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MSK II > Final > Flashcards

Final Flashcards

1
Q

When do you screen for developmental delays

A

Status done at every visit; more thorough screening at 9,18, and 24 or 30 months; autism screen at 18 and 24 months

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2
Q

What are the domains of development

A

Gross motor, fine motor, language, cognitive/social-emotional and behavioral

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3
Q

What is M-CHAT-R

A

Modified checklist for autism in toddlers; administer at 18 and 24 months

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4
Q

What should a baby be able to do at 6 months

A

Babble; sits momentarily

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5
Q

What should a baby be able to do at 9 months

A

Mama/dada, pulls up, cruises, sits well without support

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6
Q

What can a baby do at 1 year

A

Separation anxiety, mama/dada, stacks 3 cubes, stands momentarily

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7
Q

What should a baby be able to do at 2 years

A

Walks well, runs, walks up stairs, kicks ball forward, 2 words together, 1/2 of langue understood by people who don’t live in the home, starting interest in potty training; 6 blocks stacked, copy a line

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8
Q

What should a 3 year old be able to do

A

Tricycle, 3 words together, playing in groups (3), 9 blocks, 3/4 of speech understood by strangers

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9
Q

What should a baby be able to do at 4 years

A

Balance on one foot, hop on one foot, 4 body parts, all speech understood by strangers, small sentences, use past tense, copies cross

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10
Q

What should a 6 year old be able to do

A

Tie shoes, skips, draw person with 6 parts

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11
Q

When does Becker MD present

A

After 5 years of age

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12
Q

How are congenital MDs inherited

A

AR

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13
Q

What is Pompe dz

A

AR; alpha glucosidase mutations; build up of glycogen in lysosomes; presents in infancy as hypotonia, hypertrophic cardiomyopathy, resp failure, feeding difficulty, hearing loss; treat with enzymes (myozyme) - can reduce cardiac mass and improve ejection fraction

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14
Q

What is myotonia congenita

A

Mutation in chloride channel (CLCN 1) AD or AR; first symptoms in childhood; muscle stiffness relieved by exercise; muscles hypertrophic; fainting goat syndrome

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15
Q

What is periodic paralysis

A

Repeated episodes of flaccid paralysis of extremities

  • hypokalemia: mutation in calcium and sodium channel; occurs after exercise and carb rich foods
  • hyperkalemia: mutations in sodium channel; occurs while eating potassium rich food or rest after exercise

Treat with acetezolamide

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16
Q

What is juvenile dermatomyositis

A

Most common idiopathic inflammatory myopathy in children; mean onset 7 years; proximal m weakness, heliotrope rash, gottron papules, thrombi or hemorrhage in peri-ungual cap bed; acquired

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17
Q

What can GGT tell you

A

If elevated, think liver

If normal, think muscle

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18
Q

What are the results of nerve conduction studies in Myopathies

A

Normal

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19
Q

What kind of autoab is RF

A

IgM that targets Fc portion of IgG *produced by B cells in synovial joints

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20
Q

What other conditions is RF present in

A

Sjograns, cryoglobulinemia, PBC, mixed connective tissue, endocarditis, SLE, sarcoidosis, malignancy

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21
Q

Is anti CCP or RF more specific for RA

A

CCP

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22
Q

What does a homogenous pattern of ANA suggest

A

Drug induced lupus - histone ab

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23
Q

What does a Rim pattern ANA suggest

A

anti dsDNA; SLE

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24
Q

What does a speckled ANA pattern indicate

A

Anti SM (SLE) or anti SS-a/B sjogren

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25
Q

What is anticentromere ab specific for

A

Scleroderma CREST

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26
Q

What is anti scl 70 specific for

A

CREST

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27
Q

What are the joint fluid analysis results indicative of

A

Noninflammatory: 200-2000 mononuclear cells
Inflammatory: 2000-50000; >50000 septic

