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338 Cards in this Set
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microcytic anemias, MCV<80?
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1.iron deficiency anemia (most common)
2.anemia of chornic disease 3.thalasemmias 4.sideroblastic anemia |
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Macrocytic anemia, MCV>100
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B12
folate most likley w/ an alcoholic |
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what are the nomrocytic anemias, low reticuloctye count corrected?
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1.Aplastic anemia
2.renal disease |
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normocytic anemia, corrected reticulocyte elevated
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spheroctyosis
sickle cell G6PD microangiopathic hemolytic anemia autoimmune hemolytic |
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Reticuloctye count next to complete blood count is the proper work-up of an enemia, what is a reticulocyte
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reticuloctye is immature RBC
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if you have a normocytic anemia (MCV 80-100), why is a reticulocyte count important?
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distinguishes a bone marrow from one outside the marrow-
hyerplasia is the normal response (should be greater than 3% corrected) if less then 3% corrected reticulocyte count then the bone marrow is the problem |
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VHY***
correct reticulocyte count for the degree of anemia, what is the equation? Example 15% hematocrit, retic is 9% (anything over 3 is considered high) |
hematocrit/45 * reticuloctye count
15/45 * 9 = 3 3% or greater is a good response if less a bad response |
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What does a reticulocyte look like (thats on boards)
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They contain RNA filaments because they are still making hemaglobin (looks like little black worms) takes 24 days to mature
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How do you correct the for polychromasia (very immature RBCs younger than reticuloctes)?
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divide the above question by 2
see these cells by a wrights giemsa stain |
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pateint has a 5gm hemoglobin was given 3 units of packed RBC, the next day his hemoglobin is 6 and hematocrit is 18, is this an appropriate response, why?
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NO, it should of been 8 and 24, because the patient has a bleed (MC)
for every unit of packed RBC's inc. hemaglobin 1 and hematrocrit by 3%. Note: if you multiply the Hemaglobin by 3 equals the Hct. |
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persistant ribosomes (DOTS)in a RBC are seen in?
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basophilic stippling-lead posioning
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if patient has microcytic anemia and has a increased RDW (reflects variation in the size of RBCs)?
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iron deficiency anemia
Because it develops over time |
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target cells VS spherocytes?
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Target cells are obese cells (to much membrane) so it sticks out in the middle
spherocyte - anorexic cell (have to little cell membrane) so no central pallor |
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When do you see target cells
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alcoholics and thalasemmia, sickle cells...(hemaglobinopathies)
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all of the microcytic anemias have a decrease in hemaglobin
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see a greater area of pallor
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MCHC is increased in what disease
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hereditary spherocytosis
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koilonychia is a sign of?
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iron deficiency anemia, riboflavin def...
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IRON STUDIES: define each
serum Iron serum ferritin (soluble form of iron storage) TIBC % Saturation |
iron bound to transferrin(normal about 100)
soluble iron starge protien (best overall screening test) TIBC (normal is 300) correlates w/ transferrin % saturation - serum iron/TIBC (normal is 33%) |
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what is the carrier protien of iron?
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transferrin - made in the liver
TIBC and transferrin are the same |
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what happanes when iron stores in the bone marrow are low to transferrin and TIBC?
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transferrin production by the liver increases and so does TIBC
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What happens to serum ferritin in iron deficiency anemia, anemia of chronic disease and iron overload
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dec. in iron deficiency anemia
inc. in anemia of chronic disease (macrophages make more ferretin when theres inflammation) and iron overload disease |
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What happens to serum iron if a pateint has iron deficiency anemia, ACD or iron overload disease?
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dec. in iron def. and ACD
inc. in iron overload disease |
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TIBC is directly related to?
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transferrin, when it inc. or dec. so does TIBC
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decrease in ferritin and increase in TIBC =
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Iron deficiency anemia
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Increase in ferritin and a decrease in TIBC is seen in?
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ACD and iron overload
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what is the mechanism of micocytic anemia?
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they make less hemoglobin, so the RBC's are triggered to undergo more mitoses and it causes cells to be smaller
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what is heme
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iron + protoporphyrin
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what are the different globins: A, A2 and F
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A - 2alpha, 2 beta
A2 - 2 alpha and 2 delta F- 2 alpha and 2 gamma |
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what is hemoglobin
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heme + globin
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what is MOA of iron def. anemia
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no iron...can't make heme...can't make hemoglobin...
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anemia of chronic disease MOA
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bodies assume that inflammatin is in an infection, and bugs can multiply more when there is iron...so during inflammation body stores all of the iron in macrophages (to prevent bacteria from getting it) and you can't get it out so serum iron is low but serum ferritin is eleveated. NO iron can make heme...or hemoglobin hence anemia.
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common causes of sideroblastic anemias?
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alcohol (MC but still not common) because alcohol is toxic to mitochondria...iron can then get in but can't get out.
B6 deficiency (isoniazid depletes this, B6 is an important co-factor) Lead poisioning - lead denatures Protein...especially ferrocheletase...iron can get in but not out In all of these a ringed sideroblast forms (iron deposits in mitochondria which surrounds nucleus and it can't get out) heme cannot be synthesized either. |
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what is the rate limiting rxn of heme synthesis?
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ALA synthase (B6/pryidoxine co-factor) catalyzes the rxn of succinyl-COa and glycine to form ALA (amino levulinic acid)
HEME inhibits ALA synthase as a negative feedback system |
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what is the last step in the formation of heme?
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Ferrochelastase adds iron to protoporphyrin IX to make heme
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what is the test of choice for lead poisioning?
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blood lead level
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who do we see alpha thalessemia in?
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asians and black (also sickle and G6PD)
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what is the problem in alpha thalessemia?
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problem in making alpha globin chains
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How is a patinet w/ the follwing deletions effected in alpha thalessemia:
1.one gene deletion 2.two gene deletion 3.three gene deletion 4. four gene deletion |
NOTE: four genes control alpha globin synthesis
1. no anemia - silent carrier 2. Two gene deletion - alpha thal trait (mild microcytic anemia and inc. RBC count), 3. really decreased severe anemia (form own hemaglobin, 4 beta chians called HbH disease) 4. four deletions- usually a spontaneously aboartion make there own hemaglobin (Hb barts: 4 gamma chains) |
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In what area of the world is choriocarcinoma increased?
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Far east because increased in number of spontaneous abortions as a result of alpha thalesemmia
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which of the alpha thalessmias wont show up on elctrophoresis?
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2 gene deletion because in 2 gene deletion all of the Hb types require alpha globin chains and all will be decreased together so the relative proportions will look normal on electrophoresis.
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Patient presents w/ dec. Heb A, A2 and F (normal electrophoresis) and increased RBC count, DX?
