Deficiency Anemias

Acute Blood Loss. Severe anemia may result from a deficiency of all the circulating elements, following acute blood loss. This occurs with post traumatic hemorrhage, ruptured duodenal ulcer, ectopic pregnancy and in hemophilia. The etiology of the condition is exsanguination and the sympto­matology is that of shock. The blood vol­ume is first replaced by plasma, and there is a lowering of the hemoglobin, marked increase in the platelet count and a leuko­cytosis. Rapid loss of one third of the blood volume (1500-2000 CC.) is usually fatal, but 50 per cent may be lost more slowly, over a period of more than 24 hours, without death. The administration of plasma or transfusions may be life saving.
Iron Deficiency. Patients of either sex with chronic iron deficiency usually give a history of chronic blood loss (melena, hemoptysis, epistaxis or metrorrhagia). Iron deficiency may also develop during periods of maximum growth in childhood, puberty and pregnancy because of its increased utilization. The blood picture is of the hypochromic, microcytic type. Because of the iron deficiency the red cells contain less hemoglobin and there is a low mean corpuscular hemoglobin concentration. Fatiga­bility, headache, weakness or dyspnea on exertion are outstanding symptoms. The finger nails may be brittle and spoon shaped. This type of anemia responds to iron therapy.

Deficiency of Anti-Anemic Principle (B12,) in Pernicious Anemia. The liver Under normal conditions stores an antianemic factor which is absorbed from food of high protein content, such as liver, yeast and eggs. Absorption of this extrinsic factor is aided by a factor in gastric secretion, for­merly called the intrinsic factor. The in­trinsic factor is apparently absent in pa­tients suffering achylia in pernicious anemia and in certain stomach disorders. The essential extrinsic factor is apparently vita­min B 12. The interaction of these two fac­tors and their absorption from the gastro­intestinal tract provides the antianemic principle stored in the liver. Its formation and absorption may be interfered with in cases of diarrhea or steatorrhea (sprue or celiac disease), or its storage in the liver may be reduced in hepatic diseases, such as cir­rhosis, with resultant macrocytic anemia. This anti-anemic principle, which is neces­sary for the maturation of red blood cells, has been designated vitamin B 12.
In pernicious anemia caused by vitamin B12 deficiency the patients have a characteristic lemon color tint. Neurologic symptoms, such as parathesias and difficulty in walking, may be prominent, and the anemic triad, pallor, weakness and dyspnea, is pres­ent. In sprue, celiac disease and pellagra, there are diarrhea and loss of weight. All patients with macrocytic anemia may suffer with sore tongue and a variety of gastro­intestinal disturbances. The blood findings in this type of anemia are characterized by macrocytosis, hyperchromia and marked variation in the size and shape of the red blood cells. Following specific therapy, signs of blood regeneration (reticulocytosis) are seen. There is leukopenia in which large multisegmented neutrophilic leukocytes are conspicuous. The platelet count may be lowered. In relapse, the icteric index may be raised to 20 or more units (normal, from 5 to 7) and circulating normoblasts are numerous. There is a marked hyperplasia of the bone marrow in which the count of nucleated red blood cells may reach 50 per cent or more with megaloblasts predomi nating. This group of anemias responds specifically to liver therapy or vitamin B 12.

Anemias

The anemias may be divided into threemajor groups. those resulting from a specific deficiency (deficiency anemias), those resulting from lowered hematopoietic func­tion (hypopoietic anemias), and those caused by increased blood destruction (hemolytic anemias).

Hematopoietic System

In the embryo the blood cells are formed from the mesenchyme of the blood islands. Later this mesenchyme forms the endo­thelium of blood capillaries of bone marrow, lymph nodes, spleen and liver but retains its erythropoietic functions. The mesenchyme associated with this endothe­lium forms reticulum and gives rise to granulocytes, monocytes and lymphoid ele­ments. In the bone marrow the red blood cells arise within the capillaries from endothelium, while the granulocytes are formed extravascularly from reticulum. The stromal elements about embryonal lymphatics are the antecedents of lymphoid tissue. Reticu­lum cells in this stroma form large lymphoblasts which develop into small lympho­cytes. Large phagocytic cells or histiocytes can arise either from this reticulum, from undifferentiated connective tissue or from the endothelial lining of lymphatic or venous sinuses, in the liver, spleen, lymph nodes, etc. Collectively these tissues which furnish histiocytes are referred to as the reticuloendothelial system.
The hematopoietic organs and their associated structures are divided into two classes, 1. the erythropoietic tissues and, 2. the leukopoietic tissues.
The diseases of the erythropoietic tissues include polycythemia, the various forms of anemia, the purpuras and megakaryocy-tosis. Primary neoplasia of the erythro­poietic system is not definitely established.The diseases of the leukopoietic tissue include a variety of chronic infections and neoplastic diseases which involve myeloid and lymphoid elements.

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Halitosis

Halitosis is a condition where patient feels unpleasent or a type of offensive odors in air, it may be due to poor oral hygiene or oral cavity usually seen in patients who are social handicap, some times raely it is a presentation of serious systemic illness which require diagnosis and treatment.

