Musculoskeletal and Connective Tissue Flashcards
(111 cards)
1
Q
What is the pathophysiology of this condition?
A
Costochondritis, inflammation of the costochondral or costosternal joints, causes localized pain and tenderness. Often, more than one of the seven costochondral joints is affected, especially between the second and fifth costosternal junctions. Repetitive minor trauma or repetitive activities are the likely causes, but bacterial and fungal infections (not likely here given the lack of swelling, erythema) and thoracic surgery may also be implicated.
2
Q
What is the innervation of the intercostal space?
A
The intercostal nerves (thoracic spinal and ventral rami) supply general sensory innervation to the skin of the thoracic and anterior abdominal walls. The dermatomes follow a girdle-like distribution. The sensory nerves also supply the parietal pleura and parietal peritoneum. The intercostal nerves also have motor innervation through the ventral rami of T1–T12. Intercostal nerve 1 participates in the brachial plexus; nerves 2–6 innervate the thorax; and nerves 7–12 innervate the anterior abdominal wall.
3
Q
What conditions, other than costochondritis, should be considered in the differential diagnosis?
A
Although the localized areas of tenderness suggest a musculoskeletal cause, serious conditions such as myocardial infarction and pericarditis (which has an abnormal echocardiogram, pain changes with position, and frictional rub on auscultation) need to be ruled out. Other considerations include pleuritic pain, which could be a manifestation of pneumonia, pulmonary embolism, pneumothorax, or pleuritis. Pleuritis can be seen in inflammatory conditions such as systemic lupus erythematosus (abnormal serology), fibromyalgia (tender points), and gastroesophageal reflux disorder.
4
Q
What is the blood supply of the intercostal space?
A
At each space, there is a posterior artery and anterior set of arteries (Figure 9-1). The bottom nine posterior arteries originate from the descending thoracic aorta, whereas the anterior artery originates from the internal thoracic. The posterior intercostal vein, artery, and nerve run together as a neurovascular bundle along the lower border of each rib. Therefore, during thoracentesis the needle must be inserted just above the lower rib in the intercostal space to avoid injury to the vessels and nerve.
5
Q
What is the most likely diagnosis?
A
The patient’s biopsy shows atypical keratinocytes that have invaded the basement membrane; therefore, malignancy is present. Although basal cell carcinoma (BCC) is the most common type of skin cancer, the description of the lesion suggests squamous cell carcinoma (SCC).
Cutaneous SCC is the second most common tumor of the skin. It arises from the malignant proliferation of epidermal keratinocytes. The condition typically presents as a firm, well-demarcated lesion that is scaling, crusting, or ulcerated. Histologic examination is necessary for a diagnosis.
6
Q
What precursor lesion can lead to cutaneous squamous cell carcinoma (SCC)?
A
Actinic keratosis (AK), a dysplastic lesion of the epidermis, can lead to SCC. These lesions occur only on sun-exposed skin and consist of hyperkeratotic papules that have a coarse, sandpaper feel; some may present as a “cutaneous horn.”
7
Q
What risk factors are associated with Cutaneous SCC?
A
The most important risk factor for SCC is sunlight exposure in which ultraviolet (UV) rays cause DNA damage. Other exogenous factors include ionizing radiation, immunosuppression, chronic inflammation (from burns, scars, or ulcers), and arsenic exposure.
8
Q
What inherited disorders predispose patients to Cutaneous SCC?
A
Xeroderma pigmentosum is a rare autosomal recessive disorder that displays a defect in DNA excision repair, which impairs the ability to repair UV-induced DNA damage. Albinism is also associated with SCC because of the generalized pigment loss due to dysfunction and deficiency of melanocytes.
9
Q
What is the prognosis for patients with cutaneous SCC?
A
Even though cutaneous SCC can be locally invasive, it rarely metastasizes (1%–5% of cases). Therefore, more than 90% of patients can be cured with local excision.
10
Q
What retroperitoneal structures of the abdomen could the bullet have hit?
A
11
Q
What layers of the lateral and anterior abdominal wall would the bullet have to penetrate to reach the peritoneum?
A
12
Q
What is the blood supply to the kidney?
A
Renal artery → segmental artery → lobar artery → arcuate artery → afferent arteriole → glomerulus → efferent arteriole → vasa recta → segmental vein → renal vein
13
Q
What is the blood supply to the spleen?
A
The main blood supply is from the splenic artery, which is a branch of the celiac trunk (the other two branches are the L gastric and common hepatic arteries). The L gastro-omental and short gastric are branches off the splenic artery.
14
Q
What organs supply the splenic vein?
A
The splenic vein starts at the hilus of the spleen and receives blood from the stomach, pancreas, and inferior mesenteric vein. The splenic vein joins with the superior mesenteric vein to form the hepatic portal vein.
