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176 Cards in this Set
- Front
- Back
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When do you transfuse blood?
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1. When Hb gets below 7 and symptomatic
or 2. Pt has requires an increased carrying capacity (CAD, or other cardiopulmonary disease) |
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A unit of PRBC will raise Hb by this much . . .
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Hb increases by 1
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Cryoprecipitate contains. . .
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Factor VIII and fibrinogen
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Warfarin cannot be reversed with vitamin K in pts with . . .
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. . . liver failure. (they can't produce the coagulation proteins)
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1 unit of platelets raises the platelet count by . . .
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10,000
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Whole blood is used only for . . .
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massive blood loss
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for a pt with massive blood loss, the ideal ratio of platelets: FFP : PRBCs should be
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1 : 1 : 1
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INtravascular hemolysis is . .
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. . . very serious and needs IMmediate attention
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Extravascular hemolysis . . .
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Everything is ok, and no treatment is required. (Due to foreign antigen the body built up immunity to . . . Kell antigen
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What type of anemia will present with ring sideroblastic anemia?
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Microcytic
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What are the causes of ring sideroblastic anemia?
Mechanism? |
lead poisoning
pyridoxine deficiency toxic effects of alcohol Mechanism - these substances cause a defective synthesis of protoporphyrins. Iron then accumulates in the mitochondria. |
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What type of anemia is produced by liver disease?
Mechanism? |
Macrocytic anemia (MCV up to 115)
Liver disease causes an altered metabolism of plasma lipoproteins into RBC membranes, altering RBC shape (an increasing volume) |
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After noting a decreased H/H on a pt's CBC what is the next step in the work up for anemia?
Then what? |
First step is to assess volume status and hemodynamic stability. If unstable transfuse blood.
reticulocyte count (along with RBC indices eg. MCV) |
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Look at anemia chart pg 326 (Step - up to medicne)
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pg 326
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If the reticulocyte count is greater than 2 percent, what are the two possible causes of anemia?
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Blood loss
Hemolytic anemia (reticulocytes are increased due to increased production) |
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If the reticulocyte < 2% what do you examine next?
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MCV
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The most common cause of iron-deficiency anemia is . . .
The most common source is . . . . In the ederly. . . |
Blood loss
Menstrual bleeding GI blood loss if no menstration |
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Iron deficiency anemia due to dietary deficiency is seen primarily in these 3 groups. . .
Why? |
Infants - especially in being fed primarily on human milk bc human milk is low in Fe. Rapid growth increases iron requirements. This occurs mostly between 3-6 mo
Adolescents - rapid growth increases iron requirements. Pregnant Women - increased iron requirement |
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What is ferritin?
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Ferritin is an intracellular protein that stores iron and releases it in a controlled fashion. The amount of ferritin reflects the amount of iron stored. In humans, it acts as a buffer against iron deficiency and iron overload
Therefore, if iron is low ferritin will be low to prevent it from sequestering iron from the bone marrow. |
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What is transferrin?
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shuttles iron around the body to places where it is needed. Therefore it will be high in iron deficiency anemia, bc the body wants iron to go to places where it is needed most.
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What is the most reliable test for iron deficieny anemia?
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Ferritin level
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What will ferritin be in iron deficiency anemia?
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Ferritin = low = iron deficiency anemia
This is the bodys mechanism to prevent ferritin from sequestering iron in cells where it is not needed, and allows it to go to bone marrow. |
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Iron deficiency anemia, what will the happen to TIBC?
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increases
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What will happen to RDW in Fe deficiency anemia?
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High
(RDW is typically normal for other microcytic anemias) |
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What is gold standard for diagnosing Fe deficiency anemia?
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Bone marrow biopsy
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In anemia of chronic disease ferritin will be . . .
Why is iron low? Why is ferritin high? |
normal/high.
Iron is low bc it is trapped within macrophages (which are increased due to inflammation/disease). Hepcidin also reduces iron absorption Ferritin is high bc it is a defense mechanism against chronic infection. When constantly inflamed the body thinks it is infected and reduces micronutrients from feeding the perceived organism by trapping iron in cells with ferritin. |
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In anemia of chronic disease transferrin will be . . .
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low
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Thalassemia's are named for the chain that is . . .
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deficient
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Beta-thalassemia major is aka . . .
