137: Diabetes & Other Endocrine Disorders Flashcards
(295 cards)
1
Q
What are the two main types of diabetes and their characteristics?
A
- Type 1 diabetes: Insulin deficiency due to immune-mediated destruction of islet cells in the pancreas.
- Type 2 diabetes: Chronic hyperglycemia primarily due to end-organ insulin resistance and a progressive decrease in pancreatic insulin release associated with aging.
2
Q
What are some skin conditions associated with diabetes?
A
Diabetes-associated skin conditions include:
- Diabetic thick skin
- Limited joint mobility
- Eruptive xanthomas
- Acanthosis nigricans
3
Q
How does hyperglycemia affect collagen in diabetes?
A
Hyperglycemia leads to nonenzymatic glycosylation of structural and regulatory proteins, including collagen, resulting in the formation of advanced glycation end products (AGEs) that decrease the solubility and enzymatic digestion of cutaneous collagen.
4
Q
What is acanthosis nigricans and its significance in diabetes?
A
Acanthosis nigricans is a skin condition linked to obesity and insulin resistance, and it serves as a prognostic indicator for developing Type 2 diabetes mellitus.
5
Q
What are the clinical implications of macroangiopathy and microangiopathy in diabetes?
A
Macroangiopathy and microangiopathy contribute to cutaneous complications of diabetes by increasing vessel wall permeability, decreasing vascular responsiveness, and leading to diabetic ulcers and increased risk of infection and injury.
6
Q
What characterizes Type 1 diabetes?
A
Insufficiency of insulin due to immune-mediated destruction of islet cells in the pancreas.
7
Q
What is the primary cause of Type 2 diabetes?
A
Chronic hyperglycemia due to end-organ insulin resistance and decreased pancreatic insulin release.
8
Q
What leads to the formation of advanced glycation end products (AGEs) in diabetes?
A
Hyperglycemia leads to nonenzymatic glycosylation of proteins, including collagen.
9
Q
How does hyperinsulinemia contribute to cutaneous manifestations in diabetes?
A
It mediates abnormal epidermal proliferation, leading to conditions like acanthosis nigricans.
10
Q
What role does macroangiopathy play in diabetes complications?
A
It contributes to increased vessel wall permeability and predisposes patients to diabetic ulcers.
11
Q
What is the relationship between lower-extremity vibratory perception and leg amputation risk in diabetes?
A
Those lacking vibratory perception have a 15.5 times increased probability of leg amputation.
12
Q
What are the primary cutaneous manifestations of diabetes mellitus?
A
Manifestations include Acanthosis Nigricans, Limited Joint Mobility, Necrobiosis Lipoidica, Eruptive Xanthomas, and Bullous Diabeticorum.
13
Q
What are the clinical features of acanthosis nigricans?
A
- Presents as brown to gray-black papillomatous cutaneous thickening in flexural areas (posterolateral neck, axillae, groin, abdominal folds).
- Distribution is usually symmetric with a dirty, velvety texture.
- Oral, esophageal, pharyngeal, laryngeal, conjunctival, and anogenital mucosal surfaces may be involved.
- Back of the neck is the most consistently and severely affected area.
- Development of superimposed acrochordons in involved areas.
- In florid cases, (+) involvement on the back of the hands and palms (tripe palms).
14
Q
What are the potential causes of acanthosis nigricans?
A
- Loss-of-function mutations in the insulin receptor or anti-insulin receptor antibodies (Type A and Type B syndrome).
- Excess growth factor stimulation in the skin leading to aberrant proliferation of keratinocytes and fibroblasts.
- Insulin resistance and hyperinsulinemia may result from excess insulin binding to IGF1 receptors on keratinocytes and fibroblasts.
- Genetic syndromes (Crouzon and SADDAN) with mutations in fibroblast growth factor receptor 3.
- Drugs that can cause acanthosis nigricans include systemic glucocorticoids, nicotinic acid, and estrogens such as diethylstilbestrol.
15
Q
What management strategies are recommended for acanthosis nigricans?
A
- Calcipotriol, salicylic acid, glycolic acid peels, urea, systemic, and topical retinoids have anecdotal success.
- Long-pulsed alexandrite laser treatment.
- Treatment of the underlying cause may be beneficial.
- Weight loss in obese patients.
- Medications that improve insulin sensitivity, such as metformin.
- In cases associated with malignancy, treat the underlying malignancy, often gastric in origin.
16
Q
What are the clinical features of Limited Joint Mobility (LJM) and Scleroderma-like syndrome in diabetes?
A
- Presents as tightness and thickening of the skin and periarticular connective tissue of the fingers, resulting in a painless loss of joint mobility.
- Initial involvement of the DIP joints of the 5th digit usually progresses to involve all fingers.
- Larger joints of the elbow, knee, and foot may be affected.
- Characterized by the ‘prayer sign’ (inability to approximate palmar surfaces with hands pressed together).
- Skin may appear thickened, waxy, and smooth with apparent loss of adnexa, resembling scleroderma.
17
Q
What is the epidemiology of Limited Joint Mobility (LJM) in diabetes?
A
- Of adult patients with Type 1 diabetes, 30% to 50% have LJM.
- It is also common in Type 2 diabetes.
18
Q
What is the most important factor in diagnosing acanthosis nigricans?
A
Hyperinsulinemia.
19
Q
What genetic mutations are associated with acanthosis nigricans?
A
Loss-of-function mutations in the insulin receptor or anti-insulin receptor antibodies (Type A and Type B syndrome).
20
Q
What is the management approach for acanthosis nigricans associated with malignancy?
A
Treat the underlying malignancy, which is often a tumor of intraabdominal origin, usually gastric.
21
Q
What is the clinical presentation of limited joint mobility (LJM) in diabetes?
A
It presents as tightness and thickening of the skin and periarticular connective tissue of the fingers, resulting in a painless loss of joint mobility.
22
Q
What is the significance of the ‘prayer sign’ in patients with limited joint mobility?
A
It indicates an inability to approximate the palmar surfaces and interphalangeal joint spaces with the hands pressed together and fingers separated.
23
Q
What is the relationship between scleroderma-like syndrome and diabetes?
A
Scleroderma-like syndrome is not associated with systemic sclerosis but correlates with the duration of diabetes and severity of joint contractures.
24
Q
What treatments are recommended for diabetic thick skin?
A
Tight control of blood glucose and physical therapy to preserve active range of motion.
25
A patient with diabetes has a painless loss of joint mobility and thickened, waxy skin on the fingers. What is the condition, and what is the primary treatment?
The condition is Limited Joint Mobility (LJM). The primary treatment is intensive insulin therapy to control blood glucose, along with physical therapy to preserve range of motion.
26
What is the pathogenesis of Acanthosis Nigricans in insulin resistance?
In insulin resistance, excess insulin binds to IGF1 receptors on keratinocytes and fibroblasts, causing aberrant proliferation.