15
Q
What are the histologic layers of the skin?
A
Listed superficially to deep: stratum corneum, lucidum (only in palms and soles), granulosum, spinosum, basale.
16
Q
What is the most likely diagnosis?
What conditions should be considered in the differential diagnosis?
A
The young age at clinical presentation along with the tenderness, warmth, and swelling around the mass without systemic signs of infection suggests Ewing sarcoma (Figure 9-2). This diagnosis is supported by the location of the lesion and the histologic appearance (small, round, blue neuroectodermal cells), which are characteristic of this neoplasm.
17
Q
Other than Ewing sarcoma, what are the other small cell tumors?
A
Other small cell tumors include neuroblastoma, Wilms tumor, medulloblastoma, and rhabdomyosarcoma.
18
Q
What is the most likely chromosomal aberration leading to Ewing Sarcoma?
A
In total, 85% of Ewing sarcoma cases demonstrate a t(11;22) translocation. This translocation leads to an overexpression of the EWSR1 gene (encodes RNA binding proteins) on chromosome 22, which is translocated next to the FLI1 gene on chromosome 11 (encodes transcription factors).
19
Q
What is the appropriate treatment for Ewing sarcoma?
A
Ewing sarcoma is known to be a systemic disease due to the high relapse rate (80%–90%) of patients who undergo only local therapy. Therefore, most patients likely have subclinical microscopic metastatic disease at the time of diagnosis, which is treated with chemotherapy.
20
Q
What percentage of patients have metastatic disease at the time of diagnosis of Ewing sarcoma?
A
Only 25% of patients have overt metastases at the time of diagnosis.
21
Q
What is the most likely diagnosis?
A
The most common causes of lateral hip paining elderly patients include osteoarthritis, bursitis, metastases, and femoral fracture. In this patient, the sudden onset of pain after the fall and inability to walk strongly suggest a fracture of the neck of the femur (Figure 9-3). Femoral neck fractures can be incomplete or complete with no, partial, or total displacement.
22
Q
What is a potential complication of a Neck of femur fracture?
A
Fracture of the neck of the femur may disrupt blood supply to the head of the femur. The major arterial supply to the head of the femur is the medial and lateral circumflex femoral arteries (branches of the deep femoral artery) and the artery of the ligament of the head of the femur (branch of the obturator artery). The circumflex arteries may be disrupted by a fracture of the femoral neck, leaving only the artery of the ligament (a branch of the obturator) as a supply. Disruption of the blood supply may cause avascular necrosis of the femoral head.
23
Q
What bones form the hip joint?
A
The hip joint consists of the head of the femur articulating with the acetabulum. The acetabulum is formed by the ilium, ischium, and pubis. The fibrocartilaginous rim, the acetabular labrum, attaches to the acetabular margin and deepens the acetabular cup.
24
Q
Six weeks later, repeat x-ray shows a callus. What does the callus indicate about the patient’s stage of healing?
A
25
What is the most likely diagnosis? What would the differential diagnosis be if the patient were a child instead of a neonate?
In a newborn, a painless collection of fluid in the scrotum is almost certainly a hydrocele. It should resolve on its own by 1 year. The fact that the fluid in the scrotum is reducible indicates that the hydrocele was caused by a communication with the intraperitoneal fluid via a hernia.
26
What structures define the Hesselbach triangle?
The Hesselbach triangle is formed by the lateral border of the rectus abdominis muscle, the inguinal ligament, and the inferior epigastric vessels.
27
What distinguishes the two major types of hernia?
Direct hernias protrude through a weakness in the floor of the inguinal canal within the Hesselbach triangle (directly through the triangle) medial to the inferior epigastric vessels to enter the external ring into the scrotal sac. Indirect hernias enter the inguinal canal lateral to the Hesselbach triangle (lateral to the inferior epigastric vessels) indirectly through the internal inguinal ring (located in the fascia transversalis), then via the inguinal canal to the external inguinal ring located above and lateral to the pubic tubercle, and finally into the scrotal sac (Figure 9-4).
28
Which type of hernia is more common in infants and children?
Indirect inguinal hernias are more common in children, as they result from a congenital failure of the processus vaginalis to close.
29
What are the contents of the normal spermatic cord?
The spermatic cord in the inguinal canal contains the testicular artery and veins, lymphatic vessels, and the vas deferens. The sheath of the cord is formed by the internal spermatic fascia, the cremasteric muscle, and the external spermatic fascia. The ilioinguinal nerve is in the sheath and exits at the external ring; it is vulnerable to injury in surgical repairs of hernias. The genital branch of the genitofemoral nerve supplies the cremaster muscle. The processus vaginalis is an extension of peritoneum that normally obliterates spontaneously between the upper pole of the testes and the internal inguinal ring. In some cases, however, it remains patent, increasing the risk of hydrocele and indirect hernia.
