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112 Cards in this Set
- Front
- Back
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Growth and Development of Nervous System
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Develops from a dorsal thickening of the ectoderm (neural plate)
Neural groove and folds Neural tube Neural crest Mesoderm Blood vessels, microglial cells, dural and arachnoid layers of the meninges, the capsule of some peripheral nerve endings, and nerve coverings |
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Sulcus Limitans
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Forms the lateral boundary of the medial eminence of the 4th ventricle
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Basal Plate
Alar Plate Floor Plate |
Basal plate -contains primarily motor neurons
Alar plate - primarily associated with sensory functions Floor plate – derivative of the notocord which will separate the basal plate during neurulation |
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Defects of Neural Tube Closure
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Defects of neural tube closure
Anencephaly Encephalocele Meningocele Myelomeningocele Arnold-Chiari type II malformation Tethered cord syndrome |
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Folic Acid Link
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Environmental causes include diabetes mellitus and the antiepileptic drug valproate.
Two mutations of the folate dependent enzyme 5,10-Methylenetetrahydrofolate reductrase (MTHFR), MTHFR C677T and MTHFR A1298C, are associated with an increased risk for NTDs. |
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AFP test
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Neural tube defects can be detected in utero by determination of alpha-fetoprotein (AFP) and acetylcholinesterase in the amniotic fluid and maternal blood.
Alpha- fetoprotein, a circulating fetal protein produced by the liver, peaks at 12-14 weeks of gestation and subsequently declines. AFP leaks from the fetus into the amniotic fluid through exposed capillaries of the NTD. This results in persistently high levels of AFP in the amniotic fluid and in the maternal blood. Elevated AFP is also seen in other lesions where fetal capillaries are exposed to the amniotic fluid such as omphalocele and sacrococcygeal teratoma. Acetylcholinesterase leaks directly from exposed neural tissue into the amniotic fluid. |
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Tethered Cord Syndrome
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The cord is said to be "tethered" when it is abnormally attached within the boney spine.
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Arnold-Chiari Malformation
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Cerebellar tonsils elongate and herniate through foramen magnum into spinal canal, resulting in compression of parts of the brain and spinal cord, and disruption of cerebrospinal fluid flow.
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Spina bifida occulta
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Vertebral defect that allows the protrusion of the neural tube contents
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Cranial deformities
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Acrania, Craniosynostosis, Microcephaly, Congenital hydrocephalus
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Craniosynostosis
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bone forms too fast and new cells stop forming, so the skull bones fuse together prematurely and further growth is impossible, causing the various serious effects of the condition
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Macewin Sign
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(“cracked-pot” sign)-An indication of hydrocephalus in which percussion of the skull generates a cracked-pot sound.
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DDX
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Dandy-Walker Deformity
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Dandy-Walker symptoms
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increased head circumference, bulging at the back of the skull, problems with the nerves that control the eyes, face and neck, and abnormal breathing patterns
-bilateral abducens |
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Dandy-Walker basic info
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Dandy-Walker deformity is a rare congenital malformation that may be noticed immediately or may develop without notice. Dandy Walker Deformity involves the cerebellum (a area in the back of the brain that controls movement) and the fluid spaces around it. The focal feature of this disease is an enlargement of the fourth ventricle (a small channel that allows fluid to flow freely between the upper and lower areas of the brain and spinal cord), a partial or complete absence of the cerebellar vermis (the area between the two cerebellar hemispheres), and a cyst formation near the base of the skull. The fluid spaces may increase causing an increase in pressure in the brain.
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More Dandy-Walker info
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Dandy-Walker malformation consists of a malformation of the roof of the fourth ventricle and of the cerebellum. The cerebellum is poorly developed, displaced upwards and laterally. The enlarged fourth ventricle balloons out backward (see Image 1, Image 4). The fourth ventricle is grossly misshapen and is a membrane-wrapped cyst that extends into the foramen magnum. This cyst may lift and displace the posterior portion of the brain, as well as cause an internal obstruction of normal CSF flow with resultant hydrocephalus (see Image 2, Image 3, Image 6). Dandy-Walker malformation may be associated with atresia of the foramen of Magendie and, possibly, the foramen of Luschka.
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Static Encephalopathies
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Cerebral palsy
Spastic cerebral palsy Dyskinetic cerebral palsy Ataxic cerebral palsy |
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Cerebral Palsy (CP) basic info
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CP has three main types: spastic, ataxic, and athetoid. It may also manifest as a combination of types. Roy has spastic CP, as evidenced by his increased muscle tone. CP is caused by brain damage resulting in an inability to control muscle movements.3 This damage can be prenatal, perinatal, or postnatal, and can be due to malformation, infection, birth trauma, anoxia, accidental or non-accidental trauma, or intracranial hemorrhage. One hallmark of CP is that it is not progressive.