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28
Q

How do you treat acute gout

A

NSAIDs, colchicine, steroids

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29
Q

Is CT or MRI better for bone

A

CT

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30
Q

What is the definition of number joints involved in arthiritis

A

Oligo: 3 or <
Pauci: 5 or <
Poly: >6

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31
Q

What endocrine problems can cause arthritis

A

Diabetes: chariots and cheiroarthropathy
Thyroid: carpal tunnel
acromegaly

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32
Q

What is cANCA also called

A

PR3-ANCA

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33
Q

What is pANCA also called

A

MPO-ANCA

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34
Q

What is a speckled staining pattern indicative of

A

Sjogren’s most common

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35
Q

What is the SLE serology

A

Positive ANA, dsDNA (dz activity), smith, decreased complement

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36
Q

What are the 3 types of antiphospholipid abs

A
  • type 1: causes biologic false positive test for syphilis; VDRL
  • type 2: lupus anticoagulant; risk for venous and arterial thrombosis and misarriage; prolonged aPTT; confirmed with abnormal dilute Russell viper venom time (DRVVT) - corrects with phospholipid but not plasma
  • type 3:anti-cardiolipin abs beta2GPI

*abs should be measured on 2 occasions 12 weeks apart

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37
Q

How do you treat hypercoagulability in lupus

A

Start with LMWH/unfractionated heparin then bridge to vitamin K antagonists (warfarin) to achieve goal INR of 2.5

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38
Q

How do you treat antiphospholipid ab in pregnancy

A

Low molecular weight heparin (enoxaparin) + aspirin

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39
Q

What retinopathy is seen with SLE

A

Cotton wool spots

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40
Q

What will you seen in drug induced lupus

A

No renal or neuro sx; positive Ana, positive anti-histone abs

Causes: hydralazine, isoniazid, minocycline, TNF inhibitors, quinidine, chlorpromazine, methyldopa, procainamide

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41
Q

What drug can case an SLE flare

A

Sulfa antibiotics

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42
Q

What is neonatal lupus

A

Affects children born of mothers with lupus; anti Ro or La abs transient (rashes, thrombocytopenia, hemolytic anemia, arthritis) permanent complete heart block*

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43
Q

What is SLE treatment

A

Avoid sun exposure, NSAIDs, corticosteroids, hydroxychloroquine

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44
Q

What increases mortality in SLE patients

A

In early years: infections; kidney or CNS dz

Later: atherosclerosis; MI; leading causes of death in first decade of dz

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45
Q

What are preventative measures for SLE

A

Avoid smoking, minimize risk factors for atherosclerosis, influenza vaccine, pneumococcal q 5 years;cancer screening

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46
Q

What does systemic sclerosis affect

A

Skin, lungs, GI, kidneys, MSK , heart; obliteration of eccrine sweat and sebaceous glands leads to dry itchy skin

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47
Q

What is the treatment for systemic sclerosis

A

No disease modifying therapy; control sx and slow progression; education - warm clothing, smoking cessation; calcium channel blockers for raynauds, ACEI for HTN; antireflux, glucocorticoids for pericarditis (*high doses assoc with renal crisis), cyclophosphamide for lung function, PDE5 inhibitor or CP in patients with pulm HTN

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48
Q

What is morphea

A

Patches seen in localized scleroderma

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49
Q

What is the serology of scleroderma

A

Diffuse: anti-scl 70, anti-DNA topoisomerase, anti-RNA pol III
Limited: anti-centromere

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50
Q

What is the work up for scleroderma

A

CXR, barium swallow, hand x Ray can show distal tuft resorption and calcinosis; ECG, echo, PFT, skin bx

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51
Q

What are the sx of diffuse systemic sclerosis

A

Fatigue, stiffness, malaise, erythema, pruritis, raynaud later, inflammatory edematous phase -> fibrotic phase - skin induration, hyperpigmentation, loss of body hair and impaired sweating; renal crisis - hemolytic anemia*

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52
Q

How can diffuse scleroderma affect skin

A

Hyper/hypopigmentation, dry itchy skin, mask facies, mirostomia, telangitasia, atrophic skin, calcium deposits, raynaud

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53
Q

How can diffuse scleroderma affect GI

A 
Malnutrition - fat, b12, vit D def
Xerostomia
GERD - strictures - Barrett, hoarsnesss, chronic cough
Gastroparesis
GAVE: watermelon stomach
Chronic diarrhea
PBC: anti-mitochondrial ab
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54
Q

What is the primary cause of morbidity and mortality in diffuse and limited scleroderma

A

Pulm involvement

Increased incidence of bronchoalveolar carcinoma

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55
Q

What MSK findings can you seen in scleroderma

A

Carpal tunnel, tendon friction rubs, hypothyroidism

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56
Q

What cancer is sjogrens assoc with

A

B cell NHL

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57
Q

What serology would you see for sjogren

A

Positive ANA, RF, hypergammaglobulinemia, anti-SSA (can lead to newborn complete heart block)/SSB; low C4, high ESR, anemia of chronic dz

