Complete Text (Part 17)

cells : (a) Histological differences. (b) Morphological differences. (c) Chemical differences. (d) Biological differences. (e) Embryological differences. (f) Comparative anatomy differences. (g) Pathological differences. Remarks on Xomenclature — confusing terms. (a) Acidophile cells — eosinophiles. (b) Basophile cells — two varieties meant: 1. Cells with basic protoplasm. 2. Cells with basic granulations : a. old, b. new. (c) Hematoblast has two meanings: 1. Blood platelet — Hayem. 2. Megakaryocytes. ( d ) Leukoblast ( Pappenheim ) — Promyelocyte, (e) Lymphoblast is used in two ways: 1. Parent cells of lymphocyte. 2. Large cells of germ centers. (f ) Lymphoid cells — a bad term. (g) Marrow cells— white bone marrow cells, gran- ular and non-granular. (h) Mast cells — basophilic leucocytes. (i) Myeloblasts referred to as: 1. Lymphoid bone marrow cells. 2. Bone marrow lyuiphocytes. (j) Rieder cells. • Remarks on tlie varieties of bone marrow. 220 Occurrence of each : ~i (a) Erythroblastic marrow — red. (b) Myelocytic marrow — grayish. (cj Myeloblastic marrow — gray. (d) LjTiiphatic marrow — grayish. (e) Aplastic or regenerative — yellow. i Kemarks on differential blood counts. Normal cells : P. M. N. P. M. B. • > P. M. E. Lymphocytes — small and large (small mono- nuclears). Transitionals. Large mononuclears. Pathological cells : Myelocytes — neutrophilic. Myelocytes — basophilic. ^klyelocytes — eosinojDhilic. Pathological Ijanphocytes. Myeloblasts. Always note abnormal red blood cells and plate- lets. Possible changes in W. B. C. count : 1. Unchanged, 2. Decreased — leucopaenia. 3. Increased — leucocytosis. Leucocytosis mild — mild infection — good resist- ance. Leucocytosis moderate — severe infection — poor re- sistance. Leucocytosis high — severe infection — good resist- ance. Leucocytosis low — severe infection — poor resist- ance. 221 Occurrence of Leiicoc3'tosi.s : 1. Physiological. (a) New-born (12 to 20,000). (b) Digestion. (c) Pregnancy. (d) Cold and exercise. 2, Pathological. (a) Post hemorrhagic. (b) Inflammatory. (c) Toxic — acidosis, gout, lead poisoning. (d) Many inectious diseases, eucopenia occurs in: (a) Emaciation. (b) Infectious diseases, malaria, influenza,, measles, pertussis, typhoid, (c) Chronic lues, tuberculosis. Differential blood pictures : 1. W. B. C. increased — formula normal or in- creased in any cell type; (a) Leucocytosis with normal balance — in in- fectious diseases not associated with pus (mumps). (b) Leucocytosis Avith P. M. X. increase — pus. (c) Leucocytosis with P. M. E. increase — para- sitic, skin infections, anaphylactic. (d) Leucocytosis with mononuclear increase — infection of lymphatic system. 2. W. B. C. Normal — with cells of one or other variety increased. (a) Leucocytosis — poor resistance. (b) P. M. E.— parasites. (c) Lymphocytes — in children, lues., tbc, etc. 3. W. B. C. Decreased — formula relatively nor- mal, one or another cell increased. (a) Leucopaenia with normal P. M. N. count in overwhelming infection (high % P. M. N.) 222 (b) Increased V. M. E.— particularly in severe anaemias starting to improve. ( c ) Lymphocytosis — pertussis, tvplioid, nui- laria, tbc"., P. A. ((1) Large Mononuclears and Transitionals — typhoid and leukaemias. .\ Consideration of Blood Platelets. Blood platelets originate from Megakaryocytes. Tliey disintegrate rapidly. -In stained specimens there is a mend)rane with purple staining chromatin inside the cell. They have amoeboid activity, which accounts for their bizai-re shapes. Function of platelets : To form thrond)in and neu- tralize antithrombin. Tlie}^ are also thought to play same role in immunity. They can be studied: 1. In good smears, '2. Indirectly — drop into normal metaphosphate and count platelets and R. B. C. Calculate number of platelets by proportion. 