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T. Porgan, M.A.S., M.D.

Assistant Professor, University of California, Davis School of Medicine

Dystrophic calcification is characterized by calcification in abnormal (dystrophic) tissue allergy medicine kroger trusted promethazine 25mg, while metastatic calcification is characterized by calcification in normal tissue allergy austin generic promethazine 25 mg amex. Examples of dystrophic calcification include calcification within severe atherosclerosis allergy medicine kids buy discount promethazine 25 mg online, calcification of damaged or abnormal heart valves allergy journals list order promethazine 25 mg on-line, and calcification within tumors. Small (microscopic) laminated calcifications within tumors are called psammoma bodies and are due to single-cell necrosis. Psammoma bodies are characteristically found in papillary tumors, such as papillary carcinomas of the thyroid and papillary tumors of the ovary (especially papillary serous cystadenocarcinomas), but they can also be found in meningiomas or mesotheliomas. For example, calcification of a tumor of the cortex in an adult is suggestive of an oligodendroglioma, while calcification of a hypothalamus tumor is suggestive of a craniopharyngioma. With dystrophic calcification the serum calcium levels are normal, while with metastatic calcification the serum calcium levels are elevated (hypercalcemia). Causes of hypercalcemia include certain paraneoplastic syndromes, such as secretion of parathyroid hormone­related peptide, hyperparathyroidism, iatrogenic causes (drugs), immobilization, multiple myeloma, increased milk consumption (milk-alkali syndrome), and sarcoidosis. Apoptosis as originally defined is a purely morphologic process that differs from necrosis in several respects. Apoptosis involves single cells, not large groups of cells, and with apoptosis the cells shrink and there is increased eosinophilia of cytoplasm. The shrunken apoptotic cells form apoptotic bodies, which may be engulfed by adjacent cells or macrophages. With apoptosis there is no inflammatory response, the cell membranes do not rupture, and there is no release of macromolecules. One mechanism of apoptosis involves cytochrome c being released into the cytoplasm from mitochondria via bax channels, which are upregulated by p53. Cytochrome c then binds to and activates apoptosis activating factor 1 (Apaf-1), which then stimulates a caspase cascade. The product of bcl-2 is normally located on the outer mitochondrial membrane, endoplasmic reticulum, and nuclear envelope. This product inhibits apoptosis by blocking bax channels and by binding to and sequestering Apaf-1. Cytotoxic T lymphocytes stimulate apoptosis by expressing FasL or secreting substances like perforin (which forms pores) or granzyme B. Apoptosis is the type of cell death seen with embryonic development, death of immune cells, hormone-induced atrophy, and some bacterial toxins or viral infections. Examples of apoptosis of immune cells include the involution of the thymus with aging and the destruction of proliferating B cells in germinal centers of lymph nodes. Examples of apoptosis resulting from hormone-induced atrophy exclude the death of endometrial cells during menses, ovarian follicular atresia after menopause, and regression of the lactating breast after weaning. An example of a viral infection causing apoptosis is the formation of Councilman bodies in the livers of patients with viral hepatitis. Coagulative necrosis, characterized by loss of the cell nucleus, acidophilic change 98 Pathology of the cytoplasm, and preservation of the outline of the cell, is seen in sudden, severe ischemia of many organs. Myocardial infarction resulting from the sudden occlusion of the coronary artery is a classic example of coagulative necrosis. In contrast, with liquefactive necrosis the dead cells are completely dissolved by hydrolytic enzymes. This type of necrosis can be seen in ischemic necrosis of the brain, but classically it is associated with acute bacterial infections. Fat necrosis, seen with acute pancreatic necrosis, is fat cell death caused by lipases. Fibrinoid necrosis is an abnormality seen sometimes in injured blood vessels where plasma proteins abnormally accumulate within the vessel walls. Caseous necrosis is a combination of coagulative and liquefactive necrosis, but the necrotic cells are not totally dissolved and remain as amorphic, coarsely granular, eosinophilic debris. Gangrenous necrosis of extremities is also a combination of coagulative and liquefactive necrosis. In dry gangrene the coagulative pattern is predominate, while in wet gangrene the liquefactive pattern is predominate.

Motor responses at rest and to stimulation Appropriate motor response to noxious orbital roof pressure Paratonic resistance Figure 3­11 allergy symptoms 2013 cheap promethazine 25 mg mastercard. Signs of central transtentorial herniation or lateral displacement of the diencephalon wheat allergy symptoms uk purchase promethazine 25 mg mastercard, early diencephalic stage which allergy medicine works quickest generic promethazine 25mg fast delivery. In some cases allergy shots for bee stings discount promethazine 25mg with mastercard, extensor posturing appears spontaneously, or in response to internal stimuli. Motor tone and tendon reflexes may be heightened, and plantar responses are extensor. After the midbrain stage becomes complete, it is rare for patients to recover fully. Most patients in whom the herniation can be reversed suffer chronic neurologic disability. As the patient enters the pontine stage (Figure 3­14) of herniation, breathing becomes more shallow and irregular, as the upper pontine structures that modulate breathing are lost. As the damage approaches the lower pons, the lateral eye movements produced by cold water caloric stimulation are also lost. Motor responses at rest and to stimulation Motionless Legs stiffen and arms rigidly flex (decorticate rigidity) Figure 3­12. Signs of central transtentorial herniation, or lateral displacement of the diencephalon, late diencephalic stage. As breathing fails, sympathetic reflexes may cause adrenalin release, and the pupils may transiently dilate. However, as cerebral hypoxic and baroreceptor reflexes also become impaired, autonomic reflexes fail and blood pressure drops to levels seen after high spinal transection (systolic pressures of 60 to 70 mm Hg). At this point, intervening with artificial ventilation and pressor drugs may keep the body alive, and all too often this is the reflexive response in a busy intensive care unit. It is important to recognize, however, that once herniation progresses to respiratory compromise, there is no chance of useful recovery. Motor responses at rest and to stimulation Usually motionless Arms and legs extend and pronate (decerebrate rigidity) particularly on side opposite primary lesion or Figure 3­13. Clinical Findings in Dorsal Midbrain Syndrome the midbrain may be forced downward through the tentorial opening by a mass lesion impinging upon it from the dorsal surface (Figure 3­15). The most common causes are masses in the pineal gland (pinealocytoma or germ cell line tumors) or in the posterior thalamus (tumor or hemorrhage into the pulvinar, which normally overhangs the quadrigeminal plate at the posterior opening of the tentorial notch). Pressure from this direction produces the characteristic dorsal midbrain syndrome. A similar picture may be seen during upward transtentorial herniation, which kinks the midbrain (Figure 3­8). Respiratory pattern Eupneic, although often more shallow and rapid than normal or Slow and irregular in rate and amplitude (ataxic) b. Motor responses at rest and to stimulation or No response to noxious orbital stimulus; bilateral Babinski signs or occasional flexor response in lower extremities when feet stroked Motionless and flaccid Figure 3­14. Pressure on the olivary pretectal nucleus and the posterior commissure produces slightly enlarged (typically 4 to 6 mm in diameter) pupils that are fixed to light. If the patient is awake, there may also be a deficit of convergent eye movements and associated pupilloconstriction. The presence of retractory nystagmus, in which all of the eye muscles contract simultaneously to pull the globe back into the orbit, is characteristic. Deficits of arousal are present in only about 15% of patients with pineal region tumors, but these are due to early central herniation. Motor responses at rest and to stimulation Appropriate motor response to noxious orbital roof pressure Paratonic resistance Figure 3­15. Safety of Lumbar Puncture in Comatose Patients A common question encountered clinically is, ``Under what circumstances is lumbar puncture safe in a patient with an intracranial mass lesion? The actual frequency of cases in which this hypothetical risk causes transtentorial herniation is difficult to ascertain. If a patient has no evidence of compartmental shift on the study, it is quite safe to obtain a lumbar puncture.

Some congenital cataracts are caused by teratogenic agents allergy to zpack symptoms buy generic promethazine 25 mg line, particularly the rubella virus allergy shots gluten cheap 25 mg promethazine. The lenses are vulnerable to rubella virus between the fourth and seventh weeks allergyworx promethazine 25 mg fast delivery, when primary lens fibers are forming allergy testing nashville buy discount promethazine 25mg line. These cataracts are not present at birth, but may appear as early as the second week after birth. In most cases, corrective eyewear is required, although some studies have shown that artificial intraocular lenses may be safely implanted. More than 70% of patients with bilateral congenital cataracts can attain reasonable visual acuity. Extended treatment with refractive correction and additional surgery may be required. Richard Bargy, Department of Ophthalmology, Cornell-New York Hospital, New York, New York. The cornea is formed from three sources: the external corneal epithelium, derived from surface ectoderm the mesenchyme, derived from mesoderm, which is continuous with the developing sclera Neural crest cells that migrate from the lip of the optic cup and differentiate into the corneal endothelium Integration link: Cornea - histology Edema of the Optic Disc the optic nerve is surrounded by three sheaths that evaginated with the optic vesicle and stalk; consequently, they are continuous with the meninges of the brain. The outer dural sheath from the dura mater is thick and fibrous and blends with the sclera. The relationship of the sheaths of the optic nerve to the meninges of the brain and the subarachnoid space is important clinically. This occurs because the retinal vessels are covered by pia mater and lie in the extension of the subarachnoid space that surrounds the optic nerve. Development of the Choroid and Sclera the mesenchyme surrounding the optic cup (largely of neural crest origin) reacts to the inductive influence of the retinal pigment epithelium by differentiating into an inner vascular layer, the choroid, and an outer fibrous layer, the sclera. The sclera develops from a condensation of mesenchyme external to the choroid and is continuous with the stroma (supporting tissue) of the cornea. Toward the rim of the optic cup, the choroid becomes modified to form the cores of the ciliary processes, consisting chiefly of capillaries supported by delicate connective tissue. The first choroidal blood vessels appear during the 15th week; by the 23rd week, arteries and veins can be easily distinguished. Development of the Eyelids the eyelids develop during the sixth week from neural crest cell mesenchyme and from two cutaneous folds of ectoderm that grow over the cornea. As the eyelids open, the bulbar conjunctiva is reflected over the anterior part of the sclera and the surface epithelium of the cornea. Congenital Ptosis of the Eyelid Drooping of the superior (upper) eyelids at birth is relatively common. Ptosis (blepharoptosis) may result from failure of normal development of the levator palpebrae superioris muscle. Drooping of the superior eyelids usually results from abnormal development or failure of development of the levator palpebrae superioris, the muscle that elevates the eyelid. In bilateral cases, as here, the infant contracts the frontalis muscle of the forehead in an attempt to raise the eyelids. Palpebral colobomas appear to result from local developmental disturbances in the formation and growth of the eyelids. Fundamentally, the defect means absence of the palpebral fissure (slit) between eyelids; usually there is varying absence of eyelashes and eyebrows and other eye defects. Development of the Lacrimal Glands At the superolateral angles of the orbits, the lacrimal glands develop from a number of solid buds from the surface ectoderm. Early in the fourth week, a thickening of surface ectoderm, the otic placode, appears on each side of the myelencephalon, the caudal part of the hindbrain. Inductive signals from the paraxial mesoderm and notochord stimulate the surface ectoderm to form the placodes. Each otic placode soon invaginates and sinks deep to the surface ectoderm into the under-lying mesenchyme. The edges of the otic pit soon come together and fuse to form an otic vesicle-the primordium of the membranous labyrinth. The otic vesicle then loses its connection with the surface ectoderm, and a diverticulum grows from the vesicle and elongates to form the endolymphatic duct and sac.