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58
Q

What is the treatment for sjogren

A

Dentist and eye doc; cyclosporine drops (cyclin adenosine monophosphate), sips of water, sugarless candy; pilocarpine or cevimeline, hydroxychloroquine for myalgias, glucocorticoids for extra glandular manifestations; avoid atropine drugs and decongestants; no immunomodulatory drug is effective

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59
Q

Who are inflammatory Myopathies more common in

A

AA Women

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60
Q

What are the typical dermal features of inflammatory Myopathies

A

Gottron, heliotrope, periungual erythema, v neck erythema (shawl sign)

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61
Q

What serology would you see in dermatomyositis

A

Elevated CK and aldolase; anti-Jo, anti Mi2, anti-MDA5, anti-P155/140

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62
Q

What is the most common malignancy assoc with dermatomyositis

A

Ovarian - do transvaginal US, CT ab/pelvis, CA-125

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63
Q

What serology would you see with polymyositis

A

Elevated CK, anti-jo; muscle bx: endomysial inflammation

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64
Q

What are the treatment steps for PM and DM

A

Glucocorticoids, taper, IV Ig, trial of rituximab, cyclosporine, cyclophosphamide or tacrolimus

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65
Q

Which myopathy is more common in men

A

Inclusion body myositis and more common in whites

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66
Q

What are the sx of inclusion body myositis

A

Finger flexion or quad weakening; CK mild elevation or normal; bx: endomysial inflammation rimmed vacuoles - anti-cN1A abs

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67
Q

What are some differentials for prox m weakness

A
  • hypothyroid: elevated CK
  • hyperthyroid normal CK
  • cushing: Normal CK
  • polymyalgia rheumatica: pain but no weakness, CK normal
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68
Q

What does takayasu arteritis affect

A

Women; large vessels (aorta and branches - subclavian and innominate), age <40; long smooth tapered stenosis; no UE peripheral pulses; pulm involvement; reintophaty(copper wire), aortic dilation, aortic regurgitation, AAA; *diagnose with MRI or CT; hx: granuloma with giant cells; treat with glucocorticoids

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69
Q

What are the features of behcet syndrome

A

HLA-B5; Asia; recurrent mouth ulcers, genital ulcers, uveitis; large vessel - aneurysms; venous involvement - DVT; pathergy -> pustules at site of sterile needle pricks; mimics MS;ulcers in ileum or cecum; treat with low dose glucocorticoids

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70
Q

Who is PAN more common in

A

Men

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71
Q

What are the sx of PAN

A

Skin- liver reticularis, subcutaneous nodules, ulcers, digital gangrene; vasculitis neuropathy; intestinal angina (postprandial ab pain); renin mediated HTN, renal infarct; CHF; lungs are spared

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72
Q

Ho do you confirm dx of PAN

A

Bx: destruction of bv by inflammatory cells; fibrinoid necrosis; no granulomas
Angio: micro aneurysms
Treat with steroids

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73
Q

How do you treat Kawasaki

A

IVIG w/in 10 days of sx and high ASA

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74
Q

What are the features of Wegners

A

Small vessels; males; ANCA+ (PR3); saddle nose; nodule -> alveolar hem; cavitary lesions on XR; kidney; hearing loss orbital masses, keratitis, venous thrombosis, granulomatous inflammation, necrotizing vasculitis, segmental glomerulonephritis

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75
Q

How do you treat wegners

A

Cyclophosphamide and high dose glucocorticoids or rituximab; methotrexate considered if renal function normal

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76
Q

What is eosinophilic granulomatosis with polyangitis

A

Churg-Strauss; MPO-ANCA; granulomas with eosinophilia; asthma; necrotizing vasculitis; palpable purpura; treat with steroids

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77
Q

What is thromboangiitis obliterans

A

Burger dz; medium vessels; males; smokers; distal vessels first; thrombosis; diagnose with angio: corkscrew appearance

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78
Q

What is nailfold capillaroscopy used to diagnose

A

Raynauds; primary will be normal; in secondary, will show distorted and widened and irregular loops, dilated lumen and areas of vascular dropout

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79
Q

What can cause secondary raynaud

A

Beta blockers, cisplatin or bleomycin; if u/l think thoracic outlet or carpal tunnel

