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First Aid Chs Part 2 > Musculoskeletal > Flashcards

Musculoskeletal Flashcards

1
Q

What is the mutation seen in achondroplasia and what is its inheritance pattern?

A

Activating mutation in fibroblast growth factor receptor 3 (FGFR3), it is autosomal dominant. Gain of function mutation inhibits growth of cartilage and long bones.

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2
Q

What are the clinical features of achondroplasia?

A

Short extremities with normal sized head and chest. (Due to loss of endochondral long bone formation)

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3
Q

Why is the sclera blue in osteogenesis imperfecta?

A

Exposure of the choroidal veins because of thin sclera, which contains type I collagen.

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4
Q

Which type of collagen is defective in osteogenesis imperfecta?

A

Type I (collagen in bone - Autosomal dominant)

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5
Q

Which cells are dysfunctional in osteopetrosis?

A

Osteoclasts (can’t resorb bone)

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6
Q

What is the most common enzyme mutation resulting in osteopetrosis and why does it cause the disease?

A

Carbonic anhydrase II mutations result in osteopetrosis because the enzyme is normally used to produce H+ ions which allow for the breakdown of bone and resorption of calcium by osteoclasts. Without it, bone can’t be broken down.

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7
Q

What will be seen on X-ray of a patient with osteopetrosis?

A

Very thick bone with no medulla (bone-in-bone appearance)

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8
Q

Why do patients with osteopetrosis commonly have renal tubular acidosis?

A

Because the most common mutation seen in osteopetrosis is carbonic anhydrase, which, when lost, also causes RTA.

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9
Q

What is the treatment for osteopetrosis?

A

Bone marrow transplant (get new monocytes, which eventually become osteoclasts).

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10
Q

What is the pathophysiology of rickets/osteomalacia?

A

Defective mineralization of osteoid due to vitamin D deficiency. Results in deposition of osteoid throughout the body.

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11
Q

What enzyme is a marker for osteoblast activity?

A

Alkaline phosphatase (alkaline environment needed to lay down calcium in bone)

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12
Q

Why are postmenopausal women at higher risk for osteoporosis?

A

Estrogen levels decline. Estrogen is protective of bone mass.

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13
Q

Describe the changes seen in serum calcium, phosphate, PTH, and alkaline phosphate seen in a woman with severe osteoporosis.

A

All will be normal!

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14
Q

Which type of bone is lost in osteoporosis?

A

Trabecular (spongy) bone

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15
Q

What are the two types of osteoporosis?

A

Postmenopausal (due to loss of estrogen) Senile (loss of bone density with age)

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16
Q

Explain how PTH works on bone.

A

PTH activates osteoblasts, which activate the osteoclasts to resorb bone.

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17
Q

Explain the pathophysiology of Paget’s disease of bone.

A

Increase in osteoclast activity results in increase in osteoblast activity. Osteoclast burns out before the osteoblast, and the osteoblast lays down as much bone as possible, in a mosaic fashion. Results in a thick, sclerotic bone that fractures easily.

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18
Q

Is Paget’s disease diffuse or localized?

A

Localized - it does not affect the entire skeleton.

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19
Q

Isolated elevated alkaline phosphatase is seen with what disease?

A

Paget’s disease of bone (calcium, phosphorous, PTH normal)

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20
Q

What are the two main complications of Paget’s disease of bone?

A

High output cardiac failure (due to AV shunts) Osteosarcoma (malignant tumor of osteoblasts)

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21
Q

Where in the bone is osteomyelitis seen in kids?

A

Metaphysis (highly vascularized)

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22
Q

Where in the bone is osteomyelitis seen in adults?

A

Epiphysis

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23
Q

What is the #1 overall cause of osteomyelitis?

A

S. aureus

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24
Q

What is the #1 cause of osteomyelitis in sickle cell disease?

A

Salmonella

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25
Q

What is the #1 cause of osteomyelitis in an IVDU or patient with diabetes?

A

Pseudomonas

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26
Q

What causes osteomyelitis in a patient that has been bitten by a dog or cat?

A

Pasturella

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27
Q

What will be seen on x-ray in a patient with osteomyelitis?

A

Lytic focus surrounded by sclerosis

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28
Q

Where are osteomas most commonly located?

A

Facial bones

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29
Q

What is the triad seen with Gardner syndrome?

A

Familial adenomous polyposis (colon polyps), retroperitoneal fibromatosis, facial bone osteomas.

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30
Q

What is an osteoid osteoma?

A

Benign tumor of osteoblasts surrounded by rim of reactive bone seen in diaphysis of long bones. It causes bone pain that responds to aspirin.

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31
Q

What is significant about the pain in an osteoid osteoma?

A

It resolves with aspirin

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32
Q

What will be seen on x-ray in an osteoid osteoma?

A

Bony mass with radiolucent core (center core of osteoid that is surrounded by reactive bone).

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33
Q

What is the most common benign tumor of bone?

A

Osteochondroma (mature bone with a cartilagenous cap)

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34
Q

What is significant about the pain in an osteoblastoma?

A

It does NOT respond to aspirin (osteoid osteoma pain responds to aspirin)

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35
Q

What are the two benign tumors of osteoblasts and how are they differentiated?

A

Osteoid osteoma (small, arises in diaphyses, pain resolves with ASA) Osteoblastoma (large, arises in vertebrae, pain does not resolve with ASA)

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36
Q

Describe the morphology of an osteochondroma.

A

A benign tumor of bone with an overlying cartilage cap. Arises from a lateral projection of growth plate.

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37
Q

An osteochondroma can transform into which malignancy?

A

Chondrosarcoma

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38
Q

Osteosarcoma is a malignancy of which type of cells?

A

Osteoblasts

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39
Q

In which two age groups is osteosarcoma seen?

A

Teens and elderly.

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40
Q

Mutation of which tumor suppressor gene increases risk for osteosarcoma?

A

Rb

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41
Q

What are two predisposing factors to osteosarcoma in the elderly?

A

Radiation, Paget’s disease of the bone.

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42
Q

Where do osteosarcomas most commonly arise?

A

Metaphysis of long bones

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43
Q

What is Codman’s angle?

A

Elevation of the periosteum seen with rapidly growing osteosarcoma invading the surrounding soft tissue.

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44
Q

What is the hallmark of biopsy in osteosarcoma?

A

Pleiomorphic cells producing pink osteoid

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45
Q

Giant cell tumors (osteoclastoma) arise in which part of the bone?

A

Epiphysis (only tumor that arises in the epiphysis!)

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46
Q

What is the only tumor that arises in the epiphysis?

A

Giant cell tumor (osteoclastoma)

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47
Q

What is the “soap bubble” sign and what is it associated with?

A

Appearance of dark spots in the epiphysis due to reactive bone formation in a giant cell tumor (osteoclastoma).

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48
Q

Ewing sarcoma is derived from…

A

Neuroectoderm

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49
Q

Where does Ewing sarcoma arise in the bone?

A

Diaphysis (grows in medullary cavity)

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50
Q

What is seen on x-ray in Ewing sarcoma?

A

Onion skin appearance due to laying down of new periosteum.

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51
Q

What is seen on biopsy of Ewing sarcoma?

A

Small round blue cells

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52
Q

What is the translocation seen in Ewing sarcoma?

A

t(11;22) (11 + 22 = 33, Patrick Ewing’s number)

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53
Q

Where do chondromas typically arise?

A

Small bones of hands and feet (in the medulla)

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54
Q

Where do chondrosarcomas typically arise?

A

The medulla of the pelvis or central skeleton

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55
Q

Tumors that metastasize to the bone typically form which type of lesions?

A

Osteolytic (punched out)

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56
Q

What type of lesions do prostate cancer metastases produce in the bone?

A

Osteoblastic lesions - get sclerosis of the bone due to laying down of new bone (exception to the rule - normally mets give osteolytic lesions).

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57
Q

Cartilage contains which type of collagen?

A

Type II

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58
Q

Osteoarthritis (DJD) typically occurs in which joints?

A

Hip, lumbar spine, knees, DIP/PIP of fingers.

