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House Hemat > Megallo > Flashcards

Megallo Flashcards

1
Q

Megaloblastic anemia is characterized by RBCs that are (smaller or larger?) than normal.

A

Larger

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2
Q

In Megaloblastic anemia , There are enough of the megaloblasts.

T/F

A

F

also aren’t enough of them.

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3
Q

When RBCs aren’t produced properly, it results in megaloblastic anaemia.
Because the blood cells are too large, they may not be able to ___________________________

A

exit the bone marrow to enter the bloodstream and deliver oxygen.

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4
Q

An increase in MCV can be due to a number of reasons but careful review of the _________ and _______ can narrow the diagnostic possibilities.

A

patient’s history and blood smear

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5
Q

The differential can be divided into two broad categories based on RBC morphology.

____ macrocytosis

______ macrocytosis

A

Round

Oval

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6
Q

Round macrocytosis: as a result of abnomal ———— in the ________. Round macrocytosis

Common etiologies include:
1.________.
2. _____ Disease.
3. _____ Disease.
4. _________ (“_________ of the red cell”).

A

deposition of lipids

erythrocyte membrane

Alcoholism; liver; kidney; Hypothyroidism

myxedema

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7
Q

Oval macrocytosis (macroovalocytes) is a sign of problem with cell _________.

A

DNA replica tion.

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8
Q

Oval macrocytosis

The developing red cell has difficulty in undergoing _______ but RNA continues to be translated and transcribed into protein leading to _______ while the ______ lags behind.

Often _____________ are skipped leading to a larger than normal cell.

A

cell division

growth of the cytoplasm

nucleus; one or more cell division

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9
Q

macrocytic anaemia

MCV > _____fl

A

100

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10
Q

macrocytic anaemia

Impaired ____ formation due to lack of —— or _______ in ultimatly active form
Therefore the, _________ is delayed to that of the cytoplasm

A

DNA

vit.B12 or folate

maturation of nucleus

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11
Q

Causes of megaloblastic anaemia
The two most common causes of megaloblastic anemia are deficiencies of _________ and ______

A

vitamin B12 and folate.

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12
Q

Which is affected more by cooking?

Vitamin B12 or folate

A

Folate is destroyed by cooking

Little effect on vitb12

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13
Q

Usual therapeutic form of vitamin B12

Usual therapeutic form of folate

A

Hydroxycobalamin

Folic acid

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14
Q

Major intracellular physiological form of

Vitamin B12 and folic acid

A

Methy and deoxyadenosylcobalamin

Reduced polyglutamate derivatives

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15
Q

VITAMIN B12 AND FOLATE-
METABOLIC PATHWAYS
Both vitamin B12 and folate are key components in the synthesis of DNA due to their role in conversion of ______ and ________

A

uridine to thymidine.

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16
Q

VITAMIN B12 AND FOLATE-
METABOLIC PATHWAYS
vitamin B12 and folate role in conversion of uridine to thymidine.

When ________ loses a methyl group to form ________, vitamin B12 “_____” the methyl group to _____ converting it to _____.

Tetrahydrofolate is eventually converted to ________ which is required for thymidine synthase.

A

methyltetrahydrofolate

tetrahyrodrofolate; shuttles

homocysteine; methionine

methylenetetrahydrofolate

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17
Q

Vitamin B12 other role is a co-factor in the conversion of _________ to _______

A

methymalonyl-CoA to succinyl-CoA.

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18
Q

ABSORPTION AND METABOLISM OF
FOLATE

Folate:
The body stores very (little or large?) folate (for several _____) and maintenance of folate stores is dependent on adequate _______.

Folate is found in ____________, and ______

Folate is absorbed in the ______ and circulates in a ____ form or (loosely or tightly?) bond to ______.

A

Little ; weeks; dietary intake

green leafy vegetables, and liver.

small bowel ; free

Loosely ; albumin

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19
Q

ABSORPTION AND METABOLISM OF VITAMIN B12 AND
FOLATE

Vitamin B12:
In contrast to folate the body stores copious amounts of vitamin B12 (for ___-___).
Absorption of vitamin B12 is complex and can be interrupted by a variety of mechanisms.

Vitamin B12 is synthesized by ____ and the major dietary source is _____.