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Cooley's anemia
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What will be elevated on Hb electrophoresis with Beta-thalassemia?
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Hb F and Hb A2
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"Crew-cut" appearance is shown on skull X-ray with . . .
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Beta-thalassemia major
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peripheral blood smear may show these cells in Beta-thalassemia major.
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target cells
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What is the next step in someone who is suspected of having iron deficiency anemia, but does NOT respond to iron therapy?
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Hb electrophoresis to rule out thalassemia
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What is Hb H disease?
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sub-type of alpha thalassemia which involves deletion/mutation of three alpha thalassemia loci
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What is the treatment for sideroblastic anemia?
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Remove the offending agent
Consider pyridoxine |
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What do you NOT give in anemia of chronic disease?
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do NOT give Iron
Anemia is usually well tolerated |
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What viruses cause an aplastic anemia?
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Human parvovirus
Hep C Hep B Epstein-Barr Virus CMV Zoster HIV |
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What is the most common cause of B12 deficiency in the western hemisphere?
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Pernicious anemia
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Can a person with a normal CBC and MCV have a B12 deficiency?
What is the significance of this? |
YES, these individuals can still suffer the neurological impairements of B12 deficiency due to delayed treatment
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What parasite can cause B12 deficiency?
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Diphyllobothrium latum (fish tapeworm)
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In a person who is B12 deficient, where does the neurological damage occur?
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posterior columns
lateral corticospinal tracts spinocerebellar tracts |
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What neurologic symptoms will present in a person with neurological damage due to B12 deficiency?
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loss of position and vibratory sensation in the lower extremities
ataxia upper motor neuron signs (increased deep tendon reflexes, spasticity, weakness, Babinski sign) |
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What are the later manifestations of B12 deficiency?
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Urinary and fecal incontinence, impotence
Dementia |
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What level of B12 will be found if someone is deficient?
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<100 pg/mL
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If B12 is borderline, what other labs can you order?
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methylmalonic acid (high) and homocysteine levels(high)
antibodies against intrinsic factor Schilling test |
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What treatment is preferred for B12 deficiency?
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Parenteral therapy (IM dose once per month)
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How long will it take for folate to deplete ones body if they have inadequate intake?
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3 mo
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What is the most common cause of folate deficiency?
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"tea and toast" diet
(all dietary deficiency) |
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What lab test help determine the difference between B12 deficiency and folate deficiency?
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Homocysteine levels will be high in both,
but methylmalonic acid levels are only increased with vitamin B12 deficiency. |
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What anticonvulsant medication causes folate deficiency?
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phenytoin
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What are the two ways to classify hemolytic anemia?
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1. In relation to the RBC (intrinsic vs extrinsic)
2. In relation to the site of hemolysis (intravascular vs extravascular) |
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What is extrinsic hemolytic anemia?
Ex? |
hemoylsis due to factors external to RBC defects (most cases are acquired)
Immune mediated mechanical medications, burns, toxins |
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What is intrinsic hemolytic anemia?
Exs? |
hemolyisis occurs due to intrinsic RBC defects (inherited)
Hb Abnormaility (sickel cell, Hb C, thalassemias) Enzyme defects (G6PD deficiency, pyruvate kinase deficiency) |
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Where does extravascular hemolysis occur?
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reticuloendothelial system (spleen)
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Dark urine during hemolytic anemia suggest?
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Intravascular process
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What is Direct Coombs test?
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detects antibody or complement on RBC membrane
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If Coombs test is positive then . . .
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autoimmune hemolytic anemia
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What vitamin is needs to be repleted during hemolysis?
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Folate
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What is hand-foot syndrome (dactylitis) in context of sickle cell?
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Painful swelling of the dorsa of hands and feet seen in infancy and early childhood (4-6 months)
often the first presenting syptom caused by avascular necrosis of the metacarpal and metatarsal bones |
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What particular type of bacteria are pts without a spleen prone to?
What three in particular? What to do? |
Encapsulated organisms
1. Step pneumo 2. H. influenza 3. Neisseria Early vaccination and prophylactic PCN |
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What infectious complication and organism are pts with sickle cell prone?
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Salmonella osteomyelitis
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What are 3 medications given routinely to sickle cell pts
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1. Prophylactic PCN - for children until 6 years of age start at 4 mo
2. Folic acid supplementation (chronic hemolysis) 3. Hydroxurea - induces HbF |
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What is the inheritance pattern of G6PD deficiency?
