or macro)
Patho: altered mitochondrial heme synthesis in erythryoid cells in bone marrow
Hereditary: Rare, x-linked recessive but doesnt show til mid life when diabetes or cardiac failure occur due to iron overload
Dimorphism: normo cells seen with micro/hypo cells (mild anemia, female carriers, those receiving pyridoxine)
Anisocytosis & poikilocytosis also seen
Acquired SA: most common; two type Primary: caused by myelodysplatic syndrom
Secondary: Reversible SA (most prevalent form) caused by alcohol abuse, TB drug reactions, copper deficiency, hypothermia
SX: Hgb 4-10; signs of iron overload is known as erythropoietic hemochromatosis; mild to moderate enlargement of spleen & liver; bronze skin; neruo & epitheleal Sx not seen
Complications: CHF & rhythm disturbances
Children and infants may have growth and developmental impairment |
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Term
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Definition
excessive RBC production (Relative & absolute (primary & secondary (vera)))
Relative: hemoconcentration; caused by dehydration = blood becomes concentrated - more RBCs smaller amount of plasma
Absolut secondary: most commonly seen; response to hypoxia - seen in high altitudes, heavy smokers, COPD, CHF; it is the bodies attempt to compensate for lowered oxygen
Primary:fairly rare, abnormal proliferation of bone marrow stem cells with self destructive expansion of RBCs; cause unknown
Patho: increased RBCs, WBC, and platelets; splenomegaly
95% express JAK2 an aquired mutation which harms the self-regulation of erythropoietin |
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Term
| Clinical Manifestations & diagnostics of Polycythemia vera |
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Definition
perk age 60-80; more in males;more in whites of Northern European or Jewish descent
Enlarged spleen, thrombus, vessel occlusion, ischemia, infarction, ab pain, increased risk of bleeding, plethora (ruddy red color); headahces, drowsiness, delirium, mania, depression, chorea, visual distrubances, 5x increase risk of cerebral thrombosis
Risk of: Raynaud phenomenon, angina, stroke, MI; high BP, thromboangitis obliterans, GI or duodenal thrombosis, portal HTN
Diagnostics: extreme painful itching intensified by water - not responsive to histamines or lotions |
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Term
| Post-hemmorhagic anemia vs hemolytic anemia |
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Definition
PHA: acute blood loss; lowered RBC count Hgb, Hct; normo-cytic and -chromic
normal adult can tolerate 500-1000mL; above 1500mL causes Sx
If blood loss is internal, iron recovery may occur
HA: premature accelerated destruction of erythrocytes
Elevated levels of erythropoietin and increase in products of HgB catabolism
Congenital (intrinsic defects in erythrocytes) or acquired (immunologic)
unconjugated bilirubin released causing SEVERE JAUNDICE |
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Term
| Anemia of chronic disease vs IDA |
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Definition
in ACD iron stores are sufficient but low in circulation, where IDA iron stores are insufficient!!!
ACD: 50% of those in nursing homes have ACD
results from erythropoiesis in people with chronic systemic diseases of inflammation (AIDs, arthritis, SLE, malaria, hepatitis, Chronic renal failure, CHF)
develops within 1-2mo of disease activity
ACD is initially normo -cytic & -chromic, but as it progresses they become hypo/micro
ACD characterized by noraml iron stores with low circulating iron
Patho: results from 1. decreased erythrocyte life span 2. suppressed production of erythropoietin 3. ineffective bone marrow erythroid progenitor response to erythropoietn 4.altered iron metabolism & iron sequestration in macrophages
Fewer sx than most anemias; Hgb drops alot than IDA sx appear |
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Term
| Neutrophilia (granulocytosis) |
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Definition
- occurs in early stages of infection and inflammation (Ex. Surgery)
- count exceeds 7500
- Other examples: exercise, 3rd trimester, acute hemmorage, epinephrine or steroid reaction, eclampsia, bone marrow neoplasm |
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Term
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Definition
<2000; seen in prolonged infection
- when production does not meet demand (Ex: radiation)
Causes: gram- bacteria, typhoid, severe viral or protozoal infections
- in absence of infection: 1. decreased production & ineffective granulopoiesis 2. reduced survival 3. abnormal distribution & sequestration
- increased destruction (splenomegaly)
- causes leukomoid reaction |
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Term
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Definition
| an increase in immature leukocytes aka body is respoinding to new infection by increasing band cells, shift to the left |
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Term
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Definition
ECF-A from mast cells is released to attract eosinophils to the site & IL-5 is released to stimulate bone marrow to produce & secrete more
- Causes: allergy, parasites, malignancy (Hodgkins), dermatosis, drugs (digoxin) |
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Term
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Definition
migration of eosinophils into inflammatory sites therefore low in blood.