3. Aqueous solution of cresyl violet 1-800. Aqueous solution of KCN 1-UOO. Mix before use in proportion of two parts of the first to three of second. Keep iced before hand. AYait from 15 to 20 minutes, and then platelets are plainh^ seen. Normal count is 250.000 to 300,000. Increased in : Toxic or infectious states if nuld. Stronger ones decrease them. (Increase is good omen.) Clironic diseases. In secondary anaemia unless there is bone niarrow aplasia. In myeloid leukemia. Critically after hemorrhage. After splenectomy^ in two to four days. 223 Decreased in : OverwJielming infection. Lymphoid leukamia. Pernicions anaemia. True aplastic anaemias. Purpura hemorrhagica. Hemophilia. After benzol. Considerable emphasis laid upon the studies of Duke and Minot. The Anaemias or Er^^thropaenias. 1. General definition of anaemias and other terms, Oligaemia — oligocythaemia . Oligochromaemia — hydraemia. 2. General symptomatology of anaemic states : (a) Color — is only judged in terms of mucus membranes. The color of the skin in S. A. tends to be doughy white, while in P. A.. with the same or lower per cent of Hb, the skin tends to be a lemon color. (bj Eyes — eye grounds with loss of vision and floating spots from hemorrhages in the retina. (c) Dyspnoea — weakness. (d) Oastro-intestinal symptoms — lo^s of appe- tite, 8016 tongue or mouth, dermatitis ffom underlying anaemia or achylia. (Flatu- lence— especially in people over 3o.) Jaun- dice. (e) Oedema — swelling in feet and ankles. Swelling of feet and ankles not ahvays orthostatic. (f ) Neurasthenia. . 3. Classifications of anaemias. (a) Etiological: Defective forniation — hypoplastic. Increased destruction — consumptive. (I)) Haeiiiatological: Chlorotic (low index ». Pernicious (high index). (ci Histological: lriniary myelogenous — primary — embry- onic erythropoesis. Sc^condary myelogenous — secondary — post embryonic erythropoesis. ( d I Clinical grouping : - Primary. Secondary. Chlorosis Acute hemorrhagic I'ernicious Chronic hemorrhagic Primary aplasia Chronic secondary Leukanaemia Secondary aplastic Leukaemia Hemolytic Anaemias of children. Klood picture in stages of secondary anaemia. 1. Oligaemia Avithout anaemia — proportional de- crease (C. I. normal) — inhibition on the part of the bone marroAv. 2. Hydraemia — AA'ith thirst — reduced cell count A\dth low C. I. characteristic. 3. LoAA' C. I. — regeneration — metaplasia — imma- ture cells---normoblasts, macrocytes, intense marrow actiAdty. Megaloblasts occur infre- quently in true secondary anaemia. Ked cell formation exceeds hemoglobin. 4^. Normal — formation of red blood cells stops — restitution of Hb. Hemoglobin may exceed red cell formation — index plus. Causes of S. A. 1. Loss of blood. 2. Infections — chronic. 3. Malignant tumors. 4. Chemical — paroxysmal hemoglobinuria. 5. Parasites. 6. Secondary purpura. 229 Leucocytes — no characteristic clianges, usually normal and normal differential. Platelets — constantly increased. Treatment : Much iron given. (Some anaemic peo- ple called chlorotic, but tliis is really a misnomer, j Pernicious Anaemia. There is a limitation of the term. Pernicious anaemia is best given up and the term chronic hem- lytic anaemia used or "Addison-Biermer type of anaemia." Other terms are Addison anaemia, Addi- son-Ehrlich and Biermer-Elirlich anaemia. Biermer gave the first classical description in 1868. Ehrlich showed that there is a reversion to embryological type. Pernicious anaemia is not a disease entity, but a similar picture can be caused by conditions not necessarily fatal. The typical case shows a typical blood picture, certain symptoms, etc., with a chronic, progressive, hemolytic anaemia of un- known cause. The group is activity increasing. In horses an analagous anaemia of infectious origin occurs which can be transmitted. Conditions which require exclusion : 1. Worms — mostly of the flat- worm variety. (Fatty acids given off by the segments can cause anaemia in other animals.) 