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80
Q

What is treatment for raynaud

A

Keep warm, lotion, stop smoking, limit use of sympathomimetic drugs (decongestants, diet pills, amphetamines), calcium channel blockers, surgery

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81
Q

What populations does polymyalgia rheumatic and giant cell arteritis occur in

A

Women; white; frequently coexist; fever, malaise, weight loss with normal CBC

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82
Q

What are the features of giant cell arteritis

A

Large vessel; cranial aa (temporal, facial, ophthalmic); aortic arch; HA, jaw claudication, PMR, amaurosis faux or diploma; incrased ESR

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83
Q

How do you treat giant cell

A

Steroids before biopsy

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84
Q

What are the features of polymyalgia rheumatica

A

Proximal severe symmetrical morning and daylong stiffness and pain; trouble combing hair; no inflammation on muscle bx, muscle enzymes and EMG normal; elevated ESR and CRP; treat with steroids

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85
Q

What are people with RA at increased risk for

A

Infection, renal dz, GI dz, heart dz, malignancy

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86
Q

Who should be tested for RA

A

At least one joint with definite clinical synovitis not better explained by another dz

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87
Q

What is involved in the scoring system for the test for RA

A

Amount and type of joints affected, serology, acute phase reactants, duration of sx

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88
Q

What abs do you use to measure treatment response in RA

A

ESR and CRP

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89
Q

What part of the spine does RA affect

A

C1-C2

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90
Q

What is pyoderma gangrenosum

A

Tender reddish purple papule leads to necrotic non healing ulcer; seen in RA

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91
Q

What is rheumatoid vasculitis

A

Purpura, petechiae splinter hemorrhages, digital infarct

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92
Q

What is the most common pleural manifestation of RA

A

Pleuritis; nodules; Caplan syndrome - nodular densities after exposure to coal or silica dust

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93
Q

Is feltys positive for RF and CCP

A

Yes

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94
Q

What are the labs for RA

A

Anemia, thrombocytosis, hyperglobulinemia, leukopenia low glucose

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95
Q

What do you have to monitor with methotrexate

A

CBC, LFTs, Creat q 4-8 weeks

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96
Q

What should you not give leflunomide with

A

Cholestyramine

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97
Q

What is enthesitis

A

Inflammation of insertion points of tendons and ligaments; seen in seronegative spondyloarthropathise

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98
Q

What is dactylitis

A

Swelling of finger or toe seen in reactive or psoriatic arthritis

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99
Q

What is spondylitis vs spondylolisthesis vs spondylolysis

A

Spondylitis: inflammation of vertebrae
Spondylolisthesis: anterior displacement of vertebral body relative to adjacent vertebral body belo
Spondylolysis: defeat of bone btw inf and sup articular process of vertebrae

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100
Q

Which arthritides are more common in men

A

Ankylosing spondylitis, reactive arthritis

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101
Q

What manifestations besides the SI joint can ankylosing spondylitis have

A

Achilles tendinitis, plantar fasciitis; iritis (not found in RA)

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102
Q

What is schober test

A

Restricted forward flexion seen in ankylosing spondylitis; if <4 cm decreased mobility

Also will see restricted chest expansion (fabere test) if <5cm decreased

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103
Q

What will the vertebrae look like on imaging of ankylosing spondylitis

A

Squaring (loss of anterior convexity), shiny corners, sclerosis at edge of vertebral bodies

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104
Q

What is DISH

A

Diffuse idiopathic skeletal hyperosteosis - calcifications along lateral aspect of 4 continuous vertebrae bodies; men, back pain, stiffness; no SI involvement

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105
Q

What is osteitis condensans ilii

A

Young females normal SI joints; X ray shows sclerosis os iliac side of SI joint

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106
Q

What is the treatment for ank spondylitis

A

Exercise, PT, swimming, stretching, NSAID, TN alpha inhibitors, DMARD (ok but doesn’t help axial dz)

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107
Q

What is dactylitis a manifestation of

A

Reactive arthritis

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108
Q

What are the clin manifestations of reactive arthritis

A

SI pain, urethritis, conjunctivitis, oral ulcers, circunate balanitis, keratoderma blennorrhagicum (painless eruption on palms and soles), uveitis

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109
Q

What is the treatment for reactive arthritis

A

Usually self limiting; NSAIDs, steroids, if chronic progression use DMARD

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110
Q

What are the features of enteropathic arthritis

A

Parallels activity of IBD; large joints LE small joints UE; pyoderma gangrenosum, erythema nodosum, uveitis, nephrolithiasis, thromboembolism