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X-linked recessive
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What food is known to precipiate G6PD deficiency?
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Fava beans
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G6PD deficiency will produce what in RBCs?
What are they? |
Heinz bodies
denatured Hgb that precipates on the inside of RBC |
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What is the mechanism by which G6PD deficiency causes RBC destruction?
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deficiency of G6PD results in an accumulation of unneutralized peroxide, which goes on to denature Hgb. This precipiates to the inside of RBC membranes as Heinz bodies, which cause the membrane to be rigid. This rigid membrane cannot pass through the spleen causing destruction.
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What does G6PD produce are peripheral smear?
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bite cells
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What lab confirms G6PD deficiency?
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Deficient NADPH formation G6PD deficiency
Measurement of G6PD levels are dianostic |
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During a hemolytic episode G6PD may look . . .
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NORMAL . . . bc RBCs that are most deficient in G6PD have already been destroyed
repeating the test at a later date facilitates diagnosis |
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With autoimmune hemolytic anemia (AIHA), what determines the prognosis, site of RBC destruction, and response to treatment?
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The type of antibody involved . . . either IgG or IgM
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What antibody is involved with warm AIHA?
What temperature does it bind to cause AIHA? |
IgG
Binds at 37 C |
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What type of hemoylsis is involved with warm AIHA?
What is the site of hemolysis in warm AIHA? |
Extravascular
spleen (splenomegaly is a common feature) |
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What causes warm AIHA?
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Primary (idiopathic)
Secondary - results from lymphomas, leukemias, CLL, other malignancies, collagen vascular disease, and methyldopa |
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What antibody is involved with cold AIHA?
What temperature does hemolysis occur? |
IgM (MMM cold ice CreaMMM)
hemolysis (0 - 5 C) |
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What type of hemolysis is involved with cold AIHA?
What is the mechanism of cold AIHA? Where does hemolysis occur with cold AIHA? |
Intravascular
IgM results in complement activation and intravascular hemolysis the primary site of sequestration is the LIVER |
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What are the causes cold AIHA?
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idiopathic (elderly)
infection (MMMycoplasma pneumoniae or infectious MMMononucleosis) |
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What diagnostic test is used to test and determine AIHA?
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Direct Coombs Test
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With a direct coombs test, what will you see with warm AIHA?
. . . cold AIHA? |
Warm AIHA - RBCs are coated with IgG (positive direct coombs test)
Cold AIHA - if RBCs are coated with COMPLEMENT alone (Complement = Cold) |
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What might you see on a peripheral smear with warm AIHA?
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SPHEROCYTES
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What is the treatment for mild cold and warm AIHA?
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Nothing, most cases are mild and do NOT require treatment
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If warm AIHA is severe and requires treatment, what is the therapeutic approach?
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1. Glucocorticoids
2. Splenectomy - if steroirds don't work 3. Immunosuppresion - azathioprine or cyclophasphamide 4. RBC transfusions (only if necessary) 5. Folic acid supplements |
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If COLD AIHA is severe and requires treatment, what is the therapeutic approach?
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1. Avoiding cold exposure
2. RBC transfusions (only if absolutely necessary) 3. Various chemotherapeutic agents 4. STERIODS ARE NOT BENEFICIAL |
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What is Paroxysmal Nocturnal Hemoglobinuria (PNH)?
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An acquired disorder that affects hematopoietic stem cells and cells of all blood lineages
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What is the pathophysiology behind PNH?
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caused by a deficiency of anchor proteins that link complement-INactivating proteins to blood cell memebranes.
The deficieniency of this anchoring mechanism results in an unusual susceptibility to complement-mediated lysis of RBCs, WBCs, and platelets |
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What type of hemolysis occurs with PNH?
What type of anemia occurs? |
chronic INtravascular hemolysis (elevated LDH)
normochromic normocytic anemia (pancytopenia) |
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What is a potential venous complication of this disease?
What other complications may arise? |
thrombosis of the venous system. (hepatic veins - Budd Chiari syndrome)
may evolve into aplastic anemia, myelodysplasia, myelofibrosis, and acute leukemia |
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What 3 diagnostic tests are used to evaulate for PNH?
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Ham's Test
Sugar Water Test Flow cytometry |
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What is Ham's Test?