A

2-6 years

microbes

animal protein.

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20
Q

Vitamin B12

When animal protein is ingested, vitamin B12 is freed from the protein and binds to “________”.
This complex travels to the _______ where ______ destroy the _______.
This allows _______ to bind to vitamin B12.
This latest complex is absorbed only in the ___________ of ________.

Vitamin B12 binds to ____________ and is delivered to tissues

A

R proteins; duodenum

pancreatic enzymes; R protein

intrinsic factor (IF)

last 1-2 feet; terminal ileum

transcobalamin II

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21
Q

CONSEQUENCES OF VITAMIN B12 OR FOLATE
DEFICIENCY

When vitamin B12 or folate is deficient, ______ synthase function is impaired and ___ synthesis is interrupted leading to megaloblastic changes in ____________ cells.

A

thymidine; DNA

all rapidly dividing

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22
Q

CONSEQUENCES OF VITAMIN B12 OR FOLATE
DEFICIENCY

The inability to synthesized DNA leads to _________________.
There is often ________ in the marrow but most of these immature cells ____ before reaching maturity.

This process, ______________, leads to the classic biochemical picture of hemolysis-elevated ____ and indirect _____.

A

ineffectual erythropoiesis

erythroid hyperplasia; die

intramedullary hemolysis; LDH; bilirubinemia

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23
Q

The LDH level is often in the ________’s in patients with megaloblastic anemia.

A

1,000

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24
Q

In Megaloblastic Anaemia, The lack of DNA synthesis affects the neutrophils leading to nuclear ______________.

A

hypersegmentation

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25
Q

Megaloblastic Anaemia

The anemia is of (gradual or sudden?) onset and is often very (well or poorly?) tolerated despite (low or high?) hematocrits.

Often a mild _______ is seen but ________ can be severe.

A

Gradual; well ; low

pancytopenia; thrombocytopenia

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26
Q

Other rapidly dividing tissue are influenced by the megaloblastic process.
In the GI tract this can lead to ________ of the ________ and further ________.
This also leads to the classic sign of ______________.

A

atrophy of the luminal lining

malabsorption

tongue smoothing

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27
Q

AETIOLOGIES OF FOLATE
DEFICIENCY

Decreased intake- The average intake of folate in the diet is only ____-___ ug/day which is (more or less?) than the estimated daily requirement. Thus, for most people a ______ or ____ will lead to folate deficiency.

A

2-300; less

poor diet or decrease eating

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28
Q

AETIOLOGIES OF FOLATE
DEFICIENCY

Increased requirements-Patients who are _______, have _____ anemia, or ______ have increased needs for folate which can cause them to rapidly develop folate deficiency if intake is not kept up.

A

pregnant; hemolytic; psoriasis

29
Q

AETIOLOGIES OF FOLATE
DEFICIENCY

Malabsorption

T/F

A

T

30
Q

AETIOLOGIES OF FOLATE
DEFICIENCY

Drugs - Patient with underlying mild folate deficiency are more susceptible to trimethoprim/sulfa, ______ and _______toxicity.

_________ and ________ lead to increase consumption of folate.

A

pyrimethamine and methotrexate

Oral contraceptive and anticonvulsants

31
Q

AETIOLOGIES OF FOLATE
DEFICIENCY

Alcohol- Alcohol affects several aspects of folate metabolism.

Alcoholics have __________. In addition, folate metabolism is interfered with leading to a functional folate deficiency. Alcoholics have an inability to ________ and can have _______ with normal ________

A

poor intake of folate

mobilize folate stores

depleted tissue stores

serum levels of folate

32
Q

AETIOLOGIES OF VITAMIN B12 DEFICIENCY

Inadequate intake is (common or rare?) but seen in very strict _____.

Abnormal gastric events include being unable to _____________ due to lack of _______ or enzymes. This is a recently recognized group of patients which may compose a very large subset of patients with vitamin B12 deficiency. 10-30% percent of patients with ___________ will develop vitamin B12 deficiency.

A

Rare; vegans

dissociated vitamin B12 from food ; stomach acid

partial gastrectomy

33
Q

AETIOLOGIES OF VITAMIN B12 DEFICIENCY

Deficient intrinsic factor most commonly occurs due to ___________ by ______ (_______ anemia).

