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MUSCULOSKELETAL, SKIN, AND CONNECTIVE TISSUE > MUSCULOSKELETAL, SKIN, AND CONNECTIVE TISSUE- Pathology > Flashcards

MUSCULOSKELETAL, SKIN, AND CONNECTIVE TISSUE- Pathology Flashcards

1
Q

Failure of longitudinal bone growth

A

Achondroplasia

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2
Q

Which bone formation is affected in Achondroplasia?

A

Endochondral ossification

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3
Q

Clinical presentation of Achondroplasia

A

Short limbs

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4
Q

Memebranous ossification is affected in Achondroplasia

A

False, just endochondral ossification

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5
Q

What is the result that mambranous ossification is not affected in Achondroplasia

A

Large head relative to limbs

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6
Q

In Achondroplasia what inhibits chondrocyte proliferation?

A

Constitutive activation of fibroblast growth factor receptor (FGFR3)

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7
Q

Which are the explanations of Achondroplasia?

A

> 85% of mutations occur sporadically and are associated with advanced paternal age, but the conditions also demonstrates autosomal dominant inheritance

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8
Q

Common cause of dwarfism

A

Achondroplasia

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9
Q

Do patients with Achondroplasia have normal life span and feritlity?

A

Yes

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10
Q

What happens in Osteoporosis?

A

Trabecular (spongy) bone loses mass and interconnections despite normal bone mineralization and lab values (serum Ca2+ and PO4 3-)

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11
Q

How is Osteoporosis diagnosis made?

A

By a bone mineral densitiy test (DEXA) with a T score of

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12
Q

Pharmacologic cause of osteoporosis

A

By long term exogenous steroid use

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13
Q

What can osteoporosis lead to?

A

Vertebral crush fractures

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14
Q

Clinical findings of Vertebral crush fractures caused by osteoporosis

A

Acute back pain, loss of height, kyphosis

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15
Q

Type I osteoporosis

A

Postmenopausal

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16
Q

What explains Type I osteoporosis?

A

↑ bone resorption due to ↓ estrogen levels

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17
Q

Distal radius fracture

A

Colles

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18
Q

Common fractures of Type I osteoporosis

A

Femoral neck fracture, distal radius (Colles) fracture

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19
Q

Type II osteoporosis

A

Senile Osteoporosis

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20
Q

Who is mainly affected by senile osteoporosis?

A

Affects men and women > 70 years old

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21
Q

Prophylaxis of Type II osteoporosis

A

Regular weight bearing exercise and adequate calcium and vitamin D intake throughout adulthood

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22
Q

Treatment for Type II osteoporosis

A

Biphosphonates, PTH, SERMs (Selective Estrogen Receptor Modulators), rarely calcitonin; denosumab

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23
Q

What is denosumab?

A

Monoclonal antibody against RANKL

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24
Q

Marble bone disease

A

Osteopetrosis

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25
Q

What is Osteopetrosis?

A

Failure of normal bone resorption due to defective osteoclasts

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26
Q

Findings of Osteopetrosis

A

Thickened, dense bones that are prone to fracture

Bone fills marrow space

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27
Q

What happens when bone fills marrow space in Osteopetrosis?

A

Pancytopenia, extramedullary hematopoiesis

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28
Q

What mutations could cause osteopetrosis?

A

Carbonic anhydrase II mutation

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29
Q

Cause of Osteopetrosis

A

Mutations impair of osteoclast to generate acidic envirmental necessary for bone resorption

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30
Q

What do X ray show in Osteopetrosis?

A

Bone in bone apperance

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31
Q

What could be a complication of Osteopetrosis?

A

Can result in cranial nerve impingment and palsies as a result of narrowed foramina

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32
Q

What is the treatment for Osteopetrosis?

A

Bone marrow transplant is potentially curative as osteoclasts are derived from monocytes

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33
Q

Disease caused by Vitamin D deficiency

A

Osteomalacia/ rickets

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34
Q

Vitamin D deficiency in adults

A

Osteomalacia

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35
Q

Vitamin D deficiency in children

A

Rickets

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36
Q

Pathophysiology of Osteomalacia/ rickets

A

↓ Vitamin D → ↓ serum calcium → ↑ PTH secretion → ↓ serum PO4 3-

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37
Q

What is the effect of Osteomalacia/ rickets

A

Due to defective mineralization/ calcification of osteoid → soft bones that bow out

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38
Q

How are osteoclast affected in Osteomalacia/ rickets?

A

Hyperactivity of osteoblasts → ↑ ALP (osteoblasts require alkaline enviroment)

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39
Q

Osteitis Deformans

A

Paget disease of bone

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40
Q

Explanation of Paget disease of bone

A

Caused by ↑ activity in both osteoblastic and osteoclatic activity

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41
Q

Characteristics of Paget disease of bone

A

Common, localized disorder of bone remodeling

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42
Q

How are Ca2+, phosphorus and PTH in Osteitis deformans?

A

Normal

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43
Q

Which lab is abnormal in Paget disease?

A

↑ ALP

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44
Q

Microscopic findings of Osteitis deformans

A

Mosaic pattern of woven and lamellar bone

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45
Q

Fractures seen in Paget disease

A

Long bone chlak stick fractures

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46
Q

Another characteristic of Paget disease of bone

A

↑ blood flow from ↑ arteriovenous shunts

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47
Q

What could be the result of ↑ blood flow from ↑ arteriovenous shunts in Osteitis deformas?

A

May cause high output heart failure

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48
Q

What risk is increased with Paget disease of bone?

A

Osteogenic sarcoma

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49
Q

X ray findings of Paget disease

A

Hat size can be increased

Marked thickening of calvarium

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50
Q

Sensorial loss that could be seen in Paget disease

A

Hearing loss is common due to auditory foramen narrowing

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51
Q

Stages of Paget disease

A

Lytic
Mixed
Sclerotic
Quiescent

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52
Q

Who carries Lytic phase in Osteitis deformans?

A

Osteoclasts

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53
Q

Cells responsables of Mixed phase of Paget diease

A

Osteoclasts and Osteoblasts

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54
Q

This Osteitis deformans phase is carried by Osteoblasts alone

A

Sclerotic

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55
Q

How are cells affected in Quiescent phase of Paget diease?

A

Minimal osteoclast/ osteoblast activity

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56
Q

Alternative name for Avascular necrosis

A

Osteonecrosis

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57
Q

What happens in avascular necrosis?

A

Infarction of bone and marrow

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58
Q

Symptoms of avascular necrosis

A

Usually very painful

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59
Q

Causes of Avascular necrosis

A

Trauma, high dose corticosteroids, alcoholism, sickle cell

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60
Q

Most common site of Osteonecrosis

A

Femoral head

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61
Q

Why does avascular necrosis is common in femoral head?