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HAM's TEST - the pt's cells are incubated in acidified serum, triggering the alternative complement pathway, resulting in lysis of PNH cells but not normal cells
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What is the Sugar Water Test?
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Sugar Water Test - pt's serum is mixed with sucrose. In PNH, hemolysis ensues.
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What does Flow cytometry look for in PNH?
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Flow cytometry looks for anchored cell surface proteins (CD-55, CD59) - much more sensitive and specific for PNH
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What is the treatment for PNH?
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1. Glucocorticoids (but many pts do not respond
2. Bone marrow transplantation |
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What is the mechanism of HIT Type 1?
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Heparin DIRECTLY causes platelet aggregation. This is seen <48 hrs after initiating heparin.
NO treatment is needed. |
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What is the mechanism of HIT Type 2?
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Heparin induces ANTI-BODY-mediated injury to platelets.
Seen 3 to 12 days after initiating heparin. Heparin should be discontinued immediately |
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Refer to platelet disorder chart chart on pg 339 of STEP-up to medicine
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Pg 339
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What is first assessed when dealing with platelet disorders?
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Is the disorder QUANTITATIVE or QUALITATIVE
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If quantitative (abnormal platelet count) what is assessed
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Is the platelet disorder a THROMBOCYTOPENIA (too low) or THROMBOCYTOSIS (too many)
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What are the three main inherited platelet disorders?
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1. vWD
2. Bernard-Soulier syndrome 3. Glanzmann's thromnASTHENIA |
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confluent petechiae are referred to as. . .
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purpura
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Unlike coagulation disorders, heavy bleeding into tissues (hematoma) and joints (hemarthroses) . . .
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is NOT seen in thrombocytopenia
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Abnormal bleeding (even after trauma or surgery) is UNUSUAL when the platelet count is . . .
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Platelets >100,000
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There is an INCREASED bleeding hemorrhage during surgery or trauma when the platelet count is . . .
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Platelets 20,000 - 70,000
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Minor spontaneous bleeding: easy bruising, petechiae, epistaxis, menorrhagia, bleeding gums starts to occur when the platelet count is . . .
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Platelets <20,000
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Major spontaneous bleeding: intracranial bleeding, heavy GI bleeding may start to occur when the platelet count is . . .
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Platelet < 5,000
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Multiple myeloma causes a dysproteinemia which causes . . .
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a normal platelet count, but the platelets are dysfunctional.
(as well as leukemia, and myeloproliferative disorders) |
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What is the mechanism for Idiopathic Thrombocytopenic Purpura?
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This results from an autoimmune antibody formation against host platelets. These antiplatelet antibodies (IgG) coat and damge platelets, whichare then removed by splenic macrophages. (reticuolendothelial synstem binds self-immunoglobins attached to the platelet).
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What are the two main forms that ITP will present, and in what population will you see them?
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ITP Acute Form - seen in children. Preceded by a viral infection (in most cases). Usually self-limited.
ITP Chronic Form - seen in adults, most commonly in women between 20 and 40 years of age. (spontaneous remissions are rare) |
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What is involved in the diagnosis of ITP?
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1. Platelet count is typically less than 20,000, which an otherwise normal CBC (peripheral smear shows decreased platelets)
2. bone marrow aspiration shows increased MEGAKARYOCYTES 3. Increased amount of IgG of platelet associated IgG |
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What is the treatment for ITP?
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1. Adrenal Corticosteroids
2. IV immune globulin - saturates the reticuloendothelial symstem binding sites for platelet-bound self-immunoglobin, so there is less platelet uptake and destruction. 3. Splenectomy 4. Platelet transfusions - for life threatening and serious hemorrhagic episodes 5. eltrombopag and romiplastim - thrombopoietin receptor agonists increases platelet production |
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What is the mechanism for TTP?
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TTP results from inhibition of the enzyme ADAMTS13, which is the enzyme that breaks down vW factor. Very large vWF multimers are more prone to lead to coagulation. Hence, without proper cleavage of vWF by ADAMTS13, coagulation occurs at a higher rate, especially in the microvasculature, part of the blood vessel system where vWF is most active due to high shear stress.[5]
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What is produced with TTP, and where are they found?
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Hyaline microthrombi (mostly platelet thrombi) occlude small vessels - any organ may be involved.