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alpha thalassemia trait
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patient has decreased iron, % saturation, and TIBC and increased serum ferritin, DX?
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Anemia of chronic disease
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what is the most common anemia of hospitalized patients?
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Anemia of chronic disease - most likley to have a chronic disease
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what is iron deficiency anemia usually caused by
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bleeding
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Defects in the synthesis of Hb (heme + globin) is what class of anemias
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microcytic anemias
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patient has dec. serum iron, ferritin, and % saturation but increased TIBC and RDW?
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iron defciency anemia
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how do you treat alpha thalessemia?
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leave them alone, they will be ok, don't give them iron
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beta thalessemia effects what population
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black, greek and itialian
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what is the pathogenesis of Beta-thal?
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decreased beta globin chain synthesis
mild-due to a DNA splicing defect severe-anemia is due to a nonsense mutation (stop codon made) normal sythesis of alpha, delta and gamma-globin chians |
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VHY***
patient has dec. in HbA, and an increas in RBC count, HbA2, HbF (seen on electrophoresis) Treatment |
Beta thalasemmia minor
treatment - just watch them, very common |
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If a patient has no HbA, and increased HbA2, and F what is the DX?
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beta thal major
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where do you get lead posioning from?
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paint and batteries
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Patient presents w/ abdominal colic and diarrhea, and foot drop On peripheral blood smear you see a coarse basophilic stippling what is the DX
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Pb posioning, the ribosomes cannot be degrded and persist
the foot drop is from peripharal neuropathy cause by the iron |
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where does lead deposit in the body in children?
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the epiphyses and causes growth retardation
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what are the causes of iron deficiency anemia, easiest to understand by age group:
1. prematurity 2. newborns 3. Women under 50 4. Men under 50 5. Men and women over 50 |
p- because every day not in utero it is losing iron, they all must be given supplements
newborn - MCC is bleeding from meckels diverticulum W-menorrahagia (polyp, pregnancy...) M-peptic ulcer (probalby duodenal) MandN -colon cancer |
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A cousre basophilic stippling is seen in? what are they?
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Lead posioning and it denatures ribonuclease that break downs ribosomes so they persist
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Little guy lives in a poor area and is eating paint from off the wall, they have cerebral edema (maybe convulsions), pain in there abdomnen and severe microcytic anemia, DX?
How would you confirm your diagnosis? |
Lead posioning
Test the blood for lead (to confirm B6 or alcoholic induced microcytic anemia you have to do a bone marrow to find a sideroblast) |
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why does cerebral edema result form lead posioning?
what about the abdominal pain |
increase in delta aminolevulinic acid (back up prodcut from heme synthesis) which increases vessel permeability damages neurons and causes demyelination
abdominal pain - lead is actually visible in the GI tract on flate plate (plain film of the abdomen)irritates the GI tract |
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A guy is at work in the automible factory and gets intense abdominal pain, diarrhea and develops a microcytic anemia,DX?
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pb posioning
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guy who makes alcohol in an old radiator (moonshining) and develops severe abdominal pain, diarrhea and microcytic anemia, DX?
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Pb posioning
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A pottery painter presents w/ severe abdominal pain and microcytic anemia?
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Pb posioning
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what are some of the other symptoms that adults can get w/ Pb posioning?
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peripheral neuropathies (foot drop...)
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patient has high serum iron, low TIBC, high serum ferritin, high % sat Dx?
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Iron overload states - sideroblastic anemia is considered iron overload
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what do the iron studies look like for a patient w/ a thalassemia?
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they are normal
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Why is TIBC low in anemia of chronic disease
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because ferritin stores are high, just can't get it out so transferrin is not made which = TIBC so it is low.
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Cobalamin is another name for
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B12
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what is the pathogenesis of macrocytic anemias?
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Impairs DNA synthesis...delayted nuclear maturation (the cell gets big while it is waiting), big cells are called megaloblasts
affects all rapildly dividng cells, RBCs, leukocytes, platelets and intestinal epithelium methyltetrahydrofolate |
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What do vitamin B12 and folate do in DNA synthesis
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B12 removes the methyl group from methyltetrahydrofolate (circulating form of folate) creating
1. methyl-B12 which transfers the methyl group to homocysteine making methionine. 2.Tetrahydrofolate (FH4)...this starts off the cycle for formation into DNA |
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VHY***
So what lab value would you expect to be elevated in B12 and especially folate deficiency? what can this cause |
HOMOCYSTEINE - not converted to methionine
homocysteine damages endothelial cells leading to vessel thrombosis including MI. |
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Most common cause of increased serum homocysteine
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Folate (MC) then B12
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What does methionine do?
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it is involved in one carbon group transfers
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Dihydrofolate reductase conversts Dihydrofoalte (reduced form) back to tetrahydrofolate so it can be used in DNA synthesis again, what drug blocks this step?
what will this cause |
Methotrexate
trimethoprim-sulfamethaxazole will lead to a megalobastic anemia |
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what vitamin is inovled in breaking down the end prodcut of odd chain fatty acids (propinoly CoA so that methylmalonyl CoA can become succinyl CoA and be incorportated into the TCA cycle)?
What lab do you order to tes for this? If this vitamin is not present what happens |
Vitamin B12 (co-factor for methylmalonyl mutase)
Methylmalonic acid (derived from methylmalanoyl CoA), most sensitive test for B12 deficiency see neurologic problems (dorsal route; loss of proprioreception) in B12 def. because you can't make myelin (propinoyl CoA replaces acetyl CoA in neuronal membranes causing demylination) |
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What can you not correct in a B12 deficiency anemia?
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neruologic problems once they have ocurred
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THymidylate synthase is another important enzyme used in the production of DNA, what drug inhibits it?
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5-Flurouracil
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If you are working up dementia what should you always test these patients for
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TSH and B12 because these are reversible causes of dementia
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Where does B12 come from?
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animals
ovolactovegan - they take in animal milk and they don't need B12 supplements like a pure vegan does |
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describe how B12 is metabolized starting at the mouth.
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R factor in the mouth binds to B12 to protect in from being degraded by acid in the stomach
then in the stomach intrinsic factor is made by the parital cells. (located in the body and the fundus)they also make acid Then the B12-R complex is cleaved in the stomach by enzymes released from the pancreas so that intrinsic factor can bind B12-intrinsic factor complex then travels to the terminal ileum where it is reabsorbed |
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VHY***
What things happen in the terminal ileum? |
receptors for intrinsic factor and bile salts are reabsorbed there
crohns disease also frequently ocurrs there |
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MCC of B12 deficiency
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pernicious anemia-autoantibodies against parietal cells (of the body and funds) and intrinsic factor...
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What are the findings of pernicious anemia?
