pediagenosis: Organ
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Showing posts with label Organ. Show all posts
Showing posts with label Organ. Show all posts

Monday, June 14, 2021

TIBIAL INTERCONDYLAR EMINENCE FRACTURE

TIBIAL INTERCONDYLAR EMINENCE FRACTURE

TIBIAL INTERCONDYLAR EMINENCE FRACTURE

TIBIAL INTERCONDYLAR EMINENCE FRACTURE


Fracture of the intercondylar eminence (tibial spine) indicates partial or complete detachment of the ACL from the tibia and is most commonly found in children. This fracture is usually caused by hyperextension of the knee or a sudden twisting motion. Forceful traction resulting from a direct blow to the distal femur on a flexed knee may also result in this fracture. If the fracture is displaced, the loose fragment may block motion and cause severe swelling and hemarthrosis. Type I fracture of the tibial spine is an incomplete fracture, whereas type II is complete but nondisplaced. Type III fractures are described as type IIIA (complete and displaced) and type IIIB (complete, displaced, and rotated out of position).

OSTEOCHONDRITIS DISSECANS AND OSTEONECROSIS

OSTEOCHONDRITIS DISSECANS AND OSTEONECROSIS

OSTEOCHONDRITIS DISSECANS AND OSTEONECROSIS

OSTEOCHONDRITIS DISSECANS

PROGRESSION OF OSTEOCHONDRITIS DISSECANS
PROGRESSION OF OSTEOCHONDRITIS DISSECANS


Osteochondritis dissecans (OCD) is a defect in the sub-chondral region of the apophysis or the epiphysis of a bone, often with partial or complete separation of the bone fragment. When this occurs in the distal femur, it is a common source of loose bodies in the knee. Whereas OCD most often affects the posterolateral aspect of medial femoral condyle, it can also occur in other regions of the knee, as well as the shoulder, elbow, and foot.

DISLOCATION OF KNEE JOINT

DISLOCATION OF KNEE JOINT

DISLOCATION OF KNEE JOINT

DISLOCATION OF KNEE JOINT


Dislocation of the knee joint must be distinguished from dislocation of the patella. Whereas a patella dislocation involves the patellofemoral joint, a knee dislocation involves the tibiofemoral articulation. Any dislocation is an emergency, and dislocation of the knee is no exception. Reduction should be achieved as soon as possible. Striking the knee against the dashboard during an automobile accident is the most common cause of injury, but athletic injuries are also common causes. The popliteal artery and its branches are often damaged during dislocation of the knee. Therefore, arterial injury must be suspected in every knee dislocation. A thorough neurovascular examination should be performed before and after reduction, and an ankle- brachial index (ABI) should be obtained as well. If there remains any question of arterial damage, the patient frequently will undergo arteriography or CT angiography and any necessary arterial repair should be done immediately.

DISRUPTION OF QUADRICEPS FEMORIS TENDON OR PATELLAR LIGAMENT

DISRUPTION OF QUADRICEPS FEMORIS TENDON OR PATELLAR LIGAMENT

DISRUPTION OF QUADRICEPS FEMORIS TENDON OR PATELLAR LIGAMENT

DISRUPTION OF QUADRICEPS FEMORIS TENDON OR PATELLAR LIGAMENT


Damage to the quadriceps mechanism generally occurs when there is active contraction of the quadriceps femoris muscle against forced flexion of the knee. Most ruptures of this extensor mechanism occur in older patients. At the time of injury, the patient experiences sudden pain, which may be associated with a tearing sensation about the knee. The tendon may be weakened by age-related degenerative changes or by pathologic changes due to psoriatic arthritis, rheumatoid arthritis, arteriosclerosis, gout, hyperparathyroidism, diabetes, chronic renal failure, or corticosteroid therapy.

KNEE LIGAMENT INJURY

KNEE LIGAMENT INJURY

KNEE LIGAMENT INJURY

RUPTURE OF THE ANTERIOR CRUCIATE LIGAMENT
RUPTURE OF THE ANTERIOR CRUCIATE LIGAMENT


SPRAINS OF KNEE LIGAMENTS

Ligament injuries (sprains) of the knee are very common in athletes. In first-degree sprains, the ligament is trenched, with little or no tearing. These injuries produce mild point tenderness, slight hemorrhage, and swelling. Erythema may develop over the painful area but resolves in 2 or 3 weeks after injury. Joint laxity is not present, and the injury does not produce any significant long-term disability. Appropriate treatment consists of rest and muscle rehabilitation. Seconddegree sprains are characterized by partial tearing of the ligament, resulting in joint laxity, localized pain, tenderness, and swelling. When stress is placed on a joint during examination, the examiner should still feel a definite “end point” to the joint movement. Because the ligament is only partially injured, the joint remains stable; thus, vigorous rehabilitation alone will likely be sufficient treatment. Third-degree sprains produce complete rupture of a ligament, making the joint unstable. Tenderness, instability, absence of a definite end point to stress testing, and severe ecchymosis are the hallmarks of third-degree sprains. Surgical intervention may be needed.

