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3154 Haematology > IC3+7 Anemia > Flashcards

IC3+7 Anemia Flashcards

1
Q

3 broad classification of anemia

A
  1. Hypoproliferative
  • marrow damage
  • dcr stimulation (e.g., due to renal disease, inflammation, metabolic disease)
  • iron deficiency
  1. Maturation disorder

Cytoplasmic defects

  • iron deficiency
  • thalassemia
  • sideroblastic

Nuclear maturation defect

  • folate deficiency
  • vit B12 deficiency
  1. Hemolysis/hemorrhage
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2
Q

What is the Hb cut off for females and males respectively?

A

Females <11.9
Males <12.9

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3
Q

Top 4 most common causes of anemia

A
  1. iron deficiency
  2. vit b12/folic acid deficiency
  3. anemia of inflammation/chronic disease
  4. drug-induced anemia
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4
Q

History taking for pt with suspected anemia

A
  • recent blood loss
  • duration of anemia (genetic or acquired)
  • S&S - exertional symptoms due to reduced O2 carrying capacity?
  • Comorbidities - could it be anemia of chronic diseases?
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5
Q

Physical examination of pt with suspected anemia

A
  • Pallor (nail bed, eyelid, tongue)
  • Jaundice (hemolytic anemia)
  • Bruising/bleeding (petechiae, ecchymoses)
  • Lymphadenopathy, hepatosplenomegaly, bone tenderness
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6
Q

Symptoms of anemia (acute vs chronic)

A

Acute: lightheadedness, tachycardia, dyspnea

Chronic: weakness, fatigue, headache, vertigo, pallor

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7
Q

Laboratory evaluation for pt with suspected anemia

A
  • FBC - Hb (F <11.9; M<12.9)
  • Reticulocyte count - incr count suggest body trying to produce more RBCs (note that if R count is low, it could suggests bone marrow failure)
  • Peripheral smear - observe micro/macrocytic, hypochromic etc.
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8
Q

Anemia diagnosis:

  • Iron deficiency anemia
A

Microcytic
Hypochromic
Low serum ferritin, decreased transferrin saturation

*Very few small Hb-poor erythrocytes
*Iron deficiency inhibits hemoglobin synthesis

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9
Q

Anemia diagnosis:

  • Folic acid/Vit B12 deficiency
A

Macrocytic, hyperchromic

*Very few large, Hb-rich erythrocytes
*Folic acid/Vit B12 deficiency inhibits DNA synthesis - cell multiplication

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10
Q

Anemia diagnosis:

  • Acute blood loss/Hemolysis
A

Normocytic (normal MCV)

High reticulocyte count

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11
Q

Anemia diagnosis:

  • Anemia of chronic disease (e.g., CKD, RA, IBD)
A

Microcytic

Normal/high ferritin

Low TIBC (total iron binding capacity)

Serum iron decreased

*Due to release of chemical hepcidin in chronic inflammatory states => regulates iron

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12
Q

Anemia diagnosis:

  • pt has microcytic, normal/high ferritin, normal/high TIBC
A

Lead intoxication
Thalassemia (insufficient Hb)
Sideroblastic (lack of RBC, too much iron)

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13
Q

Anemia diagnosis:

  • Drug-induced anemia
A

Macrocytic

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14
Q

[Iron deficiency anemia]

Causes of iron deficiency anemia

A

Either blood/iron loss or reduced iron absorption

*Blood loss more common

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15
Q

[Iron deficiency anemia]

What might cause reduced iron absorption

A
  • Gastric bypass
  • PPIs (incr pH causes reduced iron absorption)
  • Gastritis
  • Celiac disease
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16
Q

[Iron deficiency anemia]

Treatment of IDA

A

1000-1500mg elemental iron for complete supplementation, at least 3-6 months

Daily dose: 30-40mg to 200mg of elemental iron, divided into 2-3 doses

For patients with IDA, the generally recommended dose is about 150 to 200 mg of elemental iron daily, usually in two or three divided doses to maximize tolerability. If patients cannot tolerate this daily dose of elemental iron, smaller amounts of elemental iron (eg, single 325­mg tablet of Fe2+ sulfate) usually are sufficient to replace iron stores, although at a slower rate.

17
Q

[Iron deficiency anemia]

Which iron formulation contains 100% elemental iron

A

Iron polymaltose

18
Q

[Iron deficiency anemia] - IC3

What other oral or parenteral formulations are there?

A

Oral - ferrous sulphate

IV - iron sucrose

19
Q

[Iron deficiency anemia]

Side effects of iron supplementation

A
  • Constipation
  • GI complaints: metallic taste, nausea, flatulence, constipation, diarrhea, epigastric distress, vomiting
20
Q

[Iron deficiency anemia] - IC3

Overdose can lead to toxicity as there is minimal elimination of iron in the feces, bile, urine, and sweat

What are the acute and chronic toxicities that may result?

A

Acute:

  • Necrotizing gastroenteritis with vomiting, abdominal pain
  • Bloody diarrhea followed by shock, lethargy, dyspnea, metabolic acidosis, coma and death

Chronic:

  • Hemochromatosis - iron deposit in heart, liver, pancreas, other organs => resulting in organ failure and death
21
Q

[Iron deficiency anemia] - IC3

Treatment of iron overdose

A

Iron chelators:

  • Parenteral deferoxamine
  • Oral deferasirox
22
Q

[Anemia of inflammation]

List some conditions a/w anemia of chronic diseases

A
  • Malignancy
  • HIV infection
  • Rheumatologic disorders
  • Inflammatory bowel disease
  • Castleman disease
  • Heart failure
  • Renal insufficiency
  • COPD
23
Q

[Vit B12 deficiency]

Vit B12 is almost exclusively found in ____

A

Meats

*Not found in vegetables

24
Q

[Vit B12 deficiency]

Common causes

A
  1. Reduced absorption (due to lack of intrinsic factor or gastric disruption)
  2. Nutritional (lack of Vit B12 intake from diet)
  • PPIs, H2RAs may increase gastric pH, reduce absorption
  • H. pylori infection may disrupt gatric mucosa, reduce absorption
  • Metformin increases the risk of Vit b12 malformation
25
Q

[Vit B12 deficiency]

What is pernicious anemia?

