Trace element : Iron

Ans. is ‘a’ i.e., Thalassemia; ‘c’ i.e., Anemia in chronic disease

Ans. is None

In normal individuals transferrin is about 33% saturated with iron, yielding serum iron levels that average 120 g/dl in men and 100 g/dl in women. Thus the total iron binding capacity of serum is in the range of 300 to 350 g/dl (30-35 mg/litre).

Ans. is ‘c’ i.e., MCHC

Ans. is `c’ i.e., Testis

In hemochromatosis, hypogonadism is caused by impairment of hypothalamic pituitary function and not due to deposition of Iron in the Testis.

Hemochromatosis

• Hemochromatosis is characterized by the excessive accumulation of body iron, most of which is deposited in parenchymal organs such as liver and pancreas.

o The total body content of the iron is tightly regulated, as the daily losses are matched by gastrointestinal absorption. In hereditary hemochromatosis, regulation of intestinal absorption of dietary iron is lost, leading to net iron accumulation of 0.5 to 1.0 gm/year.

o It may be recalled that the total body iron pool ranges from 2-6 gm in normal adults; about 0.5 gm is stored in the liver 98% of which is hepatocytes. In hemochromatosis the iron accumulation may exceed 50 gm, over one third of which accumulates in the liver.

o The iron accumulation is life long, the rate of net iron accumulation is 0.5 to 1.0 gm/year. The disease manifests itself typically after 20 gm of storage iron have accumulated. The disease first mainfests itself in the fifth to sixth decades of life.

o Excessive iron is directly toxic to host tissues

o The clinical features of hemochromatosis are characterized principally by deposition of excess iron in the following organs in decreasing order of severity.

Liver (95%)                   

o Usually the first organ to be affected.

• Hepatomegaly seen in most of the cases.
• Micronodular cirrhosis is characteristic
• Hepatocellular carcinoma develops in 30% patients Skin (90%)                     

o Excessive skin pigmentation (Bronzing of the skin)

o Skin pigmentation results partially due to hemosiderin deposition and mainly due to melanin deposition

• Usually diffuse or generalized, but more pronounced on the face, neck and extensor aspects of lower forearms Pancreas (65%)            

o Leads to diabetes mellitus Joints (25-50%)            

o Arthropathy

• Polyarthritis

Cardiac                        

o Congestive heart failure o Arryhthmia

• Cardiomyopathy (Restrictive)

Hypogonadism o These changes are primarily the result of decreased production of gonadotropins due to impairment of hypothalamic-pitui tary function by iron deposition however, primary testicular dysfunction may be seen in some cases

A i.e. Desferoxamine

Ans. is ‘b’ i.e., Duodenum

Iron is absorbed in the duodenum and proximal jejunum.

Ans. is ‘b’ i.e., Iron dextran

o Iron dextran can be given i.m. or i.v., while iron-sorbitol-citric acid is given only i.m.

Ans. is ‘a’ i.e., 4.4 body weight (kg) Hb deficit (g/dl)

• Total parenteral iron requirement can be calculated by :‑ 4.3 x Body weight (kg) x Hb deficit (g/dl)

Ans. is ‘c’ i.e., Vitamin C

o Factors facilitating iron absorption – Acid, ascorbic acid (Vit C), amino acids containing SH radical, meat.

Ans. is ‘b’ i.e., Deferiprone; ‘c’ i.e., Deferasirox

Ans. is None

Correct answer is 6 months.

Ans. is ‘c’ i.e., Serum ferritin depletes first

o Iron is absorbed from proximal small intestine mainly from duodenum.

o Cow milk has slightly more amount of iron than breast milk. However, bioavailability of iron of breast milk is much greater than cow milk.

Clinical manifestations

o Pallor is most important sign of iron deficiency. Infact WHO recommended the use of palmar pallor as screening measure for anemia.

o Pagophagia, the desire to ingest unusual substances such as ice or dirt may be present.

o In some children, the ingestion of lead containing substances may lead to concomitant plumbism & helminthic parasitic infection.

o In severe anemia, irratibility and anorexia are prominent. Tachycardia and cardiac dilatation occur. Systolic murmur is often present.

o Iron deficiency affects attention span, alertness and learning in both infant and adolescents.

Laboratory findings

o S. ferritin depletes first

o Next, serum iron level decreases, the iron binding capacity of serum (serum transferrin) increases, and percent saturation (transferrin saturation) is reduced.

o RDW is increased in iron deficiency anemia.

