ECA Clinical examples Chapter 1 Flashcards

1
Q

Tension lines

A

Tension lines (cleavage lines) keep the skin taut yet allow for creasing with movement. Lacerations or surgical incisions that parallel the tension lines usually heal well with little scarring because there is minimal disruption of the collagen fibers. An incision or laceration across tension lines disrupts a greater number of collagen fibers, causing the wound to gape and possibly heal with excessive (keloid) scarring. Surgeons make their incisions parallel with the tension lines when other considerations (e.g., adequate exposure, avoiding nerves) are not of greater importance.

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2
Q

Stretch Marks in Skin

A

The collagen and elastic fibers in the dermis form a tough, flexible meshwork of tissue. The skin can distend considerably when the abdomen enlarges, as during pregnancy, for example. However, if stretched too far or too rapidly, it can result in damage to the collagen fibers in the dermis. Bands of thin wrinkled skin, initially red, become purple and later white. Stretch marks appear on the abdomen, buttocks, thighs, and breasts during pregnancy. These marks also form in obese individuals. Stretch marks generally fade (but never disappear completely) after pregnancy and weight loss.

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3
Q

Burns

A

Burns are tissue injuries caused by thermal, electrical, radioactive, or chemical agents.

*In superficial burns, the damage is limited to the superficial part of the epidermis.

*In partial thickness burns, the damage extends through the epidermis into the superficial part of the dermis. However, except for their most superficial parts, the sweat glands and hair follicles are not damaged and can provide the source of replacement cells for the basal layer of the epidermis.
In full-thickness burns, the entire epidermis and dermis, and perhaps underlying muscle, are damaged. A minor degree of healing may occur at the edges, but the open ulcerated portions require skin grafting.

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4
Q

Heterotopic Bone

A

Bone sometimes forms in soft tissues where it is not normally present. Horse riders often develop heterotopic bone in their thighs or buttocks (rider’s bones) probably because of chronic muscle strain resulting in small hemorrhagic (bloody) areas that undergo calcification and eventual ossification.

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5
Q

Bone adaptation

A

Bones are living organs that hurt when injured, bleed when fractured, remodel in relationship to stress placed on them, and change with age. Like other organs, bones have blood vessels, lymphatic vessels, and nerves, and they may become diseased. Unused bones, such as in a paralyzed or immobilized limb, atrophy (decrease in size). Bone may be absorbed, which occurs in the mandible after teeth are extracted. Bones undergo hypertrophy (enlarge) when they have increased weight to support for a long period.

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6
Q

Bone Trauma and Repair

A

Trauma to a bone may fracture (break) it. For a fracture to heal properly, the broken ends must be brought together, approximating their normal position (reduction of fracture). During bone healing, the surrounding fibroblasts (connective tissue cells) proliferate and secrete collagen that forms a collar of callus to hold the bones together. Remodeling of bone occurs in the fracture area, and the callus calcifies. Eventually, the callus is resorbed and replaced by bone.

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7
Q

Degeneration—Osteoporosis

A

As people age, both the organic and inorganic components of bone decrease, often resulting in osteoporosis, an abnormal reduction in the quantity of bone, or atrophy of skeletal tissue. The bones become brittle, lose their elasticity, and fracture easily.

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8
Q

Accessory Bones

A

Accessory (supernumerary) bones develop when additional ossification centers appear and form extra bones. Many bones develop from several centers of ossification, and the separate parts normally fuse. Sometimes, one of these centers fails to fuse with the main bone, giving the appearance of an extra bone; however, careful study shows that the apparent extra bone is a missing part of the main bone. Accessory bones are common in the foot and calvarium.

