Patofisiologi Gizi Gangguan Sistem Hematologi & Defisiensi
Gizi Mikro Hematopoesis Anemia Defisiensi Gizi Mikro Slide 2 Blood:
Formed Elements Erythrocytes = red blood cells Leukocytes = white
blood cells Platelets = cell fragments Slide 3 Hematopoiesis In the
adult, all blood cell formation (i.e., synthesis of RBCs, WBCs, and
platelets) occurs in the red bone marrow Red bone marrow is
primarily found in bones of the axial skeleton, pelvic and pectoral
girdles, and in the proximal epiphyses of the humerus and femur.
The formation of blood cell is referred to as hematopoiesis or
hemopoiesis Slide 4 Red bone marrow Slide 5 Slide 6 Hematopoiesis
Hematopoiesis begins with a stem cell known as the hemocytoblast
the hemocytoblast goes through a series of morphological changes
Slide 7 Erythopoiesis The formation of erythrocytes is called
erythropoiesis Slide 8 Erythrocytes (Red Blood Cells) Anatomy of
circulating erythrocytes Biconcave disks Essentially bags of
hemoglobin Anucleate (no nucleus) Contain very few organelles
Outnumber white blood cells 1000:1 Slide 9 Erythrocytes Slide 10
Erythrocyte Slide 11 Erythrocyte: Hemoglobin Hemoglobin is a
protein that is essential to RBC function. Hemoglobin levels are
reported in grams of Hb per 100mL of whole blood, i.e., grams per
deciliter or g/dL. Typical values are: 14-18g/dL in adult males.
12-16g/dL in adult females. 14-20g/dL in infants. Slide 12 Slide 13
Leukocytes (White Blood Cells) Crucial in the bodys defense against
disease These are complete cells, with a nucleus and organelles
Able to move into and out of blood vessels (diapedesis) Can respond
to chemicals released by damaged tissues Slide 14 Types of
Leukocytes Copyright 2003 Pearson Education, Inc. publishing as
Benjamin Cummings Granulocytes Granules in their cytoplasm can be
stained Include neutrophils, eosinophils, and basophils Slide 15
Types of Leukocytes Copyright 2003 Pearson Education, Inc.
publishing as Benjamin Cummings Agranulocytes Lack visible
cytoplasmic granules Include lymphocytes and monocytes Slide 16
Neutrophil Slide 17 Eosinophil Slide 18 Basophil Slide 19 Monocyte
and Lymphocyte Slide 20 Platelets Derived from ruptured
multinucleate cells (megakaryocytes) Normal platelet count =
200,000-400,000/mm 3 Slide 21 Thrombopoiesis The formation of
thrombocyte Slide 22 Thrombocyte Slide 23 Anemia Anemia is a common
blood disorder that occurs when there are fewer red blood cells
than normal, or there is a low concentration of hemoglobin in the
blood. Slide 24 Anemia Anemia is often a symptom of a disease
rather than a disease itself. Anemia usually develops due to the
presence of one of the following: excessive blood loss or
hemorrhaging deficient production of red cells excessive red cell
destruction both decreased production and excessive destruction of
red blood cells Slide 25 Anemia Generally, anemia may be caused by
several problems, including the following: infections certain
diseases certain medications poor nutrition blood loss Slide 26
Anemia Symptoms: abnormal paleness or lack of color of the skin
dizziness, or vertigo, especially when standing lack of energy, or
tiring easily (fatigue) headache Slide 27 Anemia Symptoms (cont.)
irritability irregular menstruation cycles absent or delayed
menstruation (amenorrhea) sore or swollen tongue (glossitis)
jaundice, or yellowing of skin, eyes, and mouth enlarged spleen or
liver (splenomegaly, hepatomegaly) impaired wound and tissue
healing Slide 28 Anemia: the types There are several different
types of anemia, each with a specific cause and treatment,
including the following: Deficiency: iron folic acid piridoksin
(hipokrom) kobalamin Zinc (hipokrom) Slide 29 Iron deficiency
anaemia The RBC's are smaller than normal and have an increased
zone of central pallor. This is indicative of a hypochromic (less
hemoglobin in each RBC) microcytic (smaller size of each RBC)
anemia. Slide 30 Fe deficiency microcytic hypochrome Slide 31
Megaloblastic (perniciousa) anemia Due to folate or to B12
deficiency. Can be caused by inadequate intake or absorption of
vitamin B 12. The stomach lining produces a chemical called
intrinsic factor which is necessary for the absorption of ingested
vitamin B 12. It is often a lack of intrinsic factor that causes
pernicious anemia. Hypersegmented neutrophil that is present with
megaloblastic anemias. There are 8 lobes instead of the usual 3 or
4. The size of the RBC's is also increased (macrocytosis). Slide 32
Megaloblastic Slide 33 Types of Anemia Hemolytic RBCs rupture
(lyse) prematurely. Can be due to Hb abnormalities, mismatched
blood transfusion, parasitic or bacterial infection, or as an
autoimmune condition. Slide 34 Types of Anemia Aplastic Results
from destruction of red bone marrow by bacterial toxins, drugs or
radiation. Impacts all blood cells, leading to clotting
difficulties and immune problems. Slide 35 Types of Anemia
Sickle-Cell A mutation in the gene for the beta chain of Hb results
in an abnormal hemoglobin called HbS. Under low-oxygen conditions,
the beta chains link together and become stiff rods - this gives
the RBC a sickle shape. Sickled RBCs can then block and clog small
blood vessels. Slide 36 Sickle cell anemia Slide 37 Anaemia :
treatment treatment of the causative disease vitamin and mineral
supplements change in diet medication blood transfusion bone marrow
transplant surgery (to remove the spleen, if related to hemolytic
anemia) antibiotics (if an infection is the causative agent) Slide
38 Micronutrition Deficiency Thiamine Riboflavin (B2) Pyridoxine
(B6) Niacin Vitamin C Vitamin E Vitamin K Trace elements Slide 39
Thiamine Deficiency Thiamine - as the majority of the B complex -
is found in green vegetables, milk and liver. Thiamine is the
co-factor for many enzymes in the glycolytic pathway. Lack of
thiamine inadequate glucose metabolism accumulation of lactate and
pyruvate peripheral vasodilatation oedema. Slide 40 Thiamine
Deficiency Thiamine deficiency (beri-beri) is found in persons
consuming polished rice (classical beri-beri), in chronic
alcoholics, and in marasmus Dry beri-beri is symmetrical
polyneuropathy (ie, paresthesia, weakness, heaviness, and paresis
of the legs). CNS involvement with ischaemic damage results in the
Wernicke-Korsakoff syndrome (ie, ataxia, confusion and
ophtalmoplegia). Wet beri-beri : oedemas of the legs, pleural
effusions and ascites. - These disorders respond immediately to
thiamine treatment. Slide 41 Vitamin B2 (riboflavin) deficiency
Riboflavin is widely distributed in animal and vegetable foods. In
the human body riboflavin is converted into flavin mono- and
di-nucleotides. These compounds are of crucial importance in the
electron transport chain. Riboflavin deficiency is frequently only
part of a combined vitamin B deficiency, but the classical
manifestations are lesions around the natural openings: 1.