A

Due to inssuficiency of medial circumflex artery

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62
Q

What is the main problem of osteoporosis?

A

↓ Bone mass

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63
Q

Characterized by dense, brittle bones

A

Osteopetrosis

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64
Q

When is Ca2+ ↓ in Osteopetrosis?

A

In severe, malignant disease

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65
Q

Which lab alteration is seen in Paget disease?

A

↑ ALP

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66
Q

Abnormal “mosaic” bone architecture

A

Paget disease

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67
Q

Lab characterisitics of Osteomalacia/ rickests

A

↓ Serum CA2+
↓ PO4 3-
↑ ALP
↑ PTH

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68
Q

How are the bones in Osteomalacia/ rickests

A

Soft bones

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69
Q

When you see Serum ↑ CA2+, ↑ PO4 3-, Normal ALP, ↓ PTH. you suspect of….

A

Hypervitaminosis D

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70
Q

Causes of Hypervitaminosis D

A

By over supplementation or granulomatous disease (sarcoidosis)

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71
Q

How is Osteitis Fibrosa Cystica classified?

A

1º Hyperparathyroidism

2º Hyperparathyroidism

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72
Q

“Brown tumors” of bone

A

Osteitis Fibrosa cystica

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73
Q

Why does Osteitis Fibrosa cystica present as “Brown tumors” of bone?

A

Due to fibrous replacement of bone, subperiostal thining

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74
Q

↑Serum CA2+
↓ PO4 3-
↑ ALP
↑ PTH

A

1º Hyperparathyroidism

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75
Q

↓ Serum CA2+
↑ PO4 3-
↑ ALP
↑ PTH

A

2º Hyperparathyroidism

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76
Q

Cause of 1º Hyperparathyroidism

A

Idiopathic or parathyroid hyperplasia, adenoma, carcinoma

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77
Q

When is 2º Hyperparathyroidism seen?

A

Often as compensation for End Stage Renal Disease (ESRD) (↓ PO4 3- excretion and production of activated vitamin D)

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78
Q

Why End Stage Renal Disease (ESRD) causes 2º Hyperparathyroidism?

A

↓ PO4 3- excretion and production of activated vitamin D

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79
Q

Primary Benign bone tumors

A

Giant cell tumor

Osteochondroma

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80
Q

Age of apperance of Giant cell tumor of bones

A

20-40 years old

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81
Q

Where is commonly seen Giant cell tumor of bones?

A

Epiphyseal end of long bones

Often around knee

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82
Q

How is Giant cell tumor of bones consider?

A

Locally agressive benign tumor

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83
Q

Apearance on X ray of “Soap bubble”

A

Giant cell tumor

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84
Q

Hystology of Giant cell tumor of bone

A

Multinucleated giant cells

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85
Q

Bening bone tumor that causes Exostosis

A

Osteochondroma

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86
Q

What is exostosis?

A

Is the formation of new bone on the surface of a bone, because of excess calcium forming

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87
Q

Characteristic of Osteochondroma

A

Mature bone with cartilaginous cap

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88
Q

How often Osteochondroma progresses to Chondrosarcoma?

A

Rarely

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89
Q

Primary Malignant tumors of Bone

A

Osteosarcoma
Ewing sarcoma
Chondrosarcoma

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90
Q

Second most common primary malingnant bone tumor

A

Osteosarcoma

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91
Q

Most common primary malingnant bone tumor

A

Multiple myeloma

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92
Q

Alternative name for Osteosarcoma

A

Osteogenic Sarcoma

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93
Q

Predisposing factors to Osteosarcoma

A

Paget disease of bone, bone infarcts, radiation, familial retinoblastoma, Li Fraumeni syndrome

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94
Q

Which form of Li Fraumeni syndrome predisposes to Osteosarcoma?

A

Germline P53 mutation

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95
Q

Where is the common site of apperance of Osteosarcoma?

A

Metaphysis of long bones, often around knee

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96
Q

Codman triangle is seen on X ray on this pathology of bone

A

Osteosarcoma

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97
Q

How is Codman triangle formed?

A

From elevation of periostum

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98
Q

Which X ray pattern can Osteosarcoma present?

A

Codman triangle or sunburst pattern

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99
Q

How is Osteosarcoma consider?

A

Aggressive

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100
Q

How is Osteosarcoma treated?

A

With surgical en bloc resection (with limb salvage) and chemotherapy

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101
Q

How are lesion seen on X ray in Osteosarcoma?

A

Lucent lesion

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102
Q

What is seen in Osteosarcoma on MRI?

A

Heterogeneous mass with periosteal elevation

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103
Q

Who commonly present Ewing sarcoma?

A

Boys

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104
Q

Where does Ewing sarcoma commonly appear?

A

In diaphysis of long bones, pelvis, scapula, and ribs

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105
Q

Hystology of Ewing sarcoma

A

Anaplastic small blue cell malignant tumor

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106
Q

How is Ewing sarcoma consider?

A

Extremely aggressive with early metastases

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107
Q

Which is the good point of Ewing sarcoma?

A

Responsive to chemotherapy

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108
Q

How is the Ewing sarcoma apperance on bone?

A

“Onion Skin”

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109
Q

Which gene translocation is associated to Ewing sarcoma?

A

t (11;22) translocation

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110
Q

How common is Chondrosarcoma seen?

A

Rare

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111
Q

How is Chondrosarcoma consider?

A

Malignant, cartilaginous tumor

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112
Q

Who are at higher risk to present Chondrosarcoma?

A

Men 30-60 years old

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113
Q

Where is Chondrosarcoma often located?

A

Pelvis, spine, scapula, humerus, tibia, or femur

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114
Q

How can Chondrosarcoma appears?

A

May be of primary origin or from osteochondroma

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115
Q

Evolution of Chondrosarcoma

A

Expansile glistening mass within the medullary cavity

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116
Q

Etiology of Osteoarthritis

A

Mechanical-joint wear and tear destroys articular cartilage

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117
Q

Joint findings of Osteoarthritis

A

Subchondral cysts, sclerosis, osteophytes (bone spurs), eburnation, Herbenden nodes, and Bouchard nodes

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118
Q

What are Herbenden nodes?

A

Are hard or bony swellings that can develop in the distal interphalangeal joints (DIP)

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119
Q

What are Bouchard nodes?

A

Bouchard’s nodes are hard, bony outgrowths or gelatinous cysts on the proximal interphalangeal joints

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120
Q

Does Osteoarthritis presents with metacarpophalangeal (MCP) joints involvement?

A

No

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121
Q

Predisposing factors for Osteoarthritis

A

Age, obesity, joint deformity, trauma

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122
Q

What is Eburnation?