2. Malignant tumors. 3. Syphilis (clears up under therapy). 4. Severe chronic types of malaria. 5. Toxin given off' during puerperium. 6. Toxins due to metals — lead, etc. The cause of the disease is unknown, but there are various theories : 1. Toxins arising from gastrointestinal tract. This is a favorite theory, emphasized by Sir William Hunter. Bad teeth and mouths responsible. 2. Achylia gastrica — not true gastric atrophy. 3. Primary cause in spleen. (Comparatively re- 226 Enmiiercition of the distinguishing features : 1. Usually the histoiy is helpful. Never omit careful gastric, stool, sputum, urine examinations for occult blood. 2. K. B. C. not usually so low as in P. A. Stained smears show characteristic degree of pallor, shadows of cells. (Bone marrow may throw out deej) staining cells.) Smaller K. B. C. — degree of anisocytosis and poikilocytosis less. Normoblasts rather than megaloblasts (therefore C. I. very generally definiteh^ be- low 1 — watch C. I. carefully). 3. Platelets increased, or, at least, more than in P. A. 4. ^Y. B. ,C. either slightly increased (early stages), normal, or decreased (later stages), but not as much as in P. A. and less reduc- tion of P. M. X. Seems a sliding down of whole picture rather than repression of leucocytes. ril. Secondary Aplastic Group — Aregenerative Anaemias. Enumeration of the causes — bone marrow not changed to red. 1. Drugs, benzol, lead, arsenic, etc. 2. Long hemorrhagic state. 3. Severe septic conditions. Chief interest resides in the ability to diag- nose cases from aplastic forms of P. A. History very important. Blood picture, as a rule, shows: 1 . Parallel reduction of E. B. C. and hemo- globin. 2. Color index nearly normal (perhaps a little under j . 227 0. Anisocytosis and poikilocytosis usually slight. 4. Absence of myeloid elements with leuko- paenia. 5. Few or no nucleated K. B. C. Platelets gone. TV. Hemolytic Anaemias or Hemolytic Icterus. Described by French : congenital family dis- ease. Clinically a disease often present from early life with periods of fever, icteric tint, weakness, anaemia, urobilinuria and splenome- galy. A. Chronic icterus. 1. Congenital. 2. Acquired. B. Acute forms — new-born, infections, hepatic diseases.' Blood findings : 1. Anaemia is variable; usually moderate (rarely below 2,500,000). 2. X^sually many regenerative evidences, espe- cially basophilic cells. 3. Large numbers of vitally staining K. B. C. 4. C. I. around normal — sometimes greater thanl. . 5. Characteristic microcytosis. 6. Punctate basophilia — uncommon. 7. Usually W. B. C. slightly plus. 8. Platelets increased. 9. Diminished resistance of K. B. C. Good x3rognosis. Secondary anaemia occurs often in people who live under poor hygienic conditions. Marked improvement with fresh air, good food, etc. Secondary anaemia develops rapidly in pa- tients stricken with acute infections. (Typhoid, l)neumonia, rheumatic fever, etc.j 232 I. Patient's history — can't pin onset to any defi nite time. '2. Physical examination. (a) Characteristically well nourished. (b) Lemon or straw color. (c) Complete achylia gastrica. ( d ) Urobilinnria — constant. (e) Frequent retinal hemorrhages. 3. Blood side. (a) R. B. C. reduction out of proportion to hemoglobin. (b) Anisocytosis and poikilocytosis, Ayith prev- alence of macrocytes. (c) High C. T. (d) Leukopaenia. (e) Diminution in blood pressure. Differential diagnosis : T. Anaemias of Childhood. 1. Occur in young children. 1\ Tendency to revert to embryological blood picture ( megaloblasts predominate ) . 