They cause mechanical damge to RBCs (producing schistocytes on peripheral smear) |
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What is HUS a comination of?
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TTP = HUS + fever + altered mental status
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What is HUS?
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HUS = microangiopathic hemolytic anemia + thrombocytopenia + renal failure
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What will the coagulation profile look like in TTP?
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There is no comsumption of clotting factors so PT and PTT are normal. Bleeding time is prolonged.
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What are the clinical features of TTP?
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1. hemolytic anemia
2. thrombocytopenia 3. acute renal failure (mild) 4. fever 5. fluctuating transient neurologic signs - can range from mental status changes to hemiplegia |
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What is the treatment for TTP?
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1. plasmapheresis (large volume) - begin as soon as diagnosis is established. (delay is treatment is life threatening
2. Corticosteroids and splenectomy 3. platelet transfusions are CONTRAINDICATED |
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Do you treat TTP with platelets?
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NEVER! Platelets are an absolute contraindication in TTP, because worsens the thrombocytopenia.
The problem is a deficiency of ADAMTS13, which results in thrombi consisting of platelts. Giving more platelets will worsen the problem. |
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Heparin induced thrombocytopenia (HIT type 2) can occur with . . .
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any amount of Heparin. Ususally unfractionated heparin
LMW heparin has a much lower risk of occurance. |
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What is the main complication with HIT (type 2)?
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DVT or PE
Look for a drop in platelets a few days after heparin administration. Platelets aggregate "clump" leading to venous thrombosis or PE. |
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HIT is suggested when the platelet cound decreases by . . .
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50% or more
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What are diagnostic tests that are used to evaluate for HIT?
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1. antiplatelet factor IV
2. serotonin release assay |
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What is the treatment for HIT?
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Stop heparin
If anticoagulation is indicated (venous thrombosis), give a thrombin inhibitor such as LEPIRUDIN |
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What is Bernard-Soulier Syndrome?
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Disorder of platelet adhesion (to SUBENDOTHELIUM) due to deficiency of platelet GLYCOPROTEIN GPIb-IX
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What is the inheritance of Bernard-Soulier Syndrome?
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Recessive
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What will you see in peripheral smear with Bernard-Sloulier syndrome?
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platelets are ABNORMALLY LARGE
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What will you see on CBC with Bernard-Sloulier syndrome?
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platelet count is mildly low
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What is Glanzmann's Thrombasthenia?
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Disorder of platelet aggregation due to deficinecy in platelet glycoprotein GPIIb-IIIa.
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What will the coagulation profile look like with Glannzman's Thrombasthenia?
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increased bleeding time.
Everything else is unchanged |
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What will CBC look like with Glanzman's Thrombasthenia?
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Platelet count is normal
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What is von Willebrand's disease (vWD)?
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disorder characterized by deficiency or defect of factor VIII-related antigen.
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What is von Willebrand's factor?
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Factor VIII (8) has two portions: the coagulant portion (factor VIII coagulant protein - Hemophilia A)
and an antigenic portion (VIII antigenic protein) - this latter protein is synonymous with vWF |
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What is the inheritance pattern of vWD?
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Autosomal Dominant
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What is the function of von Willebrand's factor?
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vWF enhances platelet aggregation and adhesion (the first step in clot formation)
It also acts as a carrier of factor VIII in blood |
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Where if vWF produced in the body?
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Edothelial cells and megakaryocytes
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What is the most common inherited bleeding disorder?
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vWD - affects 1% to 3% of population.
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What diagnostic tests will evaluate for vWD?
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1. Prolonged Bleeding time
2. Prolonged PTT (may not be) 3. reduced ristocetin-induced platelet aggregation |
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What is the tx for vWF?
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1. DDAVP (desmopressin) - induces endothelial cells to secrete vWF
(always works for type I, possibly for type 2, type 3 requries Factor VIII concentrate) |
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Is cryoprecipitate a recommended option for vWD?
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Crycoprecipitate is not recommended for vWD because it carries the risk of viral transmission
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What is hemophilia A?
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deficiency or defect of factor VIII coagulant protein
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What is the inheritance pattern of Hemophilia A?
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X-linked recessive (mostly male patients)
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What clinical features are common with hemophilia A?
