Iron Deficiency And Overload Flashcards
Haemosiderosis
– Increased _______
Primary Haemochromatosis
– Increased _______
Secondary Haemochromatosis
– Increased ________
Storage Iron
Tissue Iron
Storage Iron
IRON ___-__mg/day in diet
__-__% absorbed Heme iron absorbed best
10-15
5-10
Iron Absorption is ___eased in iron deficiency
Incr
Iron Absorption in pregnancy is??
increased or decreased?
increased
Iron Absorption is (increased or decreased ?) in
erythroid hyperplasia
hypoxia
Increased
Increased
Heme iron is absorbed best as ____ much better than ____
Fe2+
Fe3+
IRON TRANSPORT AND STORAGE
Absorbed iron is (oxidized or reduced?) to _____ form Bound tightly to _____ in blood
Iron is transferred to cells and (oxidized or reduced?) to _____ form, then inserted into heme or stored
Oxidized; Fe3+
transferrin
Reduced; Fe2+
Storage iron (Fe___) bound to ____
3+
ferritin
Small amount of ferritin in blood (nanograms) correlates with body iron stores
T/F
T
ASSESSMENT OF BODY IRON
Serum iron is (low or high?) in irondeficiency
TIBC (low or high?) in iron deficiency
Serum ferritin (low or high?) in iron deficiency
Marrow iron stores is (low or high?) in iron deficiency
Low
High
Low
absent
Assessment of body iron
Serum iron is (low or high?) in Inflammation
TIBC is (low or high?) in inflammation
Serum ferritin _____eases in inflammation
Low
normal or low
Increases
IRON BALANCE
___mg/day lost via desquamation, GI blood loss in adult
Normally we absorb about _____ amount per day
1-2; the same
desquamation is ______
Skin peeling
Negative iron balance possible in __________, _______, _______, ______ etc promote negative balance
Positive balance (and eventual iron overload) can occur in inherited disorders (_________), or as a result of ___________
early childhood, Menstruation, pregnancy, lactation
hemochromatosis; repeated blood transfusions
____ of iron per day required for erythropoiesis
Most of this iron is __________ after they are eaten by macrophages
20mg
recycled from old RBC
_____ mg of “new” iron absorbed from gut
_____ mg of iron lost via sloughing of enterocytes
1-2
1-2
Excess iron stored – mainly in ____
liver
__________ is the Most common cause of anemia worldwide
IRON DEFICIENCY
IRON DEFICIENCY
Usually due to _____________
Exceptions: _______ child, ________, and In young women this is usually due to ___________ and/or _______
chronic blood loss
rapidly growing ; malabsorption
menstrual blood loss ; pregnancy
IRON DEFICIENCY
In anyone else: rule out ___ blood loss _____ disease, _____ hernia, ulcer, inflammatory bowel disease, angiodysplasia, hemorrhoids, cancer
GI; Esophageal
hiatal
Pathogenesis of Iron Deficiency
Blood loss
-by —— or ____ losses, _____ or ______ losses
Failure to meet increased requirements
-Rapid growth in _______ and ___
–Menstruation, pregnancy
Inadequate iron absorption
-_____ low in heme iron
–_______ disease or surgery
-Excessive ______ intake in infants
Occult or overt GI
traumatic or surgical
infancy and adolescence
Diet; Gastrointestinal; cow’s milk
Features of Iron Deficiency Anaemia
Depends on the _________ and ____ of anemia
Symptoms common to all anemias:
– ________________________
degree and the rate of development
pallor, fatigability, weakness, dizziness, irritability
Other features of iron deficiency Anaemia
•_______- craving ___
•Pica - craving of _________
– e.g., __________
•_____- _____ tongue
•_______ Legs
Pagophagia; ice
nonfood substances; dirt, clay, laundry starch
Glossitis; smooth; Restless
Other features of iron deficiency Anaemia
_________ - cracking of corners of mouth
___________- thin, brittle, spoon-shaped fingernails
angular stomatitis
Koilonychia
Tests for Iron Deficiency
•___________ smear
•Red cell indices (__,____)
•Serum ______
•______________= iron saturation
•Bone marrow iron stain (___________)
Peripheral blood
MCV, MCH
ferritin
Serum iron / transferrin
Prussian blue
The evolution of iron deficiency anemia
During transition from iron-deficient erythropoiesis to overt iron deficiency anemia, anemia is initially ___________/__________ and gradually becomes _____/_______
Normocytic/normochroic
Microcytic/hypochromic
The evolution of iron deficiency anemia
NORMAL -________ - _______ - _________
DEPLETED IRON STORES
IRON DEFICIENCY
IRON DEFICIENCY ANEMIA
IRON DEFICIENCY ANEMIA
•___cytic, ___chromic
•Reticulocyte count (increased or not increased ?)