MENISCAL VARIATIONS AND TEARS

MENISCAL VARIATIONS AND TEARS

MENISCAL VARIATIONS AND TEARS

TYPES OF MENISCAL TEARS AND DISCOID MENISCUS VARIATIONS
TYPES OF MENISCAL TEARS AND DISCOID MENISCUS VARIATIONS


DISCOID MENISCUS

The meniscus is normally a crescentic structure, although several forms of discoid lateral menisci have been described. These range from a complete disc to a very rare ring-shaped meniscus with abnormal thickness. The common explanation for these variant discoid forms assumes that the normal meniscus is formed from an original discoid shape and that the discoid lateral meniscus is a congenital variant in which the central portion does not degenerate with time. This theory would explain the variously shaped menisci found at surgery. However, no discoid menisci have been found in fetuses and a review of comparative anatomy shows no mammal with such a pattern of formation.

DOWN SYNDROME

DOWN SYNDROME

DOWN SYNDROME

DOWN SYNDROME


Down syndrome is a genetic disorder caused by trisomy of chromosome 21. Trisomy 21 occurs in approximately 1 of every 1000 births. Chromosome 21 is an acrocentric chromosome, and trisomy 21 is the most common form of chromosomal trisomy. Trisomy 21 most often occurs as the result of nondisjunction of meiosis, which leads to an extra copy of chromosome 21. Some patients with Down syndrome have a Robertsonian translocation to chromosome 14 or chromosome 22, which are two other acrocentric chromosomes. In these cases, the number of total chromosomes is normal at 46, but the extra chromosome 21 material is translocated to another chromosome. This, in effect, causes an extra chromo- some 21. All or part of chromosome 21 may be trans-located, leading to variations in phenotype. Mosaicism is a rare cause of trisomy 21 in partial cell lines, and the clinical phenotype depends on how early the genetic defect occurred during embryogenesis.

MARFAN SYNDROME

MARFAN SYNDROME

MARFAN SYNDROME

MARFAN SYNDROME


Marfan syndrome is an autosomal dominantly inherited disorder of connective tissue that is caused by a genetic defect in the FBN1 gene located on chromosome 15. The disorder leads to a defect in the fibrillin-1 protein, which is a component of the extracellular matrix of connective tissue. The defect leads to many clinical findings in the cardiovascular, ocular, skeletal, integumentary, and respiratory systems. The diagnosis is made based on multiple criteria that include major and minor features of the syndrome. Cardiovascular disease is a major cause of morbidity and mortality in this syndrome.

EHLERS-DANLOS SYNDROME

EHLERS-DANLOS SYNDROME

EHLERS-DANLOS SYNDROME

EHLERS-DANLOS SYNDROME


Ehlers-Danlos syndrome is a heterogeneous disease of defective connective tissue production. There are many subtypes, most caused by defects in collagen formation or in the posttranslational modification of collagen. This grouping of diseases has been confusing because of the variable nature of the subtypes and the lack of a universally adopted classification system. Under the most recent system, there are 7 distinct subtypes; under the historical classification, there were 11 types. The new classification system has not been universally adopted, which contributes to the confusion. As the genetic defects behind each subtype are determined, researchers and clinicians will gain a better understanding of the syndrome.

CUSHING’S SYNDROME: PATHOPHYSIOLOGY

CUSHING’S SYNDROME: PATHOPHYSIOLOGY

CUSHING’S SYNDROME: PATHOPHYSIOLOGY

CUSHING’S SYNDROME: PATHOPHYSIOLOGY


Cushing’s syndrome is directly caused by excessive amounts of glucocorticoids and their effects on numerous organ systems. Cortisol is strikingly elevated in all cases of Cushing’s syndrome. In some cases, levels of 17-ketosteroids and aldosterone are slightly elevated, and this plays a role in the clinical manifestations of the disease. There are numerous disease states that can cause hypercortisolemia, including excessive secretion of adrenocorticotropic hormone (ACTH, corticotropin), adenoma and hyperplasia of the adrenal gland, carcinoma of the adrenal gland, primary pigmented nodular adrenocortical disease (PPNAD), and exogenous cortisol use. In all cases, it is the marked elevation of cortisol that ultimately is the cause of the disease.

