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Fitzpatrick's Dermatology, 9th Edition (Entrance Exam / Board Exam Prep) > 136: Tuberous Sclerosis > Flashcards

136: Tuberous Sclerosis Flashcards

1
Q

What are the common clinical presentations of Tuberous Sclerosis Complex (TSC)?

A

TSC commonly presents with seizures during infancy and is associated with neuropsychiatric disorders (TAND) that affect cognitive, behavioral, and psychiatric functions.

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2
Q

What is the role of TSC1 and TSC2 in Tuberous Sclerosis Complex?

A

TSC1 (Hamartin) and TSC2 (Tuberin) are tumor suppressor genes that inhibit growth signaling through the mTORC1 pathway. Inactivating mutations in these genes lead to increased mTORC1 signaling and cell growth.

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3
Q

What are the cutaneous findings associated with Tuberous Sclerosis Complex?

A

The primary cutaneous finding in TSC is hypomelanotic macules, which are present in over 90% of children at birth or within the first few years of life. These may fade or disappear in adulthood, and detection can be improved with Wood’s lamp or UV light.

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4
Q

What are some worse risk factors associated with Tuberous Sclerosis Complex?

A

Worse risk factors for TSC include: TSC2 subtype, PKD2-TSC deletion leading to polycystic kidney disease, high tuber count and early onset epilepsy, skin manifestations such as angiofibromas and shagreen patches, and UV exposure.

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5
Q

What is the likely neuropsychiatric condition in a TSC patient with seizures and behavioral difficulties?

A

The likely condition is TSC-associated neuropsychiatric disorders (TAND), which affect approximately half of patients with TSC.

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6
Q

What are the risk factors for severe outcomes in a TSC patient with seizures and intellectual impairment?

A

Risk factors for severe outcomes include high tuber count, early-onset epilepsy, and TSC2 subtype.

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7
Q

What gene mutations are associated with Tuberous Sclerosis Complex (TSC)?

A

Mutations in the TSC1 or TSC2 tumor suppressor genes.

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8
Q

What are common clinical presentations of Tuberous Sclerosis Complex during infancy?

A

Seizures are commonly presented during infancy.

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9
Q

What is the transmission pattern of Tuberous Sclerosis Complex?

A

Sporadic cases are more common (2/3) compared to hereditary cases (1/3).

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10
Q

What is the role of the TSC1 and TSC2 genes in cell growth?

A

They form a complex that inhibits growth signaling through the mTORC1 pathway.

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11
Q

What are some skin manifestations associated with Tuberous Sclerosis Complex?

A

Angiofibromas, shagreen patches, and fibrous forehead plaques.

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12
Q

What is the significance of hypomelanotic macules in Tuberous Sclerosis Complex?

A

They are present in over 90% of children with TSC and can be detected using Wood’s lamp or UV light.

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13
Q

What is the clinical significance of TSC-associated neuropsychiatric disorders (TAND)?

A

They involve difficulties related to cognitive, behavioral, and psychiatric disorders.

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14
Q

What are the two types of skin lesions associated with Tuberous Sclerosis Complex (TSC)?

A
  1. Ash-leaf spots: Solitary to multiple, 0.5 to 3.0 cm in diameter, off-white and incompletely depigmented oval macules, commonly seen on the trunk and buttocks; can cause poliosis when located on the scalp.
  2. Confetti skin lesions: Multiple hypopigmented macules, 2-3 mm, typically occurring on the legs below the knees or forearms.
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15
Q

What is the major criterion for diagnosing hypopigmented macules in TSC?

A

> 3 hypopigmented macules measuring > 5 mm in longest dimension.

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16
Q

What percentage of patients with TSC develop facial angiofibromas, and at what age do they typically appear?

A

75-90% of patients develop facial angiofibromas, which typically appear between 2-5 years of age.

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17
Q

Describe the characteristics of facial angiofibromas in TSC.