Causes: Stress response/drugs; Cushings |
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Term
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Definition
response to inflammtion & immediate hypersensitivity reactions & myeloproliferative disorders
Ex: chronic myeloid leukemia, measles, myxedema |
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Term
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Definition
| physiologic decrease in basophils: pregnancy, ovulation, stress, Graves |
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Term
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Definition
called monocyte in circulation and macrophage in tissues
Causes: recovery phase of infection like chronic TB, endocarditis; hematologic disease; physiological in normal newborn |
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Term
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Definition
| Rare; seen in hairy cell leukemia |
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Term
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Definition
rare; seen in viral infection, thyrotoxicosis, malignancies, pertusis, hepatitis, mycoplasma pneumonia, typhoid
- Physiological in 4mo-4yo
-Seen in mono (EBV)
- Also with syphilis & adrenal insufficiency |
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Term
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Definition
abnormal lymphocyte destruction
Seen in AIDs, radiation, steroid reaction, lymphomas |
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Term
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Definition
acute, self-limiting, neoplastic lymphoproliferative clinical syndrome characterized by acute viral infection of B cells
- Caused mostly by EBV (85%); CMV seen in elderly causes similar symptoms
- 50-85% of kids infected with EBV by age 4
- only 35-50% of adults actually get mono; age 15-35, peak 15-19, males 18-23
-Patho: transmitted by saliva thru personal contact "kissing disease" (also present in genital, rectal, respiratory tract & blood)
-widespread infection of B lymphocytes, which all have EBV receptors
-initially infects oropharynyx, nasopharynyx, & salivary epithelial cells with later spread to lymphoid tissue & B cells (enter blood and spread fast)
- immunocompetent: unaffected B cells produce IgG IgA IgM antibodies agains the virus causing body to heal
-virus enters thru mouth & throat or nasap passage & effects that area & salivary glands & lymph nodes
-cytotoxic T cells activated, swelling caused by b & t cells & removal of WBCs all within the lymph system |
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Term
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Definition
initial Sx: sore throat & fever
Incubation usually 4-8wks (30-50days): flu like Sx may appear in 3-5days
Classic Triad: fever, pharyngitis (whitish Gray/green exudate on tonsils or posterior pharynx or pillars similar to strep), & lymphadenopathy of cervical nodes
Recover in few weeks with fatigue for 1-2months; avoid contact sports because of spleen rupture risk
Complications: spleen may rupture (50%) |
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Term
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Definition
platelet count < 150,000, significant when below 100,000, hemorrhage occurs from minor injury at 50,000, spontaneous bleeding (petechial rash, eccymosis, purpura occur under the skin at 10,000-15,000, severe bleeding below 10,000
Etiology: pseudothrombocytopenia (agglutinated platelets missed when being counted with automated cell counter in lab) must be ruled out first; miscounted when 10+ units of blood have been given in 24hr because it dilutes it; hypothermia can cause low platelets; hypersplenism as well
Patho: results from decreased platelet production, increased consumption, or both |
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Term
| Patho of thrombocytopenia (not mentioned in lecture |
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Definition
Patho: results from decreased platelet production, increased consumption, or both
PATHO: Congenital, acquired, and primary or secondary to other acquired or congenital disorders
Associated with: TAR syndrome, Wiskott-Aldrich syndrome, MYH9 mutation, X-linked thrombocytopenia, etc
Acquired is more common secondary to viral infection, drugs, nutritional deficits, chronic renal failure, bone marrow hypoplasia, radiation therapy, or bone marrow infiltration by cancer
Most occur from increased platelet consumption EX: heparin-induced (4% develop HIT, drug reaction caused by IgG against heparin factor 4 complex), idiopathic throm. Purpura, thrombotic throm. Purpura |
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Term
