Leukemoid Reaction

This is characterized by an elevated leukocyte count that closely resembles leukemia. Such leukocytic reactions have been found occasionally in various infections, chemical and drug poisonings, severe burns, severe hemorrhages or sudden hemolysis of blood and in meta­stases to bone. The clinical history, subse­quent course, or bone marrow biopsy may be necessary for differential diagnosis.

Agranulocytosis

This disease is characterized by an absence or a marked decrease in the number of neutrophils in the differ­ential count. Most cases have been re­ported in patients who have acquired a sensitivity to certain drugs, among them amidopyrine, organic arsenicals, sulfonamides, dinitrophenol, thiouracil, and gold salts. There is a low white count but no anemia. The platelet count and the bleed­ing and coagulation times are normal. The sedimentation is increased. The patient suffers from lever, weakness and usually from gangrenous ulcerations and infection of the throat (agranulocytic angina). Other severe infections and septicemia may occur unless penicillin is administered during the leukopenic phase of the disease.

LEUKOPOIETIC SYSTEM

Infectious Mononucleosis, Infectious Lymphocytosis, and Tropical Eoshiophilia.Infectious mononucleosis is usually described with hematologic diseases. It is a febrile disease of probable viral origin, affecting the reticuloendothelial system and producing lymphadenopathy, splenomegaly and an increase of mononuclear cells in the peripheral blood. The leukocyte count may be as high as 40,000 and contain 50 to 90 per cent of large lymphocytes, many of which are atypical and known as Downey cells. A positive test for heterophile antibodies distinguishes this disease from a similar one in children known as infec­tious lymphocytosis, in which this test is negative. In tropical eosinophilia the white count may be as high as 15,000 with 60 per cent or more eosinophils of the mature type. Many of the patients give a past his­tory of malarial infection and persistent respiratory complaints and at times a low grade fever. There is no demonstrable cause. Recovery occurs without specific treatment.

Abortion

Up to 20% of pregnancies abort before 20 weeks; there are usually no apparent reasons for abortion. The greater the amount of bleeding, the more likely the female is to develop shock (orthostatic drop in blood pressure; pallor and sweating); shock is a major risk during abortion.

Septic abortion-

HISTORY-Pregnant less than 20 weeks; often a history of trying to induce abortion; fever, chills, and severe pelvic pain. The woman is often unmarried and without parental support.

PHYSICAL EXAM-Fever with abortion; exquisitely tender uterus or adnexae often present. Hypotension, pallor, and sweating are frequently present.

Threatened abortion

HISTORY- Pregnant less than 20 weeks; vaginal bleeding; may have cramps.
PHYSICAL EXAM-Cervix is closed.

Imminent abortion

HISTORY-Pregnant less than 20 weeks; vaginal bleeding; may have cramps.but usually has cramps.
PHYSICAL EXAM-Cervix is dilated

Inevitable abortion

HISTORY-Pregnant less than 20 weeks; vaginal bleeding; may have cramps.
PHYSICAL EXAM-Cervix is dilated; fetal or placental tissue is protruding from cervix.

Incomplete abortion

HISTORY-As above, but may have noted passing of tissue; cramps and bleeding persist.
PHYSICAL EXAM-Cervix is dilated; fetal or placental tissue may be present.

Complete abortion

HISTORY-Pregnant less than 20 weeks; fetal or placental tissue has been passed; cramps and bleeding have ceased.
PHYSICAL EXAM-Somewhat variable, depending on time since abortion. Prompt closing of cervix expected after completed abortion.

Placenta previa or abruptio placentae

HISTORY-Excessive vaginal bleeding during the third trimester.
PHYSICAL EXAM-Hypotension from blood loss may be present; fundus of uterus consistent with third term of pregnancy.

Bloody show

HISTORY-Minimal bleeding and passage of mucus plug prior to delivery; uterine contractions.
PHYSICAL EXAM-Term pregnant uterus

Menstrual cramps

HISTORY-Nonpregnant woman; cramps and bleeding in association with menstrual period.
PHYSICAL EXAM-Normal pelvic exam