30
What are the two main intracapsular ligaments in the knee?
The anterior cruciate ligament extends from the anterior intercondylar area of the tibial plateau and traverses superior and lateral to the medial surface of the lateral femoral condyle. The posterior cruciate ligament extends from the posterior intercondylar area of the tibial plateau and traverses superior and medial to the lateral surface of the medial condyle of the femur (Figure 9-5).
31
What is the blood supply to the knee?
Blood supply to the knee consists of genicular branches of the following blood vessels:
1. Anterior recurrent tibial artery.
2. Anterior tibial artery.
3. Descending branch of the lateral circumflex artery
4. Femoral artery.
5. Patellar plexus.
6. Popliteal artery.
7. Posterior tibial artery.
32
What is the role of the meniscus?
The half-moon-shaped meniscus is cartilage that is found between the femur and tibia. The meniscus absorbs the impact load of the joint and is involved in stability. The meniscus is mostly avascular and is divided into the anterior horn, body, and posterior horn. A medial and lateral meniscus is connected by the transverse ligament.
33
How do the collateral and cruciate ligaments differ in function?
The cruciate ligaments remain tight in flexion and extension and relax at 30 degrees of flexion. The collateral ligaments are tight in extension and relaxed in flexion. Also, the cruciate ligaments prevent anterior and posterior displacement of the tibia. The collateral ligaments prevent abduction/adduction of the knee.
34
Which ligament of the knee is most often injured?
The medial collateral ligament is weaker than the anterior or the posterior cruciate ligaments, so medial collateral ligament injuries are more common. Anterior cruciate ligaments tears are much more common than posterior cruciate ligaments tears.
35
What is the terrible or unhappy triad?
This is a common contact-sport injury to the knee that occurs when lateral trauma is applied to the knee joint while the foot is fixed to the ground. Subsequently, the medial collateral ligament, lateral meniscus, and anterior cruciate ligament are damaged.
36
What is the differential diagnosis and what is the most likely diagnosis?
Benign causes of an irregularly colored lesion include hemangioma, seborrheic keratosis, compound or junctional nevus, and pigmented dermatofibroma. But given the characteristics of this lesion, the most likely diagnosis is a malignant melanoma. The ABCD rules help distinguish melanoma from other lesions (Figure 9-6):
* **Asymmetry**: Malignant lesions are usually asymmetric.
* **Border irregularity**: Most melanomas lack smooth, round, uniform boundaries.
* **Color variegation:** Malignant lesions usually have variations in pigmentation and occasionally lose pigmentation.
* **Diameter**:A diameter >6mm greatly increases the chances of malignancy, and most lesions are >10mm.
37
Which cells are responsible Melanomas and what is their embryonic origin?
Melanomas originate from melanocytes, which are derived from neural crest tissue and reside in the epidermis or, less frequently, in the dermis.
38
What is the etiology of Malignant melanomas?
Malignant melanomas are more likely to appear on areas that receive sun exposure. Other risk factors include atypical/dysplastic nevi and family history,
39
What is the most important prognostic factor for malignant melanoma?
The most concerning factor is vertical invasion, as deeper lesions have a worse prognosis. Detection of melanoma at early stages is crucial and prognosis is excellent if treated early. However, after the tumor has penetrated the basement membrane and entered the subcutaneous fat, 5-year survival is only 49%. The S-100 protein can help determine prognosis; elevated S-100 serum levels correlate with a worse prognosis.
40
How and where does melanoma tend to spread?
Initial lesions usually spread superficially and horizontally across the skin and then enter a vertical growth phase into the deeper layers of the skin. Melanomas may then spread either lymphatically or hematogenously; earliest detectable metastases occur in regional lymph nodes. Classic sites of hematogenous spread include brain, lung, liver, and bone; however, melanomas are notorious for metastasizing to odd locations.
41
What is the appropriate treatment for melanoma?
Surgical excision with optional regional node dissection for more advanced disease remains the first-line treatment.
42
What is the likely diagnosis and what is the pathogenesis of the disorder?
Duchenne muscular dystrophy (DMD) is an X-linked recessive (Xp21) disorder marked by a deficiency of functional dystrophin, a 23,000-kB protein that helps stabilize muscle fibers. Approximately one-third of cases are sporadic and due to spontaneous mutations (noninherited) that arise from a misalignment of chromosomes during a recombination event.
43
What is the prognosis for patients with Duchenne muscular dystrophy (DMD)?