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59
Q

Joint stiffness in the morning that worsens during the day is typical of which arthropathy?

A

Osteoarthritis (DJD)

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60
Q

What is the pathologic hallmark of osteoarthritis (DJD)?

A

Disruption of the cartilage that lines the articular surface with osteophyte formation.

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61
Q

Where are Heberden and Bouchard’s nodes located?

A

Bouchard’s - PIP; Heberden’s - DIP; (Bros before Hoes)

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62
Q

Which HLA is RA associated with?

A

HLA-DR4 (R4 sorta looks like RA)

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63
Q

HLA DR 4 increases the risk for…

A

RA

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64
Q

What is the pathological hallmark of RA?

A

Inflammation of the synovium leading to formation of pannus (inflamed granulation tissue)

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65
Q

What is pannus?

A

An abnormal layer of inflamed granulation tissue, which is hallmark for RA.

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66
Q

Joint stiffness in the morning that improves with activity during the day is typical of which arthropathy?

A

RA

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67
Q

Which joint is spared in RA?

A

DIP (it is involved in OA- important distinction!)

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68
Q

What type of hypersensitivity is RA?

A

Type III

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69
Q

What causes joint deformity (ulnar deviation of fingers) in RA?

A

Myofibroblasts in granulation tissue (pannus) contract and pull the joint.

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70
Q

What is rheumatoid factor?

A

IgM autoantibody against Fc portion of IgG

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71
Q

Which joints are most commonly involved in ankylosing spondylitis?

A

SI joints and spine

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72
Q

Aortic regurgitation is associated with which arthropathy?

A

Ankylosing spondylitis (AR secondary to aortitis)

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73
Q

Ankylosing spondylitis is associated with what HLA marker?

A

HLA B-27

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74
Q

What is the classic triad seen in reactive arthritis (Reiter syndrome)?

A

Uveitis, urethritis, arthritis.

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75
Q

Reactive arthritis (Reiter syndrome) typically occurs after infection with…

A

Chlamydia or GI bugs (campylobacter, shigella, salmonella).

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76
Q

What is “sausage finger” and with what arthropathy is it associated?

A

Swelling of the DIP joints of hands associated with psoriatic arthritis.

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77
Q

Name 3 subsets of arthropathy associated with HLA B-27

A

Ankylosing spondylitis; Psoriatic arthritis; Reactive arthritis (Reiter syndrome). These are referred to as seronegative arthropathies

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78
Q

What is “bamboo spine”?

A

Fusion of spine segments seen in ankylosing spondylitis.

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79
Q

Infectious arthritis in a sexually active young adult is associated with what bacteria?

A

N. gonorrheae

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80
Q

Describe the arthritis seen with Neisseria infection.

A

Unilateral, migratory, usually involving the knee.

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81
Q

What is deposited in the joints in gout?

A

Monosodium urate crystals (NOT uric acid!)

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82
Q

Does breakdown of purines or pyrimidines lead to gout?

A

Purines (AMP and GMP)

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83
Q

What are the two basic ways that hyperuricemia can occur?

A

Overproduction of uric acid (high protein diet, myeloproliferative disorder, Lesch-Nyhan) Failure to filter and excrete uric acid from the kidney (renal insufficiency, thiazide/loop diuretics, alcohol binge)

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84
Q

From what compound and with what enzyme does the body make uric acid?

A

Xanthine oxidase metabolizes xanthine (product of purine metabolism) into uric acid.

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85
Q

What enzyme is deficient in Lesch-Nyhan syndrome and what happens in the disease?

A

HGPRT deficiency. As a result, the body can’t salvage hypoxanthine (from AMP) and guanine (from GMP). As a result, xanthine, and thus uric acid production is greatly increased. This results in gout, self-mutilation, and developmental delay.

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86
Q

What is podagra?

A

Painful arthritis of the MTP joint of the great toe seen in acute gout.

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87
Q

What causes the acute inflammatory reaction in acute gout?

A

Monosodium urate crystals activating neutrophils.

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88
Q

Give two dietary triggers for an acute gout attack.

A

Consumption of excess meat (more purines) Consumption of excess alcohol (alcohol competes with uric acid for excretion in the kidney)

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89
Q

What is the hallmark of chronic gout?

A

Formation of tophi - white, chalky deposits of monosodium urate crystals in soft tissue or joints.

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90
Q

What are tophi?

A

White chalky deposits of monosodium urate crystals in soft tissues or joints seen in chronic gout.

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91
Q

What will be seen under the microscope with examination of gout crystals?

A

Needle-shaped crystals with negative birefringence (when crystals lay flat, they are yellow) under polarized light.

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92
Q

Needle-shaped crystals with negative birefringence under polarized light.

A

Gout

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93
Q

What color are gout crystals under parallel light?

A

Yellow

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94
Q

What deposits in the joints in pseudogout?

A

Calcium pyrophosphate

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95
Q

What will be seen under the microscope with examination of pseudogout crystals?

A

Rhomboid shaped crystals with weak positive birefringence under polarized light

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96
Q

Rhomboid shaped crystals with weak positive birefringence under polarized light.

A

Pseudogout.

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97
Q

What color are pseudogout crystals under parallel light?

A

Blue

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98
Q

What causes hypercalcemia in sarcoidosis?

A

Increased 1 alpha hydroxylation of vitamin D in epithelioid macrophages.

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99
Q

What else do you need to look for in a patient presenting with dermatomyositis?

A

Underlying cancer (particularly stomach)

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100
Q

Describe the weakness seen in a patient with dermatomyositis/polymyositis.

A

Bilateral proximal weakness (can’t climb stairs or comb hair)

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101
Q

What is a heliotrope rash and with what disease is it associated?

A

Purple rash on the eyelids and face seen in dermatomyositis. (Note: it may be described as a malar rash - don’t jump on SLE!)

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102
Q

What are Gottron’s papules?

A

Red papules on the elbows, knuckles, and knees seen in dermatomyositis.

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103
Q

Describe the skin findings in dermatomyositis.

A

Heliotrope rash (purple rash on face and eyelids) and Gottron’s papules (red papules seen on fingers, elbows, knuckles).

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104
Q

What antibody is seen in dermatomyositis?

A

Anti-Jo-1 antibody

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105
Q

Anti-Jo-1 antibody

A

Dermatomyositis/polymyositis

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106
Q

What is inflamed in dermatomyositis?

A

Perimisium

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107
Q

What antibody is seen in polymyositis?

A

Anti-Jo-1 antibody

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108
Q

What is the treatment for dermatomyositis/polymyositis?

A

Steroids

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109
Q

How is polymyositis differentiated from dermatomyositis?

A

Polymyositis has the same muscle symptoms (proximal weakness), but it will not have a heliotrope rash or Gottron’s papules.

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110
Q

Describe the skin findings in polymyositis.

A

No skin findings - only have skin findings in dermatomyositis.

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111
Q

What cells cause inflammation in dermatomyositis?

A

CD4

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112
Q

What cells cause inflammation in polymyositis?

A

CD8

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113
Q

What is inflamed in polymyositis?

A

Endomysium of muscle

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114
Q

What replaces muscle in DMD?

A

Adipose tissue (causes pseudohypertrophy of calves)

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115
Q

What is deleted in DMD?

A

Dystrophin

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116
Q

What is the largest gene in the genome and why does this matter clinically?

A

Dystrophin gene - its size predisposes it to mutations (DMD/Becker).

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117
Q

What is the function of dystrophin?

A

Anchors muscle cytoskeleton to ECM.

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118
Q

What antibody is seen in MG?

A

Autoantibody against the postsynaptic Ach receptor at the NMJ.

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119
Q

List some clinical features of myasthenia gravis.

A

Muscle weakness that worsens with use and improves with rest, ptosis, diplopia, THYMOMA.

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120
Q

Thymoma or thymic hyperplasia is associated with..

A

Myasthenia gravis

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121
Q

Surgically, what can be done to improve symptoms of a patient with myasthenia gravis?

A

Removal of the thymus (thymoma or thymic hyperplasia).