•____________ in more severe cases
Micro; hypo
not increased
Aniso- and poikilocytosis
Iron deficiency Anaemia
Serum ferritin usually (low or high?)
Serum iron (low or high?)
TIBC usually (low or high?)
Low
Low
High
IRON DEFICIENCY ANEMIA Treatment
•_________ salts
•Many patients have GI side effects, the “Slow-release” forms often not well absorbed, so _____________ can be taken
•_______ or _____, If oral iron not absorbed or not tolerated
•Slight risk of anaphylaxis Should see __________ within 2-3 week
• In severe cases ________ is indicated
Oral ferrous
Oral iron-polysaccharide complex
IV iron dextran or iron sucrose
increased hemoglobin
blood transfusion
Response to oral Iron Therapy
____ reticulocyte count In ________
________ Hb and Hct in ________
_____ Hb and Hct in _______
_______ iron stores in _______
Peak ; 7 - 10 days
Increased; 14 - 21 days
Normal ; 2 months
Normal; 4 - 5 months
Indications for IV IRON
•(Mild or Severe?) (asymptomatic or symptomatic?) anemia requiring accelerated erythropoesis
•Failure of ____ from ________
•Failure of ______ due to _____ issues
Severe; symptomatic
oral iron; g.i intolerance
oral iron; absorption
Indications for IV IRON
•_____ and ______ associated anemia
•Anemia with ____ disease (with or without dialysis dependance)
•Heavy ongoing _____ or _______ losses
Cancer and chemotherapy
chronic renal
g.i or menstrual blood
Intravenous Iron formulations
High molecular weight Iron _____ is not routinely used anymore due to a much ________________ (_______ reactions) in comparison to newer iron preparations
Dextran
poorer safety profile
anaphalyctoid
Other causes of microcytic anemia
Decreased hemoglobin production due to:
•___ withheld from red cell precursors (increased ____ - anemia of inflammation)
•_____ gene defects (______)
•Defects in ______ pathway (_____ anemias)
•Inherited conditions
•_____ poisoning
•Myelodysplasia (usually ____cytic/____blastic)
Iron; hepcidin
Globin; thalassemias
heme synthetic; sideroblastic
Heavy metal
macro; megalo
Iron overload
It is characterised by _____ to ______ increase in body iron level that has _____ effect in the body.
moderate to severe
negative
Iron overload of the parenchymal cell of the liver commonly arises due to _______ of iron, where iron is administered parenterally eg ________
excessive absorption
multiple blood transfusion
IRON OVERLOAD Hereditary
hemochromatosis
(Autosomal or Sex-linked?)
(Dominant or Recessive?)
Defective _____ gene
genotype is (common or rare?)