Patients with DMD are usually unable to walk by the end of the first decade and are confined to a wheelchair by 12 years of age. Most patients die by the end of the second decade; respiratory failure is the leading cause of death. Dilated cardiomyopathy and/or conduction abnormalities are common and can be fatal.
44
What tests are used to diagnose Duchenne muscular dystrophy (DMD)?
If DMD is clinically suspected, serum creatine kinase levels are markedly elevated, and electromyography shows myopathic changes, genetic testing or a muscle biopsy can confirm the diagnosis. Muscle biopsy shows atrophic muscle fibers of various sizes in disarray, degeneration, and necrosis of individual muscle fibers with fibrous replacement.
45
The patient’s parents have a second son who is 6 months of age. What is the chance that he, too, will develop Duchenne muscular dystrophy (DMD)?
The chances are 50% (assuming that the first case was not sporadic). Because the mother is a carrier of this disorder, each son has a 50% chance of inheriting the X chromosome with the mutated allele from her.
46
Which band in a sarcomere stays constant in length during muscle contraction?
The A band, which corresponds to the length of the thick myosin filaments.
47
How would the presentation of a patient with Becker muscular dystrophy (BMD) differ from that of a patient with Duchenne muscular dystrophy (DMD)?
The most obvious difference is the age of onset of symptoms and degree of clinical involvement. BMD patients typically remain ambulatory until at least 15 years of age and commonly into adulthood. Mental retardation and contractures are more common in BMD.
48
What is the likely diagnosis?
What conditions should be considered in the differential?
The asymmetric, gradually progressive joint pain and stiffness in this case point to osteoarthritis (x-ray findings confirm). Physical examination findings in osteoarthritis include tenderness to palpation without signs of inflammation, joint effusions, crepitus, and bony enlargement of affected joints.
49
What are the radiographic features of osteoarthritis?
Radiographic findings in osteoarthritis can be summarized by the mnemonic LOSS: Loss of joint space, Osteophytes, and Subchondral Sclerosis.
50
What is the characteristic distribution of osteoarthritis?
Osteoarthritis most often affects large weight-bearing joints including the knees, hip, and spine, as well as the distal interphalangeal joint. In contrast, RA commonly affects the proximal interphalangeal and
metacarpophalangeal joints. Osteoarthritis only rarely affects the elbows, wrists, and ankles.
51
What is the pathophysiology of osteoarthritis?
Osteoarthritis is characterized by degenerative noninflammatory changes in articular cartilage secondary to chondrocyte dysfunction. These changes may be caused by a complex interaction between metabolic, biochemical, and biomechanical factors with secondary components of inflammation. The result is progressive mechanical damage to the joint and bone eburnation, particularly in weight-bearing joints. This degeneration also causes reactive bone formation subchondrally and at the margins of affected joints.
52
What would arthrocentesis (tapping of the joint) likely show in OA?
Arthrocentesis is mostly normal with perhaps mild pleocytosis, and modestly elevated protein.
53
What is the appropriate treatment for Osteoarthritis?
Acetaminophen and nonsteroidal anti-inflammatory drugs remain the mainstays for analgesia. In a patient with a history of gastroduodenal disease, a gastroprotective agent could also be given. Occasionally, intra-articular glucocorticoids are used when symptoms persist in a few joints. Surgery may be required for refractory cases (joint replacement or fusion).
54
What risk factors are associated with Osteoarthritis?
Risk factors for osteoarthritis include increased age, obesity, female gender, lack of osteoporosis, physically demanding occupations, previous injury, or genetic disorder such as Wilson disease and hemochromatosis.
55
What genetic syndromes do this man and woman have?
The woman has neurofibromatosis type 1 (NF1, or von Recklinghausen neurofibromatosis), and the man has neurofibromatosis type 2 (NF2). NF1 is characterized by café-au-lait spots, meningiomas, neurofibromas (subcutaneous nodules), and axillary freckling. NF2 presents with bilateral acoustic neuromas (vestibular schwannomas).
56
What is the probability that the couple will have an asymptomatic child?
NF1 and NF2 are both autosomal dominant genes. On the basis of their family histories, the man and woman must be heterozygous for NF2 and NF1, respectively. Thus, each mutant gene has a 50% chance of being inherited by the child. NF1 is on chromosome 17, and NF2 is on chromosome 22; therefore, the inheritance of each mutant gene occurs independently of the other. The probability of two independent events occurring at once is the product of the probability of each event: 50% × 50% = 25%.
57
Which cell line is implicated in the formation of lesions in neurofibromatosis type 1?
Neural crest cells are involved. Most clinical signs of NF1 are related to abnormal descendants of neural crest cells.
58
What is the mechanism of tumour formation in neurofibromatosis type 1?