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122
Q

What antibodies are seen in Lambert-Eaton syndrome?

A

Antibody against presynaptic calcium channel, which prevents calcium influx and release of Ach.

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123
Q

Patient is diagnosed with Lambert-Eaton syndrome. What else should you look for?

A

Small cell lung cancer.

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124
Q

Describe the weakness seen with Lambert-Eaton syndrome.

A

Proximal muscle weakness that improves with use. Eyes are spared.

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125
Q

What is the most common benign soft tissue tumor in adults?

A

Lipoma

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126
Q

What is the most common malignant soft tissue tumor in adults?

A

Liposarcoma

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127
Q

What is the characteristic cell in liposarcoma?

A

Lipoblast

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128
Q

Cardiac rhabdomyoma is associated with what disorder?

A

Tuberous sclerosis

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129
Q

What is the most common malignant soft tissue tumor in children?

A

Rhabdomyosarcoma

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130
Q

Biopsy shows desmin positive cells. Diagnosis?

A

Rhabdomyosarcoma (rhabdomyoblasts are desmin positive).

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131
Q

What is sarcoma botryoides?

A

Rhabdomyosarcoma in the vaginal canal in young females.

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132
Q

What is the MOA of allopurinol?

A

Inhibits Xanthine oxidase

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133
Q

What is the MOA of febuxostat?

A

Inhibits xanthine oxidase

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134
Q

What is the MOA of probenicid?

A

Decreases reabsorption of uric acid in the PCT

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135
Q

What is the MOA of colchicine?

A

Inhibits microtubule polymerization through stabilization of tubulin, resulting in decreased chemotaxis and degranulation of neutrophils.

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136
Q

What two drugs can be used in an attack of acute gout?

A

Indomethacin (NSAID) or colchicine (inhibits microtubule polymerization. Used in those that NSAIDs aren’t tolerated)

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137
Q

What is etanercept?

A

A fusion protein that acts as a receptor for TNF-alpha used in inflammatory conditions (decoy receptor).

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138
Q

What are adalimumab/infliximab?

A

Anti- TNF alpha monoclonal anibodies used in inflammatory conditions.

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139
Q

What 3 drugs are used in chronic gout?

A

Allopurinol/febuxostat (xanthine oxidase inhibitors) Probenecid (decreases reabsorption of uric acid in PCT)

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140
Q

What is polymyalgia rheumatica?

A

Pain and stiffness in shoulders/hips with fever/malaise/weight loss. Does not cause muscular weakness. Associated with giant cell arteritis.

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141
Q

MOA/Use/SFX of bisphosphonates

A

MOA: Bind hydroxyapatite in bone, inhibiting osteoclasts; Uses: Osteoporosis, hypercalcemia, Paget’s disease of the bone; SFX: corrosive esophagitis, osteonecrosis of the jaw.

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142
Q

MOA of zileuton

A

Inhibits lipooxygenase and production of all leukotrienes

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143
Q

<p>MOA of zafirleukast/monteleukast</p>

A

<p>Inhibit production of LTC4, LTD4 specifically (inhibit bronchoconstriction)</p>

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144
Q

Name the layers of the epidermis from the surface to the base

A

Californians Like Girls in String Bikinis

Stratum Corneum, Lucidum, Granulosum, Spinosum and Bassalis

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145
Q

WHat is the stem cell site in the epidermis?

A

Stratum basalis

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146
Q

Describe a sebaceous gland

A

Holocine secretion of sebum. Associated with a hair follicle

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147
Q

Describe a eccrine gland

A

Secretes sweat. Found throughout the body

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148
Q

Describe a apocrine gland

A

Secretes milky viscous fluid. Found in the axillae, genitalia and areolae. Does not become functional until puberty. Malodorous due to bacterial action

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149
Q

What are zone occludens?

A

Tight junctions, prevents paracellular movement of solutes

Composed of claudins and occludins

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150
Q

What are zona adherens?

A

Adherens junction - located below tight junctions, forms a “belt” connecting actin cytoskeletons of adjacent cells with cadherins
Note - loss of E-cadherin promotes metastasis

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151
Q

What are macula adherens?

A

Desmosomes - structural support via keratin interactions

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152
Q

What are the autoantibodies against in pemphigus vulgaris?

A

Desmosomes

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153
Q

What are gap junctions?

A

Channel proteins called connexons permit electrical and chemical communication between cells

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154
Q

What are hemidesmosomes?

A

Connects keratin in basal cells to underlying basement membrane

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155
Q

What are the autoantibodies against in Bullous pemphigoid?

A

Hemidesmosomes

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156
Q

What are integrins?

A

Membrane proteins that maintain integrity of the basement membrane by binding to laminin in the basement membrane

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157
Q

What is the triad in a knee injury?

A

ACL, MCL and meniscus (classically the medial but lateral is more common)

due to a lateral force applied to a planted leg

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158
Q

If a patient has an abnormal passive abduction of the lower limb - what is wrong?

A

MCL tear

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159
Q

What does a positive McMurray circumduction test mean?

A

Medial meniscus injury

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160
Q

What is the landmark for a pudendal nerve block?

A

Ischial spine

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161
Q

What is the landmark for the appendix?

A

2/3 of the way from the umbilicus to the ASIS

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162
Q

What are the 4 muscles of the rotator cuff AND what is their action?

A

Supraspinatus - abducts the arm initially before the deltoid
Infraspinatus - laterally rotates the arm
Teres minor - adducts and laterally rotates the arm
Subscapularis - medially (internally) rotates and adducts the arm

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163
Q

What is most commonly injured of the rotator cuff muscles?

A

Supraspinatus

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164
Q

which rotator cuff muscle is most commonly injured in a pitching injury?

A

Infraspinatus

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165
Q

What nerves innervate the rotator cuff muscles?

A

C5-C6

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166
Q

Where does the supraspinatus muscle insert?

A

Greater tubercle of the humerus

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167
Q

What is a Hawkin’s kennedy test?

A

impingement test - forward flex the shoulder and elbow to 90 degrees while passively internally rotating the shoulder - pain is positive
Usually positive with a supraspinatus muscle injury

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168
Q

A patient has an anterior shoulder dislocation - what have they most likely injured?

A

Axillary nerve and posterior circumflex artery

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169
Q

Which two wrist bones articulate with the distal radius?

A

Scaphoid and lunate - articulate only with the distal radius so they transmit the force of a FOOSH

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170
Q

What is the most commonly fractured carpal bone?

A

Scaphoid - prone to avascular necrosis owing to retrograde blood supply

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171
Q

What can occur with dislocation of the lunate bone?

A

Carpal tunnel syndrome

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172
Q

What nerve can be compressed in the axilla with incorrect use of a crutch?

A

Radial nerve

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173
Q

What nerve is compressed by supracondylar fracture of the humerus?

A

Median nerve

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174
Q

What nerve is compressed in pronator teres syndrome?

A

Median nerve

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175
Q

What nerve is injured with a fracture of the medial epicondyle of the humerus?

A

Ulnar nerve

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176
Q

where in the wrist can the ulnar nerve be injured?

A

Guyon’s canal

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177
Q

What nerve can be injured by a fracture of the hook of hamate?

A

Ulnar nerve

can also be lesioned by trauma to the heel of the hand

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178
Q

Which nerve can be inured by a midshaft fracture of the humerus?

A

Radial nerve - it runs through the spiral groove ere

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179
Q

Which nerve can be injured by subluxation of the radius?

A

The deep branch of the radial nerve can be stretched

180
Q

What is a Holstein-Lewis fracture?

A

Distal spiral humeral shaft fracture = radial nerve injury

181
Q

What nerve is injured with fracture to the surgical neck of the humerus?

A

Axillary nerve and posterior humeral artery

Axillary nerve can also be injured with dislocation of the humerus and with intramuscular injections

182
Q

How many tendons run through the carpal tunnel?

A

9 tendons

183
Q

A patient has carpal tunnel syndrome how would you treat them with OMM?

A

Stretch the flexor retinaculum

184
Q

what is seen with injury to the upper trunk of the brachial plexus?

