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Inflammatory Connective Tissue Disease > 30 Raynaud Phenomenon and Vasomotor Syndromes > Flashcards

30 Raynaud Phenomenon and Vasomotor Syndromes Flashcards

1
Q

MC reported initiators of RP

A

1) Cold
2) Emotional stress
3) Exercise

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2
Q

Relative shifts from cool to warmer temp can trigger RP

A

T

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3
Q

Primary vs Secondary RP: Raynaud sign

A

Primary

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4
Q

Primary vs Secondary RP: Raynaud syndrome

A

Secondary

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5
Q

Generally, RP is more common among

A

1) Women
2) Younger age groups
3) Family members of patients with RP

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6
Q

T/F Majority of patients with RP do not have, nor will have, an associated rheumatologic or vascular disorder

A

T

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7
Q

RP occurs at high freq in these rheumatic conditions and is often the initial symptom of these disorders

A

SSc or MCTD

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8
Q

Primary vs Secondary RP: Older age of onset

A

Secondary

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9
Q

Primary vs Secondary RP: Male gender

A

Secondary

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10
Q

Primary vs Secondary RP: Symmetrical involvement

A

Primary

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11
Q

Primary vs Secondary RP: Asymmetrical

A

Secondary

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12
Q

Primary vs Secondary RP: Absence of tissue necrosis, digital pitting, gangrene

A

Primary

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13
Q

Primary vs Secondary RP: Absence of dilated loops on nailfold capillary exam

A

Primary

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14
Q

Primary vs Secondary RP: Signs and symptoms of ischemia proximal to fingers or toes

A

Secondary

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15
Q

Primary vs Secondary RP: Abnormal lab parameters

A

Secondary

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16
Q

Factors influencing vascular reactivity

A

Box 30.2 (p.429)
1) Arterial smooth muscle cells
2) Endothelial cell products
3) Sympathetic nervous system
4) Neuropeptides
5) Other

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17
Q

T/F Primary RP is fully reversible

A

T

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18
Q

Effect of decreased temp to blood vessels

A

Selectively increases response of arterial smooth muscle cells to norepinephrine

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19
Q

Endothelial cell products that influences vascular reactivity and their effects

A

1) NO (vasodilation)
2) Prostacyclin (vasodilation)
3) Endothelin-1 (vasoconstriction)

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20
Q

Effect of sympathetic nervous system to blood vessels

A

NE causes vasoconstriction

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21
Q

Neuropeptide-effect to blood vessel: Substance P

A

Vasodilation

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22
Q

Neuropeptide-effect to blood vessel: Vasoactive intestinal peptide

A

Vasodilation

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23
Q

Neuropeptide-effect to blood vessel: Calcitonin gene-related peptide

A

Vasodilation

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24
Q

Neuropeptide-effect to blood vessel: Neurokinin A

A

Vasodilation

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25
Q

Neuropeptide-effect to blood vessel: Somatostatin

A

Vasoconstriction

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26
Q

Neuropeptide-effect to blood vessel: Neuropeptide Y

A

Vasoconstriction

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27
Q

Effect of angiotensin to blood vessel

A

Vasoconstriction

28
Q

SSc-associated RP fundamentally differs from primary RP because of its associated vasculopathy involving

A

1) Fibrous intimal proliferation
2) Intrvascular thrombi

29
Q

Potent vasoconstrictors with profibrotic activities that have been shown to be overexpressed in the skin of patients with SSc and other forms of secondary RP

A

1) Endothelin-1
2) Angiotensin

30
Q

3 main classes of neurons that can innervate blood vessels

A

1) Sympathetic vasoconstrictor neurons
2) Sympathetic or parasympathetic vasodilator neurons
3) Sensory neurons that can also mediate vasodilation

31
Q

Local nerve endings can also sense the microenvironment and release these vasodilating substances