8. R. B. C. count reduced markedly and hemo- globin reduced i)roportionately. Low C. L Poililocytosis and anisocytosis marked. Polychromatic cells. 4. W. B. C. Leucocytosis (20,000). Predominant cell — ^P. M. X. Some abnormal W. B. C.'s. 5. Platelets about normal. Clinically : No characteristic lemon color to the skin- rather pasty. No urobilinnria. Rapid febrile course. Enlargement of liver and spleen. II. Aleukemic states of leukemia. 225 7. Cachexia with poor hygiene. I. Acute Hemorrhagic Anaemias. Enumeration of common causes. ( a ) Severe hemorrhage. (a» (t. I. tract. (Eoophageal, pharyngeal — acute haem. — gastric ulcer. I (c) Kespiratory (tbc, erosions of aneurisms, parasitic ) . (d) (t. F. (renal epistaxis, renal neoplasm t b, bladder conditions). Regeneration quickest in men ( 25 to 40 ) . Slowest in children. Minimum C. I. occurs around ninth day: nucleated K. B. C. 7-8 days. Rapidity of regeneration after hemorrhage. Blood loss — 4.5% body weight — entirely re- formed within 8 days. Blood loss :*% body weight — within 8 days. II. Chronic Hemorrhagic Anaemia. Succession of hemorrhages without recovery between. Enumeration of common causes : ( a I Mild hemoptysis. (b) Tbc. (c) Hemorrhoids. (d) Extreme and too frequent menstruation. (e) Xose irritation, etc. Blood findings : R. B. C. down to 1,000,000, usually small and pale. Nucleated R. B. C. not abundant. Platelets increased or not. Leukopaenia common. Picture varies Avith duration of anaemia; long-continued insults, bone marrow exhaus- tion and aregeneration becomes poor. Ultimately blood picture may resemble P. A. 230 cent theory.) There is said to be much fatty acid in the circuhition, which disappears after spleenectomy. No theory holds good for all anaemias. It is a toxic anaemia, probably the expression of absorption or the action of one or several toxins of varied origin (probably related to the fatty acid or lipoid group), causing morphological and functional changes in the bone marrow and constant reversion to embryonic type. The disease occurs in people of middle years (35-40), but can occur in people much older (in the 70s) and has been known in children. It is no re- spector of persons, occurring among the rich as well as the poor, but probably more in the male sex. It sometimes has a family tendency. Clinical symptoms and picture. 1 . Gastro-intestinal symptoms : (a) Sore tongue. (b) Active stomatitis. (c) Achlorhydria. (d) Loss of appetite, indigestion, weight in ■ stomach after eating, (e) Frequently diarrhea. 2. Cardio — respiratory system. (a) Dyspnoea. (b) Swelling of ankles. 3. Nervous system. (a) Numbness or tingling of hands or feet. (Exclude syphilis.) (b) Depressed, easily fatigued. (c) Changes in the cord (unsteadiness of gait, cushion under feet, etc.) 4. Urine. (a) Slight albuminuria. (b) Urobilinuria, prolonged and persistent. 5. Slight irregular fever. 231 C). Other findings (a) Yellow tint to the skin and conjunctiva. (b) Petechiae, not characteristic. (c) Liver and spleen may be slightly enlarged. (d) Good nutrition. (e) Patients don't come to doctor till blood is way down. Blood Picture. Total volume reduced. Hydraemia, pale, coagula- tion often delayed. Sj)reads quickly, corpuscles seem to settle quickly. Clot small (Brilliant yellowish green tint to serum-urobilin ) . Formed elements. Red blood cells reduced to 1,500,000. (As low as 113,000, with recovery.) Striking anisocytosis — gen- eral tendency to predominance of deeply staining macrocytes. High percentage of poikilocytes. Mod- erate basophilia. Nucleated reds in small numbers, megaloblasts predominating. Platelets decreased. Hemoglobin per cell high. C. I. .95 to 1.5. W. B. C. decreased per cent of P. M. X., P. M. E., P. M. B., L. M., and transitionals while the per cent of