CUSHING’S SYNDROME AND CUSHING’S DISEASE

CUSHING’S SYNDROME AND CUSHING’S DISEASE

CUSHING’S SYNDROME AND CUSHING’S DISEASE

CUSHING’S SYNDROME AND CUSHING’S DISEASE


Cushing’s syndrome is caused by excessive secretion of endogenous glucocorticoids or, more frequently, by intake of excessive exogenous glucocorticoids. The latter type is typically iatrogenic in nature. The excessive glucocorticoid levels lead to the many cutaneous and systemic signs and symptoms of Cushing’s syndrome and Cushing’s disease. Endogenous glucocorticoids are made and secreted by the adrenal glands, and benign adrenal adenomas are the most frequently implicated adrenal tumors causing Cushing’s syndrome. Cushing’s disease is caused by excessive secretion from the anterior pituitary of adrenocorticotropic hormone (ACTH, corticotropin) as the result of a basophilic or chromophobe adenoma. The increased amount of ACTH causes the adrenal glands to hypertrophy and boost their production of cortisol, eventually leading to a state of hypercortisolism. Excessive release of corticotropin-releasing hormone (CRH) from the para- ventricular nucleus of the hypothalamus can also cause the syndrome. Any tumor that has the ability to produce ACTH also has the potential to cause Cushing’s syndrome. The most frequently reported such tumor is the small cell tumor of the lung, which is able to produce many neuroendocrine hormones including ACTH in large amounts.

CARNEY COMPLEX

CARNEY COMPLEX

CARNEY COMPLEX

CARNEY COMPLEX


Carney complex, also known as NAME syndrome (nevi, atrial myxomas, myxoid neurofibromas, ephelides) or LAMB syndrome (lentigines, atrial myxomas, mucocutaneous myxomas, blue nevi), is an autosomal dominantly inherited disorder that affects the integumentary, endocrine, cardiovascular, and central nervous systems. This rare disorder is primarily caused by a genetic mutation in the tumor suppressor gene, PRKAR1A. Approximately 20% of patients have defects in an undescribed gene located at 2p16. Various genotypes and phenotypes exist, and the diagnosis is based on a complex list of major, supplemental, and minor criteria.

Friday, June 11, 2021

The “Acute Abdomen”

The “Acute Abdomen”

The “Acute Abdomen”

CAUSES OF ACUTE ABDOMEN
CAUSES OF ACUTE ABDOMEN


An acute abdominal condition should be described as acute abdomen when a patient complains of abdominal pain that persists for more than a few hours and is associated with tenderness or other evidence of an inflammatory reaction or a visceral dysfunction. The diagnosis of the cause of acute abdominal conditions remains one of the most challenging problems in medicine. Many pathologic processes, both intraabdominal and extra-abdominal, may result in an acute abdomen. An accurate history, thorough physical examination, and proper laboratory examinations help to make the broad differential diagnosis of causes.

Overview of Digestive Tract Obstructions

Overview of Digestive Tract Obstructions

Overview of Digestive Tract Obstructions

Overview of Digestive Tract Obstructions


Any organic or functional condition that primarily or indirectly impedes the normal propulsion of luminal contents from the esophagus to the anus could be considered a partial or complete obstruction. In the newborn, a variety of congenital anomalies (esophageal, intestinal, anal atresias, colonic malrotation, volvulus of the midgut, meconium ileus, aganglionic megacolon) resulting in obstruction are illustrated here. Other causes of mechanical interference of intestinal function in early infancy include incarceration in an internal or external (inguinal) hernia, congenital peritoneal bands, intestinal duplications, volvulus due to mesenteric cysts, and annular pancreas, though the latter may not become clinically manifested until the patient is an adult or an aged adult.

