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Heme > Lec 3 Nutritional Anemia > Flashcards

Lec 3 Nutritional Anemia Flashcards

1
Q

What is the pathology that causes megaloblastic anemia?

A

impaired DNA synthesis

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2
Q

What are 3 complications of impaired DNA synthesis?

A
  • megaloblastic anemia
  • malabsorption b/c GI mucosal cells affected
  • increased risk of thrombosis
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3
Q

hyperhomocysteinemia is a risk factor for what?

A

development of thrombosis

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4
Q

What is the ineffective erythropoiesis seen in megaloblastic anemia?

A

asynchrony between maturity of nucleus and that of cytoplasm b/c protein synthesis normal but DNA replication abnormal –> prematurely destroyed in the bone marrow = intramedullary hemolysis

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5
Q

What happens to retic count in medulloblastic anemia?

A

low retic count

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6
Q

What two cellular reactions is B12 a cofactor for?

A
  • methylmalonyl CoA mutation rxn of methylmalonyl CoA –> succinyl CoA
  • homocysteine-methionine methyltransferase rxn of n5-methyl THF + homocysteine –> methionine and THF
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7
Q

What B12, homocysteine, methylmalonic acid levels in B12 deficiency?

A
  • decreased B12
  • increased methylmalonic acid
  • increased homocysteine
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8
Q

Can humans synthesize folate?

A

nope! dependent on dietary intake

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9
Q

Where does absorption of folate occur?

A

primarily in duodenum and jejunum

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10
Q

What is pathogenesis of folate deficiency?

A

folate –> impaired generation of THF + thymidylate –> slowed DNA synthesis

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11
Q

How can you distinguish between B12 and folate deficiency?

A

indistinguishable by CBC, bone marrow, peripheral blood

both have high homocysteine

only B12 deficiency has high methylmalonic acid; only B12 has neurologic symptoms

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12
Q

What is the mech of action methotrexate?

A

inhibits dihydrofolate reductase –> kills cells by diverting metabolically active folates into inert pool of DHF –> causes megaloblastic anemia

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13
Q

What kind of hemolysis in megaloblastic anemia? signs?

A

extravascular hemolysis in spleen –> can cause jaundice and splenomegaly

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14
Q

What is the effect of decreased folate in pregnancy?

A

increased incidence of neural tube defects –> spina bifida

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15
Q

Why do you get neuro symptoms in B12 deficiency?

A

B12 is needed for myelin synthesis

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16
Q

What is the source of vit B12?

A

microorganisms

animal products + dairy

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17
Q

What is the source of folate?

A

veggies, fruits, liver

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18
Q

How much folate do we need per day? normal body stores?

A

need 50 ug/day

body stores 5 mg

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19
Q

What is the most common cause of folate deficiency?

A

dietary insufficiency or increased demand [aka pregnancy]

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20
Q

What are signs/symptoms of megaloblastic anemia?

A
  • sore mouth/tongue = glossitis b/c oral mucosa proliferation impaired
  • if malabsorption –> diarrhea/steatorrhea
  • jaundice/splenomegaly from extravascular hemolysis
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21
Q

What do you see on CBC with megaloblastic anemia?

A
  • high MCV
  • low retic count
  • low Hbg
  • low WBC
  • low RBC
  • low platelets
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22
Q

What are signs of megaloblastic anemia on peripheral smear?

A
  • macrocytic RBCs

- hypersegmentation of neutrophils

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23
Q

What do you see in bone marrow with megaloblastic anemia?

A

megaloblasts = abnormal, large erythroid precurosrs w/ persistent immaturity of nuclei even as cells mature

als have giant white cell precursors

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24
Q

What type of bilirubin do you see in megaloblastic anemia?

A

high indirect bilirubin

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25
Q

What level of LDH in megaloblastic anemia?

A

high LDH = sign of hemolysis

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26
Q

What is treatment for B12/folate deficiency?

A

make diagnosis and give whichever is missing

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27
Q

What is schilling test?

A
  • give radioactive B12 orally –> measure amount excreted in urine

decreased urinary excretion indicated absorption impaired

28
Q

What are some GI diseases that cause folate malabsorption?

A

celiac

crohns

29
Q

What are two drugs that could cause folate deficiency?

A
  • methotrexate

- trimethoprim sulfamethoxazole

30
Q

What are functions of iron normally?

A
  • needed for oxidative metabolism [krebs cycle]
  • cellular growth + proliferation
  • O2 transport
  • heme formation
31
Q

How much iron is stored in the body?

A

3.5 g in men; 2.5 g in women

32
Q

Where is iron absorbed?

A

absorbed in duodenum; inorganic iron must first be reduced from Fe3 –> Fe2 by ferric reductase before absorption

33
Q

What percent of ingested iron is normally absorbed?

A

10%

34
Q

What is hepcidin?

A

synthesized in liver; negative regulator of iron transport –> binds and internalizes ferroportin so Fe can’t be released from intracellular stores –> less Fe avaialable for Hb synthesis

35
Q

What is effect of hepcidin on iron absorption?

A

leads to decreased absorption of iron

36
Q

What are 3 things that stimulate hepcidin synthesis?