A

Erb’s palsy

185
Q

What is seen with injury to the lower trunk of the brachial plexus?

A

Klumpke’s palsy

186
Q

What is seen with injury to the posterior cord of the brachial plexus?

A

Wrist drop

187
Q

What is seen with injury to the long thoracic nerve?

A

winged scapula
due to serratus anterior loss - used for abduction above horizontal position

If this nerve was injured in mastectomy you would see winged scapula + lymphedema

188
Q

What is seen with injury to the Axillary nerve?

A

deltoid paralysis

189
Q

What is seen with injury to the radial nerve?

A

Saturday night palsy = wrist drop

190
Q

What is seen with injury to the msculocutaneous branch of the brachial plexus?

A

Difficulty flexing the elbow, variable sensory loss

191
Q

What is seen with injury to the median nerve at the brachial plexus?

A

Decreased thumb function - pope’s blessing

192
Q

What is seen with injur of the ulnar nerve at the brachial plexus?

A

Intrinsic muscles of the hand, claw hand

193
Q

If a patient has a clavicle fracture - what protects them from injuring the brachial plexus?

A

Subclavius muscle

194
Q

what is the job of the muscle spindle?

A

monitors muscle length

195
Q

What is the functional unit of the muscle?

A

Extrafusal muscle fibers

196
Q

What regulates the length of the muscle?

A

Intrafusal muscle fibers communicating with the muscle spindle

197
Q

What is the job of the Golgi tendon?

A

Monitor tension

provides inhibitory Ib afferent feedback

198
Q

What is the job of the gamma loop?

A

Regulates sensitivity of the reflex arc

199
Q

which ligament is torn most commonly in an inversion ankle sprain?

A

Lateral ligaments effected

Always Torn First ligament = Anterior TaloFibular ligament

200
Q

what are the three ligaments of the lateral ligaments?

A

Anterior talofibular ligament
Calcaneal fibular ligament
Posterior talofibular ligament

201
Q

Where do the wrist extensors attach?

A

Lateral epicondyle

tennis elbow

202
Q

Where do the wrist flexors attach?

A

medial epicondyle

golfers elbow

203
Q

what is the sympathetic innervation to the lower extremities?

A

T10-L2

204
Q

Describe concentric contractions

A

muscle contractions that result in the approximation of the muscles origin and insertion

example - biceps curl
The force generated by a muscle exceeds the force applied to it

205
Q

Describe eccentric contractions

A

Lengthening of the muscle during contraction due to an external force

206
Q

Describe isolytic contraction

A

Muscle contraction against resistance while forcing the muscle to lengthen
the operators force is greater than the patients force

207
Q

Describe isometric contraction

A

Muscle contraction that results in the increased tension without an approximation of the origin and insertion
Operators force will = the patients force
Example would be pushing against a stationary object

208
Q

Describe Isokinetic contraction

A

Force of contraction changes the speed of contraction remains constant. These are rare in the body

209
Q

Describe supination of the foot?

A

Adduction, inversion, platarflexion

210
Q

Describe pronation of the foot?

A

Abduction, eversion and dorsiflexion

211
Q

Describe the findings in erb duchenne palsy

A

Limb hands by side due to paralysis of the abductors
Limb is medially rotated due to paralysis of the lateral rotators
Forearm is pronated due to loss of the biceps

212
Q

What are the nerves injured in erb duchenne palsy?

A

Upper trunk - Suprascapular N, Musculocutaneous N. and Axillary nerve

213
Q

What is injured in a klumpke’s palsy?

A

Lower trunk of brachial plexus (C8-T1) also injured in thoracic outlet syndrome

214
Q

What are the findings in a patient with Klumpke’s palsy?

A

Atrophy of the thenar and hypothenar eminences
Atrophy of the interossous muscles
Sensory deficits on the medial side of the forearm and hand
Disappearance of the radial pulse upon moving the head toward the ipsilateral side

215
Q

What is the innervation of the axillary nerve

A

C5,6

216
Q

What is the innervation of the Radial nerve?

A

C5-T1

217
Q

What is the innervation of the median nerve?

A

C5-T1

218
Q

What is the innervation of the Ulnar nerve?

A

C8-T1

219
Q

What is the innervation of the musculocutaneous nerve?

A

C5-C7

220
Q

Which nerve pierces the coracobrachialis muscle and runs between the biceps and brachialis?

A

Musculocutaneous nerve

221
Q

Which nerve is responsible for the flexors and pronating the wrist?

A

Median nerve

222
Q

Which nerve is injured with a midshaft fracture of the humerus?

A

Radial nerve

223
Q

Which artery does the axillary nerve run with?

A

Posterior circumflex artery

224
Q

What muscles does the Axillary nerve innervate?

A

Deltoid and teres minor

225
Q

Where is the sensory deficit with a axillary nerve injury?

A

over the deltoid (lateral shoulder)

226
Q

What does the radial nerve innervate?

A 
BEST extensors 
Brachioradialis
Extensors of the wrist and fingers
Supinator
Triceps
227
Q

Which nerve innervates the abductor pollicus longus muscle?

A

Radial nerve

abductor pollicis brevis is by the median nerve

228
Q

What does the median nerve innervate?

A

Opposition of the thumb, lateral finger flexion and wrist flexion
so the wrist flexors, thenar muscles (opponens pollicis, abductor pollicis brevis and flexor pollicis brevis) and lumbricals 1 and 2

229
Q

Which nerve is responsible for medial finger flexion and wrist flexion?

A

Ulnar nerve

230
Q

What is the sign with an ulnar nerve lesion?

A

Radial deviation of the wrist upon wrist flexion

231
Q

What can cause ulnar claw?

A

Can be caused by long standing injury to the ulnar nerve at the hook of the hamate (FOOSH)
Distal ulnar nerve lesion leads to loss of medial lumbrical function leaving to inability to extend the 4th and 5th digits (clawing) when trying to open the hand

232
Q

What is the median claw?

A

You have loss of lateral lumbraical function. 2nd and 3rd digits are clawed upon attempted finger extension

233
Q

What is popes blessing?

A

Proximal median nerve lesion causes loss of lateral finger flexion and thumb opposition. When asked to make a fist, the 2nd and 3rd digits remain extended and thumb remains unopposed which looks like the hand of benediction

234
Q

What does the median nerve innervate?

A

LOAF

lumbricals 1 +2, opponens pollicis, abductor pollicis brevis and flexor pollicis brevis

235
Q

What is the function of the dorsal interosseous muscles?

A

Abduct the fingers (DAB - dorsals ABduct)

236
Q

What is the function of the palmar interosseous muscles?

A

Adduct the fingers (PAD - Palmar ADduct)

237
Q

WHat is the function of the lumbricals?

A

Flex at the MCP joint and extend at the PIP and DIP joints

238
Q

What can injure the obturator nerve? What is the result?

A

Anterior hip dislocation

Loss of thigh adduction and sensory loss on the medial thigh

239
Q

What is the nerve levels of the Obturator nerve?

A

L2-4

240
Q

What is the nerve levels of the femoral nerve?

A

L2-4

241
Q

What is the nerve levels of the common peroneal nerve?

A

L4-S2

242
Q

What is the nerve levesl of the Tibial nerve?

A

L4-S3

243
Q

What is the nerve levels of the superior gluteal nerve?

A

L4-S1

244
Q

What is the nerve levels of the inferior gluteal nerve?

A

L5-S2

245
Q

How can you injure the femoral nerve? What are the effects?

A

Pelvic fracture

Loss of thigh flexion and leg extension and loss of anterior thigh and medial leg sensory

246
Q

How can you injure the common peroneal nerve? What is the motor and sensory loss?

A

Injured by trauma or compression of the lateral aspect of the leg or a fibular neck fracture

The patient will have loss of foot eversion and dorsiflexion resulting in loss of toe extension, foot drop, foot slap, and STEPPAGE GAIT (swing out gait)
They will have sensory loss of the anterolateral leg and dorsal aspect of the foot

The Peroneal nerve Everts and Dorsiflexes - if injured the foot is dropPED

247
Q

How can you injure the Tibial nerve and what are the effects?

