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FITZPATRICK'S DERMATOLOGY 9TH EDITION (SHAMMY) > 22 - 148 - CUTANEOUS CHANGES IN ARTERIAL, VENOUS AND LYMPHATIC DYSFUNCTION > Flashcards

22 - 148 - CUTANEOUS CHANGES IN ARTERIAL, VENOUS AND LYMPHATIC DYSFUNCTION Flashcards

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1
Q

Disease in the distal superficial femoral artery causes:

a. Claudication in the thigh

b. Claudication in the calf muscle

c. Claudication in the buttocks

d. Claudication in the ankle

A

B

Page 2669. Because the disease is most common in the distal superficial femoral artery, patients most commonly present with claudication in the calf muscle area (the muscle group just distal to the arterial disease). When the disease affects the more proximal aortoiliac vessels, thigh and buttock muscle claudication predominates

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2
Q

A 65-year-old male was seen in the OPD due to ulceration on his right foot associated with intermittent claudication. He is hypertensive and diabetic. ABI was 0.89. What is the interpretation of this result?

A. Normal

B. Abnormal

C. Borderline

D. Elevated

A

B

Page 2671. Normal ABI range is 1.00 to 1.40. A value less than or equal to 0.90 is considered abnormal, and values of 0.91 to 0.99 are defined as “borderline.” Of note, patients with heavily calcified or “noncompressible” vessels, most commonly persons with diabetes or of advanced age, may have falsely elevated ABIs (greater than 1.4) despite the presence of significant PAD.

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3
Q

When the ABI is borderline or normal despite symptoms suggestive of claudication, what test is recommended?

A. Exercise ABI

B. Doppler waveform analysis

C. MRI

D. CT angiography

A

A

Page 2671. When the ABI is borderline or normal despite symptoms suggestive of claudication, an exercise ABI is recommended.

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4
Q

First line therapy for the treatment of obstructive peripheral artery disease except

A. Cilostazol

B. Clopidogrel

C. Statin therapy

D. Exercise program

A

B

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5
Q

The major risk factor for the development of atheromatous embolism is:

A. Atherosclerotic disease of the thoracic or

abdominal aorta

B. Coronary artery disease

C. Peripheral artery disease

D. Abdominal aortic aneurysm

A

A

Page 2676. The major risk factor for the development of atheromatous embolism is atherosclerotic disease of the thoracic or abdominal aorta.

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6
Q

Arteriography findings, in particular findings of corkscrew-shaped collaterals, are typical, but not pathognomonic for the condition.

A. Peripheral artery disease

B. Atheromatous embolism

C. Thromboangiitis obliterans

D. Livedo Racemosa

A

C

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7
Q

Characteristic of livedo racemosa except:

A. Symmetric, fishnet-like red or purple mottling with a pale conical core

B. May improve with warming but no complete resolution

C. Symptoms related to associated causative disorder

D. Surrounding skin shows purpura, nodules, macules, ulcerations, atrophie blanche– type scarring

A

A

Page 2682. Table 148-11. A is a characteristic of livedo reticularis. Livedo Racemosa - Asymmetric, irregular, and “broken”

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8
Q

This is the cooccurrence of primary lymphedema and myelodysplasia/acute myeloid leukemia.

A. Emberger Syndrome

B. Milroy Syndrome

C. Lymphedema-Distichiasis

D. Elephanthiasis Nostras Verrucosa

A

A

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9
Q

most classic symptom of PAD

A

intermittent claudication,

which is usually described as pain, fatigue, or tiredness in a defined muscle group distal to the diseased vascular segment upon walking that is relieved by rest

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10
Q

peripheral arterial disease is most common in what artery

A

distal superficial femoral artery

patients most commonly present with claudication in the calf muscle area (the muscle group just distal to the arterial disease)

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11
Q

Features of Acute limb ischemia

A
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12
Q

hallmark noncutaneous finding in PAD

A

Decreased or absent pulses distal to the stenotic arterial segment

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13
Q

How do you test for collateral circulation

A

With the patient supine, elevation of the limb at a 45-degree angle for 2 minutes should not produce pallor. Collateral circulation is deemed inadequate if the toes and feet become pale. The patient then assumes a sitting position with the legs dependent, and the time for filling of the foot veins and flushing of the feet is measured. The veins should fill within 20 seconds and the feet flush immediately in a warm environment. When these times exceed 30 seconds, the collateral circulation is deemed inadequate, and the patient must be observed frequently for the development of rest pain, ulcers, or gangrene.

