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The Charles R. Drew Papers

[Lecture notes for Pathology course] pdf (1,094,030 Bytes) transcript of pdf
[Lecture notes for Pathology course]
Item is handwritten.
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8 (1,094,030 Bytes)
1936-01-07 (January 7, 1936)
Drew, Charles R.
Original Repository: Howard University. Moorland-Spingarn Research Center. Charles R. Drew Papers
Reproduced with permission of the Moorland-Spingarn Research Center.
Exhibit Category:
Education and Early Medical Career, 1922-1938
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Document Type:
Lecture notes
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Pathology #170 Jan. 7, 1935 C. R. Drew
Pathology is the study of disease producing constellations and their effect on living organisms. It has reared itself since the time of Virchow to the status of a science, if any field in biology may be truly called a science, and as such has and can divorce itself from the previous servile position as the hand maid of medicine; yet, for us its greatest raison d'être is the part it plays in elucidating the processes of disease in man. It is well to remember from the very beginning however that the purpose of any science is to reconstruct physical experience into a system of law and order; to bring natural phenomena closer to our comprehension.
The domain of science is one of "causal explanations". Purpose, as such, lies outside this realm, teleology must find its proper scope elsewhere. The moon was not hung aloft in the heavens to keep our gas bills down, neither does blood clot to prevent man from bleeding to death. The formation of the clot may be the saving factor, but its formation is the result of a definite series of genetically related processes or steps, the absence of any one of which precludes the possibility of success, the presence of them all is tantamount to completion. So again, bacteria, per se, are not the cause of disease, but rather are they but a single link in a long concatenation of causally connected events which include such other links as hereditary background, environment, age, sex, mental attitude, previous state of health and the variable factors such as type, morphology, mass and virulence of the bacteria themselves.
What is disease? It may be considered as the reflection of a pathological process or lesion upon the organism as a whole. What is a pathological lesion? It may be defined as morphological expression of disproportion of values between stimuli and living cells. All living processes may be considered as a resultant of the interplay between various stimuli and the response of living tissue to these stimuli. If the stimulation is of short duration and of mild intensity and the activated tissue returns quickly to a state of equilibrium, -- then the process may be considered as physiological. If on the other hand the stimuli are of great intensity and prolonged in time, the result may usually be considered as pathological. To state this in another way -- irritants are environmental factors which are responsible for the emancipation of organismic potentialities. The degree of disproportion between the stimulating effect of an irritant and the response on the part of the organism determines physiology or pathology. A cloth dipped in water heated to 55 degrees centigrade and applied to a part causes the physiological increase in activity of a part with a pleasing effect and a rapid return to its previous state when the mild irritant is removed. Increase the temperature to 100 degrees centigrade and it stimulated just a bit too much, and on removal there is no rapid return to the status quo ante because actual damage has been done to the tissue and this "burn" is pathological.
As beginning pathologists let us take a part of our early guidance from that great pathologist, Virchow, who said many years ago:
(1) All knowledge of disease must be based upon objective, anatomical experience.
(2) Conclusions as to the nature of disease must be based on this experience and be made strictly according to natural laws of cause and effect.
There may be exceptions to these rules at the present time but they still serve as a sure foundation for accurate, restrained, scientific thinking in pathology. At times, perchance we shall leave our special field and indulge in theorizing and interpretation and where facts fail us to take the perfectly legitimate heuristic, a somewhat circuitous route to truth, but when so doing we knowingly leave the sphere of pure science and enter the domain of philosophy and metaphysics.
With these few introductory remarks let us begin our work with a consideration of some of the changes that take place in tissues.
Progressive Movements
Morphological Fluidity
The basic factor in growth; characteristic of higher forms; ante eates birth, postdates death.
Differentiation - a function of environment
1. Mitotic - at rest
2. Amniotic - inactive cells
Growth Requisites
1. Transudation - increased nutritive supply
2. Assimilation - ability of the tissue to use it; depends on the permeability of the cell
3. Procreation - formation of new protoplasm
Smallest living units which have all of the characteristics of living protoplasm. These increase in geometrical progression from generation, the nuclear plasma material, however, remaining in constant proportion.
Cloudy Swelling
When on the positive side it is the first step in the process of greater assimilation and increase in protoplasmic content.