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Tay-Sachs basic info
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-cherry red spot on macula
-Results in accumulation of lipids in retinal ganglion cells of the eye -Red spot is result of RGC displacement in the fovea No cure. -If a child is suspected of having tay-sachs, parents are tested for hexoaminase activity – parents usually have lower than normal values of activity for the enzyme |
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Tay-Sachs etiology
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Tay-Sachs is an autosomal recessive disorder, resulting from a mutation in the HEXA gene, which codes for beta-hexoaminidase A, a multisubunit enzyme responsible for transport and degradation of gangliosides. The mutation results in storage of the gangliosides, instead of degradation. This causes nerve distension and thus, deterioriation of mental and physical abilities.
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Symptoms of Tay-Sachs
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Patients become blind, deaf, and unable to swallow.
Muscular atrophy and paralysis Dementia, seizures, increased startle reflex to noise cherry red spot surrounded by white on macula |
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ddx
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tay-sachs
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Reyes syndrome
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potentially fatal disease that causes numerous detrimental effects to many organs, especially the brain and liver. It is associated with aspirin consumption by children with viral diseases such as chicken pox.
The disease causes fatty liver with minimal inflammation, and severe encephalopathy (with swelling of the brain). The liver may become slightly enlarged and firm, and there is a change in the appearance of the kidneys. Jaundice is not usually present. |
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Tests to diagnose Reye's
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Blood chemistry tests show low blood sugar (glucose) levels
Liver function tests show higher than normal levels of liver enzymes Serum ammonia test may be higher than normal Liver biopsy Spinal tap Head CT or head MRI scan help rule out other causes of mental status changes |
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Childhood Brain tumors
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Medulloblastoma
Ependymoma Cerebellar astrocytoma Brain stem glioma Craniopharyngioma Optic glioma |
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Neuroblastoma
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A specific type of urine test will also be done. Nearly all (9 out of 10) children with neuroblastoma will have substances called vanillylmandelic acid (VMA), or homovanillic acid (HVA), in their urine.
x-rays, ct scans |
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Ganglioneuroma
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NF-1 with choroidal ganglioneuroma: external photograph of the face showing bupthalmos of the left eye and multiple café-au-lait spots on the face (left) and an axial CT scan showing enlargement of the left eye and absence of the greater wing of sphenoid (right).
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Gliomas
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develop from the supporting cells of the brain (which hold the nerve cells in place). They can be subdivided into two main types in children: astrocytomas and ependymomas.
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Medullablastomas
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develop in the cerebellum at the back of the brain. They may spread to other parts of the brain or into the spinal cord.
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DDX
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Ganglioma
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ddx
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Tethered Cord Syndrome
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Fracture
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break in the continuity of a bone
Classifications Complete or incomplete Closed or open Comminuted Linear Oblique Spiral Transverse Greenstick Torus Bowing Pathologic Stress |
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Bone Fractures manifestations and treatment
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Manifestations
Unnatural alignment, swelling, muscle spasm, tenderness, pain, impaired sensation, and possible muscle spasms Treatment Closed manipulation, traction, and open reduction Internal and external fixation |
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Dislocation and Subluxation
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Dislocation - Temporary displacement of two bones
Loss of contact between articular cartilage Sub - Contact between articular surfaces is only partially lost Dislocation and subluxation are associated with fractures, muscle imbalance, rheumatoid arthritis, or other forms of joint instability |
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ddx
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Paget's Disease
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Paget's Diagnosis
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Physical symptoms of nerve pain, headaches or hearing loss when affecting the skull, damage to cartilage of joints, bowing or swelling of the limbs.
X-ray-- Pagetic bone has a very characteristic appearance on x-rays. Alkaline phosphatase test -- An elevated level of alkaline phosphatase in the blood can be suggestive of Paget's disease, but can be found in other conditions |
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Osteoporosis
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Porous bone
Poorly mineralized bone Bone density Normal bone 833 mg/cm2 Osteopenic bone 833 to 648 mg/cm2 Osteoporosis <648 mg/cm2 Potential causes Decreased levels of estrogen and testosterone Decreased activity level Inadequate levels of vitamins D and C, or Mg++ |
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Reticulocytes
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immature red blood cells, typically composing about 1% of the red cells in the human body. Reticulocytes develop and mature in the red bone marrow and then circulate for about a day in the blood stream before developing into mature red blood cells. Like mature red blood cells, reticulocytes do not have a cell nucleus. They are called reticulocytes because of a reticular (mesh-like) network of ribosomal RNA that becomes visible under a microscope with certain stains such as new methylene blue.
