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Blood > Haem 10 > Flashcards

Haem 10 Flashcards

1
Q

Role of B12 and folate

A

Required for DNA synthesis

Absence leads to severe anaemia which can be fatal

Known as haematinics

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2
Q

What is b12 needed for

A
  1. DNA synthesis

2. Integrity of the nervous system (both CNS and PNS, independent of the effect on DNA synthesis)

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3
Q

What is folic acid needed for

A

DNA Synthesis

Homocystine metabolism

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4
Q

How is b12 and folate involved in DNA synthesis

A

dUMP–> dTMP

This methylation from deoxyuridinemonophosphate to deoxythymidine monophosphate requires donation of CH3 from folate intermediaries from the dietary folate.

B12 is needed to convert methyl-THF to THF from which these folate intermediaries are formed

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5
Q

Areas affected by b12 and folate deficiency

A

ALL RAPIDLY DIVIDING CELLS ARE AFFECTED

  • Bone marrow
  • Epithelial surfaces of mouth and gut
  • Gonads
  • embryos
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6
Q

Clinical features of b12 or folate deficiency

A 
Anemia: weak, tired, short of breath
Jaundice
Glossitis and angular cheilosis
Weight loss, change of bowel habit
Sterility
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7
Q

Type of anaemia associated with b12 or folate deficiency

A

Macrocytic and megaloblasic (BIG cells, not small like in iron deficiency)

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8
Q

Causes of macrocytic anaemia

A 
Vitamin B12/folate deficiency
Liver disease or alcohol
Hypothyroid
Drugs e.g. azathioprine (immune suppressive)
-Haematological disorders:
  -Myelodysplasia, 
  -aplastic anemia
  -Reticulocytosis e.g. chronic haemolytic anemia
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9
Q

What does megaloblastic refer to

A

Describes a morphological change in the red cell precursors within the bone marrow

NOT size of blood cells

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10
Q

Maturation of red cells

What happens to the nucleus and the cytoplasm in megaloblastic anaemia

A

Erythroblast
Normoblast: early/intermediate/late
Reticulocyte
Circulating red blood cell

Defined by asynchronous maturation of the nucleus and cytoplasm in the erythroid series.

We start of with a nucleus, which gets smaller and smaller through development, until it becomes pyknotic and is extruded.

Meanwhile, the cytoplasm is getting more and more pink because of increasing haemoglobin (red) and then the other proteins are not produced anymore .

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11
Q

What changes is seen in normal red cell development on slides

A

Cytoplasm from blue (when there are lots of protein types) to pink (just Hb)

Nucleus condenses and then is ejected…..

Megaloblastic change is lack of synchronisation between cytoplasm and nucleus maturaton

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12
Q

Indication of megaloblastic change in peripheral blood vs in blood marrow

A

Anisocytosis
Large red cells (oval macrocytes)
Hypersegmented neutrophils
Giant metamyelocytes

In marrow… mature red cells

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13
Q

t/f thyroid disease can cause megaloblastic RBC

A

F!! Macrocytic red cells

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14
Q

Tests with high MCV

A

b12/folate
LFT
TSH/T3/T4
Reticulocyte count

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15
Q

Cause of hypersegmented neutrophil

A

folate deficiency or b12 deficiency (pernicious)

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16
Q

Megaloblastic change cause

A

ONLY FOLATE AND B12 DEFICIENCY

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17
Q

Where is dietary folate present but what is the catch

A

Fresh leafy vegetables

Destroyed by overcooking/canning/processing

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18
Q

What causes decreased folate

A

IGNORANCE
POVERTY
APATHY

and elderly and alcoholics

OR

Increased demand

19
Q

When can there be increased folate demand

A 
PHYSIOLOGICAL
-Pregnancy
-Adolescence
-Premature babies
PATHOLOGICAL
-Malignancy
-Erythoderma (red skin, big turnover of skin cells)
-Haemolytic anaemias
20
Q

Lab diagnosis of folate

A

FBC and film
Folate levels in the blood
(doesn’t necessarily mean anaemic yet, but want to then prevent anaemia so give folae)

21
Q

Consequences of folate deficiency

A

1,Megaloblastic, macrocytic anemia

  1. Neural tube defects in developing fetus
  2. Increased risk of thrombosis in association with variant enzymes involved in homocysteine metabolism
22
Q

Neural tube defects associated with folate deficiency

A

Pregnant women with folate deficiency more likely to have kid with

spina bifida
acencephaly

23
Q

Role of folate in homocysteine

A

homocysteine is toxic, and converted to methionine with folate and b12

So note that the dietary methyl-THF is converted to THF using b12 as a cofactor to then allow THF to form the intermediates that can methylate dUMP–>dTMP.