A

Knee trauma

results in loss of foot inversion and plantarflexion, toe flexion
loss of sensory on the sole of the foot

The Tibial nerve Inverts and Plantarflexes - if injured can’t step on TIPtoes

248
Q

How can you injure the superior gluteal nerve and what is the effect?

A

Posterior hip dislocation or polio.

Loss of thigh abduction (positive trendelenburg sign - CL hip drops when standing on leg ipsilateral to site of lesion)

249
Q

How can you injure the inferior gluteal nerve and what is the effect?

A

Posterior hip dislocation

Can’t jump, climb stairs or rise from a seated position. Can’t push inferiorly (downward)

250
Q

What are the levels of the sciatic nerve?

A

L4-S3 - runs down the posterior thigh and splits into the common peroneal and tibial nerves

251
Q

How is the posterior cruciate ligament commonly injured?

A

Hyperflexion injury

Hyperextension injury causes an ACL tear

252
Q

When the quads tighten - what happens in a posterior cruciate ligament tear?

A

The tibia translates anteriorly

The quads insert on the tibia

253
Q

What is the Q angle?

A

Angle between the femur axis and tibia axis - is normally 10-12 degrees

A Q angle > 20: genu valgus (knock knee) can occur due to weak vastus medialis muscles

A Q angle <10: genu carum

254
Q

What are the angles of inclination?

A

Angles between the shaft of the fermur and femoral neck

normal is 120-135

> 135: coxa valgus
<120: coxa varum

255
Q

What muscles make up the hamstrings?

A

Semitendinosus, semimembranosus, biceps femoris

256
Q

What is the sural nerve?

A

Sensory only to the posterior lateral leg and lateral side of foot

257
Q

how do you test the IT band?

A

Ober’s test

258
Q

What happens to membrane excitability if you decreased extracellular calcium?

A

Increased membrane excitability

259
Q

What in the muscle fiber shortens with contraction?

A

H band and I band

260
Q

what drug blocks the ryanodine receptor?

A

Dantrolene

ryanodine receptor is located on the sarcoplasmic reticulum

261
Q

What remains a constant length with contraction of a muscle fiber?

A

A band remainds constant length

262
Q

Describe Type 1 muscle fibers

A

Slow twitch - red fibers, resulting from increased mitochondria and myoglobin concentration (increased oxidative phosphorylation) leading to sustained contraction

examples -calf muscles or abdominal muscles

263
Q

Describe Type 2 muscle fibers

A

Fast twitch muscles - white fibers resulting from decreased mitochondria and myoglobin concentration (increased anaerobic glycolysis) - weight training results in hypertrophy of fast-twitch muscle fibers

264
Q

what happens when ATP binds the myosin head?

A

Causes released of myosin from the actin filament

this is why a lack of ATP results in rigor mortis

265
Q

WHat bones participate in endochrondal ossification?

A

Bones of the axial and appendicular skeleton, and base of the skull

Cartilagenous model of bone is first made by chrondrocytes - osteoclasts and osteoblasts later replace with woven bone and then remodel to lamellar bone. In adults woven bone occurs after fractures and in Paget’s disease

266
Q

What is Membranous ossification?

A

Occurs in the bones of the calvarium and facial bones. Woven bone is formed directly without cartilage. Later remodeled to lamellar bone

267
Q

What are osteoblasts?

A

Build bone by secreting collagen and catalyzing mineralization - osteoblasts get incorporated into the bone and become osteocytes

268
Q

What are osteoclasts

A

Multinucleated cells that dissolve bone by secreting acid and collagenases - type of macrophage

269
Q

What is the difference between high and low levels of PTH?

A

At low, intermittent levels, exerts anabolic effects (building bone) on osteoblasts and clasts

Chronic high levels (primary hyperparathyroidism) causes catabolic effects (osteitis fibrosa cystica)

270
Q

What are the effects on bone by estrogen?

A

estrogen inhibits apoptosis in bone-forming osteoblasts and induces apoptosis in bone resorbing osteoclasts. Under estrogen deficiency - excess remodeling cycles and bone resorption leads to osteoporosis

271
Q

what is responsible for linear growth?

A

Epiphyseal cartilage - growth plate

linear growth stops when the epiphysis fuses with the metaphysis (plates close)

272
Q

What is the effect of sex steroids on linear growth?

A

sex steroids initially increased linear growth but they also encourage closure of the epiphyseal growth plates

273
Q

failure of longitudinal bone growth (endochrondral ossification) but normal membranous ossification

A

Achondroplasia - most common cause of dwarfism

failed endochrondral ossification = short limbs
normal membranous ossification = normal (large) head compared to limbs

274
Q

What is the defect in Achondroplasia?

A

Constitutive activation of fibroblast growth factor receptor (FGFR3) actually inhibits chondrocyte proliferation (you don’t get the laying down of the cartilage frame)

due to advanced paternal age and also is autosomal dominant inheritance

275
Q

Describe osteoporosis

A

Trabecular (spongy) bone loses mass and interconnections despite normal bone mineralization and lab values
can lead to acute vertebral crush fractures - acute back pain loss of height and kyphosis

276
Q

Describe Type 1 osteoporosis?

A

Postmenopausal - increased bone resportion due to decreased estrogen levels

examples - femoral neck fracture, distal radius fracture (colles’ fracture)

277
Q

Describe Type 2 osteoporosis?

A

Senile osteoporosis - affects men and women over the age of 70

278
Q

Describe Osteopetrosis

A

Failure of normal bone resportion due to defective osteoclasts leading to thickened dense bones that are prone to fracture.

The bone fills the marrow space leading to pancytopenia and extramedullary hematopoiesis

279
Q

What is the mutation in Osteopetrosis?

A

Impaired osteoclasts
Commonly due to carbonic anhydrase II mutation leading to impaired ability of osteoclasts to generate an acidic environment for resorbing bone

bone marrow transplant would be potentially curative

280
Q

Describe osteomalacia and rickets

A

Vitamin D deficiency
Osteomalacia is seen in adults and rickets in kids

due to defective mineralization/calcification of osteoid leading to soft bones that bow out

281
Q

what is hyperactive in osteomalacia and rickets?

A

osteoblast - you have increased alkaline phosphatase (since osteoblast require alkaline environment to work)

282
Q

What is Paget’s disease of bone (Osteitis deformans)?

A

Common, localized disorder of bone remodeling caused by increase in both osteoblastic and osteoclastic activity

283
Q

What is the pattern seen in Paget’s disease (Osteitis deformans)?

A

Mosaic (“woven” bone pattern - long bone chalk-stick fractures.

284
Q

What are possible risks seen in Paget’s disease (Osteitis deformans)?

A

High cardiac output heart failure - due to increased blood flow from increased arteriovenous shunts

also increased risk of osteogenic sarcoma

285
Q

How can phenytoin lead to deficiencies in Vitamin D?

A

Phenytoin induces P450 system which metabolizes Vitamin D

286
Q

A patient with both lytic and sclerotic areas of bone

A

Paget’s disease of bone (Osteitis deformans)

287
Q

What are the lab findings in a patient with Osteoporosis?

A

all NORMAL! just a decreased in bone mass due to decreased osteoblast activity

288
Q

What are the lab findings in a patient with Osteopetrosis?

A

Decreased serum calcium and increased ALP - has thickened denes bone due to decreased osteoclast activity

289
Q

What are the lab findings in a patient with Osteomalacia/Rickets?

A

Decreased serum calcium and phosphate and increased ALP and PTH
patient will have soft bones due to defective mineralization

290
Q

What are the lab findings in a patient with Osteitis fibrosa cystica?

A

Increased serum calcium, ALP and PTH and decreased phosphate

The patient will have brown tumors of hyperparathyroidism (due to XS osteoclast activity)

291
Q

What are the lab findings in a patient with Paget’s disease of the bone?