Laparoscopic Peritoneoscopy

Laparoscopic Peritoneoscopy

Laparoscopic Peritoneoscopy

Laparoscopic Peritoneoscopy


Laparoscopic peritoneoscopy is the direct inspection of the peritoneal cavity and its contents by means of an endoscopic instrument introduced through the abdominal wall. Laparoscopic surgery has revolutionized the field of surgery and has gradually been replacing many conventional surgical procedures. The procedure is used in gastroenterologic, general surgical, and gynecologic disorders in which a positive diagnosis cannot be established by simpler methods. Its value lies in the fact that it can frequently supply information that otherwise would be obtained only by exploratory laparotomy. In addition to being a surgical method, it is particularly valuable as a diagnostic tool for visualizing and obtaining biopsies from peritoneal surfaces, the liver, the omentum, and the small bowel, as well as the pelvic organs. Intraabdominal adhesions, peritoneal carcinomatosis or tuberculosis, ascites, or hemorrhage can readily be recognized and sampled via a laparo- scope. In malignant disease, laparoscopy is useful for staging.

Overview of Gastrointestinal Hemorrhage

Overview of Gastrointestinal Hemorrhage

Overview of Gastrointestinal Hemorrhage

CAUSES OF GASTROINTESTINAL HEMORRHAGE
CAUSES OF GASTROINTESTINAL HEMORRHAGE


Many gastrointestinal disorders manifest themselves by bleeding. Intestinal bleeding may present as bright-red blood, suggesting gross lower bleeding (hematochezia), passage of black stool (melena), or other findings of bleeding but no change in stool color (occult bleeding). When no cause of bleeding can be detected with the usual examinations, obscure gastrointestinal bleeding is occurring.

Secretory, Digestive, and Absorptive Functions of Small and Large Intestines

Secretory, Digestive, and Absorptive Functions of Small and Large Intestines

Secretory, Digestive, and Absorptive Functions of Small and Large Intestines

DIGESTION OF PROTEIN
DIGESTION OF PROTEIN


The purpose of the complex enzymatic reactions to which foodstuffs are exposed within the intestinal lumen is to prepare nutrients for transfer into and assimilation within the organism. The lumen of the digestive system, which is the space encompassed by the wall of the digestive tube, belongs, fundamentally speaking, to the outside world, and the processes by which the products of digestion enter and pass through the intestinal wall into the circulation are called secretion and absorption, respectively. The mucosa of the small intestine throughout its length is lined by cells involved with both secretion and absorption: mucus-secreting cells, neuroendocrine cells, and immune active cells. The incredible efficiency of intestinal function is emphasized by the fact that of the approximately 8 L of fluid that enters the small intestine, only 100 to 200 mL is excreted from the rectum, for an efficiency rate in excess of 98%. In disease states, the large and small intestines absorb even more fluid, sometimes exceeding 25 L per day. Alternatively, in secretory dis- orders and infection, the volume of diarrhea lost may rapidly pose a life-threatening risk of dehydration, with the loss of many liters of fluids and their accompanying electrolytes.

Thursday, June 10, 2021

Coronary Arteries and Cardiac Veins

Coronary Arteries and Cardiac Veins

Coronary Arteries and Cardiac Veins

BLOOD SUPPLY OF THE HEART

STERNOCOSTAL AND DIAPHRAGMATIC SURFACES
STERNOCOSTAL AND DIAPHRAGMATIC SURFACES


The normal heart and the proximal portions of the great vessels receive their blood supply from two coronary arteries. The left coronary artery (LCA) originates from the left sinus of Valsalva near its upper border, at about the level of the free edge of the valve cusp. The LCA usually has a short (0.5-2 cm) common stem that bifurcates or trifurcates. One branch, the anterior inter- ventricular (descending) branch, courses downward in the anterior interventricular groove (largely embedded in fat), rounds the acute margin of the heart just to the right of the apex, and ascends a short distance up the posterior interventricular groove.

Specialized Conduction System of Heart

Specialized Conduction System of Heart

Specialized Conduction System of Heart

Specialized Conduction System of Heart


The specialized heart tissues include the sinoatrial (SA) node, atrioventricular (AV) node, common atrioventricular bundle or bundle of His, right and left bundle branches, and peripheral ramifications of these bundle branches, which make up the subendocardial and intra- myocardial Purkinje network. In addition, other fiber groups in the atria meet some of the histologic and electrophysiologic criteria for specialization. These tissues constitute Bachmann’s bundle and the inter- nodal conducting paths of the right atrium.

Valves

Valves

Valves

CARDIAC VALVES OPEN AND CLOSED
CARDIAC VALVES OPEN AND CLOSED


Each atrioventricular (AV) valve apparatus consists of a number of cusps, chordae tendineae, and papillary muscles. The cusps are thin, yellowish white, glistening trapezoid-shaped membranes with fine, irregular edges. They originate from the annulus fibrosus, a poorly defined and unimpressive fibrous ring around each AV orifice. The amount of fibrous tissue increases only at the right and left fibrous trigones.

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