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14
Q

Most significant atherosclerotic risk factors

A

DM and smoking

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15
Q

Under resting conditions, normal blood flow to extremity muscle groups

A

300 to 400 mL/min

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16
Q

normal ABI

A

1.00 to 1.40

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17
Q

Abnormal ABI

A

less than or equal to 0.90

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18
Q

Borderline ABI

A

0.91 to 0.99

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19
Q
A
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20
Q

How can you differentiate diabetic neuropathy ulcer from arterial limb ulcers

A

Diabetic neuropathic ulcers:
- may develop on the heel, toes, or shin in the presence of normal pulses. These painless (neurotrophic) ulcers are caused by repetitive trauma not noticed by the patient because of the peripheral neuropathy. With regard to the foot, ulcers often occur over pressure points with a surrounding callus.

Arterial limb ulcer
- exquisitely tender, do not have a preference for pressure points on the foot, and lack a surrounding callus.

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21
Q

most feared consequence of PAD

A

severe limbthreatening ischemia leading to amputation

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22
Q

Differential Diagnosis of Foot Ulcers

A
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23
Q
A
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24
Q

Identify the type of ulcer

A

Arterial

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25
Q

Identify the type of ulcer

A

Venous ulcer

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26
Q

Identify the type of ulcer

A

Neuropathic ulcer

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27
Q

Goal of medical management of PAD

A

measures to halt the progression of the disease as well as to alleviate the symptoms

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28
Q

measures to halt the progression of PAD

A
  • cessation of smoking
  • optimization of risk factors, such as diabetes mellitus, hypertension, and hyperlipidemia
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29
Q

Treatment of choice for patients with symptoms of intermittent claudication

A

Exercise program

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30
Q

Patients with intermittent claudication often are instructed to exercise to the threshold of tolerable pain, briefly rest, and then exercise again for a total duration of ___________

A

30 to 60 minutes a day in excess of their normal activity, 3 or more times a week.

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31
Q

First line treatment for Obstructive Peripheral Arterial Disease

A
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32
Q
A
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33
Q

Target LDL for PAOD

A

< 100 mg/dL

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34
Q

Two agents have been approved for the indication of intermittent claudication in the United States

A

Cilostazol
Pentoxifylline

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35
Q

phosphodiesterase inhibitor with antiplatelet and vasodilatory properties, is an effective treatment to improve symptoms and increase walking distance in patients with obstructive peripheral arterial disease

A

Cilostazol

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36
Q

affects red cell deformability and blood viscosity and can be considered as second-line alternative therapy to cilostazol

A

Pentoxifylline

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37
Q

highly effective for aortoiliac disease and is often indicated for moderate, or lifestyle-limiting claudication

A

Endovascular intervention with angioplasty or stenting

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38
Q

most consistent adverse risk factor associated with the progression of occlusive peripheral artery disease

A

Continued smoking

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39
Q

Target LDL in PAOD if with uncontrolled or multiple risk factors

A

<70 mg/dL

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40
Q

embolization of small pieces of atheromatous debris from the more proximal arteries to the smaller distal arteries

A

Atheromatous embolism

Synonyms include cholesterol embolism, atheroembolism, blue toe syndrome, and pseudovasculitis syndrome.

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41
Q

major risk factor for the development of atheromatous embolism

A

atherosclerotic disease of the thoracic or abdominal aorta

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42
Q
A
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43
Q

In atheromatous embolism, What do you call the Funduscopic examination, revealing cholesterol embolus within branching points of the retinal arteries

A

Hollenhorst plaques

It. is a specific but insensitive finding because most atheromatous emboli arise from a source distal to the aortic arch

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44
Q

Organ systems that can be involved in atheromatous embolism

A
  1. Renal
  2. CNS
  3. Gastrointestinal; colon - most commonly affected
45
Q

rare, progressive, inflammatory and thrombotic disease that predominately affects small- and medium-sized arteries of the extremities

A

Thromboangiitis obliterans (TAO), also known as Buerger disease

It is strongly associated with the use of tobacco products, and seen mostly in men between the ages of 20 and 40 years.

46
Q
A
47
Q

First-line therapy for Thromboangiitis obliterans

A
48
Q
A
49
Q

only strategy proven to prevent the progression of thromboangiitis obliterans

A

Absolute discontinuation of tobacco use

50
Q

ischemic dermopathy characterized by a violaceous reticular or “net-like” mottling of the skin

A

Livedo

51
Q

primary disorder affecting young to middle-aged females that is benign. The livid conical discoloration is symmetric, reversible, and uniform

A

Livedo reticularis

52
Q

secondary disorder that is pathologic and permanent.