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Basophilic stippling
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numerous thin and dark granules scattered throughout the RBC, related to abnormal hemoglobin synthesis representing aggregated ribosomes can be seen in thalassemia syndromes, iron deficiency and lead poisoning.
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Howell-Jolly bodies
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one chromosome that escaped during the mitotic process. Dark, round, and usually unique within the RBC In normal patients, RBC cells that contain one HJ body are eliminated from the blood stream by the spleen within a few minutes. Seen in asplenia, pernicious anemia and severe iron deficiency.
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Cabot's ring bodies
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remnants of the mitotic spindle, appearing as purple rings or loops within RBC in lead toxicity, pernicious anemia and hemolytic anemias
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Heinz's bodies
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denatured aggregated hemoglobin and can be seen in thalassemia, asplenia and chronic liver disease.
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ddx each
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A. basophilic stippling
B. Howell-jolly bodies c. Cabot's ring bodies d. heinz's bodies |
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ddx
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anisocytosis
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ddx
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poikilocytosis
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Normochromic-Macrocytic Anemia
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stem cells are abnormally large
unusually large erythrocytes Normal Hgb large erythrocytes have a small nucleus compared to the size of the cell. The chromatin in the nucleus does not clump properly which means that the DNA cannot effectively replicate itself. This causes ineffective erythropoiesis which in the formation of red blood cells. The defective DNA synthesis is caused by a deficiency in either vitamin B12 or folate. This deficiency causes premature cell death which results in a reduced number of mature erythrocytes. |
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Pernicious Anemia
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Caused by a lack of intrinsic factor from the gastric parietal cells which is required for vitamin B12 absorption
Results in vitamin B12 deficiency Typical anemia symptoms Neurologic manifestations Nerve demyelination Others Loss of appetite, abdominal pain, beefy red tongue (atrophic glossitis), icterus, and splenic enlargement Treatment Parenteral or high oral doses of vitamin B12 |
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Microcytic-Hypochromic Anemia
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Characterized by red cells that are abnormally small and contain reduced amounts of hemoglobin
Related to: Disorders of iron metabolism Disorders of porphyrin and heme synthesis Disorders of globin synthesis In this type of anemia the erythrocytes are abnormally small and the amount of hemoglobin is reduced. |
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Iron & Erythropoeisis
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Iron stores include the bone marrow, reticuloendothelial system (liver and spleen) and RBCs.
Transferrin (total iron-binding capacity) transports iron (Fe) to developing erythrocytes. Iron is deposited in the RBC, and transferrin returns to storage sites to bind more Fe for transport. Lactoferrin is a competitor of transferrin; it takes Fe that is free and returns it to storage sites Lactoferrin levels are elevated in anemia of chronic disease. |
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Sideroblastic Anemia
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Altered mitochondrial metabolism causing ineffective iron uptake and resulting in dysfunctional hemoglobin synthesis
Ringed sideroblasts within the bone marrow are diagnostic Sideroblasts are erythroblasts that contain iron granules that have not been synthesized into hemoglobin |
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ddx
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Sideroblastic Anemia
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Normocytic-normochromic anemia
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Characterized by red cells that are relatively normal in size and hemoglobin content but insufficient in number
Aplastic anemia Pancytopenia Fanconi anemia Posthemorrhagic anemia Acute blood loss from the vascular space Hemolytic anemia Sickle cell anemia Anemia of chronic inflammation |
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Schistocytes
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RBC fragmentation may be caused by RBCs striking against abnormal surfaces (aortic stenosis; atherosclerosis) or artificial surfaces (prosthetic heart valves; arterial grafts).
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what type of cells are these?
