28 Disorders of Nutrition Flashcards

1
Q

Erythropoiesis
Building blocks:
?, ?, ?, ?

Regulation:
?

A

Erythropoiesis
Building blocks:
Hemoglobin, Iron, Vitamin B12, Folate (B9)

Regulation:
kidney erythropoietin

A higher than normal reticulocytes count may indicate: Anemia due to red blood cells being destroyed earlier than normal (hemolytic anemia) Bleeding. Blood disorder in a fetus or newborn (erythroblastosis fetalis)

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2
Q

Review the metabolism and biological functions of iron

Metabolism:
- ? are responsible for ?.
- Upon absorption, iron circulates around the body bound to the protein ? and is taken up by different tissues for utilisation.
- The ? system, which includes the splenic macrophages, recycles iron from ?.
- Among many other functions, the liver produces the ?.
- ? controls the release of iron from enterocytes and macrophages into the circulation and is regarded as the master regulator of systemic iron metabolism.

Low Demand:
- absorbed iron is stored within the ? in the form of ?

High Demand:
- absorbed ferrous iron is transported across the ? into blood controlled by ? (?), a ferrous iron export protein that modulates how much of the enterocyte iron is absorbed into circulation and made available to the body
- expression is tightly regulated by the hepatic hormone heparin.

A

Metabolism:
- Duodenal enterocytes are responsible for dietary iron absorption.
- Upon absorption, iron circulates around the body bound to the protein transferrin and is taken up by different tissues for utilisation.
- The reticuloendothelial system, which includes the splenic macrophages, recycles iron from senescent erythrocytes.
- Among many other functions, the liver produces the hormone hepcidin.
- Hepcidin controls the release of iron from enterocytes and macrophages into the circulation and is regarded as the master regulator of systemic iron metabolism.

Low Demand:
- absorbed iron is stored within the enterocyte in the form of ferritin

High Demand:
- absorbed ferrous iron is transported across the basolateral membrane into blood controlled by ferroportin 1 (FPN1), a ferrous iron export protein that modulates how much of the enterocyte iron is absorbed into circulation and made available to the body
- FPN1 expression is tightly regulated by the hepatic hormone hepcidin.

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3
Q

Iron Deficiency Anemia (IDA)

Possible Causes? 3

A

Increased requirements
- Growth, pregnancy

Limited Supply
- Poor intake (malnutrition)
- Malabsorption

Increased loss:
- Bleeding
- Phlebotomy (hospital acquire anemia)

A phlebotomy is a procedure to remove a specific amount of blood from a vein in your arm.

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4
Q

Clinical presentation of IDA
9

A
  • fatigue
  • pallor
  • weak
  • dizzy
  • headaches
  • incr. HR & breathing
  • poor growth & neurodevelopment
  • impaired immune response
  • reduced cognitive ability & physical performance
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5
Q

How is iron deficiency anemia (IDA) treated?

A

1.Oral iron therapy
- nutrients and medications influence bioavailability
- Gastrointestinal tract toxicity

2.Parenteral Iron
- Iron injections are administered either directly into the blood stream through an IV line or into the muscle
- Faster repletion of iron stores
- Allergic reactions

3.Recombinant human erythropoietin

4.Blood transfusion

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6
Q

What are four iron status markers?

A
  1. Serum Iron: Lots of variability (not a good marker)
  2. Serum Ferritin (FER): Long term stores
  3. Total iron binding capacity (TIBC) : indirect measurement of transferrin
  4. Transferrin saturation: %= Iron/TIBC x 100

High TIBC means that you have low levels of iron. When there isn’t much iron to attach to, you’ll have a lot of free transferrin in your blood

Low TIBC means that you don’t have very much transferrin available to bind to iron. In other words, you have high iron levels, so most of the transferrin is bound to it, which leaves very little free in your blood.

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7
Q

What is microcytic anemia?

A

Lack of iron compromises hemoglobin production and leads to reduction in development of new RBC in the bone marrow -> smaller than normal RBCs

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8
Q

Review the metabolism and biological functions of vitamin B12

  • ? soluble vitamin
  • Structure?
  • Sources? 3
    • It is coabsorbed with ? in the ? after being extracted by ?
A

Vitamin B12 (Cobalamin)
- water-soluble vitamin
- Tetrapyrrole rings, central cobalt atom
- Humans lack enzymes to produce Vit B12 so sources include: microbial synthesis // meat // dairy
- It is coabsorbed with intrinsic factor (IF) in the terminal ileum after being extracted by gastric acid

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9
Q

Biological actions of Vitamin B12

  • Co-enzyme that carries out its actions with ? for ?, ?, ? and ?
  • Label image
  • In chronic B12 deficiency, there may be an elevation in ? and/or ?
  • In chronic folate deficiency, there is an elevation in ?
A
  • Co-enzyme that carries out its actions with folate for cell growth, DNA synthesis, RBC production, and neurological function
  • Label image
  • In chronic B12 deficiency, there may be an elevation in homocysteine and/or methylmalonyl CoA
  • In chronic folate deficiency, there is an elevation in homocysteine
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10
Q

Review the metabolism and biological functions of vitamin B12

Clinical presentation of B12 Deficiency: 2

A

1.Neuropsychiatric:
- Developmental delay, hypotonia, cognitive impairment, peripheral neuropathy, gait, irritability, fatigue, weakness

2.Gastrointestinal
- Feeding difficulties, glossitis, decreased appetite

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11
Q

Macrocytic anemia evaluation

What is Macrocytic Anemia

A

Impaired DNA synthesis leads to increased RBC growth without cell division

Macrocytic anemia is a blood disorder that causes your bone marrow to make abnormally large red blood cells. It’s also a type of vitamin deficiency anemia. This condition happens when you don’t get enough vitamin B12 and/or vitamin B9 (folate).

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12
Q

How is macrocytic anemia evaluated?

Hematology ?
Biochemistry ?

A

Hematology:
- CBC, peripheral blood smear
- MCV - high
- Reticulocyte count (Low: inadequate RBC production)

Biochemistry:
- Plasma Vit B12
- Plasma homocysteine (secondary test)
- Plasma methylmalonic acid (secondary test)
- Anti-IF/Parietal cell Ab’s
- Liver and thyroid function
- Bone marrow examination

MCV stands for mean corpuscular volume. An MCV blood test measures the average size of your red blood cells.

A complete blood count (CBC) is a blood test used to evaluate your overall health and detect a wide range of disorders, including anemia, infection and leukemia. A complete blood count test measures several components and features of your blood, including: Red blood cells, which carry oxygen

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13
Q

How is Vitamin B12 deficiency treated?

A
  • supplements
  • Intramuscular injection
  • Lifelong for pernicious anemia and malabsorption patients
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14
Q

Which of the following is incorrect about vitamin B12:
a) Deficiency is associated with microcytic anemia
b) It is a cofactor involved in DNA synthesis
c) Methylmalonic acid and homocysteine are
surrogate markers
d) The human body is unable to synthesize it
e) Lack of intrinsic factor can cause deficiency

A

Which of the following is incorrect about vitamin B12:
a) Deficiency is associated with microcytic anemia
b) It is a cofactor involved in DNA synthesis
c) Methylmalonic acid and homocysteine are
surrogate markers
d) The human body is unable to synthesize it
e) Lack of intrinsic factor can cause deficiency

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15
Q

Bone remodeling = balance between bone formation (?) and bone resorption (?)

Regulated by:
- 7

Unmineralized matrix (called ?) composed of 4 secreted by ?

Unmineralized matrix eventually undergoes ? and ? involving 3 to form ? or layers in the bone matrix (MINERALIZED MATRIX)

A

Bone remodeling = balance between bone formation (osteoblasts) and bone resorption (osteoclasts)

Regulated by:
1. Phosphorous
2. Calcium
3. Vitamin D
4. PTH
5. GH
6. Estradiol
7. Thyroid hormones

Unmineralized matrix (called OSTEOID) composed of Collagen, ALP, osteocalcin, chondroitin sulfate secreted by osteoblasts

Unmineralized matrix eventually undergoes calcification and mineralization involving Ca, phosphorous, Mgto form lamellae or layers in the bone matrix

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16
Q

Endocrine regulation of Calcium

What happens when Ca++ in ECF is decreased?

A

Parathyroid hormones secrete PTH
PTH acts on
- kidney (increase Calcium reabsorption and phosphate excretion)
- Bone (increase Ca++ pumping to ECF and increase bone resorption)

Vitamin D in small intestine increase Ca++ absorption

17
Q

Clinical presentation of calcium disorders

Hypercalcemia (4)
Hypocalcemia (4)

A

Hypercalcemia (4)
1. Moans
2. Bones
3. Groans
4. Stones

Hypocalcemia (4)
1. Muscle pain
2. Seizure
3. Tetany
4. Arrythmias

18
Q

What is Rickets?

What is Osteomalacia?

Possible Causes (3)

Presentation

A

Rickets = deficient mineralization of the Growth Plate (children)
Osteomalacia = Deficient mineralization of the Bone Matrix

  • Nutritional deficiency (Ca++ // Vitamin D)
  • Vitamin D resistance
  • Renal Phosphate wasting

Short stature, bone deformities, hypocalcemic seizures

Asymptomatic, bone pain, mm weakness, fractures; can lead to osteoporosis in adults

Rickets is the softening and weakening of bones in children, usually because of an extreme and prolonged vitamin D deficiency. Rare inherited problems also can cause rickets. Vitamin D helps your child’s body absorb calcium and phosphorus from food.

Osteomalacia is softening of the bones. It most often occurs because of a problem with vitamin D, which helps your body absorb calcium. Your body needs calcium to maintain the strength and hardness of your bones. In children, the condition is called rickets

19
Q

A common, systemic skeletal disorder
- Affects women more than men
- Compromised bone strength leading to risk of fractures
- Failure to achieve peak bone mass
- Imbalance between bone formation and bone resorption
- Osteoclasts break down too much bone before it can be replaced

What is it!!

A

Osteoporosis

20
Q

OSTEOPOROSIS
- A common, systemic ? disorder
- Affects ? more than ?
- Compromised ? leading to risk of ?
- Failure to achieve ?
- Imbalance between ? and ?
- ? break down too much bone before it can be replaced

A
  • A common, systemic skeletal disorder
  • Affects women more than men
  • Compromised bone strength leading to risk of fractures
  • Failure to achieve peak bone mass
  • Imbalance between bone formation and bone resorption
  • Osteoclasts break down too much bone before it can be replaced
21
Q

How is osteoporosis diagnosed?

A

Personal hx of fragility fracture

Measurement of bone mineral density (BMD)
- Dual energy X-ray absorptiometry (DXA)

Assessment of clinical risk factors

22
Q

Five ways in which osteopororsis is treated?

A
  1. Balanced diet
  2. Smoking cessation, avoid alcohol abuse
  3. Regular exercise
  4. Calcium and Vitamin D supplementation
  5. Drugs
23
Q

Relationship between the kidneys and vitamin D

A

The kidneys have an important role in making vitamin D useful to the body. The kidneys convert vitamin D from supplements or the sun to the active form of vitamin D that is needed by the body.

24
Q

What is the role of PTH
a) Stimulate calcium resorption from bone
b) Stimulate vitamin D absorption from the gut
c) Stimulate synthesis of vitamin D from the
kidney
d) All of the above
e) A & C

A

What is the role of PTH
a) Stimulate calcium resorption from bone
b) Stimulate vitamin D absorption from the gut
c) Stimulate synthesis of vitamin D from the
kidney
d) All of the above
e) A & C

PTH and Vitamin D form a tightly controlled feedback cycle, PTH being a major stimulator of vitamin D synthesis in the kidney while vitamin D exerts negative feedback on PTH secretion.