Purpura

Thrombocytopenia (Purpura Hemorrhagic, Idiopathic Purpura). This disease is characterized by diminution of the platelets with prolonged bleeding time and a nonretractile blood clot. The coagu­lation time in glass is not markedly affected. Clinically, there are spontaneous hemor­rhages, epistaxis, menorrhagia and petechiae in the skin or mucous membranes. Children and young adults are most fre­quently affected. Capillary resistance is diminished and the so called tourniquet test is positive. In order to make a diag­nosis of primary purpura it is necessary to rule out acute leukemia or aplastic anemia. There is no enlarged spleen, such as occurs in Banti's disease, Gaucher's disease or hemolytic jaundice. The blood shows a re­duction of platelets, fewer than 60,000 per cubic. millimiter. and the platelets vary in size and staining characteristics. There may be an anemia due to blood loss, and a posthemorrhagic leukocytosis with relative lympho­cytosis. The marrow shows increased num­bers of megakaryocytes but inhibited plate­let production. Small, repeated transfusions of whole blood are temporarily beneficial. Splenectomy may be curative.
Anaphylactoid Purpura (Schonlein and Henoch's Purpura). this condition is due to increased permeability of the capillary endothelium which permits extravasation of blood into the tissue spaces. Henoch's variety is characterized by colic and other gastro-intestinal symptoms, which often precede the purpuric eruptions so that needless operations may be performed. Schonlein's purpura is characterized by effusion into the joints and periarticular structures, which may precede the purpuric manifes­tations so that an erroneous diagnosis of rheumatic fever may be made.

Myeloid Metaplasia (Megakaryocytic Myelosis). A number of cases have been reported which have in common megakaryocytic infiltrations of the bone marrow, liver and spleen. At times there is a marked leukocytosis with increased number of megakaryocytes in the peripheral blood, The constant features of the disease are the splenomegaly, the infiltration of the hemato­poietic organs with megakaryocytes, the tendency for the bone marrow to undergo progressive fibrosis and frequent fatal ter­mination. more recently, bacilli which take the acid-fast stain have been found in the lungs of these patients. Because of the in­volvement of the bone marrow by fibrosis, and the compensatory hematopoiesis in the spleen, splenectomy is contraindicated.

Polycythemia

The term polycythemia is applied to conditions in which the number of circulating red corpuscles is increased. Erythrocytosis indicates a symptomatic response to anoxia, which may occur in cardiac or pul­monary disease, or at high altitudes. Erythrocytosis is also produced by hypertrophy or tumors of the adrenal cortex, by certain poisons, such as aniline and its derivatives, phosphorus, and occasionally by some metals.

Erythremia or polycythemia vera is a chronic disease of obscure origin, with an increase in the total blood volume and the number of red blood cells. The patients have a plethoric complexion, splenic and hepatic enlargement and a variety of neurologic and vasomotor disturbances. Venous thromboses, bleeding tendency, varicosities and phlebitis, or arterial occlusion are common, due to alteration in the blood. Thrombi in the cerebral vessels may lead to hemiplegia or paresis. The red cell count varies from 7 to 10 million, as a rule. The hemoglobin may reach as high as 25 Gram (140%). The individual red corpuscles ap­pear normal. Leukocytosis is frequently present, and the platelet count may reach 4 million. Some patients develop leukemia.

Hemolytic Anemias

The hemolytic anemias are characterized by excessive blood destruction which results in such symptoms as jaundice, formation of gallstones, and increased amounts of urobilinogen and urobilin in the stools and urine. Phagocytosis of red blood cells undergoing destruction with deposition of hemo­siderin results in splenomegaly. The acute forms may result from bloodstream infec­tions or various types of hemolytic poisons. The chronic forms are often congenital dis­orders and include familial hemolytic icterus, Mediterranean anemia and sickle cell anemia.
Acute Hemolytic Anemia. Acute hemolytic anemia may result from mismatched transfusions, hemolytic toxins, such as snake venoms, bacterial toxins, phenyl hydrazine or phenol, and from malaria or bartonellosis. The symptoms include chills and rigor, vomiting and diarrhea, pain in the back and legs, hemoglobinuria, albuminuria and anuria. The red blood cells show marked variation in size and staining re­action. There is striking evidence of regen­eration, including reticulocytosis and cir­culating normoblasts. Treatment consists of removal of the cause.