111
Q

What spondyloarthropathy are DMARDS useful for

A

Psoriatic

112
Q

What would the lab serology show for OA

A

Normal; ESR can be elevated

113
Q

What would you see on XR of OA

A

Asymmetric joint - space narrowing, subchondral sclerosis, osteophytes and marginal lipping, bone cyst, joint mice

114
Q

What is erosive OA

A

Inflammatory; affects DIP and PIP; see seagull appearance central erosions on radiograph (RA is marginal erosions)

115
Q

Where would you see secondary OA

A

Hemochromatosis, joint infection, trauma, surgery, pseudogout, hyperparathyroidism

116
Q

What is the treatment for OA

A

Joint protection, strength training, NSAIDs, duloxetine, tramadol, acetominophen, topical capsaicin

117
Q

What are the most common cervical nerve root compressions

A

C6 and C7

118
Q

What are the most common lumbar nerve compressions

A

L5. And S1

119
Q

What would you see with C5 radiculopathy

A

Pain in scapula and shoulder; loss of sensation in lateral arm; weakness of shoulder abd; loss of biceps reflex

120
Q

What would you see in C6 radiculopathy

A

Pain in scapula, proximal arm and shoulder; loss of sensation in 1st and 2nd digit an lateral arm; weakness in shoulder abd and elbow flexion; loss of biceps and BR reflex

121
Q

What would you see with C7 radiculopathy

A

Pain in scapula, shoulder, elbow and forearm; loss of sensation in 3rd digit; weakness in elbow ext and wrist ext; loss of triceps reflex

122
Q

What would you see with C8 radiculopathy

A

Pain in scapula, shoulder, medial forearm; loss of sensation in 4th and 5th digit; finger abd and flexion weakness, loss of finger flexor reflex

123
Q

What would you see with L4 radiculopathy

A

Pain in anterior lateral thigh, kneee and medial calf; loss of sensation in medial calf; weakness of hip flexion and knee extention; DTR loss patella

124
Q

What would you see with L5 radiculopathy

A

Pain in dorsal thigh and lateral calf; sensory loss in lateral calf and dorsum of foot; weakness in hamstrings, foot dorsiflexion, inversion and eversion; no loss of DTRs

125
Q

What would you see with S1 radiculopathy

A

Pain in posterior thigh and calf; sensory loss in posterior lateral calf and lateral foot; weakness in hamstrings and foot plantarflexion; loss of Achilles reflex

126
Q

What is the dermatome for medial forearm

A

T1

127
Q

What is the dermatome for inguinal area

A

L1

128
Q

What are some etiologies of brachial plexopathy

A

Stretch from surgery (CABG), inflammatory (parsonage-turner), radiation injury (upper trunk, lateral cord, painless), neoplastic (medial cord, painful), traumatic injury, ischemia (diabetic, usually lumbar)

129
Q

What causes positive sx in peripheral neuropathies

A

Paresthesias caused by injury to large myelinated fibers (pins and needles)
Pain secondary to small unmyelinated dz (dysesthesias - pain upon gentle touch, hyperalgesia, hyperpathia)

130
Q

What would loss of large myelinated sensory fibers do

A

Impairment of light touch (cotton swab), two point, vibration, joint position sense

131
Q

What would loss of small unmyelinated fibers lead to

A

Impairment of temperature perception, pain perception (pin prick)

132
Q

What is pronator syndrome

A

Diffuse dull ache of prox forearm; pain exacerbated with forced forearm pronation; easy fatigue of forearm mm; diffuse numbness of hand (particularly median n distribution); no nocturnal awakening

133
Q

What would a needle EMG show in anterior interosseous syndrome

A

Abnormalities in FPL, FDP, PQ

134
Q

What would an EMG should abnormalities in for ulnar mononeuropathy

A

1st dorsal interosseous, abd digiti minimi, add policis, flexor carpi ulnaris, flexor digitorum profundus