A

A degenerative process of bone commonly found in patients with osteoarthritis or non-union of fractures

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123
Q

Clinical presentation of Osteoarthritis

A

Pain in weight bearing joints after use (eg at the end of the day), improving with rest

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124
Q

How does Knee cartilage loss begins in Osteoarthritis?

A

Medially (“bow legged”) Noninflammatory

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125
Q

Which systemic symptoms are found in Osteoarthritis?

A

None

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126
Q

Treatment for Osteoarthritis

A

NSAIDs, intra-articular glucocorticoids

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127
Q

Etiology of Rheumatoid arthritis

A

Autoimmune- inflammatory destruction of synovial joints

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128
Q

Who mediates inflammatory destruction in Rheumatoid arthritis?

A

By cytokines and type III and type IV hypersensitivity reactions

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129
Q

Joint findings of Rheumatoid arthritis

A

Pannus formation in joints (MCP, PIP), subcutaneous rheumatoid nodules (fibrinoid necrosis), ulnar deviation of fingers, subluxation, Bakers cyst (in poploteal fossa)

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130
Q

Which joint are not included in Rheumatoid arthritis?

A

No DIP involvement (Distal interphalangeal joint)

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131
Q

Predisposing factors for Rheumatoid arthritis

A

Females > males

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132
Q

How many patients of Rheumatoid arthritis present with + rheumatoid factor?

A

80%

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133
Q

Antibodies of Rheumatoid factor

A

Anti- IgG antibody

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134
Q

Which is the most specific marker of Rheumatoid arthritis?

A

Anti-cyclic citrullinated peptide antibody

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135
Q

Which factor is very associated to Rheumatoid arthritis?

A

HLA-DR4

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136
Q

Classical presentation of Rheumatoid arthritis

A

Morning Stiffness lasting > 30 minutes and improving with use, symmetric joint involvement, systemic symptoms

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137
Q

Systemic symptoms of Rheumatoid arthritis

A

Fever, fatigue, pleuritis, pericarditis

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138
Q

Treatment for Rheumatoid arthritis

A

NSAIDs, glucocorticoids, disease modifying agents

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139
Q

Examples of disease modifying agents when treating Rheumatoid arthritis

A

Methotrexate, sulfasalazine, TNF- α inhibitors

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140
Q

Characteristics of a Rheumatoid arthritis joint damage

A

Bone and cartilage erosion
Increased synovial fluid
Pannus formation

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141
Q

Characteristics of a Osteoarthritis joint damage

A 
Thickened capsule
Slight synovial hypertrophy
Osteophyte
Ulcerated cartilage
Sclerotic bone
Joint space narrowing
Subchondral bone cyst
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142
Q

Findings on X ray of the knee on Osteoarthritis

A

Joint space narrowing and sclerosis

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143
Q

Possible hand manifestation of Rheumatoid arthritis

A

Boutonniere deformitis of PIP joints with ulnar deviation

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144
Q

Autoimmune disorder characterized by destruction of exocrine glands

A

Sjogren syndrome

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145
Q

Which glands are mainly affected in Sjogren syndrome?

A

Exocrine (especially lacrimal and salivary)

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146
Q

Who are mainly affected by Sjogren syndrome?

A

Females 40-60 years old

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147
Q

Findings of Sjogren syndrome

A

Xerophthalmia
Xerostomia (Decrease Salivary production)
Bilateral Parotid enlargement

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148
Q

Which antibodies are present in Sjogren syndrome?

A

Antinuclear antibodies: SS-A (anti-RO and/or SS-B (anti-La)

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149
Q

How can Sjogren syndrome be acquired?

A

Can be a primary disorder or a secondary syndrome associated with other autoimmune disorders (eg. rheumatoid arthritis)

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150
Q

Complications of Sjogren syndrome

A

Dental carie, mucosa-associated lymphoid tissue (MALT) lymphoma

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151
Q

How can a MALT lymphoma be pressented in Sjogren syndrome?

A

May present as unilateral parotid enlargement

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152
Q

Explain Xerophthalmia in Sjogren syndrome… which is the risk?

A

Decreased tear production and subsequent corneal damage

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153
Q

What is gout?

A

Acute inflammatory monoarthritis caused by precipitation of monosodium urate crystals in joints

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154
Q

What is associated to gout?

A

Hyperuricemia

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155
Q

What causes hyperuricemia in gout?

A

Underexcretion of uric acid

Overproduction of uric acid

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156
Q

Percentage of undersecretion of uric acid causing hyperuricemia in gout

A

90% of patients

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157
Q

Percentage of Overproduction of uric acid causing hyperuricemia in gout

A

10% of patients

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158
Q

Causes of undersecretion of uric acid causing hyperuricemia in gout

A

Largely idiopathic

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159
Q

What can excacerbates undersecretion of uric acid causing hyperuricemia in gout?

A

By certain medications (eg. thiazide diuretics)

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160
Q

Causes of Overproduction of uric acid causing hyperuricemia in gout

A

Lesch Nyhan syndrome, Phosphoribosyl pyrophosphate (PRPP) excess, ↑ cell turnover, (eg. tumor lysis syndrome), von Gierke disease

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161
Q

Characteristics if crystals in Gout

A

Crystals are needle shapped and - birefrigent

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162
Q

What does - birefrigent crystals means?

A

Yellow under parallel light, blue under perpendicular light

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163
Q

In whom is it more common gout?

A

In males

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164
Q

Symptoms of gout

A

Asymmetric joint distribution. Joint is swollen, red and painful

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165
Q

Classic manifestation of Gout

A

Is painful Metatarsophalangeal Joint of the big toe (podagra)

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166
Q

What is tophus?

A

Localized deposition of crystalline monosodium urate monohydrate in peripheral tissues
Are pathognomonic for the disease gout

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167
Q

Where are Tophus commonly found in Gout paitents?

A

Often on external ear, olecranon bursa, or Achiles tendon

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168
Q

When can an acute attack of gout tends to occur?

A

After a large meal or alcohol consuption

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169
Q

Which is the explanation of Alcohol causing gout?

A

Alcohol metabolites compete for same excretion sites in kidneys as uric acid, causing ↓ uric acid secretion and subsequent buildup in blood

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170
Q

Treatment for Acute Gout

A

NSAIDs (eg. indomethacin), glucocorticoids, colchicine

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171
Q

For Chronic gout, what helps to prevent it?

A

Xanthine oxidase inhibitors

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172
Q

Example of Xanthine oxidase inhibitors for chronic gout

A

eg. Allupirinol, Febuxostat

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173
Q

How are tophi seen in microscope in Gout disease?

A

Aggregates of urate cystals surrounded by inflammation

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174
Q

How is Pseudogout presented?