Lym- phocytes is increased. During a remission the eosinophilic cells are increased together with other cells of myeloid origin, while tlie lymphocytes fall. Clinical course of disease: The onset is usually gradual and progressive. The disease may last from 1 to 10 years. It is charac- terized by a feeling of well-being till the R. B. C. count drops markedly low. Wave-like remissions occur, which may last from 1 to 6 years. An occa- sional cure is reported. The end usually comes from an intercurrent infection or from an acute exacer- bation. A gradual mental stupidity and toxaemia comes near the end and the patients die similar to those with hepatic disease. Valuable poiijts in diagnosis and ]3rognosis. 228 Primary' Anaemia. An anaemia for which there is no ascertainable cause. Chlorosis. A very rare disease of unknown etiol- og3\ Scarcely ever found in the United States, some- times in Germany. Limited to female sex and usu- ally appears at onset of adolescence (14 to 20), but has been known to occur up to 35. Distinct family and recurrent tendency, especially if individual ever has anaemia. Numerous theories as to cause — "love- sick anaemia" — also some think due to constitu- tional deficiency of tlie bone marrow to synthesize hemoglobin. Xo typical ])athological lindings; Chlorosis is a distinct disease and anaemia is only a symptom of it. Xo actual destruction of K. B. C. Symptoms : Weakness, fatigue, fainting periods, dizziness, G. I. symptoms (perverted taste, fondness for pickles, etc. ) , menstrual function is disturbed. Chlorosis is possibly an internal secretion dis- turbance. Hysteria is common. Characteristic green ( sea-sick green i color to pa- tient's face. (It was once thought to be du to i^oor nutrition, but this theory is probably wrong.) Blood findings: R. B. C. decreased; however, this decrease is relatively slight and wholly out of pro- portion with the great decrease in Hb. (Here Dr. Thayer gives the R. B. C. as 4,000,000 and Hb. as 42%.) This consequently results in a phenomenally low C. I. (beloAv 0.5). Pale R. B. C. Anisocytosis and poikilocytosis slight and often absent. If there is anisocytosis, the common cells are microcytes. Xucleated R. B. C. are few, and those that occur are of the late normoblastic type. The occurrence of a megaloblast is extremely rare. 237 ble, not caseous, and often have multiple hem- oiTliages in the acute forms. They rarely give rise to obstruction, as there is no tissue reaction around them. Spleen: The form is smooth, with the notch pre- served. Rarely reaches to the umbilicus, and rarely produces abdominal discomfort. Bones : Pain present in the late stages. Skin : There may be present multiple lymphomata, especially on the face and upper throat. They are small, painless, and never break down. Lympho- dermia perniciosa, a disease with great itching, may be the first symptom. Mouth: Affections of the mouth are relatively un- common. Mikulicz's disease is symmetrical tumor formation of lacrimal and salivary glands. Heart and lungs : Negative. Urine: Bence- Jones proteinuria and uria acid notable. Temperature: Fever not predominant. Duration: 3-5 years before use of X-ray. There is a tendency to intercurrent infections, which oblit- erate picture. Blood findings : Gross appearance — creamy, almost ptirulent. E. B. C. normal or slightly reduced. C. I. about normal. Slight anisocytosis and poikilosytosis with poly- chromasia — normoblasts. W. B. C. leucocytosis may reach 000,000. Lym- phocytes, 90-96%. Reider cells may be present. Azure granules are absent. Otherwise cells look like normal, except that they stain with a "Heller Farburg." The nucleus is less picnotic, therefore the nucleoli can be seen. Many of the cells crush indicating youth. The 234 IJemoglobiii low. C. I. .0