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9
Q

Assessment of Bone Age

A

Knowledge of the sites where ossification centers occur, the times of their appearance, the rate at which they grow, and the times of fusion (synostosis) of the sites is used to determine the age of a person in clinical medicine, forensic science, and anthropology (Fig. B1.1). The main criteria for determining bone age are (1) the appearance of calcified material in the diaphysis and/or epiphyses and (2) the disappearance of the dark line representing the epiphysial plate (absence of this line indicates epiphysial fusion has occurred; fusion occurs at specific times for each epiphysis). The fusion of epiphyses with the diaphysis occurs 1 to 2 years earlier in girls than in boys. Bone age (achieved level of skeletal development) during the growing years can be determined by radiographic study of the ossification centers of the hand.

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10
Q

Displacement and Separation of Epiphyses

A

An injury that causes a fracture in an adult usually causes the displacement of an epiphysis in a child. Without knowledge of bone growth and the appearance of bones in radiographic and other diagnostic images at various ages, a displaced epiphysial plate could be mistaken for a fracture, and separation of an epiphysis could be interpreted as a displaced piece of fractured bone. Bone is smoothly curved on each side of the epiphysial plate, whereas fractures leave sharp, often uneven edges of bone.

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11
Q

Avascular Necrosis

A

Loss of blood supply to an epiphysis or other parts of a bone results in death of bone tissue, or avascular necrosis (G. nekrosis, deadness). After every fracture, small areas of adjacent bone undergo necrosis. In some fractures, avascular necrosis of a large fragment of bone may occur.

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12
Q

Degenerative Joint Disease

A

Synovial joints are well designed to withstand wear, but heavy use over many years can cause degenerative changes. Beginning early in adult life and progressing slowly thereafter, aging of articular cartilage occurs on the ends of the articulating bones, particularly those of the hip, knee, vertebral column, and hands. These irreversible degenerative changes in joints result in the articular cartilage becoming less effective as a shock absorber and low-friction surface. As a result, the articulation becomes vulnerable to the repeated impacts and friction that occur during joint movements (e.g., during running). In some people, these changes cause considerable pain. Degenerative joint disease, or osteoarthritis (osteoarthrosis), is often accompanied by stiffness, discomfort, and pain. Osteoarthritis is common in older people and usually affects joints that support the weight of their bodies (e.g., hips and knees).

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13
Q

Muscle Testing

A

Muscle testing helps an examiner diagnose nerve injuries. This technique enables the examiner to gauge the power of the person’s movement. Usually, muscles are tested in bilateral pairs for comparison. There are two common testing methods:

1.The person performs movements that resist those produced by the examiner (active). When testing flexion of the forearm, the examiner asks the person to flex their forearm while the examiner resists the effort.

2.The examiner performs movements against resistance produced by the person. For example, the person keeps the forearm flexed while the examiner attempts to extend it.

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14
Q

Electromyography

A

The electrical recording of muscles through electromyography (EMG) is another method for testing muscle action. The examiner places surface electrodes over a muscle and asks the person to perform certain movements. The examiner then amplifies and records the differences in electrical action potentials of the muscles. A normal resting muscle shows only a baseline activity (tonus), which disappears only during sleep, during paralysis, and when under anesthesia. Contracting muscles demonstrate variable peaks of phasic activity. EMG makes it possible to analyze the activity of an individual muscle during different movements. EMG may also be part of the treatment program for restoring the action of muscles.

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15
Q

Muscular Atrophy

A

Wasting of the muscular tissue (atrophy) of a limb, for example, may result from a primary disorder of the muscle or from a lesion of a nerve. Muscle atrophy may also be caused by prolonged immobilization of a limb, such as with a cast or sling.

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16
Q

Compensatory Hypertrophy and Myocardial Infarction

A

In compensatory hypertrophy, the myocardium responds to increasing demands by increasing the size of its fibers (cells). When cardiac muscle fibers are damaged during a heart attack, the tissue becomes necrotic (dies) and the fibrous scar tissue that develops forms a myocardial infarction (MI), an area of myocardial necrosis (pathological death of myocardial tissue). Smooth muscle cells also undergo compensatory hypertrophy in response to increased demands. During pregnancy, the smooth muscle cells in the wall of the uterus increase not only in size (hypertrophy) but also in number (hyperplasia).