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Achlorhydria (loss of gastric acid) due to destruction of perietal cells...predispose you to cancer
chronic atrophic gastritis (increased incedence of gastric adenocarcinoma |
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what are the causes of B12 deficeincy?
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1. pernicious anemia
2. bacterial overgrowth (when there is stasis bacteria grow and eat b12 and bile salts) 3.terminal ileum disease (crohns) 4.pure vegan 5. chronic pancreatitis (alcoholic) 6. Fish tape worm from fish in michigan diphyllobothrium latum (eats B12)*****always on the test. |
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MCC of folate deficeincy?
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alcohol - blocks the reabsorption of monoglutamate
Remeber folate is not stored very long B12 is for years |
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what is the most sensitive test for B12 deficiency?
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increased methylmalonic acid
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where do you get folate from?
How is it absrobed? |
plants and animals
converted to monoglutamtes by intestinal conjugase so it can be absorbed. once absorbed converted to methyltetrahydrofolate (circulating form of folate) |
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A patient is taking drug for seizures and develops a macrocytic anemia w/ hypersegmented neutrophils but there neurological exam is normal what is the drug?
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phenytoin - blocks the intestinal conjugase causing folate deficiency
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What blocks monoglutamate (intestinal absorption form of folate) from being absorbed?
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Alcohol and oral contraceptives
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On peripheral smear you see hypersegmented neutrophil (more than 5 lobes), DX
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macrocytic anemia B12 or folate deficiency if no neurologic problems then B12 problem if its a boards question
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What is the romberg test?
what does it mean |
patient is standing w/ arms out and then they close there eyes, they fall over because loss of proprioreception (posterior column)
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What is a shilling test used For?
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defines the causes of B12 deficiency
Administer radioactive B12 |
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What do the following findings mean:
Shilling test is preformed and patient pies out a lot or radioactive B12? |
dietary deficiency of B12 (pure vegan)
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What do the following findings mean:
Shilling test is preformed w/ intrinisic factor and radioactive B12 appears in the urine? |
Pernicious anemia w/ a lack of IF
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What do the following findings mean:
Shilling test is preformed w/ antibiotics? |
overgrowth of bacteria causing destruction of B12
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What do the following findings mean:
Shilling test is preformed w/ pancreatic extract? |
chronic pancreatic disease w/ lack of enzymes to cleave off R-binder and make B12 available
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what is the best indicator of folate stors?
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RBC folate (not stored very long)
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what are the different causes of normocytic anemia w/ a corrected reticulocyte count below 3%?
So the bone marrow is not responding. |
1. Blood loss less than a week(bone marrow has not had time to respond)
2.early iron deficiency anemia 3. Aplastic anemia 4. Chronic renal failure (CRF) (dec. EPO most common cause) 5. cancer |
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Patient presents w/ fever, neutropenia, bleeding, and fatigue...lab values show pancytopenia, DX?
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aplatic crisis
hypocellular bone marrow |
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What are the main causes of aplastic anemia
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MOST cases are idiopathic
DURGS (MCC) infection: Hepatitis C, Parvovirus (destruction of just RBC's usually) radiation |
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what are the signs of volume depletion?
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decreased blood pressure but increased pulse
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what is the most common cause of anemia associated w/ chronic renal failure?
how do you treat them what might you see on peripheral smear? |
dereased synthesis of EPO
Treat w/ EPO simple burr cells (RBCs w/ an undulating membrane) |
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what are the mechanisms of hemolysis
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can kill it intravascularly (inside the blood vessel)
extravasulcar hemolysis-outside the blood vessel (macrophage destruction) |
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what are the causes of extravascular hemolysis?
what labratory signs point to this? |
IgG or C3b on surface-autoimmune hemolysis
abnormal shape (sickle cells or spherocytosis) jaundice (increased unconjugated bilirubin), but none in the urine because Macrophages spit out unconjugated RBCs |
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what is the end product of macrophage destruction of RBCs
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unconjugated RBC
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Normocytic anemias: w/ corrected reticulocyte counts above 3% are caused by?
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hemolytic anemias w/ defectes inside the RBCs (intrinsic) or w/o the RBC (extrinsic)
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what causes intrinsic hemolysis?
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1.enzyme deficiency (G6PD)
2.mechanical damage (calcified aortic valve) 3.complement destruction -IgM hemolysis, punches holes and destroys it |
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VHY***
what 2 lab values point to intravascular hemolysis? |
1.decreased serum haptoglobin (combines w/ hemoglobin and is not detected when it combines)
hemoglobinuria-hemoglbin is released when RBC is destroyed and it gets in blood and urine don't usually get jaundiced |
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most common intrinsic RBC defects (3), they have normocytic anemia w/ a corrected reticulocyte count greater than 3%?
HINT: the problem is not w/ the marrow thats why the corrected reticuloctye count is normal. |
MAD is the Pneumonic:
M-membrane defect (sphercocytosis) A-abnormal hemoglobin (hemaglobinopathies) D-deficeincy enzyme (G6PD) |
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AD disease, splenomegaly, jaundice, gallbladder (calcium bilirubinate anemia)disease and peripheral smear shows RBCs w/ loss of central pallor
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hereditary spherocytosis
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what is the diagnostic test for herdeitary spherocytosis?
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osmotic fragility test (to little membrane)membrane allows water and salt in and in cells rupture in mildly hypotonic salt solutions
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what is the treatment for Hereditary spherocytosis?
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Splenectomy
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what is the defect in hereditary spheroctyosis
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mutation in ankyrin or spectrin in the cell membrane
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what can cause an aplastic crisis in children w/ spherocytosis?
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infection w/ parvovirus B19
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black individual w/ microhematuria, what is the frist step in working them up?
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sickle cell screen
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SICKLE CELL DISEASE VHY***
what is the inheritance of sickle cell anemia? |
AR
most common hemaglobinopathy in adults |
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Does the heterozygote HbAS have anemia?
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NO only the homozygote HbSS
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What type of defect and hemolysis do sickle cell patients have?
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Intrinsic defect
Extravascular hemolysis |
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what is the pathogenesis of sickle cell anemia
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sustitution of valine for glutamic acid at the 6th position of B-globin chain
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what causes sickling in sickle cell patients?
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increase in HbS (greater than 60%), they aggregate and polymerize into long needle like fibers and assume the shape we see on peripheral blood
Increase in deoxyhemoglobin |
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At what age do you start to see sickle cell disease, why?
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5-6 months because HbF protects them
hydroxyurea increases the synthesis of HbF |
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What are the key pathologic processes in HbSS?
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1.severe hemolytic anemia
2.vaso-occlusive crisis-causes ischemia and pain |
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what is the most common presentation of sickle cells anemia in infants
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Dactylitis
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How can you tell that the patient has a non-functioning spleen at a 2 yrs of age?