Etiology
Physiologic halitosis, such as with eating onions and garlic or with morning breath, is temporary. These odors are reversible, transient, and responsive to Simple oral hygiene. pathologic halitosis is more intense and not easily reversible. It may arise from similar mechanisms but results more frequently from regional or systemic pathology, leading to persistent odors that ultimately require treatment.Persistent halitosis (usually noted by individuals around the patient) is more severe than physiologic halitosis. The important task initially is to categorize the halitosis as either localized to the oral cavity or originating systemically. In 80% to 90% of patients, halitosis is due to bacterial activity from disorders
of the oral cavity, and in the remainder of patients, the condition is attributed to nonoral or systemic sources. Volatile sulfur compounds arising through the microbia degradation of amino acids are the presumed source of most offending odors. Bad breath may originate from the following areas: oral cavity 85% to 88%, nasal passages 8%, tonsils 3%, and other sites 2% to 3% . In addition, the causes of halitosis can be subcategorized into pathologic and nonpathologic types.
Nonpathologic causes Morning breath is due to decreased salivary flow overnight associated with increased fluid pH, elevated gram-negative bacterial growth, and volatile sulfur
compounds production. Xerostomia of any cause (e.g., sleep, diseases, medication, mouth breathing, and especially age-related declines in salivary quantity and quality) can contribute to halitosis. Missed meals can lead to halitosis secondary to decreased salivary flow and the absence of the mechanical action of the food on the tongue surface to wear down filiform papillae. Tobacco or alcohol can be a contributing cause of halitosis. Metabolites from ingested food (onions, garlic, alcohol, pastrami, and other meats) are absorbed into the circulation and then excreted through the lungs. Medications such as anticholinergic drugs can cause xerostomia, especially in the elderly. Other agents include amphetamines, psychiatric drugs,
antihistamines, decongestants, narcotics, antihypertensives, anti-parkinsonian agents, chemotherapy, and radiation therapy.
Pathologic causes Local oropharynx Chronic periodontal disease and gingivitis are common sources through the promotion of bacterial overgrowth. In their absence, the most likely oral source is the posterior dorsum of the tongue with posterior nasal drainage being a frequent contributing factor to local bacterial overgrowth. Stomatitis and glossitis caused by systemic disease, medication, or vitamin deficiencies can lead to trapped food particles and desquamated tissue. An improperly cleaned prosthetic appliance can be a local contributor, as can primary pharyngeal cancer. Other conditions associated with parotid dysfunction (e.g., viral and bacterial infections, calculi, drug reactions, systemic conditions including 'sgren's syndrome) are also important. Tonsils infrequently cause halitosis (found in 7% of the population), even with crypt tonsillitis. These may alarm patients but are usually asymptomatic and not associated with any
pathology. Gastrointestinal tract Gastrointestinal sources occasionally contribute to intermittent bad breath. Potential sources include gastroesophageal reflux disease, gastrointestinal bleeding, gastric cancer, malabsorption syndromes, and enteric infections. Respiratory tract Chronic sinusitis, nasal foreign bodies or tumors, postnasal drip, bronchitis, pneumonia, bronchiectasis, tuberculosis, and malignancies may cause halitosis. Psychiatric Halitophobia is imaginary halitosis associated with psychiatric disorders. Systemic sources include diabetic ketoacidosis (sweet, fruity, acetone breath), renal failure (ammonia or fishy odor), hepatic failure (fetor hepaticus a sweet amine odor), high fever with dehydration, and vitamin or mineral deficiencies leading to a dry mouth

Epidemiology

The prevalence of halitosis is not known, but many individuals worry about it. In one study, 20% of adults worried about bad breath, when little was measured. Approximately 25% of individuals seeking help for halitosis may be halitophobic or suffering from pseudohalitosis.
History

Focus on the characteristics of the bad breath, although the patient is often unable to describe his or her condition accurately because of olfactory desensitization. Is the odor transient or constant? Constant odor suggests chronic systemic disease or serious disorders of the oral cavity. What are the precipitating, aggravating, or relieving factors? Ask about smoking habits, diet, drugs, dentures, mouth breathing, snoring, hay fever, and nasal obstruction. Because the therapy for halitosis of oral origin, beyond the limitation of aggravating factors, is proper oral hygiene and vigorous tongue brushing, an evaluation of the patient's tooth brushing and flossing regimen is imperative.
Physical examination

This should be undertaken with an emphasis on the oral cavity, particularly looking for ulceration, dryness, trauma, postnasal drainage, infections, inflamed cryptic tonsils, or neoplasms. Techniques for localizing the odor source (systemic vs. oral cavity) include: Seal the lips and blow air through the nose. If a fetid odor is noted, this is suggestive of a systemic source. If an odor is only noted from the nose, then a nasal source is likely. Pinch the nose with the lips closed. Hold respiration and exhale gently through the mouth. Odors detected in this fashion generally are local in origin. If a similar odor is noted from both sources then a systemic source may be suspected.
Testing

For most patients, clinical laboratory testing and diagnostic imaging are unnecessary, and should only be pursued on the basis of specific findings indicated by the history and physical examination. The Schirmer's test may be useful in identifying xerophthalmia and associated xerostomia seen with Sjgren's syndrome and some other rheumatologic conditions. If indicated, radiologic studies and imaging procedures of the sinuses, thorax, and abdomen may be used to
identify infectious processes and neoplasms.
In addition to fetid odor, there may be ulceration, dryness, trauma, postnasal drainage, infections, inflamed cryptic tonsils, or neoplasms.