A

Facial angiofibromas are solitary to multiple, 1-3 mm pink to red papules with a smooth surface occurring on the central face, particularly concentrated on the alar grooves, cheeks, nose, and chin, with relative sparing of the upper lip and lateral face. They may increase in size and number during puberty and tend to be stable in size in adulthood.

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18
Q

What is a fibrous cephalic plaque and its prevalence in TSC patients?

A

A fibrous cephalic plaque is an irregular, soft to firm connective tissue nevus that may be congenital or develop gradually over years, occurring in 40% of patients. It typically develops on the forehead but can also occur on the scalp, cheeks, and face.

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19
Q

What is a shagreen patch and its common locations in TSC patients?

A

A shagreen patch is a 1-10 cm firm or rubbery irregular plaque with coalescing papules and nodules, creating a bumpy or orange skin appearance. It is most commonly seen on the lower back to sacral region, and less commonly on the mid/upper back, buttocks, or thighs.

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20
Q

What are ungual fibromas and their prevalence in adults with TSC?

A

Ungual fibromas, also known as Koenen tumors, are common in 85% of adults with TSC, primarily found on the toes more than the fingers.

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21
Q

What are periungual fibromas and their characteristics?

A

Periungual fibromas are red firm, pointed, hyperkeratotic or soft and round papules/nodules that arise in the proximal nail fold and can press on the nail matrix, causing a longitudinal groove.

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22
Q

What is the typical appearance and diagnostic significance of a Shagreen patch?

A

A Shagreen patch is a firm or rubbery irregular plaque with coalescing papules and nodules, creating a bumpy or orange skin appearance. It is a major diagnostic feature of TSC.

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23
Q

What is the typical location and diagnostic significance of a fibrous cephalic plaque?

A

A fibrous cephalic plaque is typically located on the forehead and is a major diagnostic feature of TSC.

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24
Q

How can hypomelanotic macules be better visualized?

A

Hypomelanotic macules can be better visualized using a Wood’s lamp or UV light.