Ans is ‘a’ i.e., Decreased irritability

“When specific iron therapy is given, patients often show rapid subjective improvment, with disappearance or marked diminution offatigue, lassitude, and other nonspecificc symptoms (e.g. irritability). This response may occur before any improvement in anemia observed” Wintrobe’s

o The earliest hematological evidence of response of treatment is an increase in the percentage of reticulocytes and their hemoglobin content.

o So,

          Overall earliest indicator of improvement       decreased fatigue, lassitude and other nonspecific symptoms

          Earliest hematological evidence of improvement —> Increased reticulocyte count.

. Ans. is ‘a’ i.e., Increased Reticulocyte count

Reticulocyte count is the first to rise. This is followed by elevation of haemoglobin levels. Body iron stores are restored after correction of haemoglobin levels.

`Rise in Reticulocyte count occurs by the second or third day. This is followed by elevation of haemoglobin levels. Body iron stores are repleted after correction of haemoglobin levels. – Ghai

Ans. is ‘c’ i.e., 4 x wt (kg) x Hb deficit (gm/dl)

o Blood volume averages 75 to 80 ml/kg. Each gram of hemoglobin contains 3.4 mg of iron. 50% of more iron should be given to replenish iron stores. Therefore iron requirements are determined from the equation.

Iron (mg) = wt (kg) x Hb deficit (g/dl) x 80/100 x 3.4 x 1.5 = wt (kg) x Hb deficit (g/dl) x 4

Ans. is ‘b’ i.e., Desferrioxamine IV 100 mg & ‘c’ i.e., X-ray abdomen

Iron poisoning

• Ingestion of a number of ferrous sulphate tablets may cause acute iron poisoning.

Clinical features

• Severe vomiting                          o Diarrhea

o GI bleeding                                      o There may be severe shock, hepatic & renal failure

Treatment of Iron poisoning

o Because iron is radio opaque an abdominal radiography may confirm the ingestion. Repeat radiograph may help with assessment of efficiency of gastric decontamination methods.

o Ipecac-induce emesis may be used to remove tablets from the stomach.

o Gastric lavage is not recommended in children because of its inefficiency.

o Activated charcoal does not adsorb iron and should not be used.

• Whole bowel irrigation may be of benefit.

o If tablets adhere to gastric mucosa, removal by endoscopy.

Desferrioxamine is a specific shelter of iron and is the antidote of choice.

Ans. is ‘d’ i.e., Milk

“Iron content of milk is law in all mammalian speles”. – Park

Source of iron

There are two major forms of iron.

1. Haeni-iron

• Better absorbed
• Less important source of iron in Indian diet.

a Sources are —> Liver, meat, pouliy and fish (hods of animal origin).

2. Non-haem iron

Poorly absorbed but is the important source of iron in the diet of a large majority of Indian people.

Sources are —> Vegetable origin, i..e, cereals, green leafy vegetables, Leugumes, nuts, oilseeds, jaggery and dried fruits.

Ans. is ‘b’ i.e., Meat

“Red meat is the richest source of iron” – Artcle

Ans. is ‘c’ i.e., Meat

Ans. is ‘d’ i.e., Cashew nut

o Among the given options cashew nut has maximum iron (9%). Almonds (7%), Pistachos (7%) and ground nut have iron less than cashew nut.

Ans. is ‘c’ i.e., Mucosal block in the intestinal cells according to iron requirement

 “Iron absorption is regulated according to the demand, e.g., when thee is iron deficiency, absorption increases” Robbins 644

• Various other factors also influence the absorption of iron ‑

Factors affecting iron almrption

A) Decreasing absorption

By complexing (Forming chelate) with iron

• Phytates                  
• Milk                     
• Tetracycline
• Phosphates        
• EDTA

o By opposing reduction of ferric form to ferrous form.

• Pancreatic secretions          
• Antacids            
• Alkalies 

B) Increasing absorption

By enhancing reduction of ferric form to ferrous firm.

Ans. is b i.e., 35 mg

Ans. is ‘a’ i.e., 15 mg

o Normal iron requirement in an adult female is 21 mg/day.

In pregnancy, iron requirement is 35 mg/day.

hus extra requirement is 14 mg/day (35 minus 21).

Ans. is ‘b i.e., 17 mg

Ans. is ‘b’ i.e., Serum ferritin

“The single most sensitive tool for evaluating the iron status is by measurement of serum jerritin” – Park

“It is the most usefill indicator of iron status in a population where the Prevalence” of iron deficiency is not high.