But at the same time as converting methyl-THF to THF , you convert homocysteine to methionine.

24
Q

What is homocysteine levels assocaite with

A

Very high homocysteine levels are associated with
-atherosclerosis
-premature vascular disease
(thrombosis)

25
Q

Increased risk of what with mildly elevatted homocysteine levels

Why is food fortified with folate in the US

A

Mildly elevated levels of homocysteine are associated with:
cardiovascular disease DEFINITELY
arterial thrombosis PROBABLY
venous thrombosis POSSIBLY

1998 food and drug administration in the USA
Grains fortified with folic acid (100micrograms/day)

26
Q

Classic presentation of b12 deficiency

Consequences of b12 deficiency

A

TINGINLING FINGERS!

ROMBERG’S SIGN=PROPRIOCEPTION (fall over when eyes closed!)

Neurological problems

  • Bilateral peripheral neuropathy
  • Subacute comined degeneration of the cord (Posterior and pyramidal tracts of the spinal cord)
  • Optic atrophy
  • dementia
27
Q

History of b12 deficiency

A 
Paraesthesiae
Muscle weakness
Difficult walking
Visual impairment
Psychiatric disturbance
28
Q

b12 deficiency on examination

A

Absent reflexes and upgoing plantar responses

showing peripheral and central nerve problems respectively

29
Q

b12 deficiency cause

A

Poor absoprion

Reduced dietary intake (stores large and last 3-4 years, in animal produce so only vegans at risk)

Infections/infestations (Abnormal bacterial flora (stagnant loops), Tropical sprue, Fish tapeworm)

30
Q

Normal b12 absorptin

A

Method 1: In duodenum (slow and inefficient)

Method 2: B12 must combine with intrinsic factor
Intrinsic factor is made in the stomach
(parietal cells)
B12-IF binds to ileal receptors

31
Q

What is required for b12 absorption

A

Intact Stomach
Intrinsic factor
Functioning small intestine

32
Q

3 causes of reduction in instrinsic factor

A

a) post gastrectomy
b) gastric atrophy
c) antibodies to intrinsic factor or parietal cells

33
Q

What is pernicious anaemia

A

Autoimmune condition associated with very low IF… very gradual onset

Peak age: 60 family history

34
Q

How do you solve pernicious anaemia

A

Injectins of b12 (oral won’t be absorbed as no IF!)

35
Q

Males and pernicious anaemia

A

Males have a decreased life expectancy

- stomach cancer

36
Q

How can you check antibodies in pernicious anaemia

A

Intrinsic factor antibodies
(Occasionally found in other conditions)

(not great): Parietal cell antibodies
-90% adults with PA
-16% normal females over age of 60
Increased in relative of patients with PA

37
Q

Cuase of decreased b12 absorption (NOT pernicious anaemia)

A
  1. Diseases of small bowel (terminal ileum)
    a) Crohns
    b) Coeliac disease
    c) surgical resection
38
Q

Infections predisposing you to b12 deficiency

A

H pylori,
giardia
fish tapeworm
bacterial overgrowth

39
Q

Drugs associated with low b12

A

Metformin
Proton pump inhibitors e.g. omeprazole
Oral contraceptive pill

40
Q

Tests for b12

A

What is the cause of B12 deficiency?
Antibodies to parietal cells and intrinsic factor
Anitbodies for coeliac disease
Breath test for bacterial overgrowth
Stool for H Pylori
Test for Giardia
OLDEN DAYS - Shilling test (part I and part II)

41
Q

Outline the shilling test

A

Normally, b12 should come out in urine (radioactive label)

If it doesn’t, then it may coming out in the stool

  1. Give radioactive drink in b12… if comes out in urine then they must have absorbed b12 (so no pernicious)

If no b12 in urine…. they might not be absorbing b12 properly (pernicious anaemia OR small bowel disease) or haven’t corrected b12 deficiency before test.. i.e. it will go straight to the stores

  1. Give i.v IF and another radioactive b12….. if it comes out in the urine now, it means that there is pernicious anaemia. If still none in the urine, it must mean there is some small bowel disease.
42
Q

Treatment for b12 deficiency

A 
Injections of B12…. 1000ug (i.m)
3x/week for 2 weeks
Thereafter every 3 months
IF NEUROLOGICAL INVOLVMENT
B12 injections alternate days until no further improvement – up to 3 weeks
Thereafter every 2 months
43
Q

SBA:

A 49 y old man with grey hair and blue eyes presents with anaemia. His blood count is as follows:
Hb 90g/l WBC 4 x 109/l platelets 160 x 109/l MCV 110fl

tests?

A

Answer;

Blood (12 decks)

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