The NF1 gene is a tumor suppressor gene belonging to a family of guanosine triphosphatase–activating proteins. Multiple loss-of-function mutations in this gene lead to tumor growth.
59
What is the path of the eighth cranial nerve (CN VIII) from the periphery to its site of entry into the central nervous system?
From the cochlea and vestibular canals in the petrous bone, CN VIII enters the cranial vault through the internal acoustic meatus to enter the brain stem at the junction of the pons and the medulla.
60
What other clinical features could a patient with neurofibromatosis type 1 have?
NF1 patients may have iris hamartomas (Lisch nodules), optic gliomas, distinctive bony lesions such as sphenoid dysplasia, and thinning of a long bone cortex with or without pseudarthrosis.
61
What is the differential diagnosis for recurrent fractures in children?
1. Accidental injury.
2. Birth trauma.
3. Bone fragility (including osteogenesis imperfecta and rickets).
4. Child abuse (which accounts for the vast majority of cases).
62
What is the most likely diagnosis?
The most likely diagnosis is osteogenesis imperfecta (OI), which is an inherited disorder involving defects in type I collagen, usually due to mutations in the COL1A1 or COL1A2 gene. It is also known as brittle bone disease, and its most common form has autosomal dominant inheritance.
63
What pathologic findings are associated with osteogenesis imperfecta?
OI is associated with cardiac insufficiency, mitral valve prolapse, hearing loss, basilar skull deformities (causing nerve compression and other neurological sequelae) and kyphoscoliosis. Death due to multiple fractures or pulmonary failure is common in utero or soon after birth in severe forms, which are recessively inherited.
64
What are the four major types and locations of collagen?
* Type I collagen is found in bone, skin, tendon.
* Type II collagen is found in cartilage.
* Type III collagen is found in reticular tissue, arterial walls, and uterus.
* Type IV collagen is found in the basement membrane.
65
What are the four major types and locations of collagen?
* Type I collagen is found in bone, skin, tendon.
* Type II collagen is found in cartilage.
* Type III collagen is found in reticular tissue, arterial walls, and uterus.
* Type IV collagen is found in the basement membrane.
66
What steps are involved in collagen synthesis?
Procollagen strands containing a repeating Gly-Pro-X sequence are synthesized in the ribosome, hydrolyzed by prolyl hydrolase, and glycosylated in the rough endoplasmic reticulum and Golgi complex. Three procollagen strands associate in a triple helix and are secreted into the extracellular space, where the propeptides are cleaved, allowing for polymerization with other collagen molecules to form collagen fibrils.
67
What enzymes in collagen synthesis depend on ascorbic acid?
Proline hydroxylase (which hydroxylates prolyl and lysyl residues) cross-links collagen and depends on ascorbic acid. Vitamin C deficiency can lead to scurvy, which causes ulceration of the gums, bruising, anemia, poor wound healing, and hemorrhage due to deficient collagen synthesis.
68
What is the most likely diagnosis?
**Rheumatoid arthritis (RA)**
Clinical features of RA include the followiing:
1. Morning stiffness for more than 1 hour that is present for more than 6 weeks.
2. Arthritis in three joints or more for more than 6 weeks.
3. Arthritis of hand joints for more than 6 weeks.
4. Symmetric joint swelling and involvement.
5. Rheumatoid subcutaneous nodules.
6. Positive serum rheumatoid factor and/or anti-cyclic citrullinated protein antibodies (anti-CCP).
7. Abnormal C-reactive protein (CRP) and/or erythrocyte sedimentation rate (ESR).
8. Typical radiographic changes (shown in Figure 9-9).
69
What is the pathophysiology of Rheumatoid arthritis (RA)?
RA is a chronic systemic autoimmune inflammatory disorder that destroys articular cartilage. While the etiology is unclear, the autoimmune reaction is mediated by CD4+ T cells, macrophages, and cytokines (tumor necrosis factor and interleukin-1), which promote the inflammatory response. Together these elements form a pannus that gradually erodes and disfigures joints.
70
What joints are typically affected in Rheumatoid arthritis (RA)?
Symptoms usually develop symmetrically in the small joints of the hands and feet (metacarpophalangeal, proximal interphalangeal, metatarsophalangeal joints), as well as wrist, elbows, knees, and ankles. The cervical spine may also be involved.
71
What test can help diagnose Rheumatoid arthritis (RA)?
Although no specific laboratory test is diagnostic of RA, most patients have a positive serum rheumatoid factor (RF; not perfectly sensitive nor specific) and anti-CCP (similar sensitivity and better specificity than RF).
72
What are the characteristic joint deformities in Rheumatoid arthritis?