| Idiopathic (Immune) thrombocytopenia purpura |
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Definition
- increased platelet destruction
-Acute: seen in children and lasts 1-2mo with a complete remission; secondary to viral infections (leads to large amounts of antigen (viral particles) or allergic reactions or SLE that form immune complexes with circulating antibodies - bind to receptors on platelets causing platelet destruction in spleen and resolves when antigen or cause is removed
-Chronic: associated with IgG autoantibodies against platelet-specific antigens; mainly in women 20-40yo; progressively worse
-Mainly from IgG and act against one or more of several platelet glycoproteins – removed from circulation by mononuclear phagocytes in the spleen through the Fc receptor
Sx: initially minor bleeding problems (petechial and purpura) over several days – progression to major hemorrhage of mucosal sites (epistaxis, hematuria, menorrhagia, bleeding gums
During preg: may also have newborn that is thrombocytopenic
Mother may not have ITP but has the IgG antibody against antigen inherited from father and found on fetal platelets but not on maternal platelets |
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Term
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Definition
-fat soluble vitamin necessary for synthesis and regulation of prothrombin, procoagulant factors and anticoagulant regulators within the liver
Most common cause of the deficiency is parenteral nutrition in combo with broad spectrum antibiotics that destroy normal gut flora
CM: from lab findings to significant hemorrhage due to the lack of vitK-dependent proteins |
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Term
| Effect of liver disease on coagulation |
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Definition
| Impaired hemostasis or the inability to promote coagulation and the development of a stable fibrin clot is commonly associated with liver disorders, either from lack of vitamin K or specific diseases of the liver |
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Term
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Definition
acute or chronic hepatocellular diseases, cirrhosis, vitK def.; major liver surgery – all present with hemostasis derangements that may be characterized by defects in the clotting or fibrinolytic systems or platelet function
The hepatic parenchymal cells produce most of the factors involved in hemostasis, thus damage results in diminished production of factors involved in clotting in proportion to the parenchymal cell damage |
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Term
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Definition
acquired clinical syndrome characterized by widespread activation of coagulation resulting in formation of fibrin clots in medium and small vessels throughout the body – may lead to blockage of blood flow to organs resulting in failure; simultaneous clotting (centrally) and hemorrhage (peripherally)
-Result of increased protease activity in blood caused by unregulated release of thrombin followed by fibrin formation and accelerated fibrinolysis
-Endothelial damage is the primary initiator of DIC
- Amount of activated thrombin exceeds the body’s antithrombins and the thrombin does not remain localized
-widespread thromboses created causes widespread ischemia, infarction, and organ hypoperfusion - this happens CENTRALLY
- high mortality rate
Tx is removal of the stimulus
Sx: bleeding from IV sites, A-lines, purpura, petechiae, hematomas, symmetric cyanosis of fingers & toes |
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Term
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Definition
- From book:
arterial hypotension, shock hypoxemia, acidemia, stasis of capillary blood flow
- From BBC: systemic inflammatory response to trauma, preg related (placenta abruption, severe preeclampsia, amniotic embolism), septicemia |
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Term
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Definition
By activating the fibrinolytic system (plasmin), fibrin degradation product (FDP) & D-dimer levels will increase
Labs- low platelet count, increased clotting times, presence of FDP, coagulation inhibitors |
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Term
| Virchow Triad (not mentioned in lecutre) |
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Definition
Risk of devoloping spontaneous thrombosis r/t:
Injury to vessel(atherosclerosis, HTN, radiation, smoking, cholesterol, toxins, immunologic mechanisms)
Change in blood flow (turbulence in arteries vs stasis in vessel)
hypercoaguability of blood (thrombophilia) |