A

Increased ALP is possible

due to abnormal bone architecture

292
Q

Name the Bone tumor: Occurs in 20-40 yo at the epiphyseal end of long bones

A

Giant cell tumor (Osteoclastoma)

293
Q

Name the Bone tumor: Double bubble or soap bubble appearance on X ray

A

Giant cell tumor - AKA osteoCLastoma

CL - clean = soap

294
Q

Name the Bone tumor: Locally aggressive benign tumor often around the distal femur, proximal tibial region

A

Giant cell tumor - AKA osteoclastoma

295
Q

Name the Bone tumor: Most common benign tumor and occurs in males less than 25 years old

A

Osteochondroma

malignant transformation to chondrosarcoma is rare

296
Q

Name the Bone tumor: Mature bone with cartilaginous cap that commonly originates from long metaphysis.

A

Osteochondroma

osteoCHondroma = CHunk of bone

297
Q

Name the Bone tumor: due to a defective Rb suppressor gene

A

Osteosarcoma

298
Q

Name the Bone tumor: Second most common primary malignant bone tumor (after multiple myeloma)

A

Osteosarcoma

299
Q

Name the Bone tumor: 10-20 yo more common in males than females - occurs in the metaphysis of long bones, often around the distal femur or proximal tibia. This is a malignant bone tumor

A

Osteosarcoma

300
Q

Name the Bone tumor: Has Codman’s triangle due to elevation of periosteum or sunburst pattern on Xray. It’s aggressive and treated with surgical en bloc resection (with limb salvage) and chemotherapy

A

OsteoSarComa

S- sunburst
C - codmans triangle

301
Q

Name the Bone tumor: Occurs in boys less than 15 yo, commonly appears in the diaphysis of long bones, pelvis, scapula and ribs

A

Ewing’s sarcoma

302
Q

Name the Bone tumor: Contains anaplastic small blue cell malignat tumor, extremely aggressive with early mets but it’s responsive to chemo

A

Ewing’s sarcoma

303
Q

Name the Bone tumor: Onion skin appearance in bone and associated with t(11;22) translocation

A

Ewing’s sarcoma

onion rings and wings
onion skin appearance = concentric formation of new bone layers

304
Q

Name the Bone tumor: Occurs in men 30-60 years old and is usually located in the pelvis, spine, scapula, humerus, tibia or femur

A

Chrondrosarcoma

305
Q

Name the Bone tumor: Malignant cartilaginous tumor that may occur from primary origin or from an osteochondroma.

A

Chondrosarcoma

306
Q

Name the Bone tumor: Expansile glistening mass within the medullary cavity of diaphysis

A

Chrondrosarcoma

307
Q

What part of the bone does osteomyelitis most commonly occur?

A

Metaphysis of long bones

308
Q

What is the cause of osteoarthritis?

A

Mechanical cause - joint wear and tear that destroys the articular cartilage

309
Q

What is the cause of rheumatoid arthritis?

A

Autoimmune cause - inflammatory destruction of the synovial joints - type 3 HS

310
Q

Which disease has no DIP involvement?

A

Rheumatoid arthritis

usually involves just the MCP and PIP joints

311
Q

What is rheumatoid factor?

A

IgM antibody against the Fc portion of IgG

312
Q

What HLA is associated with rheumatoid arthritis?

A

HLA-DR4

313
Q

Compare the treatment of osteoarthritis with RA?

A

Osteoarthritis - NSAIDs, intra-articular glucocoritcoids

RA - NSAIDs, glucocorticoids, disease-modifying agents (methotrexate, sulfasalazine, TNF-alpha inhibitors)

314
Q

describe a swan neck deformity

A

Extended PIP and flexed DIP

315
Q

describe a boutonniere deformity

A

Flexed PIP and extended DIP - the extensor tendon on the back of the finger splits do that the PIP sticks out

316
Q

What is the syndrome that has lymphocytic infiltration of exocrine glands especially the lacrimal and salivary glands?

A

Sjogren’s syndrome

317
Q

What are the increased risks in Sjogren’s syndrome?

A

dental caries, increased risk of B cell lymphoma

Sjogren’s can also be associated with rheumatoid arthritis
(Can’t see (dry eyes), can’t spit (dry mouth), can’t climb up a ship)

318
Q

What are the autoantibodies seen in Sjogren’s syndrome?

A

Autoantibodies to ribonucleoprotein antigens: anti-Ro and anti-La

319
Q

Why can alcohol precipitate a gout attack?

A

Alcohol metabolites compete for the same excretion sites as uric acid in the kidney

320
Q

which diuretics can exacerbate gout by decreased uric acid excretion?

A

Loop diuretics and Thiazide diuretics

321
Q

where are common locations to get tophus formation with gout?

A

external ear, olecranon bursa or Achilles tendon

note tat tophi are uric acid deposits - they are NOT inflamed

322
Q

List the treatments for acute gout

A

NSAIDs (indomethacin), glucocorticoids and colchicine

323
Q

List the treatments for chronic gout

A

Xanthine oxidase inhibitors like allopurinol or febuxostat

324
Q

can you use aspirin in a gout patient?

A

NO it’s contraindicated - both uric acid and aspirin compete at renal transporters resulting in higher serum levels of uric acid

Sulfonamides, penicillin and thiazide diuretics compete at this same spot

325
Q

What is seen in joint aspiration for a patent with gout vs a patient with pseudogout?

A

Gout - negative birefringence

pseudogout - positive birefringence

326
Q

List four causes of osteonecrosis?

A

This is infarction of the bone and marrow.

Caused by trauma, high dose corticosteroids, alcoholism and sickle cell

most common site is the femoral head

327
Q

What is seronegative spondyloarthropathies?

A

Arthritis without rheumatoid factor

associated with HLA-B27

328
Q

When do you see pencil-in-cup deformities on xray?

A

Psoriatic arthritis

along with sausage fingers

329
Q

What are syndesmophytes?

A

Like osteophytes but they are seen in ankylosing spondylitis

330
Q

What is the classic triad seen in Reiter’s syndrome?

A

Conjunctivities with anterior uveitis, urethritis, arthritis - can’t see, can’t pee can’t climb a tree

331
Q

What can cause reactive arthritis?

A

Post-GI (shigella, salmonella, Yersinia, campylobacter, clostridium) or with chlamydial infections

332
Q

How do you treat ankylosing spondylitis?

A

Indomethacin primary

secondary is sulfasalazine, or anti-TNF alpha agents

333
Q

Nephritis is the most common cause of death in SLE patients - what are the problems with the kidneys?

A

Nephrotic - membranous glomerulonephritis

Nephritic - Diffuse proliferative glomerulonephritis

334
Q

What are the autoantibodies seen in SLE?

A
  • ANA - screening but not specific
  • anti-DS DNA - specific poor prognosis
    anti-smith antibodies very specific but not prognostic
    anti-histone antibodies - drug induced lupus
335
Q

Why do SLE patients test false positive on syphilis tests?

A

due to antiphospholipid antibodies which cross react with cardiolipin used in the tests

336
Q

What are the presentations in SLE?

A

fever, fatigue, weight loss, libman sacs endocarditis, hilar adenopathy, Raynaud’s phenomenon

337
Q

What is the cause of an SLE patient developing autoimmune hemolytic anemia?

A

Warm IgG antibodies - binds to surface of RBCs

patients will have a positive direct Coombs test

338
Q

Describe Sarcoidosis

A

“A GRUELING DISEASE”

  • ACE increased
  • Granulomas (non caseating)
  • Rheumatoid arthritis
  • Uveitis
  • Erythema nodosum (tibial)
  • Lymphadenopathy (bilateral, HILAR)
  • Idiopathic
  • Noncaseating granulomas
  • Gamma globulinemia
  • Vitamin D increased - causing hypercalcemia
339
Q

A patient presents with bilateral hilar adenopathy and reticular opacities - what should you think?

A

Sarcoidosis

340
Q

Why do patients with sarcoidosis have hypercalcemia?

A

They have increased vitamin D due to elevated 1 alpha hydroxylase mediated vitamin D activation in epithelioid macrophages

341
Q

What is the treatment for a patient with sarcoidosis?