Ulnar deviation/drift, swan-neck, and Boutonniere deformities of the fingers and the “bow-string” sign (prominence of the tendons in the extensor compartment of the hand) are all characteristic of RA. Occasionally patients present with synovial cysts from increased intra-articular pressure and eventual tendon rupture.
73
What are 6 primary pharmacologic therapies for Rheumatoid arthritis?
1. Analgesics including acetaminophen.
2. Nonsteroidal anti-inflammatory drugs.
3. Glucocorticoids.
4. Disease-modifying antirheumatic drugs such as methotrexate, hydroxychloroquine, or sulfasalazine.
5. Anti-cytokine therapies such as etanercept, infliximab, and adalimumab.
6. Other biologic agents such as abatacept and
rituximab.
74
What are some nonarticular manifestations of Rheumatoid arthritis?
* Musculoskeletal manifestations include osteopenia, osteoporosis, muscle weakness, vasculitis, and skin symptoms such as rheumatoid nodules. Pulmonary manifestations include pleuritis, pleural effusion, and interstitial fibrosis.
* Cardiac manifestations include coronary artery disease and heart failure.
* Other manifestations include scleritis, anemia, and Felty syndrome (RA with splenomegaly and neutropenia).
75
What underlying condition contributed to these fractures?
Osteoporosis. This disease is characterized by reduced bone mass with microarchitectural disruption, porosity, and skeletal fragility. Osteoporosis is difficult to diagnose, as a fracture is often the first clinical manifestation.
76
What two factors contribute most to osteoporosis?
The majority of postmenopausal women with osteoporosis have bone loss related to age and/or estrogen deficiency. Estrogen naturally suppresses cytokines (such as interleukin-1 and -6) and receptor activator of nuclear κ-B ligand (RANKL,) which both increase osteoclast activity. RANKL interacts with RANK to promote development and function of osteoclasts. Denosumab is the first osteoporosis treatment that acts by blocking RANK-RANKL binding.
77
What are 5 secondary factors that increase the risk of Osteoporosis?
1. Physical inactivity.
2. Calcium and vitamin D deficiency.
3. Prolonged glucocorticoid therapy.
4. Hyperparathyroidism.
5. Hyperthyroidism.
78
What sites of fracture are most common in osteoporosis?
Vertebral compression fractures are the most common clinical manifestation of osteoporosis. Most fractures are asymptomatic and usually an incidental finding on x-ray of the chest or abdomen. However, they may manifest as spinal deformity and shortened stature. Hip and distal radius (Colles) fractures are also common.
79
What tests and/or imaging tools can be used to test bone density?
Dual-energy x-ray absorptiometry (DEXA) scans are used to compare bone density to an age-matched reference population. Density more than two standard deviations below the expected range confirms the diagnosis.
80
What are the appropriate treatments for osteoporosis?
* The mainstay of treatment and prevention of osteoporosis is **bisphosphonates** such as alendronate and risedronate. This is in addition to continuation of both calcium and vitamin D supplementation. These agents act by decreasing osteoclastic bone resorption. One of the side effects of bisphosphonates is esophagitis; thus, patients are instructed to take it with water and while standing or sitting upright (and remain so for at least 30 minutes).
* Raloxifene, a selective estrogen receptor modulator is also used in refractory cases.
* Intermittent administration of recombinant parathyroid hormone has also shown to be effective.
81
What conditions should be considered in a patient with trauma to the chest?
Direct injury can cause pulmonary or myocardial contusion, rib or sternal fractures, diaphragmatic injury, vessel laceration, and aortic damage, which is often fatal. Conditions associated with chest trauma include pneumothorax, flail chest, hemothorax, and cardiac tamponade.
82
What 5 important nerves are at risk in stab wounds to the thorax?
1. Cardiac plexus.
2. Recurrent laryngeal nerve.
3. Phrenic nerve.
4. Pulmonary plexus (contiguous with the cardiac plexus).
5. Vagus nerve
83
What are the major arteries and veins of the thorax?
84
Which side of the chest uses the thoracic duct for lymphatic drainage?
The lymphatic duct is used for lymphatic drainage for the entire lower body, left arm, left side of the head and neck, and the left side of the thorax. The right arm, right side of the head and neck, and right side of the thorax, however, use the right lymphatic duct. The thoracic duct drains into the venous system at the junction of the left jugular and subclavian veins.
85
What is the difference between the left and right mainstem bronchi?
The mainstem bronchus passes inferolaterally from the bifurcation of the trachea at the sternal angle to the hilum. The right main bronchus is shorter and wider and runs more vertically, allowing for passage of aspirates more easily than the left bronchus. The left main bronchus is longer and travels anterior to the esophagus between the thoracic aorta and the left pulmonary artery.
86
What are the clinical features in a patient with pneumothorax post trauma?