Increase in protoplasmic content and structures already present
Numerical increase in cell elements and protoplasmic content. Both content and function are constant in type.
An inherent characteristic of living matter. Young cells form an ANLAGEN whose direction of differentiation is then a function of environment. There is always a tendency to overproduce.
Connective Tissue - from fibroblasts
Cartilage - from perichondroblasts or fibroblasts
Bone - from periosteum, endosteum or chondroclasts (?)
Vessels - endothelial buds from preexisting vessels
Blood - reappearance of myeloid foci of embryonic type in bone marrow, liver, spleen
Muscles - hypertrophy rather than hyperplasia the rule
Nerve - by extension from the proximal part of the fiber only
Ganglion Cell - no true regeneration when totally destroyed
Epithelial Cells
Lining - Parenchymal - no true regeneration if integrity of the architectural plan has been disturbed
Abnormal Regeneration
Abortive or pathological, the result of destruction of normal skeletal structure by trauma or disease
Scar Tissue - substitution of lower tissue in injury
Regressive Movements
I. Atrophy - quantitative regressive movement in tissue
1. Reduced in size
2. Patchy reduction in protoplasm
3. Apparent excess of nuclear structures
4. Pigment collection
5. Reduced oxidation
6. Reduced function
7. Hydopsical dissolution
1. Interruption of nerve cell control
2. Insufficiency of self regulation
3. Nutritive interference
II. Cloudy Swelling
Granular degeneration of cell protoplasm in form of precipitated suspensoids. First stage of degeneration when on the negative side. When sever the nuclei may undergo 1. Myknosis, 2. Karryorrhexis and 3. Chromatolysis
III. Fatty Changes
1. Infiltration - extracellular collections of large fatty cells as the result of nutritive disturbances in circulatory stasis
2. Phanerosis - intracellular disintegration of cellular protoplasm as the result of toxic activity
3. Lypaemia - excess fat in the blood stream, seen in pregnancy, starvation, acidosis, anaesthesia and alcoholism
4. Adipocere - waxy transformation of dead bodies in which splitting and regenerating fat derivative replace the muscles
IV. Hyaline Transformation
Waxy, smooth, glistening, faintly bluish pink staining material is seen most frequently in the intimal lining if the blood vessels, and in the muscles in typhoid fever, trichinosis, icterous neonataorum, snake bite, etc.
V. Amyloid Substitution
Bacon like hyaloid protein degeneration product seen in chronic wasting and purulent processes like Tbc, Syphilis, osteomyelitis ect. giving staining reactions similar to starch but which is thought to be a mixture of proteid substance and chondroitin sulphuric acid.
VI. Mucoid Substitution
Drowning and disintegration of epithelial mucoid cells in their own secretions; coagulates in strings and stains basically
VII. Colloidal Degeneration
Like the others a purely descriptive term referring to substances which look like that substance seen in the thyroid gland. A desquamation of secretory cells due to retention if jelly like product which coagulates in discs and stains pink with acid dyes
VIII. Carbohydrate Changes
Glycogen content of organs is always in inverse proportion to fat.
1. Diabetes Mellitus - upset ibn COH metabolism
2. Von Clarke's Disease - excessive storage of glycogen
IX. Protein changes
Uric acid the result of breakdown of nucleoproteins
Gout 1. excessive uric acid, 2; Monosodium urate (tophi) in the cartilages 3. Arthritis
Salt and Mineral Changes
Normal - 10 mgrms. % in blood, maintained by the activity of the parathyroid glands
Two types
1. Indeffusible - firmly bound in such tissues as the bones
2. Diffusible
a. Unionized - playing very little part in the active metabolism of the body
b. Ionized - the amount in ionic form depends on the carbonic acid tension; when it is reduced the equation goes from left to right and the insoluble tricalcium phosphate is reprecipitated
Ca3(PO4)2+- 2H2CO3 2CaHPO4 + Ca(HCO3)2 2Ca++ + 2HPO4- + Ca++ = 2HCO3-
1. Blood Clotting
Prothrombin - Cephalin - Ca -- Thrombin
Thrombin - Fibrinogen -- Fibrin
2. Increases contraction of heart muscle
3. Direct relationship to nervous irritability
4. Formation of bones
5. Balance in Hydrogen ion maintenance
Causes of Increase in Calcium
1. Halisteresis - withdrawal of Ca. from bones as seen in ostemalacia. Decalcification follows in the acid juices of such tissues as the stomach and kidney in the presence of alkaline tissue juices