135
Q

What is froment sign

A

Grab piece of paper with bent thumb; ulnar neuropathy

136
Q

What would peroneal n entrapment lead to

A

Foot drop, weak eversion, sensory loss in dorsum of foot

137
Q

What would femoral neuropathy lead to

A

Weak knee extension; absent knee jerk

138
Q

What deficiencies can cause peripheral neuropathy

A

B1,6,12, E, copper

139
Q

What is paraneoplastic neuropathy

A

Only sensory

140
Q

How do you confirm small fiber polyneuropathy

A

Decreased epidermal nerve fiber density on skin bx

141
Q

What is the difff btw CMT 1 and 2

A

1 is demyelinating; 2 is neuronal

142
Q

What are the features of CMT 1

A

Onset 1st or 2nd debate; difficulty walking or running; distal symmetric atrophy (legs >arms), Areflexia, mild sensory loss, skeletal deformities (Pes cavus, hammer toes, scoliosis); EMG shows slowing of motor nerve conduction

143
Q

What is diff about CMT 2 presentation

A

Later; EMG shows normal conduction velocity

144
Q

What is fabry’s dz

A

Alpha galactosidase def

145
Q

Does guillaine barre have sensory signs

A

No

146
Q

What indicates a poor prognosis in Guillain barre

A

EMG findings of low amplitude motor n responses

147
Q

What is miller fisher syndrome

A

Ophthalmoplegia, ataxia, Areflexia, Facial weakness, dysarthria, dysphagia, GQ1b an GT1a abs

148
Q

What is multifocal motor neuropathy

A

Males; initially in distribution of single nerve; progressive distal weakness hands > feet; no sensory signs or UMN signs; elevated GM-1 ab; EMG shows conduction block; CSF normal; treatment is IVIG

149
Q

What would Hu ab test for

A

Carcinomatous sensory neuropathy

150
Q

How would you test for heavy metals

A

Urine

151
Q

When can EMG lead to a specific diagnosis

A

GBS, CMT1, MMN

152
Q

What are the presynpatic disorders of NMJ

A

Lambert Eaton, botulism, steroids, magnesium, black widow venom, congenital myasthenic syndrome, aminoglycosides, tetanus, tick paralysis

153
Q

What are the synaptic disease of NMJ

A

Organophosphate, edrophonium, neostigmine, congenital end plate AChE def, nerve agents

154
Q

What are the postsynaptic disorders of NMJ

A

Myasthenia, succinylcholine, D penicillamine, curare, classic slow channel syndrome

155
Q

What are the EMG findings for myasthenia

A

Decreased response on repetitive stimulation; increased jitter on single fiber EMG

156
Q

What’s the treatment for myasthenia

A

AChEI, prednisone, plasma exchange, IVIG, thymectomy

157
Q

What drugs can unmask or exacerbate myasthenia

A

-NMJ blockers: succinylcholine, pancuronium
-Excessive AChEI
-corticosteroids and ACTH with high initial dose*
-thyroid supplements
-BOTOX
-magnesium salt
-antiarrhythmics: lidocaine, quinine, procainamide, verapamil, beta blockers
-abx: aminoglycosides
D penicillamine

158
Q

What is MUSK syndrome

A

3 types, mainly in women
-oculopharyngeal weakness, neck, shoulder, resp weakness, poor response to AChEI and thymectomy; PLEX, IVIG and rituximab best

159
Q

What is the clinical presentation of lambert Eaton

A

Prox weakness, loss of DTRs, dry mouth, impotence

160
Q

How do you treat lambert Eaton

A

AChEI, 3-4 diaminopyridine, guanosine hydrochloride (bone marrow suppression)

161
Q

How do you treat botulism

A

ICU monitoring until toxin clears

Antitoxin - but can cause serum sickness and anaphylaxis
Guanidine hydrochloride: bone marrow suppression

162
Q

How do you treat nerve gas poisoning

A

Remove clothes, sodium hypochlorite; antidotes - atropine until secretions recede; 2-pralidoximine chloride; seizures respond to benzo only

163
Q

What are the nondepolarizing NM blocking drugs

A
  • isoquinoline derivatives: atracurium, cisatracurium, doxacurium, mivacurium, turbocharging
  • steroid derivatives: pancuronium, pipercuronium, rocuronium, vecuronium
164
Q

What is the depolarizing NM blocking drug

A

Succinylcholine

165
Q

What are the AChEI

A

Ambenonium, donepezil, echothiophate, edrophonium, galantamine, neostigmine, physostigmine, pyridostigmine, rivstigmine, tacrine

