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Digestion And Metabolism > Minerals And Nutritional Anemias > Flashcards

Minerals And Nutritional Anemias Flashcards

1
Q

What are the functions and deficiency syndromes of iron?

A

Functions: Essential component of hemoglobin and iron- containing metalloenzymes

Deficiency symptoms: Hypochromic microcytic anemia

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2
Q

What are the functions of copper and its deficiency symptoms?

A

Function: Component of cytochrome c oxidase, dopamine β- hydroxylase, tyrosinase, lysyl oxidase, and involved in cross-linking collagen and keratin

Deficuency symptoms: Muscle weakness, neurologic defects, hypopigmentation, abnormal collagen cross-linking

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3
Q

Describe the effects of copper

A
  • Cofactor in redox reactions
    • Lysyl oxidase
      • Collagen Synthesis (Covalent cross-links) – Differentiate from vitamin C
    • Tyrosinase (Melanin synthesis)
    • Cytochromes (Electron transport chain)
    • Superoxide dismutase (Scavenger of reactive oxygen species)
  • Forms ceruloplasmin in liver (copper transport protein)
    • Helps in iron metabolis
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4
Q

Summarize copper metabolism

A
  1. Dietary copper transported to liver bound to albumin
  2. In hepatocytes, forms ceruloplasmin (secreted into plasma) (requires Copper transporting ATPase)
  3. Aged ceruloplasmin taken up by liver from plasma and copper secreted into bile (requires Copper transporting ATPase)
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5
Q

What is the role of ceruloplasmin in iron metabolism?

A
  • Ceruloplasmin (ferroxidase) converts ferrous iron to ferric form
  • Converts ferrous (absorbed iron) to ferric form and incorporates ferric iron into transferrin for transport of iron
  • Mobilizes ferric ions from ferritin and hemosiderin
  • Ceruloplasmin is a serum protein (a2-globulin)
  • Acute phase protein
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6
Q

What are the manifestations of copper deficiency?

A
  • Microcytic anemia (smaller RBCs)
    • Ceruloplasmin (ferroxidase) required for iron mobilization
    • Copper deficiency affects iron mobilization
  • Degradation of vascular tissue – decreased lysyl oxidase activity.
    • Increased risk of bleeding/ hemorrhage
  • Defects in hair: Hypopigmented discolored hai
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7
Q

What is Menkes syndrome (Menke kinky hair syndrome)?

A
  • Inherited defect in dietary copper absorption
  • Low plasma copper levels
  • X-linked disorder
  • Hair twisty, grayish and “kinky” (Tyrosinase)

• Aneurysms and neurological dysfunction
(low lysyl oxidase activity)

• Early age of presentation (1-2 years)

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8
Q

What is Wilson disease?

A
  • Autosomal recessive disorder
  • Accumulation of copper in liver, brain and eye
  • Mutation of copper transporting ATPase (ATP7B gene)
  • Over 30 mutations (Allelic heterogeneity)
  • Attaches copper to ceruloplasmin and excretes copper into bile
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9
Q

Outline the cause of Wilson disease

A
  1. Defective biliary copper excretion
    Defective copper incorporation into ceruloplasmin
  2. Accumulation of toxic levels in liver
  3. Liver damage – hepatitis and cirrhosis (presenting symptom)
  4. Excess copper spills into plasma
  5. • Eye: Kayser-Fleischer rings in cornea
    • Brain: Neurological damage causing
    neuropsychiatric symptoms (basal ganglia)
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10
Q

Describe the lab diagnosis of Wilson disease

A

Lab Diagnosis

  • Decreased serum ceruloplasmin
  • Increased urinary excretion of copper
  • Increased hepatic copper content
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11
Q

What are the Corneal findings of Wilson disease?

A

Kayser-Fleischer (KF) rings – Copper deposits in cornea

Patients with Kayser-Fleischer rings usually have basal ganglia (CNS) involvement

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12
Q

What is the significance of iron?

A

-Heme synthesis- Hemoglobin, myoglobin (in muscle)

  • RBCs contain hemoglobin (Largest storage form for iron)
  • Loss of RBCs results in loss of iron
  • For Redox reactions and component of cytochromes of electron transport chain
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13
Q

Describe dietary intake

A
  • Tightly regulated by body iron stores
  • Intestinal mucosal cells are iron sensors (requires HFE)
  • Higher body iron stores; less iron absorbed in intestine
  • Heme iron (red meat) absorbed better than inorganic iron (vegetarian)
  • Inorganic iron in ferrous form is absorbed
  • Ferric iron changed to ferrous iron in stomach
  • low pH in stomach and dietary vitamin C
  • Vegans risk of iron deficiency (high content of phytate and oxalate)
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14
Q

Explain iron transport and storage

A

Ceruloplasmin (ferroxidase) converts ferrous iron to ferric iron
which is incorporated to transferrin

  • Transferrin (transport protein) for ferric ion in plasma
    • B-globulin serum protein
  • Iron stored in liver and RES as ferritin and hemosiderin (ferric)
  • Tiny amounts of ferritin in blood – Measurement of serum ferritin levels indicators of body iron s
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15
Q

What are the lab tests for iron status?

A

Serum ferritin levels indicator of iron stores (Normal: 50-300 ng/ml)
• High serum ferritin in iron overload (hemochromatosis)
• Low serum ferritin in iron deficiency anemia

  • Serum iron (remember, iron is bound to transferrin)
    • Low serum iron levels in iron deficiency anemia
    • High serum iron levels in iron overload (hemochromatosis)
  • Transferrin saturation and Total iron binding capacity
  • Hemoglobin levels and hematocrit
  • MCV, MCHC – Red cell indicators of RBC size and hemoglobin concentration
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16
Q

What is the logic behind lab tests for iron status?

A
  • Serum iron: Iron bound to transferrin (Normal: 50-150 g/dL)
    • Serum iron decreased in iron deficiency anemia
    • Serum iron increased in iron overload
    • Total iron binding capacity (TIBC): Total number of iron binding sites on transferrin (transferrin levels) Normal: 250-400
    Ug/dl
  • TIBC increased in iron deficiency anemia
    • TIBC decreased in iron overload

• Percent saturation of transferrin: Percent of transferrin binding sites occupied by iron. Normally 1⁄3 binding sites
saturated with iron (Normal: 30% transferrin saturation) Total Iron Binding Capacity (TIBC) Explained
• Transferrin saturation decreased in iron deficiency anemia
• Transferrin saturation increased in iron overload

17
Q

What causes iron deficiency anemia?

A

• Most common nutritional deficiency

• Reduced dietary iron absorption: Vegans, low dietary vitamin C, achlorhydria
(low stomach HCl), high dietary fiber

• Infants, pregnant women and blood donors at risk

• Chronic bleeding: Increased menstrual bleeding, uterine fibroids, GI bleeding
(ulcer/ cancer), parasitic infestation

18
Q

What are the clinical features of iron deficiency anemia?

A 
Clinical features:
• Iron deficiency anemia – hypochromic microcytic 
• Fatigue and pallor
• Weakness, dizziness
• Brittle nails
• Pica (appetite for soil
19
Q

What are the lab tests of iron deficiency anemia?

A

Low serum ferritin levels (indicate low body iron stores)
Low serum iron levels

  • Low percent saturation of transferrin (<20%)
  • Increased TIBC
  • Low hemoglobin levels; low hematocrit
  • Low MCV (microcytic anemia) and low MCHC (hypochromic anemia)
  • Bone marrow iron stores - low
20
Q

What are the dietary modifications for management of iron deficiency?

A
  • Supplement iron rich foods

* Increase availability of dietary iron – vitamin C; Include heme iron (animal sources); Reduce dietary fiber

21
Q

What is hereditary hemochromatosis (iron overload)?

A
  • Autosomal recessive disorder; Common in Caucasians
  • Excessive iron absorption (HFE gene mutation)
  • Most frequent mutation is C282Y allele of HFE
    • However, other mutations are known (allelic heterogeneity)
    • Many are compound heterozygotes
  • Delayed age of onset
  • Males affected earlier than females – variable expressivity • Excessive accumulation of iron in skin, liver and pancreas
22
Q

What are the clinical features of hereditary hemochromatosis(iron overload)?

A

Excess iron causes free radical formation and DNA damage

Clinical Features: http://www.hemochromatosis.org/#videos
• More common in males; presenting age 40

  • Acute synovitis or chronic joint pain (knuckles)
  • Chronic fatigue (difficult to diagnose)

• Hepatomegaly; Liver damage – cirrhosis; hepatocellular
carcinoma

  • Diabetes – destruction of beta cells of pancreas
  • Cardiac dysfunction
  • Brownish skin pigmentation (Bronze orange color of skin)
  • ‘Bronze Diabetes’
23
Q

What are the lab tests for hereditary hemochromatosis?

A
  • High serum ferritin levels – indicate excessive iron stores
  • High serum iron levels
  • Transferrin saturation (>50%)
  • TIBC is decreased
24
Q

Describe the management of hereditary hemochromatosis?

A
  • Phlebotomy – removal of blood (donation of blood)
  • Dietary modifications – Reduce dietary iron content and iron absorption from diet
    • Reduce red meat (iron in meat is better absorbed)
    • High fiber content (fiber reduces iron absorption)
25
Q

What is nutritional anemia?

A
  • Anemia is a clinical sign
  • Reduced red cell mass
  • Hemoglobin levels <12 g/dL; and/ decreased RBC count
  • Measure hemoglobin concentration, hematocrit and RBC count
  • Erythropoiesis (RBC formation) in bone marrow depends on availability of nutrients, growth factors and precursor cells
  • Reduced nutrient availability results in nutritional anemia
26
Q

How is nutritional anemia classified based on MCV?

A

• Nutritional anemias based on RBC size
• Microcytic anemia (<80) due to reduced heme synthesis.
• Also seen in lead poisoning
• Macrocytic anemia (>100) due to reduced cell
division.
• Normocytic anemia (Normal MCV) – Protein energy malnutrition (PEM

27
Q

What is the type of anemia and lab test of pyridoxine deficiency?

A

Microcytic anemia

Low MCV; Elevated Homocysteine; Iron parameters - Normal

28
Q

What type of anemia and lab tests are done for copper deficiency?

A

Microcytic anemia

Low MCV; Low serum copper

29
Q

What are the types of anemia and lab tests. Done for vitamin B12 deficiency?

A

Macrocytic, megaloblastic anemia; Neuropsychiatric manifestations

Lab test: MCV – Increased; Increased Homocysteine; Increased methylmalonate; Low Vitamin B12 levels

30
Q

What are the types of anemias and lab tests of folic acid deficiency?

A

Macrocytic, megaloblastic anemia

MCV – Increased; Increased Homocysteine; Methylmalonate - Normal; Low Folic acid levels; Normal vitamin B12 levels

31
Q

Compare macrocytic anemias in folate deficiency and vitamin B12 deficiency

A

Vitamin B12 deficiency
• Clinical features: Anemia with associated neurological features
• Anemia – Macrocytic (MCV increased) and megaloblastic bone marrow
• Serum homocysteine and serum methylmalonate levels are elevated
• Anemia is due to folate trap
• Neurological features may be due to accumulation of methylmalonate (affects myelination)
• Risk factors: Parietal cell destruction (pernicious anemia); ileal mucosal disease or resection; vegan diet
• Serum vitamin B12 levels are low

Folate deficiency

• Clinical features: Macrocytic anemia
• Anemia – Macrocytic (MCV increased)
and megaloblastic bone marrow
• Serum homocysteine levels are elevated; Serum methylmalonate levels are normal
• Anemia is due to folate deficiency
• Risk factors: pregnancy, malabsorption syndrome, folate antagonist treatment
• Serum folate levels are low

Digestion And Metabolism (57 decks)

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