Fractured ribs from trauma or trauma itself can lead to a pneumothorax. Patients will often be tachypneic, hypoxic, and/or have decreased/absent breath sounds on the side of the pneumothorax. Imaging can confirm a pneumothorax. A chest tube is usually used to manage a pneumothorax from trauma. If there is a pneumohemothorax, separate chest tubes should be used to remove the blood and the air.
87
Among the conditions that can cause shoulder pain in elderly patients, what is the most likely diagnosis in this case?
88
What events commonly precipitate Rotator cuff tears?
89
What tendons are likely involved in rotator cuff tear injuries and what is their distal attachment?
The rotator cuff is made up of the tendons of the “SITS” muscles: Supraspinatus (the most commonly affected tendon with rotator cuff tears), Infraspinatus, and Teres minor insert on the greater tuberosity, and the Subscapularis inserts on the lesser tuberosity (Figure 9-10).
90
What are the innervations and actions of the rotator cuff muscles?
91
What is the most likely diagnosis? What explains the friction rub on auscultation?
Systemic lupus erythematosus (SLE). SLE is a multisystem autoimmune connective tissue disease with a variable clinical presentation that most commonly affects young women in their 20s and 30s. Most manifestations of SLE are secondary to immune complex deposition.
SLE patients can develop pericarditis leading to friction rub.
92
What laboratory tests can be used to confirm the diagnosis of SLE?
Antibody testing including antinuclear antibodies (ANA), antiphospholipid antibodies, antibodies to double-stranded DNA (dsDNA), and anti-Smith (Sm) antibodies are used to diagnose SLE. Positive anti- dsDNA and anti-Sm test results are the most specific for SLE. A positive ANA test is sensitive but not specific. High-yield fact: antiphospholipid antibodies also bind the cardiolipin antigen used in syphilis testing; therefore, lupus patients have a false-positive syphilis test.
93
What would a positive antihistone antibody suggest?
It would suggest drug-induced lupus, but the reason for this correlation is unknown. Common medications that can cause drug-induced lupus include hydralazine, procainamide, minocycline, penicillamine, and isoniazid.
94
What are the 11 classification criteria for a diagnosis of SLE?
For SLE, remember the mnemonic SOAP BRAIN MD: Serositis, Oral ulcers, Arthritis, Photosensitivity, Blood changes (SLE patients often have leukopenia, a mild anemia, and clinically insignificant thrombocytopenia), Renal involvement (proteinuria or casts), ANA, Immunologic changes, Neurologic signs (seizures, frank psychosis), Malar rash, and Discoid rash.
For the diagnosis of SLE, a patient must display a minimum of four out of 11 characteristics.
95
What are the typical renal findings in SLE?
Most SLE patients have an abnormal urinalysis. There are six classes of renal disease in SLE, which are usually differentiated with a renal biopsy. Immune complex (anti-DNA-DNA)–mediated glomerular diseases are most common. SLE nephropathy most commonly displays a nephrotic syndrome pattern with a histologic subtype of diffuse lupus nephritis (class IV). The pathologic finding on histology that is almost pathognomonic for SLE is “wire loop” lesions (tubuloreticular structures in the glomerular endothelial cells, which may also be seen in HIV nephropathy). Other findings include subepithelial or subendothelial deposits with inflammation.
96
What is the most likely diagnosis and what are the two forms of this condition?
Systemic sclerosis (scleroderma), an autoimmune connective tissue disorder (Figure 9-11). Scleroderma exists in two forms, limited and diffuse, both of which occur in the setting of Raynaud phenomenon (exaggerated vasoconstriction in response to cold or stress leading to sharply demarcated color changes of the fingertips). This patient displays the limited form in which the skin of the fingers, forearms, and face are often affected with distinctive thickening.
Diffuse systemic sclerosis eventually involves visceral organs as well as the gastrointestinal tract (particularly the esophagus), heart (myocardial fibrosis), muscles, lungs (interstitial lung disease is seen in the majority of patients, causing dyspnea on exertion and cough), and kidneys. This results in dysphagia, respiratory difficulty, arrhythmias, and mild proteinuria. The most concerning manifestation of this disease is malignant hypertension leading to renal failure.
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What is the most likely diagnosis and what are the two forms of this condition?
Systemic sclerosis (scleroderma), an autoimmune connective tissue disorder (Figure 9-11). Scleroderma exists in two forms, limited and diffuse, both of which occur in the setting of Raynaud phenomenon (exaggerated vasoconstriction in response to cold or stress leading to sharply demarcated color changes of the fingertips). This patient displays the limited form in which the skin of the fingers, forearms, and face are often affected with distinctive thickening.