27
What are the clinical features of Acanthosis Nigricans, and what is its most consistently affected area?
Features include brown to gray-black papillomatous cutaneous thickening in flexural areas, with the back of the neck being the most consistently affected area.
28
What are the clinical features and pathogenesis of Acanthosis Nigricans?
Features include brown to gray-black papillomatous thickening in flexural areas. Pathogenesis involves excess insulin binding to IGF1 receptors, causing keratinocyte and fibroblast proliferation.
29
What is the epidemiology of Scleroderma Diabeticorum in patients with diabetes?
Affects **2.5% to 14%** of patients with diabetes, particularly associated with **longstanding diabetes** and **obesity** among patients with **Type 2 diabetes**.
30
What are the clinical features of Scleroderma Diabeticorum?
- Insidious onset of **painless**, symmetric induration and thickening of the skin on the upper back and neck.
- May spread to the face, shoulders, and anterior torso.
- Skin retains a **nonpitting**, woody, **peau d’orange** quality.
- Associated with **postinfectious scleredema** and may lead to decreased sensation and range of motion.
31
What is the management approach for Scleroderma Diabeticorum?
- **Radiotherapy**
- **Low-dose methotrexate**
- **Bath psoralen and ultraviolet A light (PUVA)**
- **Extracorporeal photopheresis**
- **Weight reduction** and **physical therapy**
32
What are the clinical features of Eruptive Xanthomas?
- Present as **1-mm to 4-mm**, reddish-yellow papules on the buttocks and extensor surfaces of the extremities.
- Lesions may coalesce into plaques over time.
- Often associated with **severe hypertriglyceridemia** and potentially undiagnosed diabetes.
33
What is the management for Eruptive Xanthomas?
- **Lifestyle modification** and control of the underlying diabetes.
- Lesions respond rapidly and usually resolve completely in **6 to 8 weeks**.
34
What are the common skin infections in diabetic patients?
- Diabetic patients experience several skin infections more commonly and with greater severity.
- **Leukocyte chemotaxis**, adherence, and phagocytosis are impaired, especially during **hyperglycemia** and **diabetic acidosis**.
35
What is the epidemiology of diabetic ulcers?
- Occurs in **15% to 25%** of diabetic patients.
- **10-30x** increased risk of lower-extremity amputation.
- Lower-extremity ulcers account for **25%** of all hospital stays for patients with diabetes.
36
What are the clinical features of diabetic ulcers?
- **Callus formation** precedes necrosis and breakdown of tissue over bony prominences of feet.
- Ulcers are surrounded by a ring of callus and may extend to underlying joint and bone.
- Complications include **soft-tissue infection** and **osteomyelitis**.
37
What are the major factors contributing to the development of diabetic ulcers?
- **Peripheral neuropathy**, pressure, and trauma.
- **Neuropathy** associated with uncontrolled hyperglycemia is a major predictor.
- **Charcot arthropathy** and ill-fitting shoes are common causes.
38
What percentage of patients with diabetes are affected by Scleroderma Diabeticorum?
2.5% to 14%.
39
What is a common cause of eruptive xanthomas?
Uncontrolled diabetes leading to severe hypertriglyceridemia.
40
What is the risk of lower-extremity ulcers in diabetic patients?
Occurs in 15% to 25% of diabetic patients with a 10-30x increased risk of lower-extremity amputation.
41
What are the complications associated with diabetic ulcers?
Soft-tissue infection and osteomyelitis.
42
What role does neuropathy play in diabetic ulcers?
Neuropathy is a major predictor of diabetic ulcers, especially when associated with uncontrolled hyperglycemia.
43
What factors are associated with foot ulceration in diabetes?
Previous foot ulceration, prior lower-extremity amputation, long duration of diabetes, impaired visual acuity, onychomycosis, and poor glycemic control.
44
How does the skin quality appear in Scleroderma Diabeticorum?
The skin retains a nonpitting, woody, peau d’orange quality.
45
What is the typical resolution time for eruptive xanthomas with management?
They usually resolve completely in 6 to 8 weeks.
46
A patient presents with painless, symmetric induration and thickening of the skin on the upper back and neck. What is the likely diagnosis, and what are the associated management strategies?
The likely diagnosis is Scleredema Diabeticorum. Management includes radiotherapy, low-dose methotrexate, bath PUVA, extracorporeal photopheresis, weight reduction, and physical therapy.
47
A patient with diabetes develops reddish-yellow papules on the buttocks and extensor surfaces of the extremities. What is the condition, and what is the underlying cause?
The condition is Eruptive Xanthomas, caused by severe hypertriglyceridemia, often associated with uncontrolled diabetes.
48
What are the key factors contributing to the development of diabetic ulcers?
Key factors include peripheral neuropathy, pressure, trauma, ill-fitting shoes, and socks. Neuropathy associated with uncontrolled hyperglycemia is a major predictor.
49
What are the clinical features and management of diabetic ulcers?
Features include callus formation, necrosis, and tissue breakdown over bony prominences. Management includes debridement, off-loading, and glycemic control.
50
What are the clinical features and management of Scleredema Diabeticorum?
Features include symmetric induration and thickening of the skin on the upper back and neck. Management includes weight reduction, physical therapy, and PUVA.
51
What are the clinical features and management of Eruptive Xanthomas?
Features include reddish-yellow papules on the buttocks and extensor surfaces, often asymptomatic but associated with severe hypertriglyceridemia. Management involves lifestyle modification and diabetes control.
52
What are the standard therapies for neuropathic diabetic ulcers?
Standard therapies include:
1. **Debridement**
53
What is the management of Scleredema Diabeticorum?
Management includes weight reduction, physical therapy, and PUVA.
54
What are the clinical features of Eruptive Xanthomas?
Features include reddish-yellow papules on the buttocks and extensor surfaces, often asymptomatic but associated with severe hypertriglyceridemia.
55
What is the management of Eruptive Xanthomas?
Management involves lifestyle modification and diabetes control.
56
What are the standard therapies for neuropathic diabetic ulcers?
Standard therapies include debridement, off-loading, moist wound care, protective dressings, recombinant platelet-derived growth factor, and biologic approaches for large or poorly responsive ulcers.
57
What is the significance of glycemic control in preventing diabetic ulcers?
Optimizing glycemic control is crucial as it prevents neuropathy, which is closely associated with foot ulceration.
58
What are the clinical features of Necrobiosis Lipoidica?
Clinical features include sharply demarcated yellow-brown plaques on the anterior pretibial region, violaceous irregular borders, early presentation as red-brown papules and nodules, and ulceration in approximately 13% to 35% of cases.
59
What management strategies are recommended for Granuloma Annulare in diabetic patients?
Management strategies include early application of potent topical glucocorticoids, intralesional injection of glucocorticoids, short-term systemic glucocorticoids, aspirin and dipyridamole, tumor necrosis factor inhibitors, topical retinoids, topical PUVA, and surgical excision as a last resort.