Ans. is ‘c’ i.e., Serum Ferritin

• During an Iron deficient state, the body will mobilize its Iron Stores & so try to maintain a near normal supply of Iron to tissues e.g. Bone Marrow.
• So the first organ to be depleted of Iron wilt be the Iron stores.

o And we know Serum Ferritin reflects the body stores of Iron.

o Therefore serum ferritin is the first to be changed (i.e. depleted).

Ans. is ‘b’ i.e., 100 mg elemental iron + 500 gFA

• Recommendations by Government of India (2007)

          Include infants 6-12 months age in the programme

          For 6-60 months age, provide liquid formulations

          Recommended daily intakes:

Ans. is ‘d’ i.e., Soyabean

Amongst Pulse

• Highest calories                                           Soyabean

         Highest protein                                            Soyabean

         Highest fat                                                    Soyabean

 Highest iron                                                          Soyabean

o Highest thiamine                                                  Soyabean

        Highest riboflavin                                           Soyabean

        Highest calcium                                             Horse gram

        Highest Niacin                                               Peas dry

Highest vit C      Bengal gram

Ans. is ‘d’ i.e., Jaggery 

Jaggery is also called as poor man’s iron as it is one of the cheaptest source of iron.

Ans. is ‘c’ i.e., 100 – 150 mg 

Ans. A: Ferritin

Ferritin is the storage form of iron.

Transferrin is iron transporter protein

70% of iron in the body is hemoglobin

Ferritin which is not combined with iron is called apoferritin.

Under steady conditions, the serum ferritin level correlates with total body iron stores; thus, the serum ferritin level is the most convenient laboratory test to estimate iron stores.

The ferritin levels measured have a direct correlation with the total amount of iron stored in the body. If ferritin is high there is iron in excess, If ferritin is low there is a risk for lack in iron.

Serum ferritin is the most sensitive lab test for iron deficiency anemia.

Ferritin is also used as a marker for iron overload disoreders, such as hemochromatosis and porphyria in which the ferritin level may be abnormally raised.

Ans. B: Transferrin

Transferrin

• They are iron-binding blood plasma glycoproteins that control the level of free iron in biological fluids.
• In humans, it is encoded by the TF gene.
• Transferrin is a glycoprotein that binds iron very tightly but reversibly.
• Although iron bound to transferrin is less than 0.1% (4 mg) of the total body iron, it is the most important iron pool, with the highest rate of turnover.
• Transferrin has a molecular weight of around 80 kDa and contains 2 specific high-affinity Fe (III) binding sites.
• The affinity of transferrin for Fe (III) is extremely high but decreases progressively with decreasing pH below neutrality.
• When not bound to iron, it is known as “apo-transferrin”

Ferritin

• It is a ubiquitous intracellular protein that stores iron and releases it in a controlled fashion.
• The amount of ferritin stored reflects the amount of iron stored.
• In humans, it acts as a buffer against iron deficiency and iron overload.
• Ferritin is a globular protein complex consisting of 24 protein subunits and is the primary intracellular iron-storage protein in both prokaryotes and eukaryotes, keeping iron in a soluble and non-toxic form.
• Ferritin that is not combined with iron is called apoferritin.

Ans: B i.e. Duodenum

Site of absorption

• Stomach is the site of absorption of water and alcohol
• Duodenum is the site of absorption of iron and calcium
• Ileum is the site of absorption of vitamin B12 and bile salt

Ans. D: Decreases following gastrectomy

Various dietary factors affect the availability of iron for absorption; for example, the phytic acid found in cereals reacts with iron to form insoluble compounds in the intestine. So do phosphates and oxalates.

Most of the iron in the diet is in the ferric (Fe3+) form, whereas it is the ferrous (Fe2+) form that is absorbed. Fe3+ reductase activity is associated with the iron transporter in the brush borders of the enterocytes

No more than a trace of iron is absorbed in the stomach, but the gastric secretions dissolve the iron and permit it to form soluble complexes with ascorbic acid and other substances that aid its reduction to the Fe2+ form. The importance of this function in humans is indicated by the fact that iron deficiency anemia is a troublesome and relatively frequent complication of partial gastrectomy.

Almost all iron absorption occurs in the duodenum. Some is stored in ferritin, and the remainder is transported out of the enterocytes by a basolateral transporter named ferroportin 1. A protein called hephaestin (Hp) is associated with ferroportin 1. It is not a transporter itself, but it facilitates basolateral transport.

In the plasma, Fe2+ is converted to Fe3+and bound to the iron transport protein transferrin. This protein has two iron-binding sites. Normally, transferrin is about 35% saturated with iron.