166
Q

What are the antimuscarinics

A

Atropine, glycopyyrolate

167
Q

What are the cholinesterase reactivators

A

Pralidoxime

168
Q

What are the centrally acting spasmolytics

A

Baclofen, carisprodol, cyclobenzaprine, diazepam, tizanidine

169
Q

What are the noncentally acting spasmolytics

A

Dantrolene and botulinum toxin

170
Q

What are the drugs for MS

A

Glucocorticoids, glatirmer acetate, IFN (beta1a and b), mitoxantrone

171
Q

What are NM blockers used for

A

Adjuncts during anesthesia

172
Q

What are the long acting NM blockers

A

Doxacurium, pancuronium, pipercuronium

173
Q

What are the short acting NM blockers

A

Mivacurium, ultra short is succinylcholine

174
Q

What are the intermediate NM blockers

A

Atracurium, cisatracurium, rocuronium, vecuronium

175
Q

How must you administer nondepolarizing NM blocking agent

A

Parenterally

176
Q

How do you reverse nondepolarizing NM blockers

A

AChE inhibitor, anticholinergics coadministered (atropine, glycopyyrolate)to minimize bradycardia, bronhoconstrition, salivation, N/V

177
Q

What are the adverse effects of nondepolarizing agents

A

Some produce histamine release; at large doses, tubocurarine can produce Ach receptor blockade at autonomic ganglia and adrenal medullary which can cause decreased BP

178
Q

Which inhaled anesthetic has the largest drug interaction with nondepolarizing NM agents

A

Isoflurane potentiates NM blockade

Aminoglycosides also potentiate;

179
Q

How is atracurium eliminate

A

Hoffman reaction

180
Q

Which nondepolarizing muscle relaxant can be used in hepatic and renal failure

A

Cisatracurium

181
Q

How is mivacurium metabolized

A

Cholinesterase

182
Q

Which NM blocking gents have the least tendency to cause histamine release

A

Steroidal; vecuronium, rocuronium (used more often), pancuronium, pipercuronium

183
Q

Which nondepolarizing agent has the most rapid time of onset and can be atlernative to succinylcholine

A

Rocuronium

184
Q

How is succinylcholine metabolized

A

Butyrlcholinesterase and pseudocholinesterase in liver and plasma

185
Q

What are the adverse effects of succinylcholine

A

Bradycardia - reverse with anticholinergic
Hyperkalemia in patients with burns or nerve damage
Increased intraocular pressure

Black box* cardiac arrest; acute rhabdo in kids with undiagnosed myopathy

186
Q

Which AChE inhibitors are irreversible

A

Echothiophate, parathion, malathion, sarin, soman

187
Q

What are the quaternary AChE inhibitors

A

Neostigmine, pyridostigmine, edrophonium, echothiophate

188
Q

What are the tertiary AChE inhibitors

A

Physostigmine, donepezil, tacrine, rivstigmine, galantamine

189
Q

What are the uses of AChE inhibitors

A

Myasathenia, atonic bladder, glaucoma

190
Q

What are the AChE inhibitors used for myasthenia

A

Pyridostigmine, neostigmine and ambenonium

191
Q

What AChE inhibitor is use to reverse pharmacological paralysis

A

Neostigmine

192
Q

What AChE inhibitors are used for Alzheimer’s

A

Donepezil, rivstigmine, galantamine, physostigmine

193
Q

Which nondepolarizing NM blocking agent is potentiated by AChE inhibitors

A

Mivacurium

194
Q

How do you treat AChE inhibitor poisoning

A

Atropine, pralidoxime and benzo

195
Q

What is baclofen

A

Centrally acting spasmolytics; MOA: agonist at GABAa receptor - hyperpolarization due to increased potassium conductance; causes less sedation than diazepam and does not reduce overall m strength; adverse effects: drowsiness and increased seizure - withdrawal slowly; slurred speech

196
Q

What is carisprodol

A

Acts as CNS depressant; addictive potential - use only short term; dizziness and drowsiness; met by CYPC19; metabolized to meprobamate

197
Q

What is cyclobenzaprine

A

Reduces motor activity by influencing alpha and gamma motor neurons; structurally related to TCAs and produces antimuscarinic side effects - section, confusion, hallucinations; met by CYP450; xerostomia

198
Q

What is diazepam

A

Long acting benzo; sedation; MOA: promotes binding of inhibitory neurotransmitter in CNS GABA to GABAa receptor; anxiolytics and anticonvulsant; controlled substance

199
Q

What is tizanidine

A

MOA alpha 2 agonist; decreases excitatory input to alpha motor neurons; causes drowsiness, hypotension, dry mouth, muscle weakness