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Howell jolly bodies**(nucleus remnant) - if the spleen were working then the macrophages would of taken it out
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VHY***
sickle cell patients w/o a spleen are likley to get what type of infections? |
streptococcus pneumoniae sepsis and salmonella paratyphi osteomyelitis (remember staph A is the usual cause)
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most common cause of death in a little dude w/ sickle cell anemia
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Strep. penumoniae sepsis
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Sickle cell smear and howell jolli bodies on a smear, what does it mean.
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spleen is disfunctional
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when would you see dactylitis
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after 6-9 months is when they have high enough concentrations of HbS...before HbF inhibits sickling
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what usually destroys salmonella in sickle cell patients?
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splenic macrophages
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what is the most common cause of death in a sickle cell adults?
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acute Chest syndrome-vaso oclussive polumonary capillaries, chest pain, lung infiltrates and hypoxemia
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what is the inheritance of G6PD def.
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sex-linked recessive (most enzyme def.)
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VHY***
what is the most common enzyme deficency causing hemolysis? |
G6PD
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what is the problem in G6PD?
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decresed synthesis of NADPH and glutathione so you can't neutralize peroxide...this damages Hb (heinz bodies) and damages the RBC membrane resulting in intravascular hemolysis (intrinsic defect as well)
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VHY***ON EVERY TEST
what would cause so much peroxide to be produced that you would damge RBC's in G6PD deficeincy? |
1. infection
2. drugs (primaquine**,DAPSONE**(used to treat leprosy)) Fava beans can also percipitate it |
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VHY****
Medical missionary going to africa does not develop malaria but later developed a hemolytic anemia, what drug caused this, what is the diagnosis? |
Primaquine
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who gets G6PD (group of people)
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black, greek and itialian
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how is the diagnosis of G6PD made
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never enzyme essay during an acut hemolytic episode.
specail stain to identify heinz bodies then enzyme essay later to confirm |
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what is the most common autoimmune hemolytic anemia, and what is the most common cause of this?
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Autoimmue warm type (IgG) and Lupus is the most common cause will have IgG and C3b on the RBC - extravascular hemolysis (macrophages get ride of them)
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How can you tell that a RBC cell is coated w/ IgG and C3b, in other words TEST OF choice for autoimmune hemolytic anemia
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DIRECT COOMBS TEST (DAT)- test for those ON RBCs ONLY
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Indirect coombs, when is it used?
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when looking for antibody in the serum
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What is the second most common cause of autoimmune hemolytic anemia
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drugs
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VHY**ON EVERY BOARD
what are the 3 drugs that cause autoimmune hemolytic anemia, what is the mechanims of each? |
Penicillin - little piece of penicillin attaches to RBC and IgG attaches to it and eaten in spleen (extravascular hemolysis)
methyldopa- alters Rh antigen, so you make antibodies against your own Rh antigens...then removed in spleen Quinidine - acts as hapten and IgM attaches to drug and forms a complex and fixes complement (intravascular hemolysis) |
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Person is on penicillin develops rash what type of hypersensitivity?
Differen person develops hemolytic anemia, what type of hypersensitivity? |
Type I
Type II |
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what are the anti-hypertensive drugs that can be used in women and what are there complications?
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methyldopa - autoimmiune hemolytic anemia
Hydralazine - drug induced lupus |
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VHY***
what type of Hypersensitivity do you see w/ each of the drug induced automimmune hemolytic anemias? |
Pencillin - type II
methyldopa - Type II Quinidine - Type III |
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VHY***ON EVERY BOARD
patient has a systolic injection murmur, increased PMI, increases on inspiration and the following CBC: low MCV, fragmented RBCC... what happen? |
microangiopathic hemolytic anemia from aortic stenosis
low MCV is from it being chronic and they got iron deficeincy anemia as well |
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what are some other causes of of microangiopathic hemolytic anemia?
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DIC, HUS and TTP
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what is the most common cause of macroangiopathic hemolytic anemia (MHA)?
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aortic stenosis
prothestic heart valves can also cause this |
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schistocytes result from...?
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MHA
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VHY****
Rings formed in RBC, DX? what are the symptoms seen |
plasmodium falciparum, produce hemolytic anemia causing fever spikes
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VHY****
who do you usually see leukemoid reactions in? |
KIds...
WHooping cough pertusis will usually cause (tons of lymphocytes) |
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what is a leukomoid rxn
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exagerated response to an infection, usually WBC above 50,00/0uL.
May involve Neuts, lymphs or eosinophils |
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atypical lymphocytes are seen in what infections
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CMV,
taxoplasmosis, any cause of hepatitis, phenytoin OF COURES MONO |
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Patient presents w/ fatigue, tonsillits, hepatosplenomegaly and generalized lymphadenopathy what is the diagnosis?
what should this patient avoid |
infectious mono (epstein barr virus)
contact sports can casue the spleen to rupture |
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what are the important features of epstien barr virus?
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Attaches to B cells via the CD21 receptor
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VHY**
How do you test for Mono: fatigue, tonsillitis, hepatosplenomegaly, lymphadenopathy, rash w/ ampicillin and increased serum transaminase from hepatitis. |
monospot test - is a heterophile (hetero-diff, phile-loving)antibody test...IgM antibodies directed against horse, sheep and bovine RBC
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what is the king WBC of chronic infections: RA, crohns, lupus...
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Macrophages
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What type of hypersensitivity is eosinophilia?
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Type 1 hypersensitivity rxn
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What are some examples of eosinophilia or type I hypersensitivity
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bronchial asthma
rash to penicillin hay fever Invasive helmnith infections (strongyloidiasis, hookworm infection...) polyarteritis nodosa and addisons disease (no cortisol) |
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people taking creatine supplments have what elevated in there serum, but BUN are normal in a patient that is a body builder?
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taking creatine supplements
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COmmon board question?
DO pin worms or amebiasis infections cause eosinophilia |
No they are non-invasive so no rxn
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IN a nut shell eosinophilia is what type of hypersensitivity and what are the two big causes of it?
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Invasive helminths and hypocortisolism
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RBC count is the number or RBCs that you have per volume.
The RBC mass the total number of RBCs in your total body. SO if you run and become volume depleted what will happen to RBC count and RBC mass? |
RBC count will go up because volume depleted but RBC mass is normal (body is not making more RBCs)
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Patient has a decrease in RBC count but RBC mass is normal, DX?
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Relative polycythemia (MC of the polycythemias) just a loss of plasma volume
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IF absolute increase in RBCs mass, when is this appropriate.
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tissue hypoxia (lung disease, COPD, high alttitudes)
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When is absolute increase in RBC mass not appropriate
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1. polycythemia rubra vera - stem cell disease in the marrow (no longer respond to checks and balances, neoplastic disease)
2. Tumor or cyts w/ excess production of EPO (renal cell carcinoma) |
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What are the myeloproliferative diseases (4)
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Polycythemia vera
chronic myelogenous leukemia myeloid metaplasia w/ myelofibrosis essential thrombocythemia - stem cell that makes platlets goes crazy. |
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what are the 4 Hs of polycythemia vera.
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HYPERVISCOSITY
Hypervolemia (only polycythemia that increases plasma volume) Histinemia (because inc. in all cell types including basophils and mast cells(found in the skin)) Hyperuricemia - because more cells are undergoing purine metabolism |
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How do you treat polycythemia vera
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phlebotomy - want to make them iron deficient to reduce making RBCs
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What is the major complication associated w/ hyperviscosity?
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inc. peripheral resistance...inc. risk of thrombosis (anywhere)...which is what people die of w/ polycythemia
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what is the most common cause of budd chiari syndrome?
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polycythemia vera - thrombosis of the hepatic vein.
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When a patient takes a hot shower they itch all over their body, DX
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polycythemia vera - from inc. release of histamine from inc. in mast cells in the skin.
NOTE: Patient who has severe jaundice can also get generalized itching |
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when treating cancer patientw w/ chemo durgs what should you give the patient to prevent renal failure?
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Allopurinol-blocks the breakdown of purines and scince you will kill a ton of cell uric acid would go way up and could destroy your kidneys
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what are the levels of RBC mass, EPO Oxygen sat and plasma volume in polycythemia vera?
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RBC mass - elevated
EPO - decreased (got plenty of oxygen and RBCs) O2 sat - normal Plasma volume - increased |
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what are the levels of RBC mass, EPO Oxygen sat and plasma volume in the following cases: COPD, high altittude or tetralogy of flow
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RBC mass high
plasma volume - normal O2 sat - low EPO - high |
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what are the levels of RBC mass, EPO Oxygen sat and plasma volume in relative polycythemia?
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RBC mass - normal
Plasma volume - low o2 sat - normal EPO - Normal |
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what are the levels of RBC mass, EPO Oxygen sat and plasma volume in renal cell carcimoa or hepatocellular carcinoma
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RBC mass - elevated
O2 sat - normal plasma volume - normal EPO - elevated |
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VHY***KNOW THIS
Features of leukemias: lymphadenopathy, hepatosplenomegaly, abnormal cells in the peripheral blood, always have anemia (usually normocytic), usually thrombocytopenia, and usually inc. in WBC count. what are the age brackets of the diffenet leukemias, w/ the above scernario, DX. |
0-14 - ALL
15-39-AML (myleoblast w/ auer rod) 40-59 (AML and CML seperate by bone marrow) geater than 60 - CLL (MC overall) |
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what seperates acute from chronic leukemia
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<30% - chronic
>30% acute |
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VHY***
what is the most common cause of generalized non-tender lymphadenopathy? |
CLL
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VHY***
what test do you get to confim CML |
philadelphia chromosome test t(9:22) abl chromosome 22
leukocyte alkaline phosphatase stain - neoplastic cells don't have it so they don't stain, it will be low |
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IF you see tear drop cells and the patient has a big spleen what is the dx?
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Agnogenic myeloid dysplasia (myelodysplastic syndrome)
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most common cancer in kids
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ALL
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what is the most common type of ALL and what are the positive marker studies thaty you need to know about it?
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Ealry pre-B-cell ALL
CD10 and CALLA positive |
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Most common cause of death in CLL
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infection caused by hypogammablobulinemia-(non-functional)
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What is the stain used to ID hairy cell leukemia
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TRAP-tartate reistant acid phosphatase
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Which leukemia infiltrates the gums
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AML - M5
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which of the leukemias is most common for producing DIC?
What is the treatment, how does it work what is the translocation. |
M3-acute promyelocytic leukemia (numerous Auer rods)
t(15:17) translocation treat w/ retinoic acid (vit A) causes blasts to mature into benign cells |
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If you have a lymphadenopathy that hurts it is never?
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malignant, because those are inflammatory rxns
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if non-tender lymphadenopathy it is?
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Cancer
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Generalied Vs local lymphadenopathy
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Gen - systemic disease or cancer (lupus, HIV,
Local (exudative tonsilitis, breast cancer) |
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what area of a lymph node will be absent in brutons A gammaglobulinemia?
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germinal follicles because thats where B cells are and they are gone
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what part of the lymph node will be gone in diGeorge syndrome?
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Paratrabeculae because thats T-cell area (specifically paracortex)
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hisotcytosis X (handcshullerchristen, or letterer sieva disease) what part of the lymph node would be reacting?
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Sinsuses
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IF you had SCID what areas of the germinal follicle would be present and which would be abscent?
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combined B and T cell deficeincy so only sinuses would be present
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What would you see in the lymph node w/ follicular hyperplasia, like in SLE, RA and early stages of HIV
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prominent germinal follicles
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patient has granulomatous microabsceses in regional lymph nodes from being scratched by a cat, what is the cause
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bartonella Henselae
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what is the most common malignant lymphoma?
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Non-Hodgins lymphomas; follicular lymphoma is the most common subtype, B cell origin t(14;18) translocation, causing overexpression of BCL2 antiapoptosis gene
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what two tissues are resistant to invasion by cancer?
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cartilage and elastic tissue
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what is the proto-oncogene in brukitts lymphoma and the translocation
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myc oncogene and t(8;14)
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what do you see on hisotology w/ burkitts lymphoma (non-hodgikns lymphoma?
where does this cancer effect |
starry sky appearnce - neoplastic B cells are the dark of night and the macrophages are the stars
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What is the neoplastic cell in mycosis fungoides, what areas does it involve?
what is it called when the malignant cells are in the peripheral blood |
Helper T cells (CD4 TH cells)
begins in the skin and progresses to the lymph nodes and other orgnas sezary's syndrome |
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what bacteria has a terminal spore so it kind of looks llike a tennis racket.
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clostridium tetani (close to tenis)
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A bribeck granule in a histiocyte looks like a _____on EM
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tennis racket
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Fever night sweats, weakness, and weight loss, reedsternburg cells (cell w/ owl eyes), what is the malignant cell?
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Hodgkins lymphoma - the reedsternburg cell is the malignant cell if it were the lymphoctes (which are all benign) then it would be a non-hodgkins lymphoma
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what is the most common cancer of lymph nodes?
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1.metastisis
2.most common primary is Non-hodgikns lymphoam (follicular |
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VHY***
Women presents w/ non-painful lymph node (above the diaphram; e.g. supraclavicular or neck...) and a mass in the anterior mediastinum the 2nd is above the diaphram, DX? CLASSICAL CASE |
nodular sclerosing hodgkins lymphoma
reedsternburg cell (malignant cell) |
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polyclonal gammaopathy what does it mean?
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many benign plasma cells are making antiboides in a chronic situation.
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what is the most abundant immunoglobulin
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GAMmma- order of abundance
G-IgG most abundant A- IgA M-IgM |
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What does monoclonal gammanopathy mean?
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almost always means malignancy of plasma cells all of the other plasma cell are suppressed.
usually IgG is whats made |
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VHY***
elderly women coughs and develops severe pain in her chest, she comes and has a fracture or her ribs, Diagnosis? |
Multiple myeloma
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Important things to know about multiple myeloma?
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Bone findings - lytic lesion (vertebral column most common), pathologic fractures and hypercalcemia
M-spike on serum protein eletrophoresis usually due to IGg kappa you can find bence joints protiens in the urine (light chains) |
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ON EM what do you see sheets of in a normal plasma cells
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SHEETS OF RER around the nucleus
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what things can be converted to amyloid?(beta pleated sheets)
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pre-albumin
calcitonin light chains in multiple myeloma Trisomy 21 (chromosomes 21 codes for beta amyloid) |
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what does beta amyloid do to neurons?
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toxic- causes you to loose neurons
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VHY*****ON EVERY TEST
Patient dies at age 40 and reveals atrophy in the brian , senile plaques in frontal and temporal lobes,who was the patient? |
down syndrome patient they either die of cardiac defects as kid or get alzhiemers from excess beta amyloid.
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Macrophage has wrinkled cytoplasm appearnce and have a build up of Glucocerebroside what is the diagnosis?
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guachers disease (AR), lysosomal storage disease
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Macrophage has bubbles in cytoplasm and severe mental retardation and a build up sphingomyelin in the lysosomes, dx
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Niemann Picks disease, lysosomal storage disease
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what's the the only glycogen stoarge disease that is lysosomal storage?
How do they die? |
Pompes - they can't break down glycogen and builds up...excess glycogen in the heart and they die
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why don't we form clots in our small arteries normally?
4 different things what are the small arteries |
small arteries - aterioles venules and capillaries
Heparin enhances anti-thrombin III (made in the liver) and neutralizes the coagulation factors PGI2-vasodilates (flow to fast for coagulation), inhibits platelet aggregation Protien C and S (vit K dependent)...inactivate V and VIII and enhane fibrinolysis. tissue plasminogen activator - activates plasminogen to release plamsin |
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what is the deadly combo that can cause women to clot?
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smoking and birth control pills
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what causes bleeding to stop when we cut small arteries
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when you cut a vessel tissue thromboplastin** is released starts the coagulation system
exposed collagen factor XII is activated (intrinsic system is started)... when endothelial cells are damaed they expose vWF*** platlets have a receptor for this and stick. when platelet sticks it releases ADP***...potent aggregator to allow more platlets to come and stick together (release rxn). Once the platlet sticks it makes and releases thromboxane A2 (only cell that has thromboxane synthase...makes TXA2 from PGH2) |
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what is the main use of bleeding time
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test platlets only*** usually 7-9 minutes
formation of the temporary platlet plug. |
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what are the three functions of thromboxane A2
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vasoconstrictor - slows the rate of blood flow so they don't get washed away
Bronchoconstictor platelet aggregator |
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what cell is analgous to function of the platlet: release rxn and then formation of its own factors?
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Mast cells
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what inhibits the precursor PGH2 for the sythesis of thromboxane A2 by binding to platlet cycloxygenase irreversibly not in other cells?
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Apspirin-prevents platlet aggregation
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what is the platelt plug
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it is temporary clot that stops bleeding (platlets stuck together by fibrinogen)
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what causes increased bleeding time?
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thrombocytopenia
Von willebrands disease (most common genetic disease, AD disease) Aspririn - most common cause of prolonged bleeding time |
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Dipyramidol blocks?
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thromboxane A2
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How do other non-steroidal anti-inflammatories differ from Apirin in how they block cycloxygenase?
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reversible takes about 48hrs
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how does the platlet plug become more stable?
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thrombin converts the fibrinogen to become fibrin and makes the platelet plug more stable and you can;t disloage it.
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what breaks down the platlet plug
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plasmin
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petechiae, epistaxis, ecchymosis, superficial bleeding are all sympotoms of? what test is elevated
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platlet disorders...you don't see these w/ coagulation disorders...its because you cant' form temporary platlet plugs...
bleeding time is increased |
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Hemophilia A is a deficiency of what factor, what are the symptoms?
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factor VIII:C
late bleeding, bleeding into joints... |
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hemarthrosis and bleeding into closed spaces, GI bleeds are seen w/ what type of bleeding problem
|
coagulation problem
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what is the most sensitive test for von willebrands disease
|
ristocetin co-factor essay
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what is platlet count
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platlet number (just because you have a normal number dosnt' mean they work)
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bleeding time is good to test for?
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platlet function
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Patient w/ OA had chronic headaches, and went in for transurethral resection and after the surgery they couldn't stop the bleedingeeding, his PTT, PT and platlet count are normal, what is going on and what is the treatment?
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Platelets don't work the patient has been on Asprin (inhibiting the function of the platlets) for OA.
Treat by giving them platlet pack transfusion because these platlets work. |
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extrnisic system has factor?
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VII
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what are the important factors of the intrinsic system
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XII, XI, IX and VIII
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what does PT test
|
VII, X, V, II (prothrmbin) and I (fibrinogen)
evaluates extrinisic system |
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PTT test for what
|
evaluates intrinsic sytem
XII, XI, IX, VIII, X, V, II and I all the way down to the clot |
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Protime (PT) is prolonged but PTT was normal what is the defect?
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VII is defective
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VHY***
PTT is prolonged and PT is normal, what is defective PLAY ODDS? |
hemophilia A factor VIII deficeincy, it is the most common coagulation disorder.
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VHY***
what is the PT and PTT of a patient w/ on warfarin? |
decreased but PT is better monitor because warfarin inhibits vitamin K dependent factors and factor VII is one of them and it has the shortest half life of the coagulation factors. (remember warfarin does not work on already synthesized coagulation factors, hald to wait for the current ones to be depeleted to start seeing its effects)
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What does tissue thromboplastin activate
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factor VII in teh extrinisic coagulation system
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what is the final common pathway of the extrinisic and intrinsic system?
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X to fibrin clot
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VHY***
what factors does warfarin inhibit |
II, XII, IX and X - the Vitamin K dependent facotrs
note: warfarin inhibits epoxide reductase |
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VHY***
what does anti thrombin III inhibit, (Heparin enhances this)? |
IX, X, XI, XII, II and VII
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VHY***
what do you evaulate when a patient is on Heparin |
PTT, PT is down to but PTT is better in following heparin because more of the factors that are inhibited are covered.
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Fibrinolytic system, what does plasmin do?
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breaks down stuff but leaves crumbs.
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VHY***
what is the single best test for DIC? |
D-dimer -detects fragments of cross-linked fibrin monomers (so proves fibrin was present) a clot was formed.
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What cross-links insouble fibrin monomers?
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Factor XIII - helping to stabalize the clot
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VHY
picture of the back of the hands of an old person what are they? when would this be an abnormal finding? |
senile purpura - as our skin thins the area of our bodies that hit things get eccymosis (unstable blood vessels), it is age dependent and normal
buttocks... |
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VHY***
patient has little red dots on tongue, fingers, lips and in the GI tract (they are all little telangiectasias)and they have iron deficiency, DX? |
osler weber rendu syndrome (hereditary telengiectasia)..iron deficient from bleeding from the telangiectasias
most common genetic vascular disorder |
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Epistaxis (MC), petechiae and ecchymosis and bleeding from superficial scratches are all signs of?
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platlet dysfunction
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VHY**
12 yr old kid w/ upper respiratory respiratory infection 1 week ago, now presents w/ epistaxis and lesions, you press on them and they don't blanch, they also have a platlet count of 220,000 DX, and pathogenesis? |
ITP-Idiopathic thrombocytopenic purpura (most common childhood cause of thrombocytopenia) usually after a upper-respiratory tract infection
IgG antibody against platlet and macrophages remove platlets from the spleen NOTE:Type II hypersensitivity |
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How can you tell a telangiectasia from a petechiae on physical exam
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telangiectasias blanch because they are AV fistuals.
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how do you treat sever ITP
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coritcosteroids
if mild just watch em' |
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women w/ positive Sm antibody test and has epistaxis, petechiae, splenomegaly and generalized tender lymphadenopthy
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SLE w/ ITP (same mechanism as the boy in the above question)
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What is the basic pathogeneis behind HUS and TTP?
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Nothing to do w/ coagulation factors (so TP AND TTP)
something in the plasma damages the small vessels throughout the body and get firm platlet plugs throughout the body...use up all of the platlets...can bleed...the RBC smash into these platlet plugs and get microangiopathic hemolytic anemia producing shistocytes. |
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what is the pentad of TTP
|
Fever, thrombocytopenia, renal failure(because platelt plugs in glomeruli as well), microangiopathic hemolytic anemia w/ shistocytes and CNS deficits (CNS deficites are not seen in HUS)
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What is the treatment for TTP
|
Plasmophoresis
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What are the two main causes of HUS?
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O157:H7 from E. coli found in beef (undercooked w/ this toxin which damages the blood vessels)
Shigella toxin also does this |
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what must be present to make the call of HUS and TTP
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Shistocytes w/ microangiopathic hemolytic anemia
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What would your PTT, PT and bleeding time to be in HUS and TTP?
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PTT and PT are normal but bleeding time is prolonged w/ thrombocytopenia
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A patient who has a molar extraction and have a constant oozing of blood out of the hole where the tooth was, DX
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coagulation disorder
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patient has platlet adhesion defect,and coagulation defect (minor def. of factor VIII), have symptoms of both problems...menorrhage, GI bleed, epistaxis, easy bruisibility...Dx?
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Von willebrands disease (vWD)
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What are the three parts to coagulation factor VIII
|
vWF
VIII coagulant VIII antigen (carrier protein) |
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Genetics of hemophilia A vs vWD?
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sex linked recessive (so its seen in males)
AD - vWD |
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what are the deficiencies seen in vWD Vs hemophilia A?
|
decrease VIII coagulant only in hemophilia A
Deficient in VIII antigen, dec. in VIII coagulant and vWF |
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What drug can be used to treat mild vWD in men and women
|
MEN - Dessmopressin (DDaTP) can cause increase in all the factors.
WOMEN w/ menorrhagia - birth control pills (also inc. sythesis of all the factors as well) |
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what tests are abnormal in vWD?
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Increased PTT and bleeding time.
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|
antiphospholipid syndrome (APLS) includes what two diseases
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SLE and HIV
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what do antiphospholipid antibodies do (APAs)?
|
directed against phospholipids bound to plasma protiens
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APAs include what two things
|
anticardiolipin antibody and lupus anticoagulant (makes people thrombogenic)
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VHY****
what false positive can anticardiolipin antibody produce? |
false-positive syphilis test
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what produces vitamin K deficiency in a hospitalized patient?
|
antibiotic therapy
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|
what is the most common cause of DIC?
|
Sepsis, E. COli is the most common and Neisseria meningitidis
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|
What malignancies can cause DIC?
|
Acute promyelocytic leukemia
pancreatic cancer w/ release of procoagulants in mucin |
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|
what is the pathogenesis of DIC?
|
Clots are forming all over the body in small vessels...fibrinogen, V, VII, II, I, and platlets are all consumed...all that is left is serum (two disesease at the same time thrombosis and coagulation deficiency)
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|
what are the common causes of DIC
|
SEPTIC shock, or rattle snake bite (High yeild on board)
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patient is in shock, and bleed form every orifice, DX?
|
DIC
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How do you test for DIC?
|
PTT and PT, thrombocytopenia, D-dimers positive (BEST TEST)***, platelt count decreased
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|
what kills a pregnanct women w/ a Amniontic fluid embolism?
|
DIC-thromboplastin is the activator
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|
How can you tell a patient has a hereditary thrombois?
what is the most common cause of this? |
young person w/ a deep vein thrombosis, seems to be a family proponderance for it.
Abnormal factor V Leiden so the body can't break it down and you clot more easily. |
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|
Antithrombin III deficeincy, most common cause
|
women on birth control
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VHY***
Patient w/ deep venous thrombosis, give them heparin, PTT is normal, give more heparin and remains normal, DX? |
Anti-thrombin III deficiency...remember heparin induces Anti-thrombin III deficiency.