17
Q

Anastomoses, Collateral Circulation, and Terminal (End) Arteries

A

Anastomoses (communicating connections) between the multiple branches of an artery provide numerous potential detours for blood flow in case the usual pathway is obstructed by compression, position of a joint, pathology, or surgical ligation. If a main channel is occluded, the smaller alternate channels can usually increase in size, providing a collateral circulation that ensures the blood supply to structures distal to the blockage. However, collateral pathways require time to develop; they are usually insufficient to compensate for sudden occlusion or ligation. There are areas where collateral circulation does not exist or is inadequate to replace the main vessel. Arteries that do not anastomose with adjacent arteries are true terminal (end) arteries. Occlusion of a terminal artery disrupts the blood supply to the structure or segment of an organ it supplies. For example, occlusion of the terminal arteries of the retina will result in blindness. Although not true terminal arteries, functional terminal arteries (arteries with ineffectual anastomoses) supply segments of the brain, liver, kidney, spleen, and intestines.

18
Q

Arteriosclerosis: Ischemia and Infarction

A

The most common acquired disease of arteries is arteriosclerosis (hardening of arteries), a group of diseases characterized by thickening and loss of elasticity of arterial walls. Atherosclerosis, a common form of arteriosclerosis, is associated with the buildup of fat (mainly cholesterol) in the arterial walls. Calcium deposits then form an atheromatous plaque, resulting in arterial narrowing and irregularity (Fig. B1.2). This may result in thrombosis (formation of a local thrombus [clot]), which may occlude the artery or be flushed into the bloodstream, resulting in ischemia (reduction of blood supply to an organ or region) and infarction (local death of an organ or tissue). Among the consequences of a thrombus are myocardial infarction (heart attack), stroke, and gangrene (necrosis in parts of the limbs).

19
Q

Varicose Veins

A

When the walls of veins lose their elasticity or the deep fascia becomes incompetent in sustaining the musculovenous pump, the veins become weak and dilate under the pressure of supporting a column of blood against gravity. This results in varicose veins, abnormally swollen, twisted veins, most often seen in the legs (Fig. B1.3A).

20
Q

Lymphangitis, Lymphadenitis, and Lymphedema

A

The terms lymphangitis and lymphadenitis refer to the secondary inflammation of lymphatic vessels and lymph nodes, respectively. These pathological processes may occur when the lymphatic system is involved in the metastasis (spread) of cancer—the lymphogenous dissemination of cancer cells. Lymphedema (the accumulation of interstitial fluid) occurs when lymph is not drained from an area of the body. For instance, if cancerous lymph nodes are surgically removed from the axilla (armpit), lymphedema of the upper limb may result.

21
Q

Damage to Central Nervous System

A

When the CNS is damaged, the injured axons do not recover in most circumstances. Their proximal stumps begin to regenerate, sending sprouts into the area of the lesion; however, growth is blocked by astrocyte (a type of glial cell) proliferation at the site of injury. As a result, permanent disability follows destruction of a tract in the CNS.

22
Q

Peripheral Nerve Degeneration

A

When peripheral nerves are crushed or severed, their axons degenerate distal to the lesion because they depend on their cell bodies for survival. A crushing nerve injury damages or kills the axons distal to the injury site; however, the nerve cell bodies usually survive and the connective tissue coverings of the nerve are intact. No surgical repair is needed for this type of nerve injury because the intact connective tissue sheaths guide the growing axons to their destinations. Surgical intervention is necessary if the nerve is cut because the regeneration of axons requires apposition of the cut ends by sutures through the epineurium. The individual fascicles (bundles of nerve fibers) are realigned as accurately as possible. Compromising a nerve’s blood supply for a long period produces ischemia by compression of the vasa nervorum (see Fig. 1.26), which can also cause nerve degeneration. Prolonged ischemia of a nerve may result in damage no less severe than that produced by crushing or even cutting the nerve.

23
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