2. Parathyroid underactivity - in case of tumor displacement of a great deal of the tissue
3. Paget's Disease of Bones - classification rather obscure at the moment but there is increase in Ca.
4. Hyperostosis Frontalis Interna - Surg., Gyn., & Obs. 61-353-35
Decrease in Calcium
1. Parathyroid over activity
2. Alkalaemia
a. Gastrointestinal - loss of HCl by vomiting
b. Hyperpnoea - blowing off of CO
c. Alkalie ingestion - excess NaO2H
3. Rickets - in complete absorption from G. I. tract
4. Nephritis - incomplete riddance?
1. Always in degenerated, necrotic, hyaline tissue such as arterial walls in hypertension, atherosclerotic plaques, avascular tumors, scar tissue, abscesses, Tbc. nodes, & exudates, cysts, incrusted parasites etc.
Why Calcification?
1. Physical deposition theory
2. Fatty acids form insoluble soaps
3. Supersaturation maintained by high CO2 tension
4. Necrosis and hyaline metamorphosis
Why in bone at all?
Growing bone contains an enzyme capable of splitting hexose phosphate into hexose & inorganic phosphate.
A. Nephrolithiasis
B. Cholelithiasis
C. Pancreatic lithiasis
avascular tumors, scar tissue, abscesses, The nodes & exudates, cysts, parasites (Trichinaelis)
Why calcification
1. Physical deposition
2. Fatty acids to form insoluble soaps
3. Super saturation maintained by high CO2 tension
4. Necrosis & hyaline metamorphosis
Why calcification in bone at all
Growing bone contains an enzyme capable of splitting hexose phosphate into hexose & inorganic phosphate ppt. Ca3 (PO4)2 85% bone.
1. Kidney Stones - Nephrolithiasis
D. Keyser J.A.M.A. 104 # 15 1299 - April 1935
J. Swift Coby J. Mol. 32: 541- 34
Experimental production (see card)
1. Oxanire
2. Excessive Ca Ox diet
3. Parathyroid or vecetiral excess
4. Uric acid crystals in animals i ech fistulas
5. Vitamin A deficiency
6. Infection c urea splitters, strep staph & B. Proteins
7. Incrustation in presence of infection
Types CaPO4 Vitamin def. - CaCO2 Alkaline diets - Uric Acid - Acid
2. Gall Bladder
1. Cholesterol - pure
2. Pigment - pure
3. Infection
4. Mixed
Theories Weiser Gray - Arch. Path. 17 - 1 - 34
1. Aschoff 1924 High blood cholesterol, + stasis
2. Confirmed 1933 - Wilkie - blood-bile cholesterol
3. Naunyer - 1892 - disintegration of epithelium of GB
4. Elman + Graham 1938 - support Naunyer - to account for crystals in strawberry gallbladder.
Schade: - The increasing impoverishment of the bill in cholate content compels small quantities of cholesterol to settle out. But owing to the presence of fal it is guttulate seperation which occurs, and since in such simple stasis, foreign substances are lacking, there is nothing to prevent aggregation of the droplets. (A. Shade Colloid Chemistry N.Y. 1928 - 2- 803
In biliary stasis from anat. or phys. abnormalities the bile collects. during this period there may be infiltration of cholesterol from hyercholesterolated blood and a decrease in the amount of the alkali cholates which are responsible for returning the fat in the form of an emulsion as well as the cholesterol in the dispensed state. In the absence of infection, a decrease in cholates may result from either or both of the following causes
1. A change in the pH of the bile from alkaline to the acid, converting the alkali salt to the insoluble glycocholic acid which is neither an emulsifying agent for fat nor a peptizing agent for cholesterol (or)
2. A physiologic change in the wall of the gall bladder which allows resorption of the alkali cholates.
The disappearance of alkali cholate, either by conversion to glycocholic acid or by resorption causes ppt of cholesterol. The excess cholesterol collects around the fat droplets which tend to coalesce as the cholate is gradually removed, then the fat acts as a solvent which is responsible for the growth of interlacing crystals.
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