A

1) Substance P
2) VIP
3) Calcitonin gene-related peptide
4) Neurokinin A

32
Q

Local nerve endings can also sense the microenvironment and release these vasoconstricting substances

A

1) Somatostatin
2) Neuropeptide Y

33
Q

These receptors in digital and cutaneous vesselsare abnormal with enhanced response to stimulation in patients with primary and secondary RP

A

Alpha adrenergic receptors

34
Q

How cold can cause vasoconstriction

A

Selectively amplifies vascular smooth muscle constriction in response to NE mediated through alpha adrenergic receptors

35
Q

How estrogen can cause vasoconstriction

A

Increase alpha-2 adrenergic receptors in vascular smooth muscle

36
Q

Conditions associated with secondary RP in children

A

Box 30.3 (p.430)

37
Q

T/F History alone is accepted as diagnostic for RP in general practice

A

T

38
Q

Diagnostic modality that is associated with danger of precipitating acute catastrophic arteriolar spasm

A

Arteriography

39
Q

T/F Tri-phasic color changes occur in a majority of patients with RP

A

F

40
Q

Frequently involved digits

A

Index, middle, and ring finger

41
Q

Digit often spared in RP

A

Thumb

42
Q

Tender red SC nodules seen in RP

A

Pernio

43
Q

In general RP is more common among: M or F

A

F

44
Q

In general RP is more common among: Young or old

A

Young

45
Q

T/F RP is more common among family members of patients with RP

A

T

46
Q

T/F A large majority of patients with RP do not have and will not develop an associated rheumatic disease

A

T

47
Q

RP occurs at a high frequency for these 2 disorders and is often the initiating symptoms

A

1) SSc
2) MCTD

48
Q

T/F ESR is necessary in the workup of RP

A

F, unnecessary and can be misleading

49
Q

T/F ANA is necessary in the workup of RP

A

F, unnecessary and can be misleading

50
Q

Autoantibodies that can be done for patients with RP that are most sensitive for predicting evolution to SSc

A

Anti-centromere, antitopoisomerase (anti-Scl70)

51
Q

T/F most pediatric patients with secondary RP have a (+) ANA

A

T, 85-100%

52
Q

T/F a significant number of patients with primary RP have a (+) ANA without evidence for assoc with a rheumatic disorder

A

T

53
Q

Compared to RP, perniosis

A

lacks blanching

54
Q

Compared to RP, acrocyanosis

A

does not present with a sharp demarcation

55
Q

General measures for mgt of RP

A

Pg 433, box 30.4

56
Q

First-line in the treatment of RP

A

Non-pharmacologic measures

57
Q

TReatment algorithm for uncomplicated RP

A

Pg 434 Fig 30.4

58
Q

TReatment algorithm for uncomplicated RP

A

Pg 434 Fig 30.5

59
Q

T/F Secondary RP is less likely to show a complete response to CCB compared to primary RP

A

T

60
Q

T/F ACEi are effective for RP

A

F

61
Q

First-line pharma agents for uncomplicated RP

A

CCB

62
Q

Second-line pharma agents for uncomplicated RP

A

Direct vasodilators: NTG, Hydralazine, Minoxidil
Indirect vasodilators: Sympatholytics (prazosin), SSRI (fluoxetine), ACEi (captopril), ARB (losartan), PDEi (sildenafil), Endothelin-1 antagonist (bosentan)

63
Q

First-line pharma agents for complicated RP

A

CCB, aspirin low dose, pain ctrl

64
Q

2nd-line pharma agents for complicated RP

A

Topical NTG (1%)
Na nitroprusside
LMW heparin
Local or regional sympathetic block

65
Q

Major goals in secondary RP

A

Reduce frequency and severity of attacks
Prevent new digital ulcerations
NOT to completely terminate attacks (unrealistic)

66
Q

Key to success in the setting of critical digital ischemia in RP

A

Early intervention

Inflammatory Connective Tissue Disease (8 decks)

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