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shistocytes
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Polycythemia
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Overproduction of red blood cells
Relative polycythemia Result of dehydration Fluid loss results in relative increases of red cell counts and Hgb and Hct values |
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Leukocyte quantitative functions
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Increases or decreases in cell numbers
Bone marrow disorders or premature destruction of cells Response to infectious microorganism invasion |
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Alteration of Leukocyte function - qualitative function
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Disruption of cellular function
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Granulocytosis
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Neutrophilia is evident in the first stages of an infection or inflammation
If the need for neutrophils increases beyond the supply, immature neutrophils (banded neutrophils) are released into the blood This premature release is detected in the manual WBC differential and is termed a shift to the left When the population returns to normal, it is termed a shift to the right |
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ddx
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granulocytosis
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ddx
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eosinophilia
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basopenia
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Occurs in acute infections, hyperthyroidism, and long-term steroid therapy
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basophilia
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Response to inflammation and hypersensitivity reactions
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monocytosis
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Poor correlation with disease
Usually occurs with neutropenia in later stages of infections Monocytes are needed to phagocytize organisms and debris |
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Signs and symptoms of leukemia
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Anemia, bleeding purpura, petechiae, ecchymosis (bruising), thrombosis, hemorrhage, DIC (Disseminated Intravascular Coagulation), infection, weight loss, bone pain, elevated uric acid, and liver, spleen, and lymph node enlargement
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acute leukemia
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Presence of undifferentiated or immature cells, usually blast cells
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chronic leukemia
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Predominant cell is mature but does not function normally
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actue lymphocytic leukemia
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A condition marked by a rapid increase in the number of immature white blood cells called "lymphoblasts," which fail to function as normal cells; leaves the body susceptible to anemia, infection, and bleeding.
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acute myelogenous leukemia
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A condition that occurs in which the infection-fighting white blood cells do not mature fast enough, leaving the body susceptible to anemia and infection.
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chronic lymphocytic leukemia
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A slowly progressing condition marked by the proliferation of abnormal white blood cells called lymphocytes; leaves the body susceptible to anemia, infection, and bleeding.
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chronic myelogenous leukemia
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A slowly progressing condition marked by the proliferation of abnormal white blood cells called granulocytes; leaves the body susceptible to anemia, infection, and bleeding.
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Philadelphia chromosome
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specific chromosomal abnormality that is associated with chronic myelogenous leukemia (CML). It is due to a reciprocal translocation designated as t(9;22)(q34;q11), which means an exchange of genetic material between region q34 of chromosome 9 and region q11 of chromosome 22. The presence of this translocation is a highly sensitive test for CML, since 95% of people with CML have this abnormality. However, the presence of the Philadelphia (Ph) chromosome is not sufficient to diagnose CML, since it is also found in acute lymphoblastic leukemia (ALL, 25–30% in adult and 2–10% in pediatric cases) and occasionally in acute myelogenous leukemia (AML).
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Local Lymphadenopathy
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Drainage of an inflammatory lesion located near the enlarged node
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General lymphadenopathy
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Occurs in the presence of malignant or nonmalignant disease
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Lymphoma
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Lymphoma is a general term for a group of cancers that originate in the lymphatic system.
The lymphomas are divided into two major categories: Hodgkin lymphoma and all other lymphomas, called non-Hodgkin lymphomas. The prefix "lymph-" indicates their origin in the malignant change of a lymphocyte and the suffix "-oma" is derived from the Greek suffix denoting "tumor." About 53 percent of the blood cancers that occur each year are lymphomas. |
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Hodgkin Lymphoma
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Reed-Sternberg Cells
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Osteomyelitis
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most often caused by a staphylococcal infection
Most common cause is open wound (exogenous); also can be from a blood-borne (endogenous) infection Manifestations Acute and chronic inflammation, fever, pain, necrotic bone Treatment Antibiotics, débridement, surgery, hyperbaric oxygen therapy |
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Osteomalacia
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Deficiency of vitamin D lowers the absorption of calcium from the intestines
Inadequate or delayed mineralization Bone formation progresses to osteoid formation but calcification does not occur; the result is soft bones Pain, bone fractures, vertebral collapse, bone malformation |
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Malignant bone tumor manifestations
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Increased nuclear/cytoplasmic ratio, irregular borders, excess chromatin, a prominent nucleolus, and an increase in the mitotic rate
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Osteosarcoma
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38% of bone tumors
Predominant in adolescents and young adults; occurs in seniors if they have a history of radiation therapy Contain masses of osteoid “Streamers”: noncalcified bone matrix and callus Located in the metaphyses of long bones 50% occur around the knees |
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Chondrosarcoma
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Tumor of middle-aged and older adults
Infiltrates trabeculae in spongy bone; frequent in the metaphyses or diaphysis of long bones The tumor contains lobules of hyaline cartilage that expand and enlarge the bone Causes erosion of the cortex and can expand into the neighboring soft tissues |
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ddx
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chondrosarcoma
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ddx
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Fibrosarcoma
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Fibrosarcoma
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Firm, fibrous mass of collagen, malignant fibroblasts, and osteoclast-like cells
Usually affects metaphyses of the femur or tibia Metastasis to the lungs is common |
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Ewing's sarcoma
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starts in the bone. Any bone can be affected, but the pelvis, thigh bone (femur) and shin bone (tibia) are the most common places.