Diffuse systemic sclerosis eventually involves visceral organs as well as the gastrointestinal tract (particularly the esophagus), heart (myocardial fibrosis), muscles, lungs (interstitial lung disease is seen in the majority of patients, causing dyspnea on exertion and cough), and kidneys. This results in dysphagia, respiratory difficulty, arrhythmias, and mild proteinuria. The most concerning manifestation of this disease is malignant hypertension leading to renal failure.
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What serologic marker is used to test for Systemic sclerosis (scleroderma)?
Anti-DNA topoisomerase I (Anti-Scl-70) antibody is highly specific for systemic sclerosis. Anticentromere antibodies are more characteristic of limited scleroderma (CREST syndrome).
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What is the pathogenesis of Systemic sclerosis (scleroderma)?
The etiology of this condition is unknown; however, symptoms begin with vascular damage and are due to excessive synthesis of extracellular matrix, increased deposition of collagen in normal tissue, fibrosis, immune activation, and vascular damage.
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What is CREST syndrome?
CREST is an acronym for the five findings in individuals with limited systemic sclerosis: Calcinosis, Raynaud phenomenon, Esophageal dysmotility, Sclerodactyly, and Telangiectasia.
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What is the appropriate treatment for Systemic sclerosis (scleroderma)?
Most therapies are supportive; skin-softening agents and gloves are used to help skin sclerosis and Raynaud phenomenon. Bosentan and prostacyclin analogs might also be useful in pulmonary hypertension. Cytotoxics have a role in treating inflammatory lung disease.
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What is the most likely diagnosis?
Klumpke palsy results from birth injury to the lower trunk of the brachial plexus (C8 and T1 nerve roots). It is a proximal brachial plexus neuropathy.
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What motor deficits are likely to result from Klumpke palsy?
The C8 and T1 nerve roots contribute to the ulnar and median nerves. The muscles affected are the medial part of the flexor digitorum profundus and the flexor carpi ulnaris (the only extrinsic muscles of the forearm supplied by the ulnar nerve), and all intrinsic muscles of the hand, including those innervated by the ulnar nerve (interosseous muscles, the second and third lumbrical muscles, and the adductor pollicis brevis muscles), and those innervated by the median nerve (thenar muscles and the first two lumbrical muscles). Over time, wasting of the thenar and hypothenar eminences occurs. Marked wasting between the metacarpals on both palmar and dorsal surfaces of the hand results from paralysis of the lumbricals and interossei.
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What motor deficits are likely to result from Klumpke palsy?
The C8 and T1 nerve roots contribute to the ulnar and median nerves. The muscles affected are the medial part of the flexor digitorum profundus and the flexor carpi ulnaris (the only extrinsic muscles of the forearm supplied by the ulnar nerve), and all intrinsic muscles of the hand, including those innervated by the ulnar nerve (interosseous muscles, the second and third lumbrical muscles, and the adductor pollicis brevis muscles), and those innervated by the median nerve (thenar muscles and the first two lumbrical muscles). Over time, wasting of the thenar and hypothenar eminences occurs. Marked wasting between the metacarpals on both palmar and dorsal surfaces of the hand results from paralysis of the lumbricals and interossei.
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What sensory deficits are involved in Klumpke palsy?
The lower trunk from C8 and T1 contributes to the medial cutaneous nerves of the arm, forearm, and the ulnar and median nerves. Thus, in this patient, loss of sensation will occur on the medial side of the arm; the forearm; the dorsal and palmar surface of the fifth finger and half of the fourth finger; the palmar surface of the first, second, and third fingers and lateral half of the fourth finger extending onto the nail beds on the dorsal surface as far as the distal interphalangeal joints; and the palmar surface of the hand.
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What are 3 other injuries that can cause Klumpke palsy?
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What is another nerve lesion that can cause claw hand?
An ulnar nerve injury will also present with claw hand. However, with ulnar nerve injury, only the little finger and the ring finger are clawed because the median nerve is spared (resulting in normal thenar muscles). Also, the sensory deficit involves only the ulnar nerve distribution: the palm and dorsal surfaces of the medial part of the hand and the dorsal and palmar surfaces of the fifth finger and half of the fourth finger.
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What is the differential diagnosis for acute joint pain? 4 categories?
What is the most likely diagnosis?
Gout, secondary to hyperuricemia. Gout characteristically causes monoarticular arthritis, often of the first metatarsophalangeal joint (podagra).
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What are common causes of gout?
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What are the most likely findings of arthrocentesis in gout?
Needle-shaped negatively birefringent crystals are diagnostic for gout. By contrast, findings of pseudogout include basophilic rhomboid crystals of calcium pyrophosphate composition.
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What are the appropriate treatments for gout?
- Acute attacks?
- Prevention?