200
Q

What is dantrolene

A

Non-centrally acting spasmolytic; reduces skeletal m strength (in contrast to centrally acting drugs); MOA; inhibitor of ryanodine receptor; sedation and hepatitis; used to treat UMN disorders

201
Q

What is botulinum toxin

A

Non-centrally acting spasmolytic; MOA cleaves SNARE complex preventing release of ACh; usd for strabismus, axillary hyperhydrosis, chronic migraine prophylaxis

202
Q

How often are glucocorticoids given for MS

A

Monthly bonus IV;

203
Q

What is glatiramer acetate

A

MS drug; MOA: mixture of AA (alanine, glutamic acid, lysine, tyrosine) - induces Treg cells specific for myelin antigen

204
Q

What is the MOA of IFN in MS

A

Acts on BBB by interfering with T cell adhesion to endothelium by binding VLA-4 on T cells or inhibiting T cell expression of MMP; reduces relapses and slows brain atrophy

205
Q

What is mitoxantrone

A

MS drug; antineoplastic; intercalated into DNA resulting in cross links and strand breaks. Related to anthracycline abx

206
Q

What infections can cause motor neuron dz

A

Polio, west Nile, HIV

207
Q

What metabolic syndromes can cause motor neuron dz

A

Alpha glucosidase def (pompe), cancer, thyroid

208
Q

What is hirayama’s dz

A

One upper limb affected; monomelic amyotrophic

209
Q

What is diagnostic testing for ALS

A

EMG shows widespread denervation and reinneration; CPK normal; CSF normal; imaging normal; assess for HIV; muscle bx only needed in confusing cases

210
Q

What are the things you will NOT SEE in ALS

A

No sensory sx; no loss of mental function, no extraocular mm involvement, no bowel or bladder sx, no decubitus, fasciulations rarely the presenting sx

211
Q

What are the common causes of death in ALS

A

Resp failure, pneumonia, pulm embolus

212
Q

What is rituzol

A

Glutamate inhibitor that may prolong life in ALS by 3 to 6 months

213
Q

What is progressive bulbar palsy

A

Selective involvement of lower cranial n motor nuclei; dysarthria, dysphagia, dysphonia, chewing difficulty, drooling, resp difficulty; rarely runs course as isolated syndrome almost always progresses to ALS

214
Q

What is spinal muscular atrophy

A

More common in males; mean onset is 64; LMN deficits predominate due to degeneration of anterior horn cells; no UMN involvement; symmetric UE involvement first; usuallly doesn’t progress to ALS; survival >15 years; better with earlier age of onset

215
Q

What is primary lateral sclerosis

A

UMN (corticospinal) deficit prevails; weakness, spasticity, hyperrreflexia, babinski; slow progression but can evolve into ALS; survival rate better than ALS

216
Q

What is Hopkins syndrome assoc with

A

Asthma; adult motor neuron dz

217
Q

What is the diff btw cream and ointment

A
  • Cream: half water half oil with emulsifier, spreads easily; well absorbed and washes off with water; can’t pump;; better than ointments for oozing skin conditions
  • ointments: more oil than water; feel greasy and are occlusive; stay on surface of the skin; not absorbed; best used for dry skin since they trap moisture ; provide for more absorption of active ingredient; less likely to cause allergic reaction
218
Q

What is important about hand hygiene

A

Should wash 15-30 seconds; should use plain soap

219
Q

What are emollients

A

Form oily layer on top of skin that traps water - petrolatum, lanolin, mineral oil and dimethicone

220
Q

What are humectants

A

Draw water into outer layer of skin; glycerin, lecithin, and propylene glycol

221
Q

What are horny substance softeners

A

Loosens bonds between top layer of cells which helps dead skin cells fall off and helps skin retain water; urea, alpha hydroxy acids, allantoin

222
Q

What are the ingredients in sunscreen

A

PABA: UVB
Benzophenones: less effective
Dibenzoylmethanes: UVA - useful for photosensitivity; and lupus

223
Q

What are sunshades

A

Opaque material that reflex light; ex: titanium dioxide

224
Q

What is glutaraldehyde

A

Antiseptic that cross links proteins

225
Q

What are the disinfectants that affect the inner membrane

A
  • quaternary amine: membrane damage involving bilateral

- chlorhexidine: congealing of cytoplasm

226
Q

What are the oxidizing antiseptics

A
  • halogens: oxidation of thiