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41 Cards in this Set
- Front
- Back
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what is the most common cause for macrocytic anemia
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1. EtOH abuse
2. Folate/B12 deficiency 3. chemo/HIV treatments 4. accelerated erythropoiesis |
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what are the 2 most common causes of megloblastic anemia
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1. B12 deficiency
2. Folate deficiency |
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what does megaloblastic anemia look like in blood smear? bone marrow?
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*mega, DNA synthesis bad due to folate or B12 missing
Blood Smear: abnormal shape/size, Howelle-Jolly Body, large oval RBC, WBC are few- hypersegmented neutrophiles Marrow: bad DNA in ALL cell lines so platelets (megakaryocytes), WBC, RBC, are in decreased number and increased size |
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what value classifies anemia as megoblastic
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MCV >100fL
**MCH is elevated due to increase in size |
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what is the difference btwn megaloblastic anemia and and non megaloblastic
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mega: impaired DNA synthesis, super big cells, caused by B12/folate deficiency
non mega: DNA synthesis is ok, problem with bone marrow, etoh abuse, liver disease, cells not quite so huge |
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what type of anemia has howelle jolly bodies
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megaloblastic
faulty DNA synthesis |
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can you distinguish megaloblastic anemia caused by B12 or folate deficiency by bone marrow or blood smeat
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nope, in both cases DNA synthesis is impaired and cells will be large and few
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megaloblastic anemias, insufficeint or ineffective? what happens to CR
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insufficent, low CR
**there will be LESS of all cells **they are HYPOproliforative |
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what 2 thigns does folate do?
what 2 thigns does B12 do? |
Folate
1. DNA synth 2. Carry CH3 for methionine synth and SAMe formation B12: 1. Homocystein Methyl Transferase (Recycle folate for DNA synthesis and Transfer CH3 from folate to homocystein so that you can make neuro things) 2. Methylmalylonly CoA mutase |
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the start product for homocystein methyltransferase is...
then end product is the required nutrient is... |
homocystein --- B12/homocyc methyltransferase--> methoinine
**so when no B12 homocystein builds up and metthonie is depleted |
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when does homocystein build up
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1. B12 deficeincy
2. folate deficiency **homocystein methyltransferase isnt working |
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does B12 or folate deficenty lead to peripheral neuropathy
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B12, no methionine so no working on peripheral neurons
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waht all accumulates with B12 defeciency
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1. Homocystein
2. N methyl THF |
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what is the folate trap, is it a problem with folate or B12
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B12 problem
B12 isnt around to recycle folate. Folate is stuck in the 5 Methly THF form and cant work. **the folate trap looks like a folate deficency but its really a B12 problem *homocycstein methyltransferase os deficient |
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why does B12 deficency look like a folate deficency
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B12 recycles folate from a useless (5 Me THF) form to a useable (THF) form
**no B12 for recycle, no folate **homocystein methyltransferase is deficent |
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what happens if folate is given to a person with a B12 defeicy
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Anemia clears up and DNA synthesis resumes but the peripheral neuropathy that occurs when you dont have Methionine persists
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increased levels of what indicate a B12 deficiency over folate
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methymalonyl CoA
(methylmalanoic acid build up from the reacion catalzyed by methymalonlyCo A mutase in which B12 is required) |
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what are the 2 ways B12 causes neuropathy
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1. Decreased Methionine means decreased methylation of myelin basic protein which myelinates neurons
2. bad methymalonyl CoA mutase means odd chain FA build up and cause abnormal FA additions to the myelin sheath |
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name the 4 proteins associated with B12 abs
list where they are made and where they are used |
Protein Made Used
1. R Binder: Mouth --> stomach 2. IF: Stomach --> duodenum 3. IF Receptor: duodenum --> enterocyte 4. Transcobalamin: circulation |
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what steps of B12 abs depend on pH (stomach, duodenum)
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1. stomach, acidic enviornment required to free B12 from protein (pepsin cleaves protein), prevents IF binder binding to B12
2. duodenum, more neutral, R binder is removed and B12 binds IF |
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B12 abs in the mouth
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B12 bound to dietary protein
R binder secreted |
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B12 abs in stomach
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pepsin cleaves B12 from dietary protein
B12 binds to R binder IF secreted |
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B12 abs in duodenum
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R binder is destroyed B12 is free
B12 binds IF |
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B12 in ileum
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IF receptor is expressed
IF/B2 is endocytosed, B12 is freed and then binds transcobalamin. B12 is picked up in the tissues by transcobalamin receptors |
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Cheif Cells
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pepsinogen
**converted into pepsin by acidic environment, pepsin frees B12 from dietary protein so it can bind R binder |
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Parietal Cells
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Secreted HCL, IF
HCL cleaves pepsinogen IF is secreted in the stomach and will bind in duodenum |
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what does parietal celld estruction do to B12
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creates a deficency
*No HCL and no IF, B12 remains bound to dietary protein. No acid no pepsin, B12 is pooed out |
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name 3 ways B12 abs is reduced by decreased HCL
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1. destroy parietal cells
2.gastric surgery 3. achlorydria |
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what is a way to decrease B12 abs in the SI
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1. tapeworm. the worm steals the B12
2. Celiac disease- flatten the villi so less abs occurs 3. partial block: bacterial growth steals b12 |
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waht causes b12 deficency
what are the causes of folate deficency |
Nts deficieny rare
**usually malabsorption, old folks, vegans, alcoholics Folate: usually a dietary difeciency, stores are no good |
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what does N2O do to B12, what does this cause
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NO oxidizes cobalt and makes B12 functionally deficient ----> megaloblastic anemia, peripheral neuropathy
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what are the 2 ways the pernicious anemia blocks IF
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1. Blocking AB, block formation of IF
2. Binding AB, prevend B12.If from binding to IF receptors in the ileum |
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what do the stages of hte shilling test measure
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1. B12 abs
2. ID if B12 deficneicy is due to IF 3. ID bacterial overgrowth 4. ID pancreatic dysfunction |
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what is stage 1 of schilling and what does it test
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measure b12 abs
**if the labeled B12 is in the pee it means its being abs, if the B12 is in the poo, its not being abs **IF EXCRETION IN URINE IS LESS THAN 7% GO TO STEP 2, if urine excretion is ok then you just werent eating enough B12 |
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explain stage 2 of schilling
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1. an individual who is not abs B12 is given B12 and IF,
*if they then have normal urinary excretion we know that there is an IF production problem, pernecious anemia **if the person STILL has low urinary excretion it means the B12 is still not being abs, and can be due to bacterial overgrowth or pancreatic deficiency |
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if you have a dietary deficiency of B12 what does scholling test look like?
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stage 1, given B12 and then you have normal urinary excretion
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if you have pernicious anemia what does a schilling test look like
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stage 1. given B12 and you still have low urinary excretion. abs isnt happening bc you are mission IF
stage 2, given B12 AND IF causes abs to be normal and excretion in urine normal *pernicious anemia, B12 deficiency due to IF problem |
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what are clinical features of Pernicious anemia
Urinary methymalonylic acid CR when B12 given Serum AB to IF Achorhydria |
Urinary methymalonylic acid: increased
CR when B12 given: increased Serum AB to IF: present Achorhydria: present |
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how do you fix B12 deficiency in PA
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give IM B12
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what are the test results for PA
MCV MCHC Schilling IF AB CR Methylmalanonic acid homocystein achlorhydria |
MCV: increase
MCHC: WNL Schilling: low in stage I, normal in stage II IF AB: present CR: decreased to normal Methylmalanonic acid: increased homocystein: increased achlorhydria: present |
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what is pernicious anemia, what cells are destroyed, what does this do to abs
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parietal cells are destroyed
no IF is made Also no HCL is secreted, achlorydria *B12 cant bind IF in the duodenum *no B12 means Anemia, no folate recycleing |