A
  • iron intake
  • inflammation
  • infection
37
Q

What are 4 things that suppress hepcidin synthesis?

A
  • anemia
  • hypoxemia
  • erythropiesis
  • iron deficiency
38
Q

What is most common cause of low iron?

A

bleeding; particularly chronic GI blood loss

39
Q

What is iron’s carrier protein in the blood? How much of it is normally saturated with iron?

A

transferrin

30% normally saturated with iron

40
Q

What happens to transferrin sat with iron deficiency?

A

transferin sat increases

41
Q

What happens to amount of transferrin receptor in iron deficiency?

A

transferrin receptor synthesis increases b/c erythroid precursors want more transferrin-iron complex!

42
Q

What does total iron binding capacity of blood measure?

A

concentration of transferrin

43
Q

What happens to transferrin level in iron deficiency?

A

iron deficiecny –> less iron binding to transferrin gene and inhibiting transcription –> increased production of transferrin –> TIBC increases

44
Q

What does amount of cellular ferritin in blood tell you?

A

correlates to body iron stores

45
Q

What happens to plasma ferritin in iron deficiency?

A

plasma ferritin decreases

46
Q

What things cause an increase in ferritin?

A

inflammation, infection, malignancy

ferritin = acute phase reactant

47
Q

What are clinical signs of iron deficiency?

A

anemia, pica [chew on things], cheilosis [dry edges of lips], pallor, glossitis, koilonychia [spoon nails]

48
Q

What is major cause of iron deficiency in developing countries?

A

GI blood loss from hookworm infection

49
Q

What is pathogenesis of iron deficiency causing anemia?

A

lack of iron incorporation into heme –> deficient heme synthesis –> poor cell growth

50
Q

What do you see on peripheral blood smear in iron deficiency anemia?

A

microcytic hypochromic RBCs
increased RDW = RBC distribution width
FEP = free erythrocyte protoporphyrin
target cells

low RBC, normal white count

51
Q

What do you see on CBC in iron deficiency anemia?

A
  • decreased Hb and hematocrit
  • decreased MCV and MCH
  • low retic count
  • increased RDW
  • decreased iron
  • increased TIBC
  • decreased ferritin
  • decreased transferrin sat
  • increased serum transferrin receptor
52
Q

Why do you get high platelets in iron deficiency anemia?

A

b/c thrombopietin similar struct to EPO –> when EPO rises can also stimulate platelet production

53
Q

What type of anemia can you see increased iron?

A

chronic hemolytic anemia –> b/c you are breaking down RBCs you will have increased iron

OR secondary yo chronic blood transfusions in severe anemia

54
Q

What is potential cause of idiopathic hereditary hemochromatosis?

A

autosomal recessive from genetic defect HFE gene on chr 6 –> iron overload through GI absorption and hepcidin deficiency

55
Q

What are symptoms of hereditary hemochromatosis?

A

cirrhosis, cardiac arrhythmias, HF 2ndary to restrictive cardiopyopathy, DM, arthralgias, bronze skin

56
Q

What do you see in blood of hereditary hemochromatosis?

A

serum Fe, transferrin sat, and ferritin will all be abnormally elevated

57
Q

What are sideroblastic anemias?

A

disorder due to impaired incorporation of iron into heme molecule –> Fe accumulates within the mitochondria fo red cell precursors in the bone marrow –> prematurely destroyed in BM –> ineffective erythropoiesis

58
Q

What are some acquired causes of sideroblastic anemia?

A

alcohol
isoniazid
toxins [lead]

all antagonists of pyridoxal phosphate = coenzyme of heme synthesis

59
Q

What is the mutation in inherited form of sideroblastic anemia?

A

defect in ALA synthase which is required for heme synthesis

60
Q

What do you see on CBC in sideroblastic anemia?

A

low MCV

low retic

61
Q

What do you see in bone marrow with sideroblastic anemia?

A

hypercellular BM with erythroid hyperplasia

ringed sideroblasts

62
Q

What do you see in labs with sideroblastic anemia?

A
  • high serum Fe
  • high transferrin saturation
  • high ferritin
  • nomral TIBC
63
Q

What is treatment for sideroblastic anemia?

A

pyridoxine [vit B6] b/c its a cofactor the ALA-synthase

64
Q

What are some common causes of anemia of inflammation?

A
  • chronic infection
  • chronic inflammatory disease [IBD, SLE, sarcoidosis, etc]
  • cancer
65
Q

What is the pathogenesis of anemia of inflammation?

A
  • cytokines of inflmmation –> inhibit EPO –> decreased RBC production

increased synthesis of hepcidin –> decreased transport of Fe; impaired Fe absorption

66
Q

What do you see on peripheral smear in anemia of inflammation?

A

RBCS normocytic/normochromic OR can be microcytic/hypochromic b/c of functional iron deficiency

67
Q

What do you see in labs in anemia of inflammation?

A
  • low retic count
  • low serum Fe
  • decreased transferrin [TIBC]
  • normal or increased serum ferritin
  • decreased transferrin sat
  • normal soluble transferrin receptor levels

Heme (20 decks)

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