A

With pain and effusion in a joint

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175
Q

What causes Pseudogout?

A

By deposition of calcium pyrophosphate crystals within the joint space

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176
Q

What is seen in Pseudogout on X ray?

A

Chondrocalcinosis

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177
Q

Characteristics of Crystals seen in Pseudogout

A

Forms Basophilic, rhomboid crystals that are weakly positively birefringent

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178
Q

Which joints are mainly affected in Pseudogout?

A

Large joints (classically the knee)

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179
Q

Who are mainly affected by pseudogout?

A

> 50 years old; both sexes affected equally

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180
Q

Diseases associted to Pseudogout

A

Hemochromatosis, hyperparathyroidism and hypoparathyroidism

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181
Q

Treatment for sudden Gout

A

NSAIDs

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182
Q

In case of Severe attacks of Gout what is recommended?

A

Steroids and Colchicine

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183
Q

Comparing Gout and Pseudogour, what is the difference between their crystals?

A

Gout- Crystals are yellow when parallel to the light

Pseudogout- Crystals are blue when parallel to the light

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184
Q

Common agents that cause Infectious arthritis

A

S. aureus, Streptococcus and Neisseria gonorrhoeae

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185
Q

Charactetristics of Gonococal arthritis

A

Is a STD that presents as migratory arthritis with asymmetric pattern

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186
Q

How is the joint affected by Infectious arhtritis?

A

Swollen, red, and painful

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187
Q

Main Findings of Infectious arthritis

A

STD
Synovitis (eg. knee)
Tenosynovitis (eg. Hand)
Dermatitis (eg Pustules)

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188
Q

Arhritis without rheumatoid factor (no anti IgG antibody)

A

Seronegative spondyloarthropathies

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189
Q

Seronegative spondyloarthropathies

A 
PAIR
Psoriatic arthritis 
Ankylosing spondylitis
Inflammatory bowel disease
Reactive arthritis
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190
Q

Which factor is strong associated to Seronegative spondyloarthropathies?

A

HLA-B27 (gene that codes for HLA MHC class I)

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191
Q

In whom does Seronegative spondyloarthropathies occurs more often?

A

In males

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192
Q

Joint pain and stiffness associated with psoriasis

A

Psoriatic arthritis

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193
Q

Characterisitics of Psoriatic arthritis

A

Asymmetric and patchy involvement

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194
Q

Possible characteristic of fingers in Psoriatic arthritis

A

Dactylitis

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195
Q

What is Dactylitis?

A

“sausage fingers”

196
Q

What is seen on X ray in Dactylitis in Psoriatic arthritis?

A

“pencil in dup” deformity in x ray

197
Q

How many patients with Psoriatic arthritis present Dactylitis?

A

Seen in fewer than 1/3 with psoriasis

198
Q

Chronic Inflammatory disease of spine and sacroiliac joints

A

Ankylosing spondylitis

199
Q

Reuslts of Chronic Inflammatory disease of spine and sacroiliac joints

A

Ankylosis (stiff spine due to fusion of joints), uveitis, and aortic regurgitation

200
Q

X ray characteristic seen in Ankylosing spondylitis

A

Bamboo spine (Vertebral fusion)

201
Q

Inflamatory bowel diseases

A

Crohn disease and Ulcerative colitis

202
Q

Which seronegative disease is also associated to Inflammatory bowel disease?

A

Ankylosing spondylitis or peripheral arthritis

203
Q

Alternative name for Reactive Arthritis

A

Reiter Syndrome

204
Q

Classic Triad of Reiter Syndrome

A

Conjuntivitis and anterior uveitis
Urethritis
Arthritis

205
Q

What do patients with Reactive Arthritis say?

A

“Can’t see, can’t pee, can’t bend my knee”

206
Q

Causes of Reactive Arthritis or Reiter Syndrome

A

Post GI (Shigella, Salmonella, Yersinia, Campylobacter) or Chlamydia infections

207
Q

Classic presentation: Rash, joint pain, and fever

A

Systemic lupus erythematous

208
Q

Classic presentation of Systemic lupus erythematous

A

Rash, joint pain, and fever

209
Q

Who suffer more often Systemic lupus erythematous?

A

In a female of reproductive age and African descent

210
Q

Wart-like vegetations on both sides of valve in Systemic lupus erythematous

A

Libman Sacks endocarditis

211
Q

What are Libman Sacks endocarditis?

A

Wart-like vegetations on both sides of valve in Systemic lupus erythematous

212
Q

Kidney finding in Systemic lupus erythematous

A

Lupus nephritis

213
Q

Which type of hypersensitivity reaction is Lupus nephritis?

A

Type III hypersensitivity reaction

214
Q

Types of Lupus nephritis

A

Nephritic

Nephrotic

215
Q

Characteristic of nephritic Lupus nephritis

A

Diffuse proliferative glomerulonephritis

216
Q

Characteristic of nephrotic Lupus nephritis

A

Membranous glomerulonephritis

217
Q

Main characteristics of Systemic Lupus erythematosus

A 
RASH OR PAIN
Rash 
Arthritis
Soft tissues/serositis
Hemathologic disorders (cytopenias)
Oral/ nasopharyngeal ulcers
Renal disease, Raynaud phenomenom
Photosensitivity / Positive VDRL/RPR
Antinuclear antibodies
Immunosuppressants
Neurologic disorders (eg. seizures, psychosis)
218
Q

Characteristics of Rash in Systemic Lupus erythematosus

A

Malar or discoid

219
Q

Which lab tests are postive in Systemic Lupus erythematosus?

A

VDRL/ RPR

Antinuclear antibodies

220
Q

Common causes of death in Systemic Lupus erythematosus

A

Cardiovascular disease
Infections
Renal disease

221
Q

Which antibodies may be positive for Systemic Lupus erythematosus?

A 
Antinuclear antibodies (ANA)
Anti-dsDNA
Anti-Smith
Antihistone
Anticardiolipin
222
Q

How are ANA consider for Systemic Lupus erythematosus?

A

Sensitive, not specific

223
Q

If Anti- dsDNA are positive in SLE, how does it translates?

A

Specific, poor prognosis (renal disease)

224
Q

How are Anti Smith antibodies are consider for SLE?

A

Specific, not prognostic

225
Q

To whom are Anti Smith antibodies directed to?

A

Against snRNPs

226
Q

When are Antihistones antibodies present in SLE?

A

Sensitive for Drug indiced lupus

227
Q

When are Anticardiolipin antibodies false positive when thinking of SLE?

A

On test for syphilis, prolonged PTT (paradoxycally, increased risk of arteriovenous thromboembolism)

228
Q

What is affected in SLE by immune complex formation?

A

↓ C3, C4 and CH50

229
Q

Why are C3, C4 and CH50 ↓ in SLE?

A

Due to immune complex formation

230
Q

Treatment for SLE

A

NSAIDs, steroids, immunosupressants, hydroxychloroquine

231
Q

Characterized by immune mediated, widespread noncaseating granulomas and Elevated ACE levels

A

Sarcoidosis

232
Q

What is Sarcoidosis?

A

Characterized by immune mediated, widespread noncaseating granulomas and Elevated ACE levels

233
Q

In whom is Sarcoidosis more common?

A

In black females

234
Q

Clinical findings of Sarcoidosis

A

Often asymptomatic except for enlarged lymph nodes

235
Q

On incidental CXR you find bilateral hilar adenophaty and/or reticular reticular opacities, and the patient is asymptommatic, what do you suspect of?

A

Sarcoidosis

236
Q

What are the CXR possible findings on Sarcoidosis?

A

Bilateral hilar adenophaty and/or reticular reticular opacities

237
Q

What is associated to Sarcoidosis?

A

With restrictive Lung disease (interstitial fibrosis), erythema nodosum, lupus pernio, Bell palsy, uveitis

238
Q

Possible Microscopic findings in Sarcoidosis

A

Epithelioid granulomas containing microscopic Schaumann and asteroid bodies

239
Q

Lab findings in Sarcoidosis

A

Hypercalcemia

240
Q

Why is Hypercalcemia present in Sarcoidosis?

A

Due to ↑ α hydroxylase- mediated vitamin D activation in macrophages

241
Q

Treatment for Sarcoidosis

A

Steroids

242
Q

Which are the clinical findings of Polymyalgia rheumatica?

A

Pain and stiffness in shoulders and hips, often with fever, malaise and weight loss

243
Q

How is the muscular weakness in Polymyalgia rheumatica?

A

Does not cause muscular weakness

244
Q

In whom is it more common seen Polymyalgia rheumatica?

A

In women > 50 years old

245
Q

What patholgy is associated to Polymyalgia rheumatica?

A

Temporal (giant cell) arteritis

246
Q

Whcih labs may be present in Polymyalgia rheumatica?

A

↑ ESR, ↑ C- reactive protein, normal CK

247
Q

Which is the treatment for Polymyalgia rheumatica?

A

Rapid response to low dose corticosteroids

248
Q

In which patients is more often seen Fibromyalgia?

A

Most commonly seen in females 20-50 years old

249
Q

Chronic, widespread musculoskeletal pain associated with stiffness, paresthesias, poor selep and fatigue

A

Fibromyalgia

250
Q

Main findings in Fibromyalgia

A

Chronic, widespread musculoskeletal pain associated with stiffness, paresthesias, poor selep and fatigue

251
Q

Which is the treatment for Fibromyalgia?

A

Treat with regular exercise, antidepressants (TCAs, SNRIs), and anticonvulsants

252
Q

Progressive symmetric proximal muscle weakness, characterized by endomysial inflammation

A

Polymyositis

253
Q

What is Polymyositis?

A

Progressive symmetric proximal muscle weakness, characterized by endomysial inflammation

254
Q

What kind of inflammation is present in Polymyositis?

A

Endomysial inflammation with CD8+ Tcells

255
Q

What is most often involved in Polymyositis?

A

Shoulders

256
Q

Clinical findings of Dermatomyositis

A

Similar to polymyositis, but also involves malar rash, Gottron papules, heliotrope rash, “shawl and face” rash, “mechanics hands”

257
Q

What is heliotrope rash?

A

Erythematous periorbital

258
Q

What risk is increased in patients with Dermatomyositis?

A

Occult malignancy

259
Q

Type of inflammation seen in Dermatomyositis

A

Perimysial inflammation and atrophy with CD4+ T cells

260
Q

LAb findings on Polymyositis and Dermatomyositis

A

↑ CK, + ANA, + anti Jo- 1, + anti SRP, + anti-Mi antibodies

261
Q

Treatment for Polymyositis and Dermatomyositis

A

Steroids

262
Q

Neuromuscular junction disease

A

Myasthenia gravis

Lambert Eaton myasthenic syndrome

263
Q

Most common Neuromuscular junction disorder

A

Myasthenia gravis

264
Q

Uncommon Neuromuscular junction

A

Lambert Eaton myasthenic syndrome

265
Q

Which kind of antibodies are present in Myasthenia gravis?

A

Autoantibodies to postsynaptic ACh receptor

266
Q

Which kind of antibodies are present in Lambert Eaton myasthenic syndrome?

A

Autoantibodies to presynaptic Ca2+ channel → ↓ ACh release

267
Q

This disease is manifested with Ptosis, diplopia and weakness

A

Myasthenia gravis

268
Q

How do symptoms worsen in Myasthenia gravis?

A

With muscle use

269
Q

Clinical symptoms on Myasthenia gravis

A

Ptosis, diplopia, and weakness

270
Q

Pathologies associated to Myasthenia gravis

A

Thymoma, thymic hyperplasia

271
Q

Which is the treatment for Myasthenia gravis?

A

AChE inhibitor

272
Q

What is the benefit of AChE inhibitors drug for Myasthenia gravis?

A

Reversal of symptoms

273
Q

Presented with proximal muscle weakness, autonomic symptoms (dry mouth, impotence)

A

Lambert Eaton myasthenic syndrome

274
Q

How do symptoms improve in Lambert Eaton myasthenic syndrome?

A

Improve with muscle use

275
Q

Clinical presentation of Lambert Eaton myasthenic syndrome

A

Presented with proximal muscle weakness, autonomic symptoms (dry mouth, impotence)

276
Q

How is the benefit of AChE inhibitors when used for Lambert Eaton myasthenic syndrome?

A

Minimal effect

277
Q

Pathology associated to Lambert Eaton myasthenic syndrome

A

Small cell lung cancer

278
Q

Metaplasia of skeletal muscle to bone following muscular trauma

A

Myositis ossificans

279
Q

What is Myositis ossificans?

A

Metaplasia of skeletal muscle to bone following muscular trauma

280
Q

Where is Myositis ossificans more often seen?

A

In upper or lower extremity

281
Q

How is Myositis ossificans may be presented on radiography?

A

May present as suspicious “mass” at site of known trauma or as incidental finding on radiography

282
Q

Excessive fibrosis and collagen deposition throughout the body

A

Scleroderma

283
Q

What is Scleroderma?

A

Systemic sclerosis

284
Q

Dermatologic findings in Scleroderma

A

Sclerosis of skin, manifestating as puffy and taunt skin with absence of wrinkles

285
Q

Most common cause of death in Scleroderma

A

Sclerosis of Pulmonary system

286
Q

Other possible findings of Scleroderma

A

Sclerosis of renal, pulmonary, cardiovascular and GI system

287
Q

Who are mainly affected by Scleroderma?

A

75% female

288
Q

2 major types of Scleroderma

A

Diffuse scleroderma

Limited scleroderma

289
Q

Characteristics of Diffuse scleroderma

A

Widespread skin involvement, rapid proggression, early visceral involvement

290
Q

Which antibodies may be present in Diffuse scleroderma?

A

Anti Scl-70 antibody

291
Q

What kind of antibody are Anti Scl-70 antibody?

A

Anti-DNA topoisomerase I antibody

292
Q

What is the limited scleroderma?

A

Limited skin involvement confined to fingers and face

293
Q

Which Scleroderma is related to CREST syndrome?

A

Limited scleroderma

294
Q

What is CREST syndrome?

A 
Calcinosis
Raynaud phenomenom
Esophageal dysmotility
Scletodactyly
Telangiectasia
295
Q

Which antibodies are associated to CREST syndrome?

A

antiCentromere antibody

296
Q

Dermatologic lesions

A 
Macule
Patch
Papule
Plaque 
Vesicle 
Bulla
Pustule
Wheal
Scale
Crust
297
Q

Flat lesion with well-circumscribed change in skin color

A

Macule

298
Q

Macule >1 cm

A

Patch

299
Q

What is a papule?

A

Elevated solid skin lesion

300
Q

Papule >1cm

A

Plaque

301
Q

Small fluid containing blister

A

Vesicle

302
Q

What is Bulla?

A

Large fluid containing blister > 1 cm

303
Q

Vesicle containing pus

A

Pustula

304
Q

What is wheal?

A

Transient smooth papule or plaque

305
Q

Flaking off of stratum corneum

A

Scale

306
Q

What is Crust?

A

Dry exudate

307
Q

When are macule seen?

A

Frecle, labial macule

308
Q

When is Patch seen?

A

Large birhtmark (congenital nevus)

309
Q

Skin lesion acne

A

Papule

310
Q

Types of diseases presented with papule

A

Mole (nevus), acne

311
Q

Type of skin lesion of Psoriasis

A

Plaque

312
Q

When are vesicles seen?

A

Chicken pox (Varicella), shingles (Zoster)

313
Q

When is Bulla seen?

A

Bullous pemphigoid

314
Q

Pathology associtated to Pustule

A

Pustular psoriasis

315
Q

Skin lesion of Hives (urticaria)

A

Wheal

316
Q

Patholgies with Scale

A

Eczema, psoriasis, Squamous Cell Carcinoma

317
Q

Skin lesion associated to Impetigo

A

Crust

318
Q

What is Hyperkeratosis?

A

↑ thickness of stratum corneum

319
Q

Examples of situations with Hyperkeratosis

A

Psoriasis, calluses

320
Q

Hyperkeratosis with retention of nuclei in stratum corneum

A

Parakeratosis

321
Q

Which pathology includes Parakeratosis?

A

Psoriasis

322
Q

What is Spongiosis?

A

Epidermal accumulation of edematous fluid in intercellular spaces

323
Q

Example of disease that has spongiosis?

A

Eczematous dermatitis

324
Q

Separation of epidermal cells

A

Acantholysis

325
Q

Which pathology presents with acantholysis?

A

Pemphigus vulgaris

326
Q

What is Acanthosis?

A

Epidermal hyperplasia (↑ spinosum)

327
Q

Pathology with Acancthosis

A

Acanthosis nigricans

328
Q

Pigmented skin disorders

A

Albinism
Melasma (chloasma)
Vitiligo

329
Q

What is the problem in albinism?

A

Normal melanocyte number with ↓ Melanin production

330
Q

What causes ↓ Melanin production in Albinism?

A

Due to ↓ Tyrosinase activity or defective tyrosine transport

331
Q

What is another cause of Albinism?

A

By failure of neural crest cell migration during development

332
Q

What risk is increased for Albinism?

A

Skin cancer

333
Q

Hyperpigmentation associated with pregnancy (“mask of pregnancy”)

A

Melasma (chloasma)

334
Q

Situations associated to Melasma

A

Pregnancy or OCP use

335
Q

Clinical characteristics of Vitiligo

A

Irregular areas of complete depigmentation

336
Q

Cause of Vitiligo

A

By autoimmune detruction of melanocytes

337
Q

Pathologies with Verrucae

A 
Warts
Epidermal hyperplasia
Hyperkeratosis
Koilocytosis
Condyloma acuminatum
338
Q

Who causes warts?

A

By HPV

339
Q

Characteristics of Warts

A

Soft, tan-colored, cauliflower like papules

340
Q

Verrucae on Genitals

A

Condyloma acumunatum

341
Q

Common mole

A

Melanocytic nevus

342
Q

How is Melanocytic nevus consider?

A

Benign, but melanoma can arise in congenital or atypical moles

343
Q

Skin lesion of intradermal nevi

A

Papula

344
Q

Skin lesion of Junctional nevi

A

Flat macules

345
Q

Alternative name for Urticaria

A

Hives

346
Q

Skin lesion in Urticaria

A

Pruritic wheals

347
Q

When are wheals form in Hives?

A

After mast cell degranulation

348
Q

Characteristics of Urticaria

A

Superficial dermal edema and lymphatic channel dilation

349
Q

Alternative name for Freckles

A

Ephelis

350
Q

What is the main point of Freckles?

A

Normal number of melanocytes, ↑ melanin pigmentation

351
Q

Alternative name for Eczema

A

Atopic Dermatitis

352
Q

How is Eczema consider?

A

Pruritic eruption

353
Q

Wheres in Atopic Dermatitis commonly found?

A

On skin flexures

354
Q

Wat else is associated to Atopic Dermatitis?

A

With other atopic diseases (asthma, allergic rhinitis)

355
Q

How is the usual evolution of Atopic Dermatitis?

A

Ussually starts on the face in infancy and often appears in the antecubital fossae thereafter

356
Q

Hypersensitivity reaction in Allergic contact dermatitis

A

Type IV hypersensitivity reaction that follows exposure to allergen

357
Q

Sites where Allergic contact dermatitis occurs

A

At site of contact

358
Q

Common causes of Allergic contact dermatitis

A

Nickel, poison ivy, neomycin

359
Q

Skin lesions characteristics on Psoriasis

A

Papules and plaques with silver scaling

360
Q

Where does Psoriasis often occur?

A

Especially on knees and elbows

361
Q

Hystologicy characteristics in Psoriasis

A

Acanthosis with parakeratosis scaling

↑ stratum spinosum, ↓ stratum granulosum

362
Q

What is parakeratosis?

A

Nuclei still in stratum corneum

363
Q

Which sign is present in Psoriasis?