A

Pernicious anemia is a type of Vit B12 deficiency anemia

Pernicious anemia is an autoimmune condition that attacks the stomach - anti-intrinsic factor antibodies (IFA) and anti-parietal cell antibodies (PCA)

Intrinsic factor binds to vitamin B12. After attaching, intrinsic factor and B12 travel to the intestines to be absorbed into the bloodstream.

Without intrinsic factor, absorption of oral Vit b12 is limited.

26
Q

[Vit B12 deficiency]

Treatment options for Vit B12 deficiency

A

Oral - Cyanocobalamin
Parenteral - Hydroxocobalamin

*Hydroxocobalamin precursor preferred to cyanocobalamin as it has more extensive protein binding, and hence retained for a longer time in circulation

27
Q

[Vit B12 deficiency]

Adverse effects of Vit B12 supplementation

A
  • Photosensitivity
  • Injection site pain (parenteral)
  • Hypertension, hot flushing, arrhythmias secondary to hypokalemia, GI disturbances, dizziness, tremor, headache, paresthesia, chromaturia, acneiform, bullous eruptions, rash, itching
28
Q

[Vit B12 deficiency]

Treatment for cobalamin deficiency due to causes other than pernicious anemia

A

Oral Vit b12 1000-2000ug daily

29
Q

[Vit B12 deficiency]

Treatment for pernicious anemia

A

Parenteral (IM/SQ) Vit B12 given 1000ug daily x1w, 1000ug weekly for 4w, 1000ug monthly for life

PO is often insufficient because some absorption of Vit B12 might depend on intrinsic factor (however, there is also mass action, hence perhaps at initial stages may still consider PO Vit B12)

*Note that: if pt as autoimmune condition, need Vit b12 supplementation for life

30
Q

[Folic acid deficiency]

Dosing and duration of folic acid supplementation

A

1mg/d folate for 1-4 months or until hematologic recovery is achieved

Note supratherapeutic dose can be used (e.g., folic acid 5mg)’; assuming normal renal function

31
Q

[Folic acid deficiency]

Folic acid metabolism

A

Folic acid is metabolised in the liver and plasma, and converted to active metabolite, 5 methyltetrahydrofolate (5MTHF); undergoes enterohepatic circulation

32
Q

[Folic acid deficiency]

Adverse effects of folic acid

A
  • GI disturbances: bitter or bad taste, nausea, abdominal distension, flatulence
  • Immune system disorders: allergic reactions (rash, pruritus, erythema, urticaria, dyspnea, shock)
  • Metabolism and nutrition disorders: anorexia (rare)
33
Q

[Folic acid deficiency]

Special precautions for folic acid use

A
  • Folate-dependent tumors, hemolytic anemia, alcoholism
  • Women with pre-existing diabetes, obesity, FH of neural tube defects, previous pregnancy affected by neural tube defect
  • Not appropriate for monotherapy in pernicious, aplastic, or normocytic anemias, when anemia is present with Vit B12 deficiency
  • Children, pregnancy and lactation
34
Q

[Folic acid deficiency]

DDIs with folic acid

A
  • Reduce plasma conc. of anticonvulsants (e.g., phenytoin, phenobarbital, carbamazepine, valproic acid)
  • Enhance efficacy of lithium
  • Decrease the therapeutic effect of methotrexate chemotherapy
  • Increased elimination with aspirin
  • Reduced absorption w sulfasalazine and triamterene
  • Chloramphenicol and Bactrim may interfere with folate metabolism
35
Q

[Erythropoiesis Stimulating Agents]

  • Used in? (where pdn of EPO is lacking)
A

The two primary FDA-approved indications for ESAs are anemia secondary to chronic kidney disease and chemotherapy-induced anemia in patients with cancer.

36
Q

[Erythropoiesis Stimulating Agents]

List the different types of ESAs

A
  • Epoetin alfa
  • Darbepoetin alfa
  • Methoxy polyethylene glycol-epoetin beta (conjugation with PEG prolongs half-life allowing 2w or 4w dosing interval)
37
Q

[Erythropoiesis Stimulating Agents]

Contraindications to the use of ESAs

A
  • Uncontrolled hypertension
  • Hypersensitivity (rare)
38
Q

[Erythropoiesis Stimulating Agents]

Adverse effects

A
  • Hypertension
  • Edema
  • Increased platelet count, thrombosis, stroke,
  • Hyperkalemia
  • Seizures
  • Myalgia, arthralgia, Iimb pain
  • GI effects: nausea and vomiting

Epoetin alfa - pruritus
Darbepoetin alfa - dyspnea, cough, bronchitis

39
Q

[Erythropoiesis Stimulating Agents]

Special precautions to the use of ESAs

A
  • Hypertension
  • History of seizures
  • Ischemic vascular disease
  • Hepatic impairment
  • Renal impairment
  • Sickle cell anemia
  • Pregnancy
  • Lactation
  • Children

3154 Haematology (14 decks)

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