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25
What are Ash-leaf spots and where are they commonly found?
Ash-leaf spots are solitary to multiple hypomelanotic macules 0.5 to 3.0 cm in diameter, typically found on the trunk and buttocks, and can cause poliosis when located on the scalp.
26
What is the major criterion for diagnosing hypopigmented macules?
> 3 hypopigmented macules measuring > 5mm in longest dimension.
27
At what age do facial angiofibromas typically appear?
Facial angiofibromas appear between 2-5 years of age in 75-90% of patients.
28
What are the characteristics of fibrous cephalic plaques?
Fibrous cephalic plaques are irregular, soft to firm connective tissue nevi that may be congenital or develop gradually, typically found on the forehead.
29
What is a shagreen patch and where is it commonly located?
A shagreen patch is a 1-10 cm firm or rubbery irregular plaque with coalescing papules, commonly seen on the lower back to sacral region.
30
What percentage of adults with TSC have ungual fibromas, and where are they most commonly found?
85% of adults with TSC have ungual fibromas, which are more common on the toes than on the fingers.
31
What are periungual fibromas and what effect do they have on the nail matrix?
Periungual fibromas are red firm, pointed, hyperkeratotic or soft and round papules/nodules that arise in the proximal nail fold and can press on the nail matrix causing a longitudinal groove.
32
What are the major and minor criteria for diagnosing ungual fibromas in Tuberous Sclerosis Complex (TSC)?
Major criterion: > 2 ungual fibromas Minor criterion: Not specified in the text.
33
What is dental pitting and how is it identified in TSC patients?
Dental pitting refers to multiple pits (tiny pinpoint or large crater-like lesions) in the enamel, observed in 100% of TSC patients. Identification is enhanced using a dental plaque stain.
34
What are the characteristics and common sites of intraoral fibromas in TSC patients?
Intraoral fibromas occur in 50% of TSC patients, more commonly in adulthood. The most common site is the gingivae, but they can also appear on the buccal, labial mucosa, hard palate, and tongue. Some patients may experience diffuse gingival overgrowth.
35
What are some non-cutaneous findings associated with Tuberous Sclerosis Complex (TSC)?
Non-cutaneous findings include: Brain: Cortical dysplasia, subependymal nodules, and subependymal giant cell astrocytomas. Seizures: Occur in 80% of patients, often starting in the first 3 years of life, with treatment options including Vigabatrin and epilepsy surgery. TAND: Behavioral, intellectual, and psychosocial difficulties, with a high prevalence of Autism spectrum disorder, ADHD, and anxiety disorders.
36
How can dental pits be identified and what is their diagnostic significance?
Dental pits can be identified using a dental plaque stain. They are a minor diagnostic criterion for TSC if more than three pits are present.
37
What are the alternative treatment options for TSC patients with seizures that are intractable to anticonvulsant therapy?
Alternative treatments include epilepsy surgery, ketogenic diet, vagus nerve stimulation, and mTOR inhibitors.
38
What is the prevalence of autism spectrum disorder and ADHD in TSC?
Nearly half of patients with TSC will have autism spectrum disorder and ADHD.
39
What is the treatment of choice for infantile spasms in TSC?
Vigabatrin is the treatment of choice for infantile spasms.
40
What percentage of TSC patients experience seizures?
Approximately 80% of TSC patients experience seizures.
41
What are some behavioral issues associated with TSC?
Behavioral issues can include Autism spectrum disorder, ADHD, and anxiety disorders.
42
What is pachydermodactyly?
Pachydermodactyly is a benign thickening of the proximal fingers.
43
What are miliary fibromas?
Miliary fibromas are patches of multiple minute papules usually on the neck or trunk that appear like 'goose-flesh'.
44
What is the prevalence of subependymal nodules in individuals with Tuberous Sclerosis Complex (TSC)?
Subependymal nodules are present in 80% of individuals with TSC.
45
What is the common treatment for cardiac rhabdomyomas in TSC patients?
The common treatment for cardiac rhabdomyomas is mTOR inhibitors, which help speed regression.
46
What percentage of TSC patients are affected by angiomyolipomas, and what is the typical treatment approach?
Angiomyolipomas affect 80% of TSC patients. The treatment approach includes selective embolization followed by corticosteroids for acute hemorrhage, and mTOR inhibitors for asymptomatic growing angiomyolipomas.
47
What are the common respiratory complications associated with lymphangioleiomyomatosis (LAM) in TSC?
Common respiratory complications of LAM include spontaneous pneumothorax, cyclothorax, dyspnea, cough, and hemoptysis.
48
What is the most common type of retinal hamartoma found in TSC patients?