Acquired and Congenital Hemolytic Icterus. In congenital hemolytic icterus repeated crises of blood destruction occur, with fever, abdominal pain and nausea. Once severe anemia and jaundice develop, they tend to persist. The spleen is enlarged, gallstones are found in 68 per cent of the cases, skeletal anomalies such as tower skull occur, and chronic leg ulcers are common. Reticulocytes, small dense red cells (sphcrocytes) and increased fragility of red cells to hypotonic salt solution are the chief blood findings. The acquired form is simi­lar to the congenital, but the increased fra­gility of the red blood cells may be absent. Both forms show an increased icteric index, at times as high as 100, and a hyperplastic bone marrow on sternal puncture. Both are benefited by splenectomy.
Sickle Cell Anemia. This is a hereditary disease in Negroes. It is characterized by the appearance of sickle-shaped red corpuscles in blood which has been standing away from oxygen two to six hours after it has been withdrawn and protected from drying. The cells show increased resistance to hypotonic salt solution. The patients suf­fer from jaundice, rheumatic pains in the extremities, leg ulcers, and irregular thick­enings of the cortex of the bones. There is no satisfactory treatment.
Mediterranean Anemia (Thalassanemia). This is a familial disease in individuals of Mediterranean stock. Those afflicted are often short in stature and have a large head. The bones about the hands and wrists may have increased density on roentgen exami­nation. Examination of the blood shows variations in the size and staining reactions of the red blood cells. Nucleated forms are common. The hemoglobin is concentrated at the periphery of the red corpuscle or as a central dot forming so-called target corpuscles. Uniformly colored cells are rare. There is often a leukocytosis. The icteric index is moderately increased. The spleen is enlarged and infarcts are common. Later the organ shrinks and is fibrosed. The bone marrow is hyperplastic. Severe forms are present in children; milder forms in adults. Transfusion is of temporary value but there is no specific treatment.

Erythroblastosis Fetalis. This is a hemolytic anemia, occuring late in fetal life or in the newborn, in a child whose blood agglutinogens differ from its mother's. As a regenerative response to blood destruction, the hematopoietic centers in the bone mar row, liver and spleen become crowded with erythroblasts, hemosiderin and foci of hematopoiesis. Nucleated red blood cells appear in the peripheral blood. The infant in severe cases is edematous and jaundiced, and hence the terms fetal hydrops and familial icterus gravis. The basal ganglia of the brain may be deeply icteric, so called kernicterus.In rare instances the incompatibility of the fetal and maternal bloods is because of the ABO grouping. However, the cause of the disease nearly always is the immunization of the RH negative mother by previ­ous transfusions with RH positive blood cells or by RH positive red cells of the fetus. The mother's RH antibodies pass into the fetal circulation and damage the child's erythrocytes. The offspring of an RH posi­tive father and RH negative mother always will be RH positive if the male is homozy­gous (all dominant genes for RH). If the RH positive father is heterozygous (one or two of the genes recessive) 50 per cent or less of the offspring will be RH positive. Levine found that 87 per cent of the white population is RH positive. The mothers of infants developing erythroblastosis fetalis belong to the 13 per cent who are RH nega­tive. The treatment consists of an adequate number of transfusions or exchange trans­fusions from a compatible RH negative donor.

Hypopoietic Anemias

Aplastic Anemias. The aplastic anemias may follow poisoning with benzol, arseni cals, gold or radiant energy (x-ray or radium). Idiopathic aplastic anemia may develop rapidly without known cause. There is a characteristic triad in these cases, con­sisting of progressively severe anemia, thrombocytopenia and leukopenia. The absence of a palpable spleen helps to distinguish this condition from aleukemic leu­kemia. The red corpuscles are normal in appearance. Nucleated and stippled forms and other signs of regeneration are absent. The bone marrow is hypoplastic. The white count usually shows 70 to 90 per cent lymphocytes. Repeated transfusions are usually the only remedy.
Repressive Anemia. This anemia is the simple chronic type, and occurs sympto matically in chronic infections, renal disease, malignancy, endocrine disorders, preg­nancy and vitamin deficiencies other than B 12. Erythropoiesis is inhibited by circula­tory toxins or other causes. The red cell count rarely Calls below 3.5 million. The number of cells, their size and the quantity of hemoglobin are proportionately decreased, so that the anemia is normocytic. Evidence of regeneration or increased blood destruction is usually absent.

Myelophthisic Anemias. This form of anemia is produced by replacement of the marrow by nonfunctioning elements. Metastatic carcinoma to bone, multiple mye­loma, myelosclerosis and lipoid storage dis­eases affecting bones are etilogic factors. Pain referred to the skeleton and spleno­megaly are often present. The anemia is variable in degree and most often normo cytic. Primitive red blood cells or leukocytes may be found in the peripheral circu­lation, together with reticulocytes and stippled cells. Roentgenography of the skeleton aids in diagnosis. Treatment must be directed to the underlying condition.

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.