Abnormal small bowel events include _____ insufficiency, ______ syndromes (bacterial absorbing vitamin B12-IF complexes) and patients infested with ___________.

A

destruction of parietal cells; autoantibodies

pernicious; pancreatic; blind loops ; Diphyllobothrium latum

34
Q

AETIOLOGIES OF VITAMIN B12 DEFICIENCY

Abnormal mucosal events including ______ syndromes and surgical removal of the ________.

Drugs -________, ____s

A

malabsorption

terminal ileum.

Metformin, PPIs

35
Q

Causes of B12 Deficiency

Pernicious Anaemia:
Auto antibodies to intrinsic factor in <___% cases
Blocks attachment of ____ to ___

Chronic gastritis

Autoantibodies against ______ cells

blocks attachment of ______ to _____

A

70

Cobalamin to IF

parietal

Cbl-IF to ileal receptors

36
Q

B12 deficiency symptoms

_______(shinny tongue)

_______ gait

Anaemia and related symptoms

______ atrophy

Malabsorption _______

A

Atrophic glositis

Shuffling

Vaginal; Jaundice

37
Q

Personality changes is a B12 deficiency symptom

T/F

A

T

38
Q

Hypohomocysteinemia is a B12 deficiency symptom

T/F

A

F

Hyperhomocysteinemia

39
Q

Neurologic symptoms is a _____ deficiency symptom

A

B12

40
Q

General Morphological features of Megaloblastic anaemia

Peripheral blood finding

haemoglobin- ____eased
Haematocrit- ____eased

RBC count- ___eased
MVC - > ____fl
MCH – _____
MCHC –_______

A

decr
decr

decr; 100; increased; normal

41
Q

General Morphological features of Megaloblastic anaemia

Peripheral blood finding

_______penia
Total WBC count –________
Platelet count –________
________penia, esp. if anaemia is severe

A

Recticulocyto

normal/low

normal/low

Pancyto

42
Q

Peripheral smear

RBC:
______ ovalocyte
_____cytic ____chromic

in severe anaemia in addition to macrocytosis, marked ______cytosis, ____philic stipplind, _____ bodies, ______may be found.

___________erthyroblast with fine open nuclear chromatin (megaloblast) may be seen in peripheral blood in severe anaemia

A

Macro

macro; normo

anisiopoikilo; baso; howell jolly

cabot’s ring

Late or intermediate

43
Q

________ is the earliest sign in vit. B12 def. and be detected even before the onset anaemia

A

Macrcytosis

44
Q

Peripheral smear in Megaloblastic Anaemia

WBC:
___________ count

____________neutrophils – is one of the earliest signs of megaloblastic haemopoeisis and can be detected even in the absence of anaemia

PLATELET:
_____________ count (severe anaemia)
______ platelet may occur

A

Normal to reduced

Hypersegemented

Normal or decreased

Giant

45
Q

Bone marrow

Markedly (hypo or hyper?) cellular marrow
Myeloid : erythroid ratio is _______ or _____
Megaloblastic erthyroid hyperplasia

Giant ___________

A

Hyper

decreased or reversed

metamyelocyte

46
Q

MEGALOBLAST

Cell and nuclear size and amount of cytoplasm (deeply ________) are ____eased

Nuclear chromatin is _____ like or ____ (____)

Nuclear-cytoplasm ______/_____

Abnormal (small or large?) precusor (promegaloblast and earl megaloblast) are increased in bone marrow as a result of _______ arrest

Abnormal mitosis (____eased)

A

basophilic royal blue; incr

sieve; stippled; open

asynchrony; dissociation

Large; maturation; incr

47
Q

Granulocytic series also display megaloblastic changes

Most prominent changes –___________ with ______ shaped nuclei and finer nuclear chromatin, and in band forms

Megakaryocytes are often (small or large?) with multiple nuclear ____ and ____ of cytoplasmic granules.

A

giant metamyelocyte; horseshoe

Large; lobes; paucity

48
Q

Biochemical findings in Megaloblastic Anaemia

___ease in serum unconjugated bilirubin

____ease LDH

______ serum iron and ferritin

A

Incr

Incr

Normal

49
Q

Diagnosing Vit. B12 & folate deficiency

measuring serum levels of B12 or folate is very adequate to diagnosis deficiency.