The most common type of retinal hamartoma in TSC patients is flat and translucent lesions, while others may be elevated, opaque, or calcified.
49
What are the potential complications of renal lesions in TSC?
Renal lesions in TSC can lead to renal insufficiency, hypertension, and retroperitoneal hemorrhage.
50
What is the risk of developing renal cell carcinoma in TSC patients?
The risk of developing renal cell carcinoma in TSC patients is approximately 2-3%.
51
What are the characteristics of retinal achromic patches in TSC?
Retinal achromic patches in TSC are characterized as hypopigmented patches in the retina.
52
What is the likely diagnosis and treatment for a TSC patient with dyspnea and spontaneous pneumothorax?
The likely diagnosis is lymphangioleiomyomatosis (LAM), which is common in adult females with TSC. Treatment includes mTOR inhibitors for patients with moderate to severe lung disease or rapid progression.
53
What is the typical course and management for cardiac rhabdomyomas in TSC?
Cardiac rhabdomyomas in TSC are often asymptomatic and spontaneously regress. If symptomatic, mTOR inhibitors can be used to speed regression.
54
What is the first-line treatment for renal angiomyolipomas with acute hemorrhage?
The first-line treatment for renal angiomyolipomas with acute hemorrhage is selective embolization followed by corticosteroids.
55
What is the treatment of choice for subependymal giant cell astrocytomas?
The treatment of choice for subependymal giant cell astrocytomas is mTOR inhibitors.
56
What are the common types of retinal hamartomas and their diagnostic significance?
The most common type of retinal hamartomas is flat and translucent. Other types include elevated, opaque, and sometimes calcified.
57
What is the first-line treatment for renal angiomyolipomas with acute hemorrhage?
The first-line treatment is selective embolization followed by corticosteroids.
58
What is the treatment of choice for subependymal giant cell astrocytomas in a patient with TSC?
The treatment of choice is mTOR inhibitors.
59
What are the common types of retinal hamartomas and their diagnostic significance in TSC?
The most common type is flat and translucent. Other types include elevated, opaque, and calcified multinodular 'mulberry' lesions. Retinal hamartomas are a diagnostic feature of TSC.
60
What genetic mutation is associated with polycystic kidney disease in TSC?
Polycystic kidney disease in TSC is associated with a contiguous TSC2-PKD1 deletion.
61
What is the typical presentation and management of cardiac arrhythmias in TSC?
Cardiac arrhythmias can be slow, fast, or irregular. Management depends on the specific type and severity.
62
What is the role of mTOR inhibitors in managing seizures and cortical dysplasia in TSC?
mTOR inhibitors are used to treat subependymal giant cell astrocytomas and may also improve seizure control.
63
What is the role of mTOR inhibitors in managing renal angiomyolipomas?
mTOR inhibitors are used for asymptomatic growing angiomyolipomas.
64
What is the role of mTOR inhibitors in managing lymphangioleiomyomatosis (LAM) in TSC?
mTOR inhibitors are used in patients with moderate to severe lung disease or rapid progression of LAM.
65
What percentage of individuals have subependymal nodules associated with TSC?
80% of individuals.
66
What is the common treatment for subependymal giant cell astrocytomas?
mTOR inhibitors.
67
What percentage of infants with multiple cardiac rhabdomyomas have TSC?
80% of infants.
68
What are the common symptoms of cardiac rhabdomyoma in fetuses?
Often asymptomatic and may cause fetal hydrops or heart failure shortly after birth.
69
What is the first-line treatment for angiomyolipomas with acute hemorrhage?
Selective embolization followed by corticosteroids.
70
What condition is associated with an increased risk of spontaneous pneumothorax in females over 40 years?
Lymphangioleiomyomatosis (LAM).
71
What percentage of TSC patients have retinal hamartomas?
30-50% of TSC patients.
72
What is the common type of retinal hamartoma found in TSC patients?
Flat and translucent lesions.
73
What is the treatment for asymptomatic growing angiomyolipomas?
mTOR inhibitors.
74
What are the potential complications of renal lesions in TSC?
Renal insufficiency, hypertension, and retroperitoneal hemorrhage.
75
What is the significance of a pathogenic mutation in the diagnosis of Tuberous Sclerosis Complex (TSC)?
A (+) pathogenic mutation is sufficient to make a definite diagnosis of TSC. However, 10-25% of patients may have no mutation identified.
76
What are the criteria for a definite diagnosis of TSC?
A definite diagnosis requires either more than 2 major features or 1 major feature and 2 minor features.
77
What imaging tests are used to confirm the diagnosis of TSC?
MRI of the brain and abdomen.
78
What is the role of molecular diagnosis in TSC?