A

Auspitz sign

364
Q

What is Auspitz sign?

A

Pinpoint bleeding spots from exposure of dermal papillae when scales are scraped off

365
Q

What is associated to Psoriasis?

A

Nail pitting and Psoriatic Arhtitis

366
Q

Skin lesions seen in Seborrheic keratosis

A

Flat, greasy

367
Q

Hystological characteristics of Seborrheic keratosis

A

Pigmented squamous epithelial proliferation with keratin filled cysts (horn cyst)

368
Q

Looks of Seborrheic keratosis

A

“Stuck on”

369
Q

Where do lesions of Seborrheic keratosis occur?

A

On head, trunk, and extremities

370
Q

Common benign neoplasm of older people

A

Seborrheic keratosis

371
Q

Which sign is possible in Seborrheic keratosis?

A

Leser Trelat sign

372
Q

What is Leser Trelat sign?

A

Sudden apperance of Multiple seborrheic keratoses

373
Q

What does Leser Trelat sign in Seborrheic keratosis indicate?

A

An underlying malignancy (eg. GI, lymphoid)

374
Q

Infectious skin disorders

A

Impetigo
Cellulitis
Necrotizing fasciitis
Staphylococcal scalded skin syndrome

375
Q

How is impetigo consider?

A

A very superficial skin infection

376
Q

Who are the main organisms that cause impetigo?

A

S. aureus or S.pyogenes

377
Q

How contagious is Impetigo?

A

Highly contagious

378
Q

Apperance of Impetigo

A

Honey colored crusting

379
Q

Variant of impetigo

A

Bullous impetigo

380
Q

Who causes bullous impetigo?

A

S. aureus

381
Q

Acute, painful, spreading infection of dermis and subcutaneous tissues

A

Cellulitis

382
Q

Clinical presentation of Cellulitis

A

Acute, painful

383
Q

Skin layers affected by cellulitis

A

Spreading infection Dermis and subcutaneous tissues

384
Q

Main bacterias that cause Cellulitis

A

S. aureus

S. pyogenes

385
Q

How does Cellulitis often starts?

A

With a break in skin from trauma or another infection

386
Q

What is Necrotizing fasciitis?

A

Deeper tissue injury, usually from anaerobic bacteria or S. pyogenes

387
Q

Main agents that cuase Necrotizing fasciitis

A

Usually from anaerobic bacteria or S. pyogenes

388
Q

Clinical finding in Necrotizing fasciitis

A

Results in crepitus

389
Q

What explains Crepitus in Necrotizing fasciitis?

A

Methane and CO2 production

390
Q

How are the bacterias of Necrotizing fasciitis consider?

A

As “Flesh eating bacterias”

391
Q

What does Necrotizing fasciitis causes?

A

Bullae and a purple color to the skin

392
Q

Pathophysiology of Staphylococcal scalded skin syndrome

A

Exotoxin destroys keratinocyte attachments in the stratum granulosum only

393
Q

What is the differecne between Staphylococcal scalded skin syndrome vs Toxic epidermal necrolysis?

A

Toxic epidermal necrolysis, destroys the epidermal junction

394
Q

Characterized by fever and generalized erythematous rash with sloughing of the upper layers of the epidermis that heals completely

A

Staphylococcal scalded skin syndrome

395
Q

Findings of Staphylococcal scalded skin syndrome

A

Characterized by fever and generalized erythematous rash with sloughing of the upper layers of the epidermis that heals completely

396
Q

Group of age when Staphylococcal scalded skin syndrome appears

A

Newborns and children

397
Q

White, painless plaques on the tongue that cannot be scraped off

A

Hairy leukoplakia

398
Q

Causant agent of Hairy leukoplakia

A

EBV

399
Q

In which patients is hairy leukoplakia seen?

A

HIV positive patients

400
Q

Blistering skin disorders

A 
Pemphigus vulgaris
Bollous pemphigoid
Dermatits herpetiformis
Erythema multiforme
Stevens Johnson syndrome
401
Q

How is Pemphigoid vulgaris consider?

A

Potentially fatal autoimmune disorder

402
Q

What is the cause of Pemphigoid vulgaris?

A

Autoimmune disorder with IgG antibody against desmoglein

403
Q

What is desmoglein?

A

Component of desmosomes

404
Q

Findings of Pemphigoid vulgaris

A

Flacid intraepidermal bullae

405
Q

What causes Flacid intraepidermal bullae in Pemphigoid vulgaris?

A

By acantholysis

406
Q

How are keratinocytes in stratum spinosum connected?

A

By desmosomes

407
Q

Which study helps to make the diangosis of Pemphigoid vulgaris? What do we see?

A

Immunofluorescence reveals antibodies around epidermal cells in a reticular (net-like pattern)

408
Q

Structure involved in Pemphigoid vulgaris, other than skin?

A

Oral mucosa

409
Q

Sign present in Pemphigoid vulgaris

A

Nikolsky sign

410
Q

What is Nikolsky sign?

A

Separation of epidermis upon manual stroking of skin

411
Q

Between Pemphigoid vulgaris and Bullous pemphigoid, which is less severe?

A

Bullous pemphigoid

412
Q

What is the problem in Bullous pemphigoid?

A

Involves IgG antibody against hemidesmosomes

413
Q

Skin layer affected in Bullous pemphigoid

A

Epidermal basement membrane

414
Q

Clinical findings on Bullous pemphigoid

A

Tense blisters containing eosinophils

415
Q

Does Bullous pemphigoid affect oral mucosa?

A

No

416
Q

Study for Bullous pemphigoid…. and what does it shows?

A

Immunofluorescence reveals linear pattern at epidermal dermal junction

417
Q

How is Nikolsky sign in Bullous pemphigoid?

A

Negative

418
Q

Skin lesion of Dermatitis herpetifomis

A

Pruritic papules, vesicles and bullae

419
Q

Where is Dermatitis herpetifomis often seen?

A

Elbows

420
Q

Deposits of IgA at the tips of demal papillae

A

Dermatitis herpetiformis

421
Q

What is the probleme Dermatitis herpetifomis?

A

Deposits of IgA at the tips of demal papillae

422
Q

Which pathology is associated to Dermatitis herpetifomis?

A

Celiac disease

423
Q

What is associated to Erythema multiforme?

A

Infections, drugs, cancers, and autoimmune disease

424
Q

Infections associated to erythema multiforme

A

Mycoplasma pneumoniae, HSV

425
Q

Drugs associated to erythema multiforme

A

Sulfa drugs, β lactams, phenytoin

426
Q

Types of lesions on Erythema multiforme

A

Macules, papules, vesicles and target lesions

427
Q

Characteristics of target lesions in Erythema multiforme

A

Looks like targets with multiple rings and a dusky center showin epithelial disruption

428
Q

Skin disease with target lesions

A

Erythema Multiforme

429
Q

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

A

Stevens Johnson syndrome

430
Q

Lesions seen in Stevens Johnson syndrome

A

Typically 2 mucous membranes are involced and skin lesions may appear like targets as seen in erythema multiforme

431
Q

Which is the main event associated to Stevens Johnson syndrome?

A

Adverse drug reaction

432
Q

More severe form of Stevens Johnson syndrome

A

Toxic epidermal Necrolysis

433
Q

When is Stevens Johnson syndrome categorized as Toxic epidermal Necrolysis

A

With > 30 % of the body surface area involved

434
Q

Miscellaneous skin disorders

A 
Acanthosis nigricans
Actinic keratosis
Erythema nodosum
Lichen planus
Pityriasis rosea
Sunburn
435
Q

Epidermal hyperplasia causing symmetrical, hyperpigmented, velvety thickening of skin

A

Acanthosis nigricans

436
Q

Where dos acanthosis nigricans especially occurs?

A

On neck or in axilla

437
Q

Situations associated to Acanthosis nigricans

A

With hyperinsulinemia (eg. diabetes, obesity, Cushing syndrome) and visceral malignancy (eg. gastric adenocarcinoma)

438
Q

How is Actinic keratosis consider?

A

Premalignant lesions

439
Q

What causes Actinic Keratosis?

A

caused by sun exposure

440
Q

Skin lesions of Actinic Keratosis

A

Small, rough, erythematous or browinish papules or plaques

441
Q

What risk is increased with Actinic Keratosis?

A

Squamous cell carcinoma is proportional to degree of epithelial dysplasia

442
Q

Painful inflammatory lesions of subcutanoeus fat

A

Erythema nodosum

443
Q

Where is Erythema nodosum commonoly found?

A

Usually on anterior shins

444
Q

Causes of Erythema nodosum

A

Often idiopathic, but can be associated to sarcoidosis, coccidioidomycosis, histoplamosis, TB, streptococcal infections, leprosy, and Crohn disease

445
Q

Clinical manifestation of Lichen Planus

A 
6 Ps of Lichen Planus
Pruritic
Purple
Polygonal Planar Papules
Plaques
446
Q

How does mucosal involvement is manifested in Lichen Planus?

A

Manifests as Wickham striae

447
Q

What are Wickham striae?

A

Reticular white lines

448
Q

Microscopic findings in Lichen Planus

A

Sawtooth infiltrate of lymphocytes at dermal epidermal junction

449
Q

Pathology associated with Lichen Planus

A

Hepatitis C

450
Q

Lesions evolution in Pityriasis rosea

A

“Herald path” followed days later by “Christmas tree”

451
Q

Types of dermal lesions in Pityriasis rosea

A

Multiple plaques with collarette scale

452
Q

Treatment for Pityriasis rosea

A

Self resolving in 6-8 weeks

453
Q

What is a Sunburn?

A

Acute cutaneous inflammatory reaction due to excessive UV irradiation

454
Q

Cellulary what are the effects of Sunburn?

A

Causes DNA mutations, indicing apoptosis of keratinocytes

455
Q

Which UV rays are dominant in tanning and photoaging?

A

UVA

456
Q

Which UV rays are seen in sunburns?

A

UVB

457
Q

Skin pathologies that sunburns can lead to…

A

Can lead to impetigo and skin cancer (basal cell carcinoma, squamous cell carcinoma, and melanoma)

458
Q

Skin cancers

A

basal cell carcinoma
squamous cell carcinoma
melanoma

459
Q

Most common skin cancer

A

Basal cell carcinoma

460
Q

Where is basal cell carcinoma found?

A

In sun exposed areas

461
Q

Prognosis of Basal cell carcinoma

A

Locally invasive, but almost never metastasizes

462
Q

Skin lesions foun in basal cell carcinoma

A

Pink, pearly nodules, commonly with telangiectasia, rolled bordersand central crusting or ulceration
Or scaling plaque

463
Q

When ypu see a nonhealing ulcers with infiltrating growth, you should suspect of…

A

Basal cell carcinoma

464
Q

Histology characteristics pf Basal cell carcinoma

A

Basal cell tumors have “Palisading” nuclei

Revelas nest of basaloid cells in dermis

465
Q

Second most common skin cances

A

Squamous cell carcinoma

466
Q

Factors associated to Squamous cell carcinoma

A

Excessive sexposure to sunlight, immunosuppression, and ocasionally arsenic exposure

467
Q

Common sites of Squamous cell carcinoma aperance

A

On face, lower lip, ears and hands

468
Q

How is squamous cell carcinoma consider?

A

Locally invasive, but may spread to lymph nodesand will rarely metastasize

469
Q

Clinical findings in Squamous cell carcinoma

A

Ulcerative red lesions with frequent scale

470
Q

What is associated to Squamous cell carcinoma?

A

Chronic draining sinuses

471
Q

Histopathology of Squamous cell carcinoma

A

Keratin pearls

472
Q

Precursor to squamous cell carcinoma

A

Actinic keratosis

473
Q

Clinical aperancer of Actinic keratosis

A

A scaly plaque

474
Q

Variant of Squamous cell carcinoma that grows rapidly (4-6 weeks) and may regress spontaneously over months

A

Keratoacanthoma

475
Q

Common skin tumor with significant risk of metastasis

A

Melanoma

476
Q

Which is the tumor marker seen in Melanoma?

A

S-100 tumor marker

477
Q

Who have higher risk of Melanoma?

A

Fair skin persons

478
Q

What is associated to Melanoma apperance?

A

With sunlight exposure

479
Q

What factor correlates with risk of Metastasis of Melanoma?

A

Depth of tumor

480
Q

Characteristics of Melanoma

A 
ABCDE
Asymmetry
Border irregularity
Color variation
Diameter > 6 mm 
Evolution over time
481
Q

4 types of Melanoma

A

Superficial spreading melanoma
Nodular melanoma
Lentigo maligna melanoma
Acrolentiginous melanoma

482
Q

Gene activated in Melanoma

A

Often driven by activating mutation in BRAF kinase

483
Q

Primary treatment for Melanoma

A

Is excision with appropriately wide margins

484
Q

Which situations of Melanoma could be treated with medication?

A

Metastatic or unresectable melanoma

485
Q

Which gene seem to be mutated in patients with Metastatic or unresectable melanoma?

A

BRAF V600E mutation

486
Q

Drug used for Metastatic or unresectable melanoma

A

Vemurafenib

487
Q

What is Vemurafenib?

A

BRAF kinase inhibitor

MUSCULOSKELETAL, SKIN, AND CONNECTIVE TISSUE (3 decks)

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