(low or high ?) penetrance
Autosomal
Recessive
HFE
common
Low
IRON OVERLOAD Other inherited disorders
•Mutations in other genes that regulate iron metabolism
•_______ and _______
•Chronic ____________
•_________
•Repeated _______ Toxicity after about 100 Units
Africans, African-Americans
ineffective erythropoiesis
Thalassemia
transfusion
HFE mutations disrupt signaling that normally increases _____ production in response to ________
hepcidin
increased iron levels
IRON OVERLOAD
____eased serum iron
(Low or High?) transferrin saturation (__%+ in hemochromatosis)
Very (low or high?) serum ferritin (over _______)
_____eased liver and marrow iron
Incr
High; 90
High; 1000
Incr
__________ is the best indicator of severity of iron overload
Quantitation of liver iron
DNA test is available for hereditary Hemochromatosis
T/F
T
IRON OVERLOAD Clinical consequences
•Liver: ____,________
•Heart: _______,_______
•endocrine: Endocrine failure (especially ______)
•bone and joint: ____
Cirrhosis, hepatocellular carcinoma
Cardiomyopathy, heart failure
diabetes
Arthropathy
Treatment of hereditary HC by _______ prevents clinical consequences of iron overload and can reverse _______ damage
phlebotomy
early tissue
Hemochromatosis-1 Disease of excess iron uptake
Defects can be in ______ , more commonly in _____ (genetic defects only really studied for northern Europeans)
Can also have acquired hemochromatosis, from _______ for other illnesses
DMT-1; HFE
transfusion
______% of population has hemochromatosis
2
Hemochromatosis
Exists worldwide, but Belt across _______ with increased incidence in Ireland, Scandinavia, _____
Northern Europe
Russia
Hemochromatosis
Defect in HFE causes decreased iron uptake by ______
Leads to increased ______ , causing increased ___________ & increased _________
crypt enterocytes
DMT-1; iron extraction from diet
iron delivery to tissues
Once iron is absorbed, very (easy or difficult ?) to remove
Difficult
Hemochromatosis-3 Sequence of events:
•Increased ______
•Increased ________: Normal c. ___%; if >___ %, often marker for disease; if > 90-95%, ________
•Increased iron _____ to ______
•Albumin Iron deposition in tissues, leading to bad stuffs
ferritin
transferrin saturation; 33;60; can start to get free iron
binding; other transport proteins
Hemochromatosis Diseases
Skin darkening
Due to __________ in skin leading to increased _______
iron deposition; melanin production
Hemochromatosis-4 Diseases
Endocrinopathy
________,________,_______
Diabetes, hypothyroidism, hypopituitarism
Hemochromatosis-4 Diseases
Liver damage
Liver damage Can lead to ____ ,_______
cirrhosis, hepatocellular CA
Hemochromatosis-4 Diseases
Cardiac damage
__________ leading to congestive heart failure
Cardiomyopathy
Hemochromatosis-5 Treatment
•Early recognition - _______
• for transfusion-induced hemochromatosis, use _______
Phlebotomy
Iron chelation
Classification of iron overload
Primary:
A. herediatary _________
B.__________
C. congenital __________
D. Neonatal __________
haemochromatosis
Aceruloplasmin
atransferrinaemia
haemchromatosis
Classification of iron overload
secondary
________ iron overload
_________ iron overload
Iron loading ______
Long term ________
Dietary
Parenteral
anaemia
haemodialysis
Thalassemia leads to iron (deficiency or overload?)
Overload
Anemia of chronic inflammation usually have ____cytic _____chromic Red cells.
normo
normo
Which of the following test is best suited for community based screening programme for identifying iron deficiency?
a. Serum ferritin
b. Red cell protoporphyrin level
c. Serum iron
d. TIBC
B
Which of the following test is best in differentiating between anemia of chronic inflammation and IDA?
a. Serum ferritin
b. Serum transferrin receptor
c. TIBC
d. Transferrin saturation
B
Which of the following is earliest recognizable change in RBC morphology in case of iron deficiency?
a. Hypochromia
b. Anisocytosis
c. Target cells
d. Poikilocytosis
B
Features of Patterson–Kelly/Plummer–Vinson Syndrome includes all of the following, except:
a. Esophageal web in post-cricoid region
b. Iron deficiency
c. Koilonychia
d. Gum Hypertrophy
D
Plummer-Vinson Syndrome (PVS), also known as Paterson-Kelly syndrome, is a rare medical condition that is characterized by a triad of symptoms consisting of _______,_________, and _________
dysphagia , iron deficiency anemia, and esophageal webs.
Macrocytic anemia may be seen with all of the following conditions, except:
a. Liver disease
b. Copper deficiency
c. Thiamine deficiency
d. Orotic aciduria
B
Anemia of chronic renal failure can be attributable to all of the following, except:
a. Low EPO level
b. Decreased RBC renewal
c. Decreased RBC supply
d. Decreased plasma volume
e. Bleeding due to platelet dysfunction
D
Erythropoietin levels will be low in all, except:
a. Polycythemia vera
b. Renal failure
c. AIHA
d. Anemia of chronic disease
C
Which is the first stage of iron deficiency?
a. Negative iron balance
b. Decreased iron stores
c. Decrease MCV
d. Decrease in Hemoglobin
A
Which statement is true regarding oral iron therapy?
a. Treatment should be given with along with vitamin C
b.Enteric coated and prolonged release preparations should be given
c. Best given after meals
d. Maximum dose is 200 mg of elemental iron/day
e. Carbonyl iron is usually not tolerated in high dose
D