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Term
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Definition
embolism (clots that don't dissolve, break from leg & travel to lung causing pulmonary embolism)
PTS (post-thrombotic syndrome -pain, swelling, ulceration of the affected limb |
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Term
| Hemolytic Disease of the Newborn |
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Definition
- Occurs only if antigen on fetal erythrocytes differ than those on maternal erythrocytes
- present Rh antigen D are positive (higher rates in whites)
- incompatability occurs if mom n baby have diff. ABO type (20-50% of all pregs.; only 1/10 end in HDN & its rare in first fetus) OR if fetus is Rh+ and mom is Rh-
-Patho: mom has antibodies against baby erythrocytes or produce them on exposure to fetal blood; IgG may enter fetal blood & bind to sufficient #s of fetal erythrocytes to cause widespread antibody-mediated hemolysis or splenic removal
- if baby is A or B type & mom is O, HDN can occur in 1st preg. |
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Term
| HDN when Rh incompatibility |
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Definition
Anti-Rh antibodies from only in Rh+ blood is circulating in an Rh- mom
Usually occurs in first pregnancy incompatibility when the placenta detaches..concurrently these antibodies affect the next fetus if it is Rh+
IgG coated fetal erythrocytes are destroyed by phagocytes in the spleen – hemolysis proceeds then anemia - erythropoiesis accelerates in the liver and spleen – immature cells called erythroblasts (hence the name) released into bloodstream
- degree of anemia depends on time the antibody has been in fetal circulation, concentration, and ability of fetus to compensate for increased hemolysis |
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Term
| Clinical manifestations of HDN |
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Definition
-Hyperbilirubinemia occurs in newborn
-Patho effects more severe in Rh incompatibility (severe life threatening anemia, death in utero, damage to CNS, extensive hemolysis increasing the bilirubin causing brain damage) than ABO (most resolve shortly after birth)
- Death in utero as early as 17wks, gross edema called hydrops fetalis occurs
-CM: mild: healthy, slightly pale, slight enlargement of spleen and liver
Pronounced pallor, splenomegaly, hepatomegaly indicate severe anemia and can lead to cardiovascular failure or shock
-Neonatal jaundice occurs shortly after birth; without transfusion the bilirubin deposits in brain called kernicterus (cerebral damage and death –icterus gravis neonatorum)
- If they survive: MR, cerebral palsy, or high-frequency deafness |
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Term
| What is the RBC deficit seen in G6PD deficiency? |
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Definition
First, G6PD is an enzyme that normall enables erythrocytes to maintain metabolic processes despite injurious conditions
- You will see hemolytic anemia (destructed RBCs)
- Asymptomatic unless:
Erythrocyte ages (common in black males)
Pregnant women ingesting aspirin may cause hemolysis in fetus with this deficiency
Oxidative stressors damage hemoglobin and the plasma membrane of erythrocytes and interfere with other enzyme activities of the cell |
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Term
| Iron Deficiency Anemia in children |
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Definition
most common blood disorder in infancy & childhood; most in 6mo-2yo, common in menstruating females
- Patho: inadequate intake in 1st few yrs of life; blood loss in children (gi lesions, parasitic infections, or hemorrhagic disease); 1/3 of infants is caused by heat-labile proteins in cow's milk
- iron stores as hemosiderin in bone marrow and liver around 4-8wks and used up to 20wks then they need supplement
Sx: mild anemia: lethargy and lassitude usually not detectable in infants and young children who cannot describe there sx
- General irritability, decreased activity intolerance, weakness, lack of interest in play
- HgB below 5: pallor, tachycardia, and systolic murmurs
- Splenomegaly in 10-15%, sutures of skull may widen; decreased physical growth; developmental delays, pica
- Attention span, alertness, and learning ability may be affected |
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Term
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Definition
homozygous (recessive) form where there is an abnormal presence of Hb S within the erythrocytes (75-95%)
Etiology: people affected with origins from central Africa, The Near East, the Mediterranean area, and parts of India; in US most common in black