Intestinal absorption of iron is regulated by three factors: recent dietary intake of iron, the state of the iron stores in the body, and the state of erythropoiesis in the bone marrow.

Ans. D i.e. Syndrome caused by systemic iron overload

Hemochromatosis

• It is the abnormal accumulation of iron in parenchymal organs, leading to organ toxicity.
• It is the most common autosomal recessive genetic disorder and
• The most common cause of severe iron overload.

Ans. D: Excess of meat in the diet

Causes of iron deficiency anemia:

• Diet

– The prevalence of iron deficiency anemia is low in geographic areas where meat is an important constituent of the diet.

Substances that diminish the absorption of ferrous and ferric iron are phytates, oxalates, phosphates, carbonates, and tannates. Ascorbic acid increases the absorption of ferric and ferrous iron.

• Hemorrhage

–  Bleeding for any reason produces iron depletion. If sufficient blood loss occurs chronically, iron deficiency anemia ensues.

• Malabsorption of iron

– Prolonged achlorhydria may produce iron deficiency because acidic conditions are required to release ferric iron from food.

– Extensive surgical removal of the proximal small bowel or chronic diseases, such as untreated sprue or celiac syndrome, can diminish iron absorption.

• Increased demand: pregnancy, lactation and growth periods.

Ans. D: Reduced ferritin

Ans. C: Ancylostoma duodenale

An adult Ancylostome (hookworm) can suck about 0.2 ml blood a day, while the smaller necator sucks in about 0.03 ml per day. These worms frequently leave one site and attach themselves to other site. As the secretions of the worm contain anticoagulant activity, bleeding from the site may continue for several days adding to the blood loss.

This chronic blood loss over a period of time leads to a microcytic hypochromic anemia. Pinworm (Enterobius vermicularis) causes irritation and pruritis in the perianal and perineal area. It may cause symptoms of chronic salpingitis and appendicitis.

Taenia solium causes cysticercus cellulosae commonly in the subcutaneous tissues and muscles. It may also affect eye, brain, heart, lung or liver.

Ans. B: BAL

Chelation with desferrioxamine is the mainstay of therapy.

• It is indicated for serum iron levels >350 mcg/ dL with evidence of toxicity or >500 mcg/ dL regardless of signs or symptoms.
• Because adsorption to activated charcoal is minimal, whole bowel irrigation is the GI decontamination (polyethylene glycol) is the method of choice.
• 1 percent Magnesium hydroxide solution orally
• Hemodialysis/exchange transfusion in severe cases.

Ans. B: Iron

Milk decreases the absorption of iron into the body.

Other factors which decreases the bio-availability of non-haem iron is presence of phytates, oxalates, carbonates, phosphates, eggs, tea and dietary fiber.

Ans. D i.e. Serum ferritin

Ans. is ‘c’ i.e., Citrus fruits

Citrus fruits are good sources of vitamin C (ascorbic acid) which increases intestinal absorption of iron.

Ans. is ‘c’ i.e., Hypochromic microcytic

Ans. is ‘c’ i.e., It binds to trnasferrin

Ans. is ‘b’ i.e., Transfer of iron into enterocytes

• Hepcidin is an iron metabolism regulatory hormone that inhibits iron absorption (transfer of iron into enterocytes).
• Ascorbic acid (vitamin C) forms soluble complexes with iron and reduces iron from the ferric to the ferrous state, thereby enhancing iron absorption.
• Tannins, present in tea, form insoluble complexes with iron and lower its absorption.

Ans. is `c’ i.e., Iron

“The level of iron in plasma is sensed by specific iron regulatory proteins which control the rate offerritin synthesis and to maintain homeostasis”  – Human physiology

Hepicidin regulates absorption of iron. But, it is also according to the serum iron level. If serum iron is deficiem, hepacidin level falls and there is increased iron absorption.

Ans. is ‘c’ i.e., Hepcidin

• By inhibiting ferroportin, hepcidin prevents enterocytes from allowing iron into the hepatic portal system, thereby reducing dietary iron absorption.

• The iron release from macrophages is also reduced by ferroportin inhibition.

Ans. is ‘a’ i.e., Iron

• Hemochromatosis is characterized by the excessive accumulation of body iron, most of which is deposited in parenchymal organs such as liver and pancreas.
• Hemochromatosis is a disorder of iron metabolism.
• Characterized by a triad of :-
• Micronodular cirrhosis

1. Diabetes mellitus
2. Skin pigmentation

• Organ not showing iron deposition in hemochromatosis

1. Testis

Ans. is ‘c’ i.e., Testis

In hemochromatosis, hypogonadism is caused by impairment of hypothalamic pituitary function and not due to deposition of Iron in the Testis.

