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NUR1142 > Module 2 - Macrocytic - Pernicious Anemia > Flashcards

Module 2 - Macrocytic - Pernicious Anemia Flashcards

1
Q

What is the most common type of macrocytic anemia?

A

PA - Pernicious anemia

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2
Q

This is caused by B12 deficiency

A

PA - Pernicious anemia

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3
Q

What is PA often associated with?

A

End stage type A chronic atrophic gastritis

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4
Q

Which population does PA commonly affect?

A

Individuals older than 30
Norther European descent
It has now been recognized in all populations and ethnic groups

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5
Q

What is the underlying problem in PA

A

Absence of intrinsic factor

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6
Q

What is intrinsic factor (IF)

A

a transporter required for gastric absorption of dietary vitamin B12

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7
Q

What is B12 needed for ?

A

a vitamin needed for nuclear maturation and DNA synthesis in red blood cells.

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8
Q

What can be some of the causes of IF deficiency?

A

-congenital or autoimmune process directed against gastric parietal cells

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9
Q

Congenital IF deficiency is a _________

A

Genetic disorder with autosomal recessive inheritance pattern.

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10
Q

Does the autoimmune form of IF deficiency have a genetic component?

A

Yes

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11
Q

What percentage of individuals related to person with PA also have PA?

A

20-30%

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12
Q

Relatives , especially first degree female relatives will show higher frequency of __________

A

the presence of gastric autoantibodies

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13
Q

PA also if often a component of what?

A

autoimmune polyendocrinopathy

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14
Q

What is autoimmune polyendocrinopathy

A

This disorder includes a cluster of autoimmune diseases of endocrine organs (e.g., chronic autoimmune thyroiditis, type 1 diabetes mellitus, Addison’s disease, primary hypoparathyroidism, Graves’ disease, and myasthenia gravis) that frequently present as comorbidities.

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15
Q

What is typically associated with PA?

A

Type 1 DM and autoimmune thyroiditis

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16
Q

Most cases of PA result from what?

A

autoimmune gastritis (Type A chronic gastritis)

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17
Q

Gastric atrophy in autoimmune gastritis results from ?

A

Destruction of parietal and zymogenic cells

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18
Q

What type of autoantibodies does an individual with PA have?

A

Individuals with PA commonly have autoantibodies against the gastric H+–K+ ATPase, which is the major protein constituent of parietal cell membranes.

19
Q

What’s the results of destruction of gastric parietal cell?

A
  • Causes gastric mucosal atrophy and results in a deficiency of all secretions of the stomach.
    -This includes hydrochloric acid, pepsin, and IF.
20
Q

Initiation of the autoimmune process may be secondary to what type of infection?

A

H.Pylori

21
Q

What are some of the environmental factors that may contribute to chronic gastritis?

A
  • excessive alcohol or hot tea ingestion and smoking
    -Complete or partial removal of the stomach (gastrectomy) causes IF deficiency.
  • ## Medications known as proton pump inhibitors (PPIs) are used to decrease gastric acidity and may decrease vitamin B12 absorption, but it is not thought that they actually cause PA.
22
Q

People with type A chronic gastritis are at risk for ?

A

developing gastric adenocarcinoma and gastric carcinoid type 1

23
Q

What is the rate of carcinoma in individuals with PA?

A

2-3%

24
Q

How long does it take for PA to develop?

A

It develops slowly: 20-30 years. By the time a person seeks treatment, it is usually severe.

25
Q

Why are early symptoms of often ignored?

A

They are non-specific and vague

26
Q

What are some of the early symptoms of PA?

A
  • infections
  • mood swings
  • and GI
  • cardiac
  • kidney diseases
27
Q

When does classic symptoms of PA usually manifests?

A

When Hgb level has decreased to 70-80 g/L

28
Q

What are the classic symptoms of PA

A
  • Weakness
  • fatigue
  • paresthesia of feet and finger
  • difficulty walking
  • loss of appetite
  • abdominal pain
  • weight loss
  • sore, smooth, beefy tongue
  • skin may become lemon yellow (sallow) – this is caused by a combination of pallor and jaundice
  • Hepatomegaly - a sign of right sided HF ( may be present in the older person along with nonpalpable splenomegaly )
29
Q

Neurological manifestation of PA results from ?

A

Nerve demyelination that may produce neuronal death.

30
Q

What parts of the spinal cord may be affected

A

Posterior and lateral columns

31
Q

Damage to the nerves can cause?

A
  • Loss of position and vibration sense
  • ataxia
  • spasticity
32
Q

Low levels of B12 have been associated with what other disorders?

A

Neurocognitive disorders

33
Q

An increased prevalence of serum vitamin B12 deficiency has been reported among individuals with
what type of disease?

A

Alzheimers

34
Q

What type of manisfestations can indicate that the cerebrum is involved?

A

Manifestations of affective disorders , most commonly depressive types.

35
Q

Diagnosis of PA are based on what?

A

Clinical Manifestations and several test resutls

36
Q

What are some of the tests ?

A
  • Blood test, bone marrow aspiration, serological studies, and gastric biopsy (reveals total achlorhydria - absence of hcl) - diagnostic for PA.
  • Presence of circulating antibody against parietal cells and IF is also useful in diagnosis
37
Q

What are some of the treatments?

A
  • Oral B12 (cobalamin) - treatment of choice. Dosing for PA or food bound cobalamin malabsorption is 1000 ug/day
  • If not corrected by the oral administration then monthly Vb12 injections.
38
Q

What determines the effectiveness of cobalamin replacement therapy?

A

rising reticulocyte count

39
Q

When does bloodcount return to normal?

A

Within 5-6 weeks

39
Q

Can PA be cured?

A

No, maintenance therapy is lifelong

40
Q

Is untreated PA fatal ?

A

Yes, usually because of HF

41
Q

What are causes of relapses?

A

results of nonadherence therapy

42
Q
A

NUR1142 (112 decks)

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