60
What is the mean age of onset for Necrobiosis Lipoidica?
Around 30 years, with women having three times more cases than men.
61
What is the association between Granuloma Annulare and diabetes?
Diabetes is present in 9.7% of patients with localized GA and 21% of patients with generalized GA.
62
What are the management strategies for Necrobiosis Lipoidica?
Management includes early application of topical glucocorticoids, intralesional injections, and prevention of ulcers.
63
What is the risk associated with intralesional injection of glucocorticoids for Necrobiosis Lipoidica?
It shows improvement but comes with the risk of ulceration.
64
What is the significance of foot examinations in diabetic patients?
Foot examinations should be done in every patient visit to detect loss of protective sensation.
65
What is the complication rate of ulceration in patients with a history of ulceration?
Patients have a high risk for reulceration, with rates of 34% at 1 year, 61% at 3 years, and 70% at 5 years.
66
What are the clinical features and management of diabetic ulcers?
Management includes debridement, off-loading, moist wound care, protective dressings, and optimizing glycemic control.
67
What are the clinical features and management of Necrobiosis Lipoidica?
Features include yellow-brown plaques with violaceous borders on the anterior pretibial region. Management includes topical glucocorticoids, intralesional injections, and ulcer prevention.
68
What are the clinical features and management of Granuloma Annulare in diabetes?
Features include annular plaques with central clearing, often on the extremities. Management includes topical or intralesional glucocorticoids.
69
What are the clinical features of atrophic tibial lesions associated with diabetes?
They present as small (<1 cm), atrophic, pink to brown, scar-like macules on the pretibial areas.
70
What is the management approach for individual atrophic tibial lesions in diabetes?
No treatment is necessary for individual atrophic tibial lesions as they are asymptomatic.
71
What are the characteristics of Bullous Diabeticorum?
Abrupt, spontaneous development of painless, non-pruritic blisters on the lower extremities, usually healing within 2 to 5 weeks.
72
What are the physiologic changes in the skin related to obesity?
Alterations in epidermal barrier function, increased sweating, larger skin folds, increased skin surface pH, poor lymphatic drainage, and impaired wound healing.
73
What are the contributing factors to the pathogenesis of obesity and metabolic syndrome?
Nutritional choices, activity/exercise, medications, inflammation, insulin resistance, depression, degenerative joint disease, obstructive sleep apnea, gonadal dysfunction, and vitamin D deficiency.
74
What is the relationship between the incidence of shin spots and diabetes?
The incidence of shin spots is correlated with the duration of diabetes and the presence of retinopathy, nephropathy, and neuropathy.
75
What characterizes acquired perforating disorders in diabetes?
They are characterized by transepidermal elimination or 'spitting' of altered dermal constituents.
76
What is the pathogenesis of diabetic bullae?
The pathogenesis is unknown, but the formation of advanced glycation end products (AGEs) may lead to increased fragility.
77
How is obesity defined in terms of body mass index (BMI)?
Obesity is defined as a BMI greater than 30 kg/m2, while overweight is defined as a BMI greater than 25.
78
What are some physiological changes in the skin related to obesity?
Physiological changes include alterations in epidermal barrier function, increased sweating, larger skin folds, and impaired wound healing.
79
What is the most important therapy for managing obesity and metabolic syndrome?
The most important therapy is weight reduction and exercise along with adequate control of cardiac risk factors.
80
What are the clinical features and management of Bullous Diabeticorum?
Clinical features include painless, non-pruritic bullae on the lower extremities. Management involves supportive treatment and ruling out other blistering diseases.
81
What is the role of leptin in regulating body weight and metabolism?
Leptin regulates energy homeostasis, neuroendocrine function, and metabolism.
82
What condition can leptin deficiency cause?
Extreme obesity, hyperphagia, diabetes, neuroendocrine abnormalities, and infertility.
83
What is the effect of leptin resistance in obese individuals?
They have high circulating levels of leptin, making pharmacologic leptin administration ineffective for weight loss.
84
What is the function of Ghrelin?
Ghrelin is a gastric-derived hormone that stimulates appetite and modulates body weight.
85
What is the most common cause of hyperthyroidism?
Graves disease, accounting for 60% to 80% of all cases.
86
What is the incidence of hypothyroidism in the U.S. population?
Hypothyroidism is present in 4.6% of the U.S. population.
87
What are common cutaneous changes associated with hyperthyroidism?
Soft, warm, and velvety skin texture.
88
What is thyroid dermopathy?
A classic manifestation of Graves disease, often associated with thyroid ophthalmopathy.
89
What is the significance of vitiligo in thyroid disease?
Vitiligo is overrepresented in patients with Graves disease and often predates the diagnosis.
90
What are the primary clinical features of hyperthyroidism-related cutaneous changes?
Features include soft, warm, and velvety skin, fine and soft scalp hair, and brittle nails.
91
What is the extreme form of diffuse thyroid dermopathy?
The extreme form is known as the elephantiasic variant, characterized by progressive thickening and gray-black hyperpigmentation of the pretibial skin.
92
What is the extreme form of diffuse thyroid dermopathy known as?
The extreme form of diffuse thyroid dermopathy is known as the elephantiasic variant. It occurs in less than 1% of patients with Graves' disease and is characterized by progressive thickening and gray-black hyperpigmentation of the pretibial skin, accompanied by woody, firm edema with nodule formation.
93
What cutaneous condition is characterized by digital clubbing, soft-tissue swelling of the hands and feet, and the presence of characteristic periosteal reactions?
The cutaneous condition characterized by digital clubbing, soft-tissue swelling of the hands and feet, and the presence of characteristic periosteal reactions is known as thyroid acropachy. It is almost always associated with thyroid dermopathy and exophthalmos.
94
What are the cardiovascular effects of thyroid hormone excess on the skin?
The cardiovascular effects of thyroid hormone excess result in:
1. Increased blood flow to the skin, manifesting as facial flushing and palmar erythema.
2. An increase in metabolism, which, along with increased peripheral blood flow and temperature dysregulation, can lead to generalized hyperhidrosis.
3. A higher incidence of chronic urticaria in patients with thyroid disease.
95
What is the significance of hyperpigmentation in patients with hyperthyroidism?
Hyperpigmentation in patients with hyperthyroidism is characterized by increased pigment in the palmar creases, gingiva, and buccal mucosa, usually more prominent in individuals with darker skin. This hyperpigmentation is a result of increased corticotropin (ACTH) due to accelerated cortisol metabolism.
96
What is the cutaneous condition characterized by rugated appearance of the palmar surface usually associated with acanthosis nigricans in the setting of malignancy?
Acanthosis nigricans.
97
What condition presents with the insidious onset of painless, symmetric induration and thickening of the skin on the upper back and neck among diabetes mellitus patients?
Diabetic dermopathy.
98
What are three genes that serve as regulators of body adiposity?
Leptin, adiponectin, and resistin.