T/F

A

F

Inadequate

50
Q

Diagnosing Vit. B12 & folate deficiency

It turns out that simply measuring serum levels of B12 or folate is very inadequate to diagnosis deficiency.

B12 deficiency.
- there would be elevated ______ level.
-also _______ acid accumulates.

A

homocysteine

methylmalonic

51
Q

Both homocysteine and methylmalonic acid assays are widely available and should be the first line tests for B12 deficiency.

T/F

A

T

52
Q

Serum folate levels are also very unreliable.

T/F

A

T

53
Q

serum homocysteine will also accumulate in folate deficiency

T/F

A

T

54
Q

Serum homocysteine is a more sensitive marker of tissue folate stores.

T/F

A

T

55
Q

Management of B12 deficiency

When vit.B12 is suspected a trial of B12 is essential
Failure to respond can only be determined after careful follow-up over a period of _______, particularly if the patient is still _______

Standard therapy for all cases of vitb12 deficiency is _________ injection of B12
Usually in the form of ____

In patient with inadequate intake, may be given by ____.

Underlying conditions should be treated.

A

several months; non-anaemic

intramuscular; hydroxycobalamin

supplements; mouth

56
Q

Vitamin B12 treatment

After initiation therapy, reticulocyte count begins to increase around ____ day –peak at ___ or ____ day gradually returns to normal by the end of ______

Hematocrit steadily rises and normalise in about ________

Blood transfusion is indicated in ______________ patients or in patients with CCF.

A

3rd; 6th or 7th

3rd week.

1-2month

severe anaemic symptomatic

57
Q

__________________ are given to patients if B12 deficiency has not been excluded.

Why?

A

Both B12 and folate

This is to prevent neurological damage, e.g subacute combined degeneration of the spinal cord.

58
Q

Elevated levels of homocysteine are associated with an decreased risk of atherosclerosis or venous thrombosis.

A

F

Increased

59
Q

Increased levels of homocysteine (reflecting lack of folic acid) in pregnant women is a risk factor for _________

A

neural tubes defects.

60
Q

Patients with alcoholism and folate deficiency can take up to _____ to respond to folate therapy.

A

three weeks

61
Q

Which is better, IM Injection or oral B13 therapy?

A

Oral therapy with 1-2000 ug/day has been tested and has been found to be just as reliable as IM therapy and is becoming more widely used.

62
Q

megaloblastic anemia often present with severe anemia, therefore transfusion therapy is often indicated.

T/F

With reason

A

F

Although patients with megaloblastic anemia often present with severe anemia, transfusion therapy is rarely indicated.

Since the anemia is rapidly reversible with therapy there is little justification for exposing the patient to the risk of transfusion except if the patient is having life- threatening symptoms such as severe ischemia.

63
Q

Megaloblastic anemia maybe caused by all of the following, except:
a. Phenytoin
b. Methotrexate
c. Pyrimethamine
d. Amoxycilline

A

D

64
Q

A 1 year old child presented with severe macrocytic anemia with sub-nephrotic range proteinuria. His vitamin B12 levels are low. The diagnosis:
a. Imerslund-Grasbeck disease
b. Thiamine deficiency
c. Roger syndrome
d. Pearson syndrome

A

A

65
Q

The earliest specific indicator of folate deficiency is:
a. Serum folate level
b. Red cell folate level
c. Anemia
d. Elevated homocysteine level

A

A

66
Q

Hypothyroidism causes pancytopenia

T/F

A

F

Hypothyroidism does not causes pancytopenia.

67
Q
  1. The earliest neurological sign of megaloblastic anemia is:
    a. Loss of position sense
    b. Loss of vibration sense
    c. Dysdiadochokinesia
    d. Romberg’s sign positive
A

A

68
Q

Cobalamin deficiency is characterized by all of the following, except:
a. Angular cheilitis
b. Glossitis
c. Cognitive impairment
d. Jaundice

A

A

That’s for iron deficiency

69
Q

megaloblastic anemia May be caused by nitrous oxide inhalation

T/F

A

T

By causing vitamin B12 deficiency

House Hemat (29 decks)

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