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hemarthrosis (knees most common site)
Intracranial bleeding (second most common cause of death. It used to be AIDS due to transfusions) Intramuscular hematomas Retroperitoneal hematomas |
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What percentage of pts with hemophilia will have HIV?
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75% with Hemophilia A
50% with hemophilia B due to blood transfusions |
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What will the coagulation profile show for someone with hemophilia A?
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Prolonged PTT
Low factor VIII normal levels of vWF |
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What is the treatment for hemophilia A?
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Factor VIII concentrate
(Desmopression (DDAVP) is used in mild cases) |
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Is cryoprecipitate and FFP recommended to use in hemophilia A?
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No, both carry an increased risk for viral transmission
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If normal plasma is mixed with plasma from a hemophiliac pt, PTT . . .
if PTT fails to . . . . then this is diagnostic for the presence of a . . . |
(PTT) becomes normal
fails to normalize. . . diagnostic for factor VIII inhibitor |
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What is hemophilia B?
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deficiency of clotting factor IX
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What is the inheritance pattern of hemophilia B?
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X - linked recessive
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What is the treatment for hemophilia B?
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treatment involves the administration of factor IX concentates.
(DDAVP does not play a role in therapy) |
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thrombin time measures. . .
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fibrinogen concentration
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Normal PT?
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11-15 sec
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normal PTT?
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25 - 40 sec
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normal bleeding time?
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2 - 7 minutes
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If a pt has a coagulopathy that is due liver dysfunction, what coagulation times will be normal and abnormal?
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abnormal:
PT (prolonged) PTT (prolonged) normal: TT (thrombin time) fibrinogen platelets |
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If a pt has a coagulopathy that is due to vitamin K deificiency what would the coagulation profile look like?
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Abnormal:
PT (porlonged) Normal: PTT TT platelet count fibrinogen level Protein S |
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Pts on TPN are at risk for . . . .
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Vitamin K deficiency (unless added)
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Broad spectrum antibiotics put pts at risk for . . .
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vitamin K deficiency, bc gut flora activate vitamin K into a form that is usable by the body
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Vitamin K deficiency is most commonly seen in . . .
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critically ill pts (who are NPO and on antibiotics)
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What is the first lab finding in a pt who is vitamin K deficient?
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. . . PT prolongation (Factor VII has the shortest half-life of the clotting factors)
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In a pt on warfarin (or vitamin K deficient),and needs immediate treatment for a hemorrhage, they are given. . .
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FFP
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What is the mechanism for a bleeding disorder due to hypersplenism caused by liver disfunction?
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Portal HTN causes splenomegaly, which leads to thrombocytopenia
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How does cholestasis cause a bleeding disorder?
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Inhibits absorption of vitamin K in the liver
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What is antithrombin III deficiency?
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A disorder that results in a hypercoagulable state
antithrombin is an inhibitor if thrombin, so a deficiency leads to increased thrombosis |
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Will heparin be effective in treating pts with antithrombin III deficiency?
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NO, heparin needs antithrombin III to work
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What is the inheritance pattern of antithrombin III deficiency?
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Autosomal Dominant
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What does protein C do?
What is protein C deficiency? |
Protein C is an inhibitor of factors V and VIII, so a deficiency leads to unregulated fibrin synthesis
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What is the inheritance pattern of Protein C deficiency?
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Autosomal Dominant
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What is Factor V Leiden?
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Protein C can no longer inactivate factor V, leading to unregulated prothrombin activation, and thus an increase in thrombotic events.
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What are the seven inherited hypercoagulable states?
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Antithrombin III deficiency
Antiphospholipid antibody syndrome Protein C deficiency Protein S deficiency Factor V Leiden Prothrombin gene mutation Hyperhomocysteinemia |
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Pts with an inherited hypercoagualable state and 2 or more thrombotic events should be treated with warfarin . . .
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permanently
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What is the mechanism for heparin?
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Potentiates the action of antithrombin to primarily inhibit clotting factors IIa and Xa.
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What is the half life of heparin?
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1 hr
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In addition to PTT, therapeutic heparin, is monitored with . . .
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antifactor Xa levels
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What is the reversal agent for heparin?
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Protamine
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What LMWH be monitored with PT or PTT?
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No, LMWH does not affect either PT or PTT
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What is used to monitor LMWH?
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Factor Xa
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Other than HIT, what is another major SE of unfractionated heparin that is not seen with LMWH?
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osteoporosis
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