PAtho: deoxygenation is the most important variable for determining the occurrence of sickling
- very stiff, dont change shape easily therefore plug BVs causing vascular occlusion, pain & organ infarction
-Undergo hemolysis in spleen & cause blood pooling and infarction of splenic vessels
-Most sickled cells regain normal shape after reoxygenation & rehydration
- Irreversible sickling caused by irreversible plasma membrane damage caused by sickling (up to 30%)
- can also be caused by increased hydrogen ion concentration in blood (decreased pH), increased plasma osmolality, decreased plasma volume, and low temp. |
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Term
| Clinical Manifestations of sickle cell anemia |
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Definition
-Sx 1st seen @ 6-12mo
-chronic with acute exacerbations
-pallor, fatigue, jaundice, and irritability
Crisis:
Vasocclusive (thrombotic) crisis: blood flow through vessel becomes halted by tangled masses of rigid sickled cells
Aplastic crisis (prolonged anemia): transient cessation of RBC production resulting in acute anemia
Sequestration crisis (in young children): blood pooled in spleen and liver
Hyperhemolytic crisis (rare): accelerated rate of RBC destruction; anemia, jaundice, reticulocytosis
Other complications: acute chest syndrome (chest pain, fever, tachypnea, wheezing, cough); glomerular disease (protein and RBC leak into urine); cholecystitis (gallstones, RUQ pain, nausea, vomiting, elevated WBC & alkaline phosphate) |
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Term
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Definition
microcytic hypochromic anemia; inherited autosomal recessive disorders that cause impaired rate of synthesis of one of the two chains a or b of Hb A
Etiology: A-chain affected is most common in Chinese, Vietnamese, Cambodians, Laotians; B-chain affect most common in Greeks, Italians, Arabs, Sephardic Jews; Both affected is common in blacks
Patho: # of genetic defects in the controlling genes determins severity of disorder (Substitution of amino acid for another, two AA substitutions, AA deletions or fusions, and synthesis of elongated chains)
Beta (more common): B chain production decreased in B minor & severly in B major - results in reduced HgB & accumulations of free chains
Alpha: trait, minor, HgB H disease, major (fatal) |
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Term
| Clinical Manifestations and Lab results of Thalassemia |
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Definition
BT minor: usually asymptomatic; mild to moderate microcytic-hypochromic anemia, mild splenomegaly, bronze skin, hyperplasia of bone marrow, increased iron
BT major:sick form birth and prone to infection; severe anemia, high output CF, death usually caused by so many transfusions, enlargement of liver and spleen, spinal impairment, deformity in facial bones (widened)
AT trait: Sx free
AT minor: momic BT minor w/ few sx
AT major: hydrops fetalis & fulminant intrauterine CHF
Children w/ either major: weakness, failure to thrive, poor development, cardiovascular compromise with high output failure; untreated they die by age 5-6
Labs: microcytic hypochromic anemia but Hgb electrophoresis to discover that problem is in synthesis of hgb |
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Term
| Hemophilia (not discussed in lecture) |
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Definition
congenital deficiencies of plasma clotting factors VIII, IX, XI account for 90-95% of hemorrhagic bleeding disorders; 1 in 5000 male births (80-85% HemA and 10-15% HemB)
A: classic, VIII deficiency, most common, x-linked recessive inheritance, affects men & transmitted by women
B: (Christmas disease), IX deficiency, x-linked recessive, clinically indistinguishable from VIII deficiency
Severe Hemophilia: spontaneous bleeding
C: XI deficiency, autosomal recessive, = in men & women, bleeding less severe
Von willebrand disease: autosomal dominant trait, infusion of plasma causes VIII activity to increase for several days because infusion of VIII temporarily induces endogenous synthese of VIII |
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Term
| PATHO & Clinical Manifestations of Hemophilia |
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Definition
PAtho: gene deletions and point mutations dominate the inheritance defects
Both types of gene defects are associated with severe HemA, where no factor VIII is circulating in blood
Point mutations: single base in the DNA is mutated to another base
CM:bleed at different ages
- During first yr of life bleeding is uncommon but hematoma formation occurs after injection of firm holding