A

steroids

342
Q

What is polymyalgia rheumatica?

A

Pain and stiffness in shoulder and hip joints often with fever, malaise and weight loss. does not cause muscular weakness.
More common in women >50yo associated with temporal giant cell arteritis
patients will have increased ESR but normal CK

343
Q

How do you treat a patient with polymyalgia rheumatica?

A

low dose corticosteroids

344
Q

Describe Polymyositis

A

Progressiev symmetric proximal muscle weakness, characterized by endomysial inflammation with CD8+ T cells - most often involves the shoulders and pelvic girdle

345
Q

Describe dermatomyositis

A

Similar to polymyositis but also involves a malar rash. Gottrons papules (red scaly papules on knuckles or knees/elbows), heliotrope rash, shawl and face rash, mechanic’s hands.
Increased risk of occul malignancy. Perimysial inflammation and atrophy with CD4+ T cells

346
Q

what are some findings in patients with Polymyositis or Dermatomyositis?

A

Increased CK, positive ANA, positive anti-Jo-1 antibodies, increased aldolase

347
Q

What is Myasthenia gravis associated with?

A

Thymoma or thymic hyperplasia

348
Q

how do you diagnose myasthenia gravis?

A

Tensilon test - edrophonium (fast acting)

349
Q

How do you treat myasthenia gravis?

A

Pyridostigmine - anticholinesterase

350
Q

Describe Myositis ossificans

A

Metaplasia of skeletal muscle to bone following muscular trauma - most often seen in upper or lower extremity. May present as suspicious mass at site of known trauma or as incidental finding on radiography

351
Q

What is scleroderma?

A

Systemic sclerosis - excessive fibrosis and collagen deposition throughout the body

352
Q

Describe diffuse scleroderma

A

Widespread skin involvement, rapid progression, early visceral involvement
associated with anti-DNA topoisomerase I antibody

353
Q

Describe CREST scleroderma

A

CREST
Calcinosis, Raynaud phenomenon, Esophgeal dysmotlity, Sclerodactyly, Telangiectasia
Limited skin involvement, often confined to fingers and face
More benign than diffuse scleroderma. associated with anti-Centromere antibody

354
Q

Describe a macule

A

flat lesion with well circumscribed change in skin color <5mm
examples: freckles, labial macule

355
Q

Describe a patch

A

Macule >5mm

examples: large birthmark (congenital nevus)

356
Q

Describe a papule

A

elevated solid skin lesion <5mm

examples: mole (nevus), acne

357
Q

Describe a plaque

A

Papule >5mm

ex: psoriasis

358
Q

Describe a vesicle

A

Small fluid containing blister <5mm

examples: chicken pox or shingles

359
Q

Describe a bulla

A

Large fluid containing blister >5mm

Examples: bullous pemphigoid

360
Q

Describe a pustule

A

Vesicle containing pus

ex: pustular psoriasis

361
Q

Describe a wheal

A

Transient smooth papule or plaque

like a hive or urticaria

362
Q

Describe a scale

A

Flaking off of stratum corneum

Ex: eczema, psoriasis, SCC

363
Q

Describe a crust?

A

Dry exudate

example: impetigo

364
Q

What is hyperkeratosis?

A

increased thickness of the stratum corneum

365
Q

What is Parakeratosis?

A

hjyperkeratosis with retention of nuclei in stratum corneum

366
Q

What is acantholysis?

A

Separation of epidermal cells

367
Q

What is acanthosis?

A

Epidermal hyperplasia with increased spinosum

368
Q

What is dermatitis

A

Inflammation of the skin

369
Q

Describe albinism

A

Normal melanocyte number with decreased melanin production due to decreased tyrosinase activity - can also be casued by fairle of neural crest cell migration

370
Q

Describe Melasma

A

AKA chloasma

Hyperpigmentation associated with pregnancy (“mask of pregnancy”) or OCP use

371
Q

Describe Vitiligo

A

Irregular areas of complete depigmentation caused by a decreased in melanocytes

372
Q

Describe Verrucae

A

Warts caused by HPV.
they are soft, tan-colored, cauliflower like papules. Epidermal hyperplasia, hyperkeratosis, KOILOCYTOSIS
Called condyloma accuminatum on the genitals

373
Q

What is melanocytic nevus?

A

common mole. Benign, but melanoma can arise in congenital or atypical moles. Intradermal nevi are popular
junctional nevi are flat macules

374
Q

What is an ephelis?

A

Freckle - normal number of melanocytes but increased melanin pigment

375
Q

What is atopic dermatitis?

A

Eczema
Pruritic eruption commonly on skin FLEXURES
often associated with other atopic diseases
usually starts ont he face in infancy and often appears in the antecubital fossa thereafter

376
Q

How can you treat atopic dermatitis?

A

Calcineurin inhibitors (tacrolimus), steroids, antihistamine

377
Q

What is allergic contact dermatitis?

A

Type IV hypesensitivity reaction that follows exposure to allergen

378
Q

Describe Psoriasis

A

Papules and plaques with silver scaling especially on knees and elbos (extensor surfaces)
Acanthosis with parakeratotic scaling (nuclei still in stratum corneum) you have increased stratum spinosum and decreased stratum granulosum

379
Q

What do you see Auspitz sign with?

A

Psoriasis

380
Q

Describe Seborrheic Keratosis

A

Flat, greasy pigmented squamous epithelial proliferation with keratin filled cysts that looks stuck on
benign

381
Q

What is lesser-Trelat sign?

A

Sudden appearance of multiple seborrheic keratosis, indicating an underlying malignancy - commonly GI or lymphoid (gastric cancer)

382
Q

Describe Pemphigus Vulgaris?

A

“DAMN is a VULGAR word”
Desmosomes - IgG antibodies against desmoglein 3
Acantholysis - loss of intracellular connections - thin intraepidermal ullae causing flaccid blisters
Mouth - involves ORAL mucosa and skin
Nikolsky’s sign - separation of epidermis upon manual stroking of skin

383
Q

Describe Bullous pemphigoid?

A

IgG antibody against hemidesmosomes - epidermal basement membrane so you have linear immunofluorescence
Eosinophils with tense blisters (negative Nikolski’s sign
does not involve oral mucosa

384
Q

Describe dermatitis herpetiformis?

A

Deposits of IgA at the tips of dermal papillae
associated with celiac disease
intensely itchy

385
Q

What is associated with erythema multiforme?

A

Infections - HSV, mycoplasma pneumonia
Drugs - sulfa drugs, beta lactams, phenytoin
cancers
autoimmune disease

386
Q

What is toxic epidermal necrolysis?

A

A more severe form of stevens-johnson syndrome with >30% of the body surface area involved

387
Q

What is stevens-johnson syndrome?

A

Characterized by fever, bulla formation and necrosis, sloughing of skin and a high mortality rate

388
Q

What is acanthosis nigricans?

A

Epidermal hyperplasia (of stratum spinosum) causing symmetrical hyperpigmented velvety thickening of the skin especially on the neck or axilla

389
Q

What can cause acanthosis nigricans?

A

Hyperinsulinemia (diabetes, obesity, Cuhsing’s syndrome)

and visceral malignancy

390
Q

What is Actinic keratosis?

A

Results from proliferation of atypical epidermal keratinocytes
premalignant lesions caused by sun exposure - small rough erythematous or brownish papules or plaques.

391
Q

What is the risk of Actinic keratosis?

A

May develop into squamous cell carcinoma - proportional to the degree of epithelial dysplasia

treat with 5-FU or cryoablation

392
Q

What is erythema nodosum?

A

Inflammatory lesions of subcutaneous fat

usually on the anterior shins

393
Q

What is erythema nodosum associated with?

A

Sarcoidosis, coccidioidomycosis, histoplasmosis, TB ,strep infections, leprosy, and crohn’s disease

394
Q

What are the findings in a patient with Lichen planus?

A 
6 Ps
Pruritic
Purple
Polygonal Planar Papules and Plaques
Sawtooth infiltrate of lymphocytes at the dermal-epidermal junction
395
Q

What is lichen planus associated with?

A

Hepatitis C

396
Q

What is pityriasis rosea?

A

“herald patch” followed days later by “Christmas tree” distribution
Multiple plaques with collarette scale
Self resolving in 6- 8 weeks

397
Q

What is pityriasis rosea due to?

A

Reactivation of HHV-7 or HHV-6

398
Q

What is a sunburn?

A

UV irradiation causes DNA mutations, inducing apoptosis of keratinocytes
UVA is dominant in tanning and photoaging
UVB is dominant in sunburn

399
Q

What can sunburn lead to?

A

Impetigo, and skin cancers

400
Q

What is cellulitis?

A

Acute painful spreading infection of the dermis and subcutaneous tissues - usually from S pyogenes or S aureus
Often starts with a break in the skin from trauma or another infection

401
Q

Describe staphylococcal scalded skin syndrome?

A

Exotoxin destroys keratinocyte attachments in the stratum granulosum only (vs toxic epidermal necrolysis which destroys the epidermal dermal junction)

The sloughing of SSSS will heal completely

402
Q

Are there bacteria in the blisters of a kin with staphylococcal scalded skin syndrome?

A

No

403
Q

What is hairy leukoplakia?

A

White, painless plaques on the tongue that cannot be scraped off - EBV mediated - occurs in HIV positive patients

404
Q

Name the skin cancer: Most common skin cancer

A

Basal cell carcinoma

405
Q

Name the skin cancer: Pink, pearly nodules with telangiectasias and rolled borders and central crusting or ulceration

A

Basal cell carcinoma

406
Q

Name the skin cancer: Palisading nuclear arrangements at the periphery of tumor cell clusters

A

Basal cell carcinoma

surgical resection is generally curative

407
Q

Name the skin cancer: Second most common skin cancer

A

Squamous cell carcinoma

408
Q

Name the skin cancer: associated with arsenic exposure commonly occurs on the face or lower lip, ears, hands

A

Squamous cell carcinoma

409
Q

Name the skin cancer: Locally invasive but may spread to lymph nodes and will rarely metastasize

A

Squamous cell carcinoma

410
Q

Name the skin cancer: Ulcerative red lesions with frequent scale. associated with chronic draining sinuses

A

Squamous cell carcinoma

411
Q

Name the skin cancer: Keratin pearls

A

Squamous cell carcinoma

412
Q

Name the skin cancer: A variant of squamous cell carcinoma that grows rapidly and may regress spontaneously

A

Keratoacanthoma

413
Q

Name the skin cancer: Common tumor with significant risk of metastasis

A

Melanoma

414
Q

Name the skin cancer: S-100 positieve

A

Melanoma

415
Q

Name the skin cancer: Often drive by activating mutation in BRAF kinase.

A

Melanoma

416
Q

Metastatic or unresectable melanoma in patients with BRAF V600E mutation may benefit from what?

A

Vemurafenib - a BRAF kinase inhibitor

417
Q

What is the function of LTB4?

A

Neutrophil chemotaxis

418
Q

What is the function of LTC4 and LTD4 and E4?

A

Bronchoconstriction, vasoconstriction, contraction of smooth muscle and increased vascular permeability

419
Q

What is the function of PGI2 (Prostacyclin)?

A

Decreases platelet aggregation, decreases vascular tone, decreases bronchial tone, decreases uterine tone

420
Q

What is the function of Prostaglandins PGE2 and PGF2alpha?

A

Increases uterine tone
decrease vascular tone
decreases bronchial tone

421
Q

What is the function of TXA2?

A

Increases platelet aggregation
increases vascular tone
increases bronchial tone

422
Q

How is aspirin different from acetaminophen?

A

Aspirin inhibits thromboxane production while acetaminophen does not
acetaminophen has NO anti-inflammatory or anti-platelet effects unlike aspirin which does

423
Q

What is the MOA of acetaminophen?

A

Reversibly inhibits cyclooxygenase mostly in the CNS - it’s inactivated peripherally
It decreases fever by reducing prostaglandin levels

424
Q

What is the clinical use of acetaminophen?

A

Antipyretic, analgesic but not anti-inflammatory

used instead of aspirin to avoid Reye’s syndrome in children with a viral infection

425
Q

What is the toxicity associated with acetaminophen overdose?

A

Hepatic necrosis - acetaminophen metabolite (NAPQI) depletes glutathione and forms toxic tissue adducts in the liver
N-acetylcysteine is the antidote which regenerates glutathione

426
Q

What is the MOA of aspirin?

A

Irreversible inhibits cyclooxygenase (COX 1 and 2) by acetylation which decreases synthesis of both TXA2 and prostaglandins
increase bleeding time but no effect on PT or PTT
It’s a type of NSAID

427
Q

What is the clinical use of aspirin?

A 
Low dose (<300 mg/day) causes decreased platelet aggregation
Intermediate dose - causes antipyretic and analgesic
high dose is anti-inflammatory
428
Q

What is the toxicity of aspirin?

A

Gastric ulcers, tinnitus
Chronic use can lead to acute renal failure, interstitial nephritis and upper GI bleeding
Risk of Reyes syndrome in children treated with aspirin for viral infection
also stimulates respiratory centers causing hyperventilation and respiratory alkalosis

429
Q

List some NSAIDs

A

Ibuprofen, naproxen, indomethacin, ketorolac, diclofenac

430
Q

what is the MOA of NSAIDs?

A

reversibly inhibits cyclooxygenase 1 and 2 - blocks prostaglandin synthesis

431
Q

What is the clinical use for NSAIDs?

A

Antipyretic analgesic and anti-inflammatory

indomethacin can be used to close PDA

432
Q

What is the toxicity of NSAIDs?

A

Interstitial nephritis, gastric ulcer (prostaglandins protect gastric mucosa), renal ischemia (PGs vasodilate afferent arteriole)

433
Q

What is celecoxib?

A

COX2 inhibitor

spares COX-1 so you shouldn’t see corrosive effects on GI lining and you also spare the platelet function since TXA2 is dependent on COX1

434
Q

What is Alendronate?

A

Bisphosphonates

435
Q

What is the MOA of bisphosphonates?

A

Pyrophosphate analog that binds hydroxyapatite in bone inhibiting osteoclast activity

436
Q

What is the clinical use of bisphosphonates?

A

osteoporosis, hypercalcemia, paget’s disease of the bone

437
Q

What is the toxicity seen in Bisphosphonates?

A

Corrosive esophagitis, osteonecrosis of the jaw

438
Q

What is one problem associated with using Allopurinol?

A

increases concentrations of azathioprine and 6-MP which are both normally metabolized by xanthine oxidase

439
Q

How does probenecid work?

A

Inhibits reabsorption of uric acid in the proximal convoluted tubule

440
Q

How does Colchicine work?

A

Binds and stabilizes tubulin to inhibit polymerization, impairing leukocyte chemotaxis and degranulation

441
Q

What is the problem with TNF-alpha inhibitors?

A

All TNF-alpha inhibitors predispose to infection including reactivation of latent TB since TNF blockage prevents activation of macrophages and destruction of phagocytosed microbes

ALWAYS CHEK A PPD BEFORE STARTING A TNFalpha INHIBITOR!

442
Q

What is the MOA of etanercept?

A 
Fusion protein (receptor for TNFalpha and IgG1 Fc) produced by recombinant DNA
EtancerCEPT is a TNF decoy reCEPTor
443
Q

What is the clinical use for etanercept?

A

Rheumatoid arthritis, psoriasis, ankylosing spondylitis

444
Q

What is the MOA of infliximab and adalimumab?

A

Anti-TNF alpha monoclonal antibody

445
Q

What is the clinical use of infliximab and adalimumab?

A

Crohn’s disease, rheumatoid arthritis, ankylosing spondylitis, psoriasis

446
Q

Describe the Thompson test

A

Squeeze the calf of the suspected injured leg while the patient lies prone

Test is positive if the foot doesn’t plantarflex in response

A popping sound is more typical for Achilles tendon rupture than an ankle problem

First Aid Chs Part 2 (6 decks)

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