Molecular diagnosis involves the identification of TSC1/2 mutations but is not sufficient for diagnosis.
79
What is the diagnostic algorithm for TSC based on skin findings?
If skin findings suggest 1 major feature, assess TSC-associated signs, symptoms, and family history.
80
What diagnostic steps should be taken for a 3-year-old child with seizures and hypomelanotic macules?
Perform a clinical evaluation for additional features and conduct imaging such as MRI of the brain.
81
What imaging modality is recommended for evaluating seizures and cortical dysplasia in TSC?
MRI of the brain.
82
What are the associated complications of ungual fibromas in TSC?
Nail dystrophy, nail loss, and pain.
83
What is the role of baseline EEG in managing seizures in TSC?
Baseline EEG is used to evaluate for seizure activity and guide management.
84
What percentage of patients with TSC may not have a mutation identified?
10-25% of patients.
85
What constitutes a definite diagnosis of TSC?
A definite diagnosis is made with 2 major features or 1 major feature plus 2 minor features.
86
What are the major features assessed in the diagnostic criteria for TSC?
Major features include angiofibromas, hypomelanotic macules, and ungual fibromas.
87
What should be done if skin findings suggestive of TSC are present?
Assess TSC associated signs and symptoms and family history.
88
What is the recommended action if a patient has additional major or minor features of TSC?
The patient should undergo TSC diagnostic evaluation.
89
What is the next step if no additional skin or oral lesions are found in a TSC evaluation?
A skin biopsy should be performed.
90
What are the differential diagnoses for hypomelanotic macules?
Conditions include Piebaldism, Vitiligo, Waardenburg syndrome, and others.
91
What histopathological features are associated with hypomelanotic macules?
Normal numbers of melanocytes with poorly developed dendritic processes.
92
What is the significance of non-specific or atypical lesions in diagnosis?
They are used to rule out other diseases.
93
What are the characteristics of angiofibromas in Tuberous Sclerosis Complex?
Angiofibromas are characterized by plump, spindle-shaped cells and increased numbers of dilated vessels.
94
What are the potential adverse effects of oral mTOR inhibitors used in TSC treatment?
Adverse effects include delayed wound healing, infections, and hypertriglyceridemia.
95
What are the recommended procedures for treating angiofibromas in TSC?
Recommended procedures include excision, curettage, and cryosurgery.
96
How often should MRI of the brain be performed in asymptomatic patients with TSC?
Every 1 to 3 years.
97
What is the role of topical mTOR inhibitors in treating TSC angiofibromas?
Topical mTOR inhibitors are safe and effective for treating TSC angiofibromas.
98
What are the treatment options for ungual fibromas in TSC?
Treatment options include excision, although recurrence is common.
99
What is the recommended screening protocol for lymphangioleiomyomatosis (LAM) in TSC?
Asymptomatic at-risk individuals should be screened with HRCT every 5-10 years.
100
What is the recommended surveillance protocol for renal angiomyolipomas in TSC?
MRI of the abdomen should be performed every 1-3 years.
101
What are the histopathological findings expected in angiofibromas?
Histopathology shows plump, spindle-shaped cells and increased numbers of dilated vessels.
102
What are the histopathological findings expected in periungual fibromas?
Histopathology shows more extensive hyperkeratosis and variable increase in vascularity.
103
What are the histopathological findings expected in Shagreen patches?
Histopathology shows sclerotic bundles of collagen in the reticular dermis.
104
What is the recommended annual screening for TSC-associated neuropsychiatric disorders?
Annual screening for TAND, blood pressure, GFR, and skin examination.
105
What is the recommended echocardiographic screening protocol for cardiac rhabdomyomas in TSC?
Echocardiographic screening is recommended for pediatric patients.
106
What distinguishes vitiligo from hypomelanotic macules in terms of melanocytes?
Vitiligo is characterized by absent melanocytes.
107
What is a common treatment for angiofibromas?
Excision, curettage, chemical peel, cryosurgery, dermabrasion, electrosurgery, or lasers.
108
What are the characteristics of fibromas?
Plump, spindle shaped or stellate fibroblastic cells in the dermis among increased numbers of dilated vessels, with collagen fibers oriented in an onion-skin pattern.
109
What is the role of oral mTOR inhibitors in treating skin lesions?
They may improve skin lesions associated with internal tumors, but can also cause adverse effects like delayed wound healing and infections.
110
What is the recommended surveillance for asymptomatic TSC patients under 25 years old?