interstitial keratitis of the cornea with vascularisation, 2.
seborrhoic dermatitis (face, vulva, and scrotum), 3. angular
stomatitis (ie, cheilosis or fissures at the angles of the mouth),
and 4. glossitis. These lesions respond to riboflavin usually given
parenterally as a vitamin B complex. Slide 42 Vitamin B6 deficiency
Vitamin B6 activity is found in three compounds found in both
vegetable and animal foods: pyrodoxine, pyridoxal, and
pyridoxamine. Pyridoxal phosphate is a co-enzyme for transaminases,
carboxylases (formation of the neurotransmitter GABA) and other
enzymes. Drugs like the antituberculosis drug, isoniazid, and the
copper-chelating agent, penicillamine, are B6- antagonists. Certain
types of polyneuropathy respond to vitamin B6 therapy. Slide 43
Vitamin B7 deficiency Niacin deficiency or pellagra (ie, roughs
skin) is recognized by the combination of the 3 diagnostic Ds:
Dermatitis, diarrhoea, and dementia. Niacin is involved in the
formation of nicotinamide adenine dinucleotide (NAD) and its
phosphate (NADP). These molecules are important in many
oxidation/reduction reactions of the intermediary metabolism.
Niacin found in different types of grains (poor content in maize),
and our endogenous synthesis is from tryptophan found in meat, eggs
and milk. Slide 44 Vitamin C deficiency (scurvy) Found in fresh
fruit and vegetables. Humans cannot synthesise ascorbic acid from
glucose as several animals. Ascorbic acid is necessary for the
production of collagen in all tissues including the vessel walls.
Vitamin C deficiency (scurvy or scorbutus) is found among food
faddists and in developing countries, where infants are fed with
excessively boiled milk. Slide 45 Vitamin C deficiency (scurvy)
Abnormal collagen without sufficient tensile strength bleedings :
bruises of the skin, haemarthron, subperiosteal bleedings, bleeding
anaemia. Infections are prolonged and the healing of wounds is
poor. Gingivitis loose teeth, Lack of normal collagen in growing
bones arrested bone growth. There is no advantage in the daily
intake of large doses of vitamin C to prevent or improve common
cold or cancer. In one controlled clinical trial there was an
accumulation of cases with kidney stones. Rebound scurvy may occur
following a sudden stop of the intake of large doses of vitamin C.
Slide 46 Vitamin E deficiency Vitamin E ( -tochoferol) is found in
fish, fish oil and vegetable oil from Soya beans and corn.
antioxidant, protects the phospholipids of the plasma membrane
against peroxidation by free radicals produced by the cell
metabolism. Prolonged vitamin E deficiency is rare, but leads to
CNS lesions, haemolytic anaemia, and muscle disorders. Patients
with fat malabsorption or patients receiving parenteral nutrition
may develop vitamin E deficiency Slide 47 Vitamin K deficiency
Vitamin K occurs in two forms in nature. Vitamin K1 is produced in
plants, and intestinal bacteria in animals synthesise vitamin K2.
Insufficient dietary intake of vitamin K is infrequent, and occurs
occasionally such as cases of anorexia nervosa. Fat malabsorption
is accompanied by vitamin K deficiency. Slide 48 Vitamin K
deficiency Newborn babies sometimes suffer from vitamin K
deficiency, because the molecule only crosses the placental barrier
with difficulty, and because the sterile gut of the baby cannot
produce vitamin K2. Destruction of the intestinal bacteria by long
term antibiotic treatment may also lead to vitamin K deficiency.
Slide 49 Vitamin K deficiency Vitamin K deficiency can lead to
terminal bleeding. This is because vitamin K normally activates
four clotting factors: prothrombin, factor VII, factor IX, and
factor X. These four proteins probably receive Ca2+ binding
properties from vitamin K Therapy with intramuscularly administered
vitamin K is rapid and effective. Slide 50 Trace Metals and
Deficiency syndromes Trace elementDeficiency syndrome
IronHypochromic microcytic anaemia ZincAcrodermatitis
enteropathica, growth retardation, infertility IodineGoiter,
hypothyroidism SeleniumMyopathy CopperMuscle weakness, neurologic
defects, hypopigmentation, abnormal collagen cross-linking
FluorideDental caries Slide 51 Any Question???