99
In acanthosis nigricans, what is the most consistently affected area?
The neck and axillae.
100
What sign indicates a patient is unable to approximate the palmar surface of the proximal and distal interphalangeal joints with palms pressed together?
LJM sign (Lateral Joint Mobility sign).
101
What gastric-derived, appetite-stimulating hormone regulates obesity?
Ghrelin.
102
What are the clinical features of thyroid dermopathy, and what is its most severe variant?
Thyroid dermopathy presents as painless, nonpitting nodules and plaques with a waxy, indurated texture, commonly on the extensor surfaces of the legs. The most severe variant is the elephantiasic form, characterized by progressive thickening and gray-black hyperpigmentation of the pretibial skin.
103
What are the clinical features of thyroid acropachy, and how is it diagnosed?
Features include digital clubbing, soft-tissue swelling of the hands and feet, and periosteal reactions. Diagnosis is aided by radiographic findings and bone scans.
104
What are the clinical features and management of thyroid dermopathy?
Features include painless, nonpitting nodules and plaques with a waxy texture, commonly on the legs. Management focuses on treating the underlying thyroid condition.
105
What are the clinical features and management of thyroid acropachy?
Features include digital clubbing and periosteal reactions. Management involves treating the underlying thyroid disease.
106
What are the risk factors for diabetic ulcers as outlined in the approach to care for diabetic foot and ulcers?
The risk factors for diabetic ulcers include:
- Elevated HbA1c
- Vision poorer than 20/40
- History of foot ulcer
- History of amputation
- Monofilament insensitivity
- Onychomycosis.
107
What is the initial step in managing a diabetic ulcer when it is present?
The initial step in managing a diabetic ulcer is to assess for palpable foot pulses. If pulses are present, further evaluation for clinical signs of cellulitis or osteomyelitis is conducted.
108
What should be done if clinical signs of cellulitis or osteomyelitis are present in a diabetic ulcer patient?
If clinical signs of cellulitis or osteomyelitis are present, the following actions should be taken:
1. Sharp debridement
2. Eliminate pressure
3. Consider osteomyelitis evaluation and begin appropriate antibiotics.
109
What are the follow-up actions if a diabetic ulcer shows improvement within 4 weeks?
If a diabetic ulcer shows improvement by 4 weeks, the follow-up actions include:
- Regular follow-up
- Education about foot care
- Addressing modifiable risk factors.
110
What should be assessed if there is no improvement in a diabetic ulcer after 4 weeks?
If there is no improvement in a diabetic ulcer after 4 weeks, the following should be assessed:
- Check compliance
- Reassess for infection
- Consider adjuvant care.
111
What should be done if an ulcer is present and there are clinical signs of cellulitis or osteomyelitis?
Perform sharp debridement and eliminate pressure.
112
What is the next step if a diabetic ulcer is present but there are no palpable foot pulses?
Conduct a noninvasive vascular assessment to check for clinically significant arterial obstruction.
113
What should be done if there is improvement in a diabetic ulcer by 4 weeks?
Continue with regular follow-up, education about foot care, and address modifiable risk factors.
114
What actions should be taken if there is no improvement in a diabetic ulcer by 4 weeks?
Check compliance, reassess for infection, and consider adjuvant care.
115
What are the characteristic facial changes associated with hypothyroidism?
Characteristic facial changes include:
- **Broadened nose**
- **Thickened lips**
- **Puffy eyelids**
- **Macroglossia** with a smooth and clumsy tongue
116
How does hypothyroidism affect hair growth and quality?
In patients with hypothyroidism, hair is:
- **Coarse, dry, and brittle**
- **Slowed growth**
- Alopecia can be either **diffuse or patchy**
- Increased numbers of hair follicles in **telogen** and **telogen effluvium** may occur when hypothyroidism onset is abrupt.
117
What is myxedema and how is it related to hypothyroidism?
Myxedema is a classic finding associated with hypothyroidism, characterized by:
- **Dermal accumulation of mucopolysaccharides** (hyaluronic acid and chondroitin sulfate)
- Tends to resolve with treatment of hypothyroidism
- Can be generalized but often appears more striking in the **extremities**.
118
What skin changes are observed in patients with hypothyroidism?
Skin changes in hypothyroidism include:
- **Cool and pale skin** due to decreased core temperature and increased peripheral vasoconstriction
- **Xerotic skin** with a poorly hydrated stratum corneum
- **Hyperkeratosis** with follicular plugging
- **Yellow-orange discoloration** due to beta-carotene accumulation, sparing the sclerae (pseudo-jaundice)
- **Fine wrinkling** of the skin
119
What are the potential complications associated with goiter in hypothyroidism?
Complications associated with goiter in hypothyroidism can include:
- **Compression of the recurrent laryngeal nerve**, leading to hoarseness
- **Tracheal or esophageal displacement**
- In extreme cases, **Pemberton sign**, which is facial plethora when arms are raised due to jugular vein compression.
120
A patient presents with cool, pale, and xerotic skin. Histological examination reveals thin epidermis and hyperkeratosis with follicular plugging. What condition might this indicate, and how can it be distinguished from atopic dermatitis?
This presentation is indicative of hypothyroidism. It can be distinguished from atopic dermatitis by the generalized distribution of findings, as opposed to the extremity-predominant distribution seen in atopic dermatitis.
121
A patient with hypothyroidism has yellow-orange skin discoloration. What is the cause of this discoloration, and how can it be differentiated from true jaundice?
The yellow-orange discoloration is due to beta-carotene accumulation in the stratum corneum, resulting from diminished hepatic conversion of beta-carotene to vitamin A. It can be differentiated from true jaundice as it spares the sclerae.
122
A patient with hypothyroidism presents with a broadened nose, thickened lips, and puffy eyelids. What is the underlying cause of these facial changes?
These facial changes are caused by myxedema, which results from dermal accumulation of mucopolysaccharides like hyaluronic acid and chondroitin sulfate.
123
A patient with hypothyroidism complains of slow-growing, brittle nails with longitudinal and transverse striations. What is the likely cause of these nail changes?
The nail changes are due to the slowed metabolic processes associated with hypothyroidism, which affect nail growth and structure.
124
A patient with a large goiter experiences facial plethora when raising their arms above their head. What is this sign called, and what causes it?
This is called the Pemberton sign, caused by compression of the jugular veins due to the large goiter.
125
A patient with hypothyroidism has alopecia involving the outer third of the eyebrows. What is the significance of this finding?
Loss of the outer third of the eyebrows is a characteristic pattern of alopecia seen in hypothyroidism.
126
A patient with hypothyroidism has impaired wound healing. What is the underlying mechanism?
Impaired wound healing in hypothyroidism is due to reduced metabolic activity and decreased protein synthesis.
127
What are the characteristic facial changes associated with hypothyroidism?
A broadened nose, thickened lips, puffy eyelids, and macroglossia with a smooth and clumsy tongue.
128
What skin changes are observed in patients with hypothyroidism?
The skin can be doughy, swollen, and waxy, but without pitting, and wound healing is impaired.
129
How does hypothyroidism affect hair growth?
Hair in patients with hypothyroidism is coarse, dry, and brittle with slowed growth, and alopecia can be either diffuse or patchy.
130
What is myxedema and how is it related to hypothyroidism?
Myxedema is a classic finding associated with hypothyroidism, resulting from dermal accumulation of mucopolysaccharides and tends to resolve with treatment.
131
What is the significance of yellow-orange discoloration of the skin in hypothyroidism?
It is secondary to the accumulation of beta-carotene in the stratum corneum, resulting from diminished hepatic conversion of beta-carotene to vitamin A.
132
What are the nail changes seen in hypothyroidism?
Nails grow slowly and can be thickened and brittle with longitudinal and transverse striations.
133
What is the relationship between hypothyroidism and goiter?
Hypothyroidism caused by iodine deficiency or Hashimoto thyroiditis can be associated with goiter.
134
What is the Pemberton sign and its association with goiter?
The Pemberton sign consists of facial plethora when patients raise their arms above their head due to compression of the jugular veins caused by large retrosternal goiters.
135
How does hypothyroidism affect the skin's temperature and hydration?
Decreased core temperature and increased peripheral vasoconstriction cause the skin to be cool and pale, and the skin is xerotic with poorly hydrated stratum corneum.
136
What is the histological finding in the skin of patients with hypothyroidism?
The epidermis is thin, and there is hyperkeratosis with follicular plugging.
137
What is the role of TSH in thyroid hormone regulation?
TSH, or Thyroid-Stimulating Hormone, is released in response to hypothalamic production of thyrotropin-releasing hormone. It binds to the TSH receptor (TSHR) on the thyroid gland, triggering the synthesis and release of thyroid hormones. Levels of TSH and thyrotropin-releasing hormone are tightly controlled by circulating levels of thyroxine (T4) and triiodothyronine (T3), which provide feedback regulation.
138
How does thyroid hormone affect skin and hair?
Thyroid hormone is essential for optimal epidermal proliferation and regulates genes involved in keratinocyte proliferation. It stimulates the expression of certain keratins and plays a crucial role in hair growth and cycling by acting on the stem cells in the hair follicle bulge.
139
What are the two categories of hyperthyroidism based on radioiodine uptake?
Hyperthyroidism can be classified into two categories:
1. **High radioiodine uptake** - indicates increased synthesis of thyroid hormone.
2. **Low radioiodine uptake** - suggests either an exogenous source of thyroid hormone or thyroid inflammation with release of preformed thyroid hormone into circulation.
140
What is the most common cause of hypothyroidism with a goiter in North America?
The most common cause of hypothyroidism with a goiter in North America is **Hashimoto thyroiditis**.
141
What is the mainstay of treatment for cutaneous findings of thyroid disease?
The mainstay of treatment for the cutaneous findings of thyroid disease is the **normalization of thyroid function**. Complete or partial remission of cutaneous findings can occur even without localized topical treatment.
142
A patient with hyperthyroidism presents with high radioiodine uptake. What does this indicate about the thyroid hormone synthesis?
High radioiodine uptake indicates increased synthesis of thyroid hormone.
143
A patient with hyperthyroidism has thin, brittle hair and diffuse alopecia. What is the role of thyroid hormones in hair growth?
Thyroid hormones regulate genes involved in keratinocyte proliferation and play an important role in hair growth and cycling by acting on stem cells in the hair follicle bulge.
144
A patient with hyperthyroidism has been treated with radioiodine ablation. What is the most common cause of hypothyroidism in such cases?
The most common cause of hypothyroidism without a goiter is the surgical or radioiodine-induced ablation of the thyroid gland for the treatment of Graves disease.
145
What triggers the release of TSH in the body?
Hypothalamic production of thyrotropin-releasing hormone.
146
How does TSH affect the thyroid gland?
By binding to the TSHR, a G-protein-coupled receptor, triggering thyroid hormone synthesis and release.
147
What regulates the levels of TSH and thyrotropin-releasing hormone?
Circulating levels of thyroxine (T4) and triiodothyronine (T3).
148
What is the major determinant of thyroid hormone binding in the blood?
Thyroid-binding globulin.
149
What are the two categories of hyperthyroidism based on radioiodine uptake?
High radioiodine uptake and low radioiodine uptake.
150
What does high radioiodine uptake indicate?
Increased synthesis of thyroid hormone.
151
What role does thyroid hormone play in the skin?
It regulates keratinocyte proliferation and affects the keratinized epithelium of the epidermis, hair, and nails.
152
What is the most common cause of hypothyroidism without a goiter?
Surgical or radioiodine-induced ablation of the thyroid gland for the treatment of Graves disease.
153
What is the mainstay of treatment for cutaneous findings of thyroid disease?
Normalization of thyroid function.
154
What can be used with some success for localized treatment of thyroid-related cutaneous findings?
Topical glucocorticoids with adjuvant compression.
155
What are the common skin manifestations associated with hyperparathyroidism?
Skin manifestations are rare but can include:
- **Cutaneous calcinosis** (calcinosis cutis or metastatic calcinosis) due to elevated calcium and phosphate levels.
- **Subcutaneous calcifications** that are skin-colored, firm to palpation, and often found in a symmetric distribution over large joints.
- **Chronic urticaria** is also associated with hyperparathyroidism.
156
What is calciphylaxis and what are its associated risk factors?
Calciphylaxis, also known as calcific uremic arteriolopathy, is a rare but life-threatening condition associated with hyperparathyroidism. It is characterized by:
- Calcium deposition in the walls of small- to medium-sized vessels, leading to vascular occlusion and skin necrosis.
**Risk factors include:**
1. Chronic renal failure
2. Secondary hyperparathyroidism
3. Obesity
4. Diabetes
5. Protein C or protein S deficiency
6. Warfarin administration
157
What is the epidemiology of parathyroid disease?
Parathyroid disease is most commonly seen in:
- Individuals older than **45 years of age**.
- There is a **2:1 female-to-male predominance**.
- **Ionizing radiation** to the neck is a known risk factor for developing primary hyperparathyroidism.
158
What clinical features are associated with parathyroid disease?
Parathyroid disease typically presents with:
- **Abnormal serum calcium levels**.
- Physical findings and symptoms associated with **hypercalcemia** and **hypocalcemia**.
159
A patient with hyperparathyroidism presents with symmetric subcutaneous calcifications overlying large joints. What is the likely diagnosis, and what causes these calcifications?
The likely diagnosis is cutaneous calcinosis, caused by the combination of elevated calcium and phosphate levels.
160
A patient with hyperparathyroidism develops chronic urticaria. What other cutaneous tumors should prompt a workup for MEN1?
Cutaneous tumors such as angiofibromas, collagenomas, café-au-lait macules, and lipomas should prompt a workup for MEN1.
161
What is a common risk factor for developing primary hyperparathyroidism?
Ionizing radiation to the neck.
162
What is the typical age demographic for most cases of parathyroid disease?
Individuals older than 45 years of age.
163
What is the female-to-male ratio in the prevalence of parathyroid disease?
2:1 female-to-male predominance.
164
What are the skin manifestations associated with hyperparathyroidism?
Skin manifestations are rare but can include cutaneous calcinosis and subcutaneous calcifications.
165
What is cutaneous calcinosis thought to be caused by?
The combination of elevated calcium and phosphate.
166
What condition is characterized by calcium deposition in the walls of small- to medium-sized vessels?
Calciphylaxis.
167
What are some risk factors for calciphylaxis?
Chronic renal failure, obesity, diabetes, protein C or S deficiency, and warfarin administration.
168
What should be considered when signs of hyperparathyroidism are present with certain cutaneous tumors?
A workup for multiple endocrine neoplasia Type 1 (MEN1) should be prompted.
169
What is the clinical presentation of parathyroid disease?
It most often presents with abnormal serum calcium levels.
170
What are the clinical features of calciphylaxis?
Calciphylaxis presents with:
1. **Tender violaceous patches** that may show a mottled or reticular pattern.
2. Areas that become **indurated and exquisitely painful**, leading to ulceration and eschar formation.
3. Common locations include the **thighs, buttocks, and breasts**.
4. Patients typically have a **normal calcium-phosphate product**, although a product greater than 70 mg/dL is a risk factor.
5. The histologic finding of **calcium deposits in vessel walls** is diagnostic.
6. High mortality rates (up to 80%) are often due to infection.
171
What skin manifestations are associated with hypoparathyroidism?
Hypoparathyroidism is associated with:
- **Scaly, hyperkeratotic, and edematous puffy skin**.
- **Paresthesias** secondary to hypocalcemia.
- **Patchy alopecia** and generalized thinning of hair.
- **Brittle nails** with transverse ridging.
- Flares of **psoriasis**, which may respond to Vitamin D analogs.
172
What is pseudohypoparathyroidism and its characteristics?
Pseudohypoparathyroidism is characterized by:
- **End-organ lack of responsiveness** to parathyroid hormone (PTH).
- Presence of **hypocalcemia** and **hyperphosphatemia** despite elevated serum PTH levels.
- Associated with **Albright hereditary osteodystrophy**, which includes:
1. **Short stature**
2. **Developmental delay**
3. **Obesity**
4. **Rounded facies**
5. **Dental hypoplasia**
6. **Shortened bones of the hands and feet**.
- Characteristic **dimpling of the fourth knuckle** known as the Albright sign.
173
A patient with chronic renal failure develops tender violaceous patches that progress to ulceration and eschar formation. What is the diagnosis, and what is the underlying pathophysiology?
The diagnosis is calciphylaxis, caused by calcium deposition in the walls of small- to medium-sized vessels, leading to vascular occlusion and overlying skin necrosis.
174
What is dental hypoplasia?
A condition characterized by underdevelopment of tooth enamel.
175
What are the shortened bones of the hands and feet associated with?
Characteristic dimpling of the fourth knuckle known as the Albright sign.
176
What is the diagnosis for a patient with chronic renal failure who develops tender violaceous patches that progress to ulceration and eschar formation?
The diagnosis is calciphylaxis, caused by calcium deposition in the walls of small- to medium-sized vessels, leading to vascular occlusion and overlying skin necrosis.
177
What skin changes are associated with hypoparathyroidism?
Scaly, hyperkeratotic, and edematous skin.
178
What is the likely cause of skin changes in a patient with hypoparathyroidism?
These changes are due to hypocalcemia resulting from hypoparathyroidism, which affects calcium homeostasis.
179
What is the Albright sign?
Dimpling of the fourth knuckle due to a shortened fourth metacarpal in pseudohypoparathyroidism.
180
What are the most common locations for calciphylaxis?
The thighs, buttocks, and breasts.
181
What are the initial clinical presentations of patients with calciphylaxis?
Tender violaceous patches that may exhibit a mottled or reticular pattern.
182
What is a common histologic finding in calciphylaxis?
Calcium deposits in vessel walls coupled with compatible clinical findings.
183
What is the prognosis for patients with calciphylaxis?
Very poor, with reported mortality rates up to 80%, usually from infection.
184
What symptoms may patients with hypocalcemia experience?
Paresthesias.
185
What hair condition is reported in patients with hypoparathyroidism?
Patchy alopecia and generalized thinning of the hair.
186
What nail condition can occur in patients with hypoparathyroidism?
Brittle nails with transverse ridging.
187
What is pseudohypoparathyroidism?
End-organ lack of responsiveness to PTH, with hypocalcemia and hyperphosphatemia present, but elevated serum PTH.
188
What are the characteristic findings in Albright hereditary osteodystrophy?
Short stature, developmental delay, obesity, rounded facies, dental hypoplasia, and shortened bones of the hands and feet.
189
What leads to the Albright sign in patients with Albright hereditary osteodystrophy?
Characteristic shortening of the fourth metacarpal leading to a dimpling of the fourth knuckle.
190
What mechanisms does PTH use to regulate calcium levels in the body?
PTH stimulates vitamin D production, calcium absorption in the GI tract, renal reabsorption of calcium and phosphate, and regulates calcium mobilization from bone.
191
What is the role of circulating free calcium in the regulation of PTH release?
Circulating free calcium acts on the parathyroid glands to control the release of PTH, ensuring that calcium levels in the blood are maintained within a normal range.
192
What are the skin manifestations associated with parathyroid disease primarily a result of?
They are primarily the result of calcium dysregulation due to abnormal levels of PTH affecting serum calcium levels.
193
What is the main treatment for hyperparathyroidism?
Partial or total parathyroidectomy.
194
What is Cushing syndrome and what is its most common cause?
Cushing syndrome describes chronic exposure to excess corticosteroids, with the most common cause being exogenous corticosteroid administration.
195
What is the significance of the relationship between POMC and ACTH in adrenal gland diseases?
The relationship of POMC to ACTH is important in diseases of the adrenal gland and the resulting skin manifestations.
196
What role does PTH play in calcium metabolism?
PTH stimulates vitamin D production, calcium absorption in the GI tract, renal reabsorption of calcium and phosphate, and regulates calcium mobilization from bone.
197
What is the most common cause of Cushing syndrome?
Exogenous corticosteroid administration.
198
What is the significance of PTHrP in skin health?
PTHrP is implicated in regulating keratinocyte growth and differentiation and uses the same receptors as PTH.
199
What is the relationship between PTH and calcium levels in patients with renal failure?
In renal failure, hyperplastic parathyroid tissue can become autoactivated, leading to tertiary hyperparathyroidism characterized by persistent hypersecretion of PTH despite hypercalcemia.
200
How is the diagnosis of parathyroid disease made?
Through measurements of serum calcium, phosphorous, and intact PTH.
201
What is the role of ACTH in the hypothalamic-pituitary-adrenal axis?
ACTH is secreted by the anterior pituitary and stimulates the production of corticosteroids.
202
What happens in secondary hyperparathyroidism?
It occurs most often in the setting of renal disease, leading to elevated PTH due to altered metabolism of calcium, vitamin D, and phosphorous.
203
What is the clinical significance of measuring PTHrP in hypercalcemia?
Measurement of PTHrP may be useful in the workup of hypercalcemia related to malignancy.
204
What are common skin findings associated with Cushing syndrome?
Common skin findings include easy bruisability and skin thinning, mild hypertrichosis, acne, frank hirsutism, and multiple violaceous striae.
205
What are the two main categories of causes for endogenous Cushing syndrome?
1. Inappropriately high secretion of ACTH, usually from a pituitary microadenoma. 2. Excess cortisol produced by the adrenal cortex independent of ACTH regulation.
206
What diagnostic tests are recommended for confirming Cushing syndrome?
24-hour urine free cortisol and late night salivary cortisol tests.
207
What is the significance of multiple violaceous striae wider than 1 cm in a patient with Cushing syndrome?
This finding is highly suggestive of Cushing syndrome.
208
What is the underlying cause of central obesity, moon facies, and buffalo hump in Cushing syndrome?
These changes are due to the effects of excess glucocorticoids on fat metabolism and distribution.
209
What is the relationship between Cushing syndrome and insulin resistance?
Cushing syndrome contributes to insulin resistance, which can lead to the development of acanthosis nigricans.
210
What is the most recognized cutaneous manifestation of Addison disease?
Hyperpigmentation of skin and mucous membranes.
211
What causes the hyperpigmentation seen in Addison disease?
It develops due to persistently low cortisol levels, leading to increased production of POMC, ACTH, and melanocyte-stimulating hormone.
212
What are some extraneous symptoms associated with adrenal insufficiency in Addison disease?
Weakness, anorexia, weight loss, abdominal pain, postural hypotension, and electrolyte abnormalities.
213
What was historically the most common cause of Addison disease?
Tuberculosis infection.
214
What autoimmune diseases are associated with Addison disease?
Autoimmune polyglandular syndromes 1 and 2.
215
What is a common infectious cause of adrenal insufficiency in Addison disease?
Infection with cytomegalovirus and Mycobacterium avium-intracellulare.
216
What is the most common cause of estrogen excess?
The pharmacologic use of estrogens for birth control, treatment of dysfunctional uterine bleeding, or postmenopausal hormone replacement.
217
What are the cutaneous manifestations of estrogen deficiency?
Epidermal atrophy and loss of cutaneous collagen, leading to dryness and increased wrinkles.
218
How does estrogen replacement therapy affect post-menopausal women?
It can reverse epidermal atrophy and restore cutaneous collagen.
219
What skin changes can occur during pregnancy due to elevated estrogen levels?
Telangiectasias, palmar erythema, spider angiomas, and hyperpigmentation of the nipples and genitalia.
220
What is melasma and how is it related to estrogen levels?
Melasma presents as irregularly shaped, hyperpigmented patches on the face and is associated with elevated estrogen levels during pregnancy or the use of oral contraceptives.
221
What is the significance of the cosyntropin stimulation test in diagnosing chronic adrenal insufficiency?
Inability to produce adequate cortisol is diagnostic for chronic adrenal insufficiency.
222
What are the characteristic features of melasma?
Irregularly shaped, hyperpigmented patches on the forehead, cheeks, nose, upper lip, chin, and neck.
223
What is the most common cause of estrogen deficiency?
Menopause.
224
What causes hyperpigmentation of the nipples and linea nigra during pregnancy?
Elevated estrogen levels during pregnancy.
225
What is Waterhouse-Friderichsen syndrome associated with?
Bilateral adrenal hemorrhage due to acute severe bacterial infection, often from meningococcal infection.
226
What is the most common cause of estrogen deficiency?
The most common cause of estrogen deficiency is menopause.
227
What causes hyperpigmentation of the nipples and linea nigra during pregnancy?
These pigmentary changes are caused by elevated estrogen levels during pregnancy.
228
What is the Waterhouse-Friderichsen syndrome associated with?
Bilateral adrenal hemorrhage due to acute severe bacterial infection, often from meningococcal infection.
229
What is the typical age range for estrogen deficiency to occur?
Around 50 years of age on average, commonly due to menopause.
230
What skin condition can occur after the discontinuation of oral contraceptives?
Telogen effluvium, characterized by diffuse loss of scalp or body hair.
231
What are some cutaneous manifestations of estrogen excess during pregnancy?
Telangiectasias, palmar erythema, spider angiomas, and pigmentary changes.
232
What is melasma and when does it typically occur?
Irregularly shaped, hyperpigmented patches on the face, often referred to as the mask of pregnancy.
233
What is the significance of the cosyntropin stimulation test in diagnosing adrenal insufficiency?
It confirms chronic adrenal insufficiency by measuring serum cortisol response to synthetic ACTH.
234
What are the clinical features of autoimmune progesterone dermatitis?
Characterized by a polymorphous eruption marked by cyclical premenstrual flares, including pruritus and urticaria.
235
What is the role of estrogen replacement therapy in post-menopausal women?
It can reverse epidermal atrophy and restore cutaneous collagen.
236
What can exacerbate acne in pregnant women despite high levels of estriol?
Relative androgen excess due to elevated progesterone.
237
What are the effects of estrogen deficiency on the skin?
Estrogen deficiency leads to skin wrinkling, xerosis, and atrophy.
238
What is Kligman's formula and its components for treating melasma?
Kligman's formula, developed in 1975, is a classic triple-ingredient preparation for melasma treatment, consisting of:
- 5% hydroquinone
- 0.1% tretinoin
- 0.1% dexamethasone in a hydrophilic ointment.
239
What are the common causes of androgen excess in women?
Androgen excess in women can occur from:
- Congenital adrenal hyperplasia (CAH)
- Polycystic ovary syndrome (PCOS).
240
How does estrogen affect sebaceous gland function and hair growth?
Estrogens suppress sebaceous gland function and tend to inhibit hair growth.
241
What is the significance of the hormone progesterone in relation to androgen receptors?
Progesterone can crossreact by binding to androgen receptors, exerting either androgenic or antiandrogenic effects.
242
What laboratory studies might help determine the source of androgen excess?
Laboratory studies may include measurements of 17-hydroxyprogesterone, testosterone, and DHEA-S levels.
243
What is the role of estrogen in skin health?
Estrogen increases epidermal and dermal thickness, water-holding capacity, and improves skin laxity.
244
What is the principal estrogen secreted by the ovaries?
Estradiol is the principal estrogen secreted by the ovaries.
245
What is Kligman's formula used for?
Kligman's formula is used for treating melasma.
246
What are the common treatments for melasma?
Topical retinoids, corticosteroids, azelaic acid, and hydroquinone-based bleaching creams.
247
What is the main hormone secreted by the corpus luteum?
Progesterone is the main hormone secreted by the corpus luteum.
248
What condition is characterized by insulin resistance and androgenic cutaneous findings?
Polycystic Ovary Syndrome (PCOS) is characterized by insulin resistance and androgenic cutaneous findings.
249
What is the most common cause of androgen excess in women?
Androgen excess in women can occur from congenital adrenal hyperplasia (CAH).
250
What is the role of androgens in males during sexual maturation?
In males, cutaneous manifestations of androgen excess occur most commonly with the onset of sexual maturation.
251
What is the significance of the gene CYP21A2 in congenital adrenal hyperplasia?
CYP21A2 encodes for 21-hydroxylase, and its deficiency accounts for more than 90% of cases of congenital adrenal hyperplasia (CAH).
252
What is the effect of estrogen replacement on skin?
Estrogen replacement improves skin laxity and wound healing.
253
What is the relationship between PCOS and metabolic syndrome?
PCOS is associated with metabolic syndrome, characterized by obesity, hypertension, lipid abnormalities, diabetes, and heart disease.
254
What are the clinical features of androgen excess related to acne?
Acne pathophysiology involves the response of sebaceous glands to androgens.
255
How does hirsutism manifest in individuals with androgen excess?
Hirsutism due to androgen excess occurs in a characteristic distribution involving the beard region of the face, chest, upper back, and suprapubic area.
256
What is the typical pattern of androgenetic alopecia in men and women?
In men, it typically presents as symmetric recession of the hairline, while in women, the frontal hairline is usually preserved with diffuse thinning.
257
What role do androgens play in skin health?
Androgens are significant regulators of hair growth and sebaceous gland function.
258
What management options are available for women with hormonally driven acne?
Management may include antiandrogens like spironolactone or oral contraceptive pills with low androgenic activity.
259
What are the potential side effects of finasteride therapy in men?
Side effects can include depression, decreased libido, and erectile dysfunction.
260
What is the underlying pathophysiology of androgenetic alopecia?
Androgenetic alopecia is caused by the conversion of scalp hairs to indeterminate and then vellus hairs due to androgen effects.
261
What are the metabolic syndrome features associated with PCOS?
The features include obesity, hypertension, lipid abnormalities, diabetes, and heart disease.
262
Why is finasteride contraindicated in women of child-bearing age?
Due to possible effects on the development of genitalia and gonads in male fetuses.
263
What percentage of men over 40 are affected by androgenetic alopecia?
Approximately 50%.
264
What is a common cause of persistent acne that should be considered in diagnosis?
Androgen excess, including conditions like CAH, PCOS, or an androgen-secreting tumor.
265
How do androgens affect sebaceous glands?
Androgens influence the response of sebaceous glands, which is part of acne pathophysiology.
266
What is the characteristic distribution of hirsutism due to androgen excess?
It typically involves the beard region of the face, chest, upper back, and suprapubic area.
267
What is the typical pattern of hair loss in men with androgenetic alopecia?
Symmetric recession of the hairline on the frontal and frontoparietal scalp.
268
How does androgenetic alopecia present in women?
The frontal hairline is usually preserved, with diffuse thinning of the crown of the scalp.
269
What role do androgens play in wound healing?
Androgens are involved in the control of wound healing and epidermal differentiation.
270
What medications can be used to treat hormonally driven acne in women?
Antiandrogens like spironolactone or oral contraceptive pills with low androgenic activity.
271
What are the clinical manifestations of acromegaly?
Overgrowth of bone and connective tissue, metabolic effects, and localized tumor mass effects.
272
What regulates the secretion of growth hormone (GH)?
GH-releasing hormone (GHRH), somatostatin, and ghrelin.
273
What is the most common cause of excessive production of growth hormone (GH)?
Excessive production is almost always caused by a pituitary adenoma.
274
What are the metabolic effects associated with acromegaly?
Diabetes, hypertension, and hyperlipidemia.
275
What histological changes are observed in the skin of patients with acromegaly?
Dense deposition of glycosaminoglycans in the dermis, coarse collagen bundles, and increased fibroblasts.
276
What is the primary hormone secreted by the pituitary gland that plays a central role in growth?
Growth hormone (GH).
277
What is the average age of diagnosis for acromegaly?
40 to 45 years.
278
What is the incidence of acromegaly in the United States?
Approximately 11 people per 1 million every year.
279
What is a rare cause of acromegaly aside from pituitary tumors?
A GH-producing tumor in the hypothalamus or an ectopic tumor such as small cell lung cancer.
280
What is the significance of serum IGF1 levels in diagnosing acromegaly?
Serum IGF1 levels can be used as a surrogate measurement of GH and are elevated in acromegaly.
281
What is the primary therapy for GH excess caused by a pituitary adenoma?
The primary therapy is surgical removal, most commonly accomplished through a selective transsphenoidal resection.
282
What are the clinical manifestations of growth hormone deficiency in children?
The primary clinical manifestation is abnormally short stature, which can be corrected by GH administration.
283
What skin findings are associated with patients who have panhypopituitarism?
Fine wrinkling of the skin, decreased pigmentation, and decreased to absent pubic and axillary hair.
284
What are the clinical presentations of GH deficiency in adults?
Decreased lean body mass, decreased strength and exercise capacity, and a loss of general vitality.
285
What is the primary clinical manifestation of GH deficiency in children?
Abnormally short stature.
286
What is the next step if residual disease is present after a transsphenoidal resection of a pituitary adenoma?
Somatostatin analogs like octreotide can be used for medical treatment.
287
What is a diagnostic test for acromegaly?
Failure to suppress the GH level to less than 1 ng/mL 1 to 2 hours after 75 g of oral glucose.
288
What is the role of somatostatin analogs like octreotide in the treatment of GH excess?
They inhibit GH secretion and are used for the medical treatment of residual disease after surgery.
289
What are plasma IGF1 levels dependent on?
Growth hormone (GH).
290
What is a diagnostic test for acromegaly?
Failure to suppress the GH level to less than 1 ng/mL 1 to 2 hours after 75 g of oral glucose.
## Footnote
This test helps confirm the diagnosis of acromegaly.
291
What is the primary therapy for GH excess caused by a pituitary adenoma?
Surgical removal.
292
What is the primary clinical manifestation of growth hormone deficiency in children?
Abnormally short stature.
293
What are some clinical presentations of GH deficiency in adults?
Decreased lean body mass, decreased strength and exercise capacity, and loss of general vitality.
294
What skin findings are associated with panhypopituitarism?
Fine wrinkling of the skin, decreased pigmentation, and decreased to absent pubic and axillary hair.
295
If residual disease is present, what can be used for medical treatment?
Somatostatin analogs like octreotide.