MRI of the brain every 1-3 years, more frequently if there are positive findings.
111
What is the disadvantage of using topical mTOR inhibitors for TSC angiofibromas?
Long-term treatment is required, and skin lesions may worsen after discontinuation.
112
What procedures may be indicated for periungual fibromas?
Excision, as they are highly recurrent.
113
What is the purpose of annual screening in patients with TSC?
To monitor for complications such as infection, hypertrophic scarring, and other health issues.
114
What is the significance of MRI of the abdomen in TSC patients?
To evaluate the progression of angiomyolipomas and renal cystic disease every 1-3 years.
115
What are the potential adverse effects of mTOR inhibitors?
May include delayed wound healing, stomatitis, mouth ulceration, and infections.
116
What is the recommended follow-up for asymptomatic patients with cardiac rhabdomyomas?
Echocardiogram screening.
117
What is the significance of a child with TSC born to parents who do not carry a TSC diagnosis?
This situation indicates a de novo mutation, parental mosaicism, or that one parent has a very mild form of TSC that went undetected.
118
What is the chance of subsequent children inheriting TSC if one parent has the condition?
There is a 50% chance that subsequent children will inherit the mutation, necessitating a 3 generation family history assessment.
119
What factors could explain a situation where neither parent has TSC but a child does?
Possible explanations include alternate paternity, undisclosed adoption, or one parent having a mosaic mutation in TSC1/2.
120
What is the prognosis for individuals with TSC compared to the general population?
Individuals with TSC have decreased overall survival compared to the general population.
121
What are some common causes of death in individuals with TSC?
Common causes of death include renal failure, intractable seizures, obstructive hydrocephalus, cardiac outflow obstruction, arrhythmia, respiratory failure, pneumothorax, and hemorrhage from an aneurysm or tumor, especially angiomyolipomas.
122
A patient with TSC has a family history of the condition. What is the inheritance pattern and recurrence risk?
TSC has an autosomal dominant inheritance pattern. If one parent has TSC, there is a 50% chance that subsequent children will inherit the mutation.
123
What is the significance of a dental examination for children with TSC?
It should be conducted every 6 months with a panoramic X-ray by 7 years old.
124
What does a positive TSC diagnosis in a child indicate about their parents' genetic status?
It may indicate a de novo mutation, parental mosaicism, or that one parent has a very mild form of TSC that escaped detection.
125
What should be considered if neither parent has TSC?
Alternate paternity, undisclosed adoption, or one parent may have a mosaic mutation in TSC1/2.
126
What is the likelihood of parents with a child who has a de novo mutation having another child with TSC?
It is unlikely for them to have another child with TSC.
127
What is the inheritance pattern of tuberous sclerosis complex (TSC)?
Tuberous sclerosis complex (TSC) follows an autosomal dominant inheritance pattern, where a mutation in the TSC2 gene can be passed from an affected parent to their offspring.
128
What are some common skin lesions associated with tuberous sclerosis complex?
Common skin lesions associated with tuberous sclerosis complex include fibrous cephalic plaque, angiofibromas, dental pitting and oral fibromas, hypomelanotic macules, shagreen patch, confetti lesions, and ungual fibromas.
129
How does the mutation in TSC2 affect cell signaling in tuberous sclerosis complex?
A mutation in TSC2 leads to the activation of Rheb-GTP, which in turn activates mTORC1, resulting in increased cell growth and protein translation.
130
What is the role of Rheb-GTP in the pathogenesis of tuberous sclerosis complex?
Rheb-GTP is an active form of the Rheb protein that activates mTORC1, a key regulator of cell growth and protein synthesis.
131
What is the relationship between TSC2 and Rheb guanosine diphosphate (GDP)?
TSC2 converts active Rheb-GTP to inactive Rheb-GDP, regulating cell growth.
132
What is the significance of germline mutations in TSC2?
Germline mutations in TSC2 can lead to the development of tumors due to loss of function at this locus.
133
How does Rheb-GTP influence mTORC1 activity?
Rheb-GTP activates mTORC1, which is a kinase that increases protein translation and cell growth.
134
What happens to Rheb-GTP levels when TSC2 function is lost?
Loss of TSC2 function results in increased levels of Rheb-GTP, leading to activation of mTORC1 and increased cell growth.
135
What type of mutation is observed in patient cells with tuberous sclerosis complex?
Somatic mutation.

Fitzpatrick's Dermatology, 9th Edition (Entrance Exam / Board Exam Prep) (213 decks)

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