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strain
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Tear or injury to a tendon
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sprain
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Tear or injury to a ligament
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avulsion
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Complete separation of a tendon or ligament from its bony attachment site
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Tendinitis
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Inflammation of a tendon
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Tendinosis
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Painful degradation of collagen fibers
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Bursitis
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Inflammation of a bursa
Skin over bone, skin over muscle, and muscle and tendon over bone Caused by repeated trauma Septic bursitis is caused by a wound infection |
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Epicondyitis
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Inflammation of a tendon where it attaches to a bone
Tennis elbow (lateral epicondylitis) Golfer’s elbow (medial epicondylitis) |
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Inflammatory Joint Disease
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Commonly called osteoarthritis
Characterized by inflammatory damage or destruction in the synovial membrane or articular cartilage and by systemic signs of inflammation Fever, leukocytosis, malaise, anorexia, and hyperfibrinogenemia Infectious or noninfectious |
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Synovitis
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Most people don't realize it, but the joint fluid can get inflamed just like the surrounding tissues. This joint fluid is known as "synovium", so inflammation of the synovium is known as "synovitis".
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Osteoarthritis
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Osteoarthritis is characterized by local areas of damage and loss of articular cartilage, new bone formation of joint margins, subchondral bone changes, and variable degrees of mild synovitis and thickening of the joint capsule
Manifestations Pain, stiffness, enlargement of the joint, tenderness, limited motion, and deformity |
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Rheumatoid Arthritis
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Inflammatory joint disease
Systemic autoimmune damage to connective tissue, primarily in the joints (synovial membrane) Similar symptoms to osteoarthritis Presence of rheumatoid factors (RA or RF test) Antibodies (IgG and IgM) against antibodies Joint fluid presents with inflammatory exudate |
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Pathogenesis of Rheumatoid Arthritis
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CD4 T helper cells and other cells in the synovial fluid become activated and release cytokines
Recruitment and retention of inflammatory cells in the joint sublining region Cycle of altered cytokine and signal transduction pathways Possible immune complex deposition and inflammatory cytokine release RANKL release and osteoclast activation. This natural and necessary surface-bound molecule activates osteoclasts, cells involved in bone resorption. Overproduction of RANKL is implicated in a variety of degenerative bone diseases, such as rheumatoid arthritis and osteomyelitis. Angiogenesis in the synovium |
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Ankylosis spondylitits
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Inflammatory joint disease of the spine or sacroiliac joints causing stiffening and fusion of the joints
Systemic, immune inflammatory disease Primary proposed site is the enthesis Site where ligaments, tendons, and the joint capsule are inserted into bone Cause unknown, but there is a strong association with HLA-B27 antigen Human Leukocyte Antigen B27 is a class I surface antigen encoded by the B locus in the major histocompatibility complex (MHC) on chromosome 6 and presents microbial antigens to T-cells. HLA-B27 strongly associated with a certain set of autoimmune diseases |
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Gout
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Metabolic disorder that disrupts the body’s control of uric acid production or excretion
Gout manifests high levels of uric acid in the blood and other body fluids Occurs when the uric acid concentration increases to high enough levels to crystallize and deposit in connective tissues throughout the body When these crystals occur in the synovial fluid, the inflammation is known as “gouty arthritis” Gout is related to purine (adenine and guanine) metabolism Affected patients can have accelerated purine synthesis, breakdown, or poor uric acid secretion in the kidneys Mechanisms for crystal deposition Lower body temperatures, decreased albumin or glycosaminoglycan levels, changes in ion concentration and pH, and trauma |
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Rhabdomyolysis
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rapid breakdown of skeletal muscle tissue due to traumatic injury, either mechanical, physical or chemical. The principal result is a large release of the creatine kinase (CK) enzymes and other cell byproducts into the blood system and acute renal failure due to accumulation of muscle breakdown products, several of which are injurious to the kidney. Treatment is with intravenous fluids, and dialysis if necessary.
Severe cases of rhabdomyolysis often result in myoglobinuria, a condition where the myoglobin from muscle breakdown spills into the urine, making it dark, or "tea colored" (myoglobin contains heme, like hemoglobin, giving muscle tissue its characteristic red color). This condition can cause serious kidney damage in severe cases. The injured muscle also leaks potassium, leading to hyperkalemia, which may cause fatal disruptions in heart rhythm. In addition, myoglobin is metabolically degraded into potentially toxic substances for the kidneys. Massive skeletal muscle necrosis may further aggravate the situation, by reducing plasma volumes and leading to shock and reduced bloodflow to the kidneys |
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Crush Syndrome (Bywaters Syndrome)
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serious medical condition characterized by major shock and renal failure following a crushing injury to skeletal muscle. Cases commonly occur in catastrophes such as earthquakes or war, where victims have been trapped under fallen masonry (the syndrome was discovered by British physician Eric Bywaters in patients during the 1941 London Blitz).
It is a reperfusion injury that appears after the release of the crushing pressure. The mechanism is believed to be the release into the bloodstream of toxic chemicals - notably myoglobin, potassium and phosphorus - that are the products of rhabdomyolysis (the breakdown of skeletal muscle damaged by ischemic conditions). The specific action on the kidneys is not fully understood, but may be due in part to nephrotoxic metabolites of myoglobin. |
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myotonia
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symptom of a small handful of certain neuromuscular disorders characterized by the slow relaxation of the muscles after voluntary contraction or electrical stimulation
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Neonatal Schwarts-Jampel
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Affected children have a characteristic facies with a fixed expression due to tonic contraction of the facial muscles.
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McArdle Disease
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Myophosphorylase deficiency
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Pompe Disease
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Pompe disease is inherited in an autosomal recessive manner, meaning that an affected individual must inherit an abnormal allele from both parents. Thus, the probability of carrier parents having a child with Pompe disease is one in four for each pregnancy.
- deficient lysosomal enzyme acid alpha-glucosidase(GAA) activity, which catalyses the breakdown of glycogen to glucose in the lyososome |
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ddx
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Pompe Disease
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Rhabdomyosarcoma
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Malignant tumor of striated muscle
Usually muscles of the tongue, neck, larynx, nasal cavity, axilla, vulva, and heart Highly malignant with rapid metastasis Types Pleomorphic, embryonal, and alveolar The embryonal form is the most common; the alveolar variety is less common and carries the worst prognosis |
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Clubfoot
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Forefoot is adducted and supinated
Positional equinovarus Idiopathic congenital equinovarus Teratologic equinovarus The majority of clubfeet result from the abnormal development of the muscles, tendons, and bones, while the fetus is forming in the uterus during the first trimester of pregnancy (about the 8-12 week). While researchers are unable to pinpoint the exact cause, both genetic and environmental conditions play a role. Clubfoot is about twice as common in males, and occurs bilaterally (both feet) in about 50% of cases. If both parents are normal with an affected child, the risk of the next child having a clubfoot is 2-5%. |
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Developmental Dysplasia of the Hip
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Abnormality of the femoral head, acetabulum, or both
Risk factors Female sex, oligohydramnios, positive family history, and breech presentation The hip can present as subluxated, dislocated, or acetabular dysplasia Manifestations Asymmetry of skinfolds at groin crease Galeazzi sign Limitation of hip abduction Positive Ortolani sign Positive Barlow test Clinical management Outcome becomes poorer with age Pavlik harness Closed reduction with spica casting Surgery |
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Galeazzi sign
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a classic identifying sign for unilateral hip dislocation. This is performed with the patient lying supine and the hips and knees flexed. Examination should demonstrate that one leg appears shorter than the other. Although this is usually due to hip dislocation, realizing that any limb length discrepancy results in a positive Galeazzi sign is important.
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Osteogenesis Imperfecta
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“Brittle bone disease”
Defect in type I collagen production Clinical manifestations Osteopenia Increased rate of fractures Bone deformity (bowing) Short stature Blue sclera and poor dentition Aortic aneurysm Clinical management Surgical Intramedullary and telescoping rod placement Medical Increased calcium and vitamin D Biphosphates |
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Legg-Calve-Perthes Disease
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Interrupted blood supply to the femoral head
Self-limiting disease Deformation due to ischemia is permanent Clinical manifestations Spasm on rotation of hip Limited internal rotation or abduction of hip “Trendelenburg” gait Clinical management Anti-inflammatories Serial radiographs Surgery |
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Osgood-Schlatter Disease
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Tendinitis of the anterior patellar tendon and osteochondrosis of the tubercle of the tibia
Clinical manifestations Pain and swelling Clinical management Restricted activity Bracing and knee immobilizer |