- By age 3-4, 90% have suffered persistent bleeding from minor injury
- Hemorrhage into elbow, knee, ankle will cause pain, limit joint movement, and predispose the child to degenerative joint changes
- Minor complications: hematuria and epistaxis
- Recurrent bleeding is a lifelong problem
- Intracranial hemorrhage and bleeding into the neck and abdomen are life threatening |
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Term
| Idiopathic thrombocytopenic purpura in children (not mentioned in lecture) |
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Definition
most common of the purpuras of childhood; disorder of platelet consumption in which antiplatelet antibodies bind to plasma membranes of platelets causing platelet sequestration & destruction by mononuclear phagocytes in spleen & other lymphoid tissue at a rate that exceeds the ability of the bone marrow to produce them
Patho: in 70% of ITP cases there is an antecedent viral disease (ex. CMV HIV EBV), suggesting viral sensitization has occurred,
- time from infection to purpura is 1-4 wks; IgG immune complexes seen on platelet surfaces
CM: bruising & petechiae rash occur with acute onset
- Asymmetric bleeding is typical, most often on legs and trunk
- Hemorrhagic bullae of gums, lips, and other mucous membranes may be prominent
- Epistaxis (nose bleeding) may be severe
- Acute phase of bleeding last 1-2 wks but thrombocytopenia persists
- Most serious complication, rare, intracranial hemorrhage |
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Term
| What test should be done when a person is suspected of having anemia? |
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Definition
CBC (RBC count, WBC count & differential and indices, and RBC distribution width)
- this test will guide what others should be done (Ex: reticulocyte count, periphereal blood smear, iron studies, Hgb electrophoresis, serum folate & serum B12 |
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Term
| What do the indices include? |
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Definition
MCV: mean corpuscular volume which is the avg. size of vol. of the RBCs & is used as the starting point in classifying an anemia
MCH: mean corpuscular hemoglobin
MCHC: mean corpuscular Hgb concentration
small: microcytic; Large: macrocytic |
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Term
| what will MCH and MCHC be in IDA? |
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Definition
low, when the defeciency is chronic
aka hypochromic |
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Term
| What are reticulocytes? If the bone marrow doesn't respond, what may be the cause? |
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Definition
they are immature RBCs and are larger than mature RBCs; during anemia the bone marrow produce more reticulocytes
If it doesnt then the anemia may be caused by aplastic anemia or pernicious anemia |
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Term
| What does a periphereal blood smear show? |
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Definition
cell size and shape
tells provider about abnormalities (that are often the most important diagnostic info) that cannot be detected by automated cell counters |
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Term
| Lab work in IDA vs. anemia of chronic disease |
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Definition
IDA: low serum iron, low serum ferritin (stores, if chronic), high Total iron binding capacity (TIBC), low transferrin saturation
Anemia of chronic disease: all will be low or normal EXCEPT ferritin is high or normal |
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Term
| Significance of serum ferritin |
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Definition
| indicator of iron stores & is most accurate diagnostic test for diagnosis of iron deficiency |
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Term
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Definition
Leukemoid reaction: premature release of immature white cells
In lab work you would see a disproportionate amount of immature leukocytes in peripheral blood smears, this would shift the distribution of cells in the blood toward those on the left side of the differentiation diagram
occurs in leukemia, infection, or inflammation |
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Term
| Reticulocyte production index tell's you what about anemia.. |
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Definition
| the actual number of reiculocytes/uL of blodd or % of reticulocytes in total red blood cell count |
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