The livid conical discoloration is asymmetric, irreversible, and “broken.”

A

Livedo racemosa

53
Q

It is the most frequent dermatologic manifestation in patients with antiphospholipid syndrome, present in 25% of patients with primary antiphospholipid syndrome, and in up to 70% of patients with systemic lupus erythematosus–associated antiphospholipid syndrome

A

Livedo Racemosa

54
Q

Differentiate Livedo Reticularis and Livedo Racemosa

A
55
Q
A

Symmetric and relatively uniform, conical rings of primary, reversible livedo reticularis (cutis marmorata).

56
Q
A

Permanent and “broken” rings of secondary livedo racemosa on the buttocks and thighs in a woman who had cerebrovascular thrombosis. This is an example of Sneddon syndrome.

57
Q
A
58
Q

marker for predicting multisystem thrombosis in the antiphospholipid antibody syndrome

A

Livedo Racemosa

59
Q

Intense, burning pain with marked erythema, typically of the lower extremity.

A

ERYTHROMELALGIA/ ERYTHERMALGIA

60
Q

ERYTHROMELALGIA commonly affects what body part

A

Lowe extremities but may affect the upper extremities as well as other body parts, such as the face and ears.

61
Q

Triggers of erythromelalgia

A

precipitated by activities that increase the body temperature, such as exercise, ambient temperature, or the use of heavy blankets at night.

The episodes also can be triggered by dependency of the limb, wearing socks, or tight shoes, and sometimes with the ingestion of alcohol or spicy foods.

There are also reports of episodes triggered by ingestion of some drugs, such as pergolide, bromocriptine, and calcium channel blockers (nifedipine, felodipine, and nicardipine)

62
Q

Relieving factor of erythromelalgia

A

cold exposure (eg, standing on a cold floor) or immersion in ice water often relieves the flares

63
Q

T/F: The peripheral pulses are usually normal or bounding in erythromelalgia

A

True

64
Q

What gene mutation is associated with inherited erythromelalgia

A

SCN9A, the gene encoding voltagegated sodium channels of sensory nerves

65
Q

Most common complication of chronic venous disease

A

Venous ulcers

66
Q

Risk factors of chronic venous disease

A

genetics,
obesity,
female gender,
pregnancy,
occupations requiring prolonged standing,
surgery,
trauma,
malignancies

67
Q

Early signs of Peripheral venous disease

A

VESH

  • Varicose Veins
  • Edema
  • Stasis Dermatitis
  • Hyperpigmentation
68
Q

Late signs of Peripheral venous disease

A

LAU

  • lipodermatosclerosis
  • atrophie blanche
  • ulcers
69
Q

Risk factors for chronic venous disease

A

heredity, age, female sex, obesity, pregnancy, prolonged standing, phlebitis, previous leg injury, and greater height

70
Q

Common Signs and Symptoms of Peripheral Venous Disease

A
71
Q

Earliest finding in chronic venous disease

A

perimalleolar edema that ascends up the leg, followed by soft tissue tenderness, even of normal appearing skin

72
Q

Characteristics of stasis dermatitis

A

erythema, scaling, pruritus, erosions, crusting, and occasional vesicles and serous drainage may occur during any stage of chronic venous insufficiency

73
Q

Area most commonly involved in stasis dermatitis

A

medial supramalleolar region where microangiopathy is most intense

74
Q

pliable subcutaneous fat is gradually replaced by fibrosis, and the skin begins to feel firm and indurated.

A

lipodermatosclerosis (sclerosing panniculitis, hypodermatitis sclerodermiformis)

75
Q

refers to skin overlying areas of fibrosis that often appears porcelain white and atrophic

A

Atrophie blanche

76
Q

purple macules, nodules, or verrucous plaques on the dorsal feet and toes of patients with longstanding venous insufficiency and mimics Kaposi sarcoma clinically and histologically

A

Acroangiodermatitis (pseudo-Kaposi sarcoma, congenital dysplastic angiopathy, arteriovenous malformation with angiodermatitis)

77
Q

Venous ulceration in chronic venous disease is classically located in what area?

A

Gaiter area

“ Although ulceration is classically located in the gaiter area (Fig. 148-13), venous ulcers have been described as ulcers occurring anywhere below the knee. Venous ulcers are typically tender, shallow, irregular, and have a red-base (Figs. 148-13 and 148-14). They are usually located on the medial ankle or along the line of the long or short saphenous veins.”

78
Q

Loss of lymphatic drainage from the lower leg may lead to verrucous changes and cutaneous hypertrophy called

A

elephantiasis nostras

79
Q

most common cause of venous valvular failure

A

Thrombosis

80
Q

nidus for venous thrombosis

A

Valve cusp

when the thrombus is lysed by plasmin, valve function is often lost as well

81
Q

Calf muscle pump failure after deep venous thrombosis is often referred to as the

A

postphlebitic syndrome

82
Q

ankle-brachial index is reliable except in the presence of

A

calcified vessels, which are noncompressible and therefore a true systolic pressure cannot be measured.

83
Q

Histologic signs of venous hypertension

A

hemosiderin deposition, lobular superficial and/or deep dermal neovascularization, and fibrosis of the dermis and subcutaneous tissue in later stages

84
Q

Contraindications to compression therapy

A

arterial occlusive disease or abnormal ankle, brachial indexes

85
Q

zincimpregnated gauze wrap

A

Unna boot

86
Q

selfadherent second layer (Coban, for example) over a zinc wrap

A

Duke boot

87
Q

cornerstone of venous ulcer management

A

fadherent second layer (Coban, for example) over a zinc wrap was introduced as the “Duke boot”.

This has proven to be easy to apply with reproducible, graduated, inelastic compression to counter the outflow from perforator incompetence, and is the cornerstone of venous ulcer management.

88
Q

cornerstone of venous ulcer management

A

fadherent second layer (Coban, for example) over a zinc wrap was introduced as the “Duke boot”.

This has proven to be easy to apply with reproducible, graduated, inelastic compression to counter the outflow from perforator incompetence, and is the cornerstone of venous ulcer management.

89
Q

mainstay of treatment for all clinical manifestations of chronic venous insufficiency

A

Mechanical therapy

Daily use of elastic compression stockings reduces swelling in some patients with postthrombotic syndrome, and may prevent worsening of established postthrombotic syndrome and reduce recurrence of healed venous ulcers

90
Q

herbal remedy that appears to be safe and effective as a short-term treatment for leg pain and swelling

A

Horse chestnut seed extract (Aesculus hippocastanum L.)

91
Q

Measurement required for graduated stockings in CVD

A

Graduated stockings that provide a minimum of 30 to 40 mm Hg at the ankle should be carefully fitted to all patients and worn for their lifetime. It is a mistake to place elastic stockings on edematous limbs, especially those limbs that are tender. Compression bandaging should be used until all edema, inflammation, and tenderness have resolved before fitting the patient with stockings.

92
Q

Once a patient develops venous thrombosis, this is the only proven method to reduce the risk of postthrombotic syndrome

A

elastic compression stockings

93
Q
A
94
Q
A
95
Q
A
96
Q

refers specifically to swelling of a part of the body due to impaired lymph transport capacity as a consequence of a malformation or malfunction of the lymphatics

A

Lymphedema

97
Q

congenitally determined intrinsic or constitutional fault in lymphatic drainage

A

Primary lymphedema

98
Q

Most common cause of secondary lymphedema

A

Paraiic infection

99
Q

cooccurrence of primary lymphedema and myelodysplasia/acute myeloid leukemia.

A

EMBERGER SYNDROME

100
Q

Mutation in EMBERGER SYNDROME

A

GATA2, which regulates the transcription of genes that are important for both development and maintenance of lymphovenous and lymphatic vessel valves

101
Q

aberrant eyelashes arising along the posterior border of the eyelid margin, which frequently leads to eyelash irritation of the cornea and photophobia

A

double row of eyelashes (distichiasis)

Seen in LYMPHEDEMA-DISTICHIASIS

102
Q

Signs and Symptoms of Lymphedema

A
103
Q

Early signs of lymphedema

A

■ Erysipelas

■ Pitting edema

104
Q

Late signs of lymphedema

A

■ Nonpitting edema

■ Papillomatosis

■ Secondary infections (bacterial, fungal, viral warts)

■ “Ski-jump” upturned toe nails

■ Thickened, woody skin

■ Verrucous tissue overgrowth

105
Q

What do you call the sign where there is Thickening of the skin overlying the digits

A

Kaposi-Stemmer sign (inability to pinch up a fold of skin between the second and third toe on the dorsum of the foot).

Seen in lymphedema

106
Q
A
107
Q

Therapeutic options for lymphedema

A
108
Q

T/F: Diuretics improves lymphedema by improving lymph drainage.

A

False.

Diuretics are frequently prescribed, and not only do they not alleviate the symptoms, they may actually worsen the condition and should not be used as a primary treatment for lymphedema

FITZPATRICK'S DERMATOLOGY 9TH EDITION (SHAMMY) (122 decks)

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