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VHY***
What disease is considered thrombohemorrhaic? what is the best screening test for this? |
DIC
D-dimers |
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|
most comon cause of thrombocytopenia in kids is?
|
IDP
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patient is on asprin what will the following lab values be: PTT, PT, bleeding time and platlet count?
|
PTT and PT normal
bleeding time is prolonged and platlet count is normal (they just don't work) |
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ITP what will the following lab values be: PTT, PT, bleeding time and platlet count?
|
PTT and PT - normal
Bleeding time - prolonged and platlet count is decreased |
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|
TTP and hemolytic uremic syndrome...what will the following lab values be: PTT, PT, bleeding time and platlet count?
|
PTT and PT are normal
Bleeding time-prolonged platlet count-prolonged |
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hemophilia A what will the following lab values be: PTT, PT, bleeding time and platlet count?
|
PTT - prolonged
PT - normal Bleeding time - normal Platlet count - normal |
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DIC what will the following lab values be: PTT, PT, bleeding time and platlet count?
|
PTT and PT increased
Bleeding time increased platlet count - decreased |
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|
warfarin or heparin use what will the following lab values be: PTT, PT, bleeding time and platlet count?
|
PTT - prolonged (better for heparin)
PT - prolonged (better for warfarin INR specifically) Bleeding time - normal Platlet count - normal |
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|
vWD what will the following lab values be: PTT, PT, bleeding time and platlet count?
|
PTT - prolonged
PT - normal platlet count - normal Bleeding time - increased |
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|
If O is the most comon blood group type what antibodies do you have in your blood?
|
anti A IgM
anti B IgM anti AB IgG |
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|
If you are BLood group A what type of antibodies do you have in your blood?
|
Anti B IgM
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If you are Blood group B what type of antibodies do you have in your blood?
|
Anti A Igm
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IF you are Blood group AB what type of antibodies do you have in your blood?
|
Anti nothing
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|
what does a new born have floating around in ther plasma in terms of blood groups?
|
Nothing it takes a little while for them to develop these once they are born
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An old person was blood group A and recieved blood group B by accident but nothing happen and why?
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Don't have a very high antibody level
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Who is the universal donor?
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Group O they don't have any antigens on the RBCs
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what is the universal recipient?
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AB - no antiboides in the serum
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what is associated w/ gastric cancer and duodenal ulcers
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A - gastric cancer
O - duodenal ulcers |
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What are the five Rh antigens?
what does mean if you are Rh + |
D, C, c, E, e
if you are positive it means you are D+ (you have the D antigen) |
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what is the duffy (Fy) antigen?
what race tends to lack this antigen? |
binding site for infestiation of RBCS by plasmodium vivax
Black americans |
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what malaria are sickle cell patients protected from?
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Plasmodium falciparum- because they can't live out their cycle in the blood cells because they are destroyed to fast
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what is a major cross match?
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pateint serum w/ the donors RBCs, i.e. is there anything in the patients serum that will attack the RBCs
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autoimmune Hemolytic anemia is what type of hypersensitivity?
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Type II
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pencillin rash is what type of hypersensitivity?
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Type I
type II if hemolytic anemia |
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What is the most common antibody in the US?
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CMV- everyone has been exposed at some time in their life
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What do they measure for in Blood when looking for HIV
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ELISA and antibodiy to Gp 120
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what is the most common infection transmitted by blood transfusion
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CMV
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what is the most common cause of post transfusion hepatitis
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Hepatitis C
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what is the safest type of transfusion?
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autologous transfussion- your own blood
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If you get an accidental needle stick what is the most likley infection you can get
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Hep D
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what is your chance of getting a HIV if you got stuck by a needle that was used to take a persons blood w/ HIV?
What do you do about it |
1:300
go on tripple therapy as if you were HIV positive (AzT and protease inhibitor and get checked.) |
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what is the most common way a medical person gets HIV?
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accidental needle stick
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don't transfuse anyone unless?
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they are symptomatic
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Fresh frozen plasma should never be used to...?
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expand plasma voulme...use normal saline
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when would you use fresh frozen plasma as a treatment
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multiple coagulation factor defects, e.g. DIC, Warfirin and are bleedin to death, cirrhosis of the liver
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Protamine sulfate is used to correct
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heparin overdose and patient is bleeding really bad
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VHY****
difference between transfusion rxn, which is most common? |
allergic transfusion rxn -itching, hives, potentially anyphylaxis,
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VHY***
After a blood transfussion a patient develops itching, hives and potentially anyphylaxis, DX what is the TX what type of hypersensitivity |
allergic transfusion
benadryl, anti-histamine Type I hypersensitivity, IgE mediated |
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anit-HLA antibodies aganist donor luekocytes, fever, chills headache, and flushing DX?
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Febrile transfusion
TYpe II hypersensitivity |
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acute hemolytic transfusion rxns are due to ?
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blood group incompatibility (operator error) or presence of atypical antiboides (some antibody titers are so low they are not caught on screening if happen a long time ago)
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VHY***
Postpardum women lost lots of blood when she delivered and got a blood transfusion, when she left she had a Hemoglobin of 10 about 1 week later she has jaundice and hemaglobin is now 8, DX? |
delayed hemolytic transfussion rxn
coombs test to confirm diagnosis. Type II hypersensitivity rxn |
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Mom is blood group O negative and baby has A or B group negative what happens in utero?
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mothers antibody crosses the placenta (anti-AB-IgG) and attaches to A antigen or RBC and is taken up in baby spleena and destroyed...the uncojugated bilirubin is taken care of by the mothers liver so no kernictuerus or anything like that.
this can happen w/ the first pregnancy. |
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what happens if Mom is blood group O negative and baby has A group negative when the baby is born?
how do you treat it? |
Mild anemia and now has to handle all of the unconjugated bilirubin on their own and there liver is inmmature...
Put under UVB light |
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what is the most common hemolytic disease of the newborn?
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ABO HDN not Rh incompatility just the blood group.
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What is the most common cause of first day (first 24 hrs) jaundice in a newborn?
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ABO incompoatibility
physiological jaundice starts on Day 3 |
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How does UVB work? The light they put babies under
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converts bilirubin in the skin to dipyrrole which is water soluble and they can pie it out
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MOM is Rh- baby is Rh + what is the problem
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mom develops antibody (sensitized) to Rh factor (D antigen) and on next pregnancy same thing happens as HDN but is much more severe so when the baby is born...bilirubin is higher and so is anemia compared to ABO HDN, they need a transfusion rxn.
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VHY***
How do you prevent Rh sensitization? If mother is Rh - |
Rh immune globulin (anti-D globulin) is given at 28 weeks, then after birth the mother is tested again to determine how much Rh immune globulin to give them?
body is tricked into thinking that they made antibodies |
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WHat if the mother is O- and baby is A+ then what do you do?
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ABO incompatibility protects against Rh sensitization because babies RBCs would be destroyed quickly but they still give the baby the typical Rh treatment to be safe...
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Free unconjugated bilirubin deposits in the basal ganglion of a new born, DX?
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kernicterus-causes severe dysfunction
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erythroblastalis fetalis what do they die of?
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high output failure (left then right side of the heart) get big livers from extrahematopoiesis
secondary to severe anemia |