Hemochromatosis

• Hemochromatosis is characterized by the excessive accumulation of body iron, most of which is deposited in parenchymal organs such as liver and pancreas.
• The total body content of the iron is tightly regulated, as the daily losses are matched by gastrointestinal absorption. In hereditary hemochromatosis, regulation of intestinal absorption of dietary iron is lost, leading to net iron accumulation of 0.5 to 1.0 gm/year.
• It may be recalled that the total body iron pool ranges from 2-6 gm in normal adults; about 0.5 gm is stored in the liver 98% of which is hepatocytes. In hemochromatosis the iron accumulation may exceed 50 gm, over one third of which accumulates in the liver.
• The iron accumulation is life long, the rate of net iron accumulation is 0.5 to 1.0 gm/year. The disease manifests itself typically after 20 gm of storage iron have accumulated. The disease first mainfests itself in the fifth to sixth decades of life.
• Excessive iron is directly toxic to host tissues
• The clinical features of hemochromatosis are characterized principally by deposition of excess iron in the following organs in decreasing order of severity.

Ans. is ‘a’ i.e., Iron deficiency Anemia

• Mentzer index more than 13 suggests a diagnosis of Iron-deficiency anemia.

Mentzer index

• The Mentzer index is used to help in differentiating iron deficiency anemia from beta thalassemia.
• The index is calculated as the quotient of the mean corpuscular volume (MCV, in fL) divided by the red blood cell count (RBC, in millions per microleter).
• If the Mentzer index is less than 13, thallassemia is said to be more likely.
• If the Mentzer Index is greater than 13, Then iron-deficiency anemia is said to be more likely.

Principle

• In iron deficiency, the marrow cannot produce as many RBCs and they are small (imcrocytic), so the RBC count and the MCV will both be low, and as a result, the index will be greater than 13. Conversely, in thalassemia, which is a disorder of globin synthesis, the number of RBCs produced is normal, but the cells are smaller and more fragile. Therefore, the RBC count is normal, but the MCV is low, so the index will be less than 13.
• In practice, the Mentzer index is not a reliable indicator and should not, by itself be used to differentiate the two conditions.

Ans. is ‘D’ i.e., Bone marrow iron is decreased earlier than serum iron

“In iron deficiency anemia the first change is decrease in iron stores ”

The decrease in iron stores is demonstrated by decreased serum ferritin level.

Remember,

Serum ferritin reflects the amount of storage iron in the body.

As the total body iron level begins to fall a characteristic, sequence of events ensue :

• First Stage or Prelatent Stage of Iron Depletion
• When iron loss exceeds absorption, a negative iron balance exists.
• Stored iron begins to be, mobilized from stores. The iron present in the macrophages of liver, spleen and bone marrow are depleted
• Decrease in stored iron is reflected by decrease in serum ferritin.
• At this stage all other parameters of iron status are normal.

Second Stage or Stage of Latent Iron Deficiency :

• Iron stores are exhausted but the blood hemoglobin level remains higher than the lower limit of normal. o After the exhaustion of iron stores :
• The plasma iron concentration fallsQ.
• Plasma iron binding capacity increases2.
• Percentage saturation falls below 15%Q.
• The percentage of sideroblast decreases in the bone marrowQ.

Third Stage or Stage of Apparent Iron Deficiency Anemia

• Supply of iron to marrow becomes inadequate for normal hemoglobin production,
• So the blood hemoglobin concentration falls^Q below the lower limit of normal and iron deficiency anemia is apparent.

Ans. is ‘a’ i.e., Intermittent Gastrointestinal blood loss

• Intravenous iron therapy is indicated in excessive continuing blood loss whose level of continued bleedin’ usually gastrointestinal or menstrual exceeds the ability of the gastrointestinal tract to absorb iron.
• Indicationspr parenteral iron supplementation  o Inability to tolerate oral iron
• Excessive continuing blood loss
• Inflammatory bowel disease
• Chronic kidney disease
• Cancer patients o Heart failure

Ans. is ‘a’ i.e., Iron dextran

• The risk of anaphylaxis is maximally associated with high molecular weight dextran (not so with low molecular weight dextran).

Intravenous iron preparations :-

Durg

• Iron dextran (high molecular weight)
• Iron dextran (low molecular weight)
• Ferric gluconate
• Iron sucrose
• Ferumoxytol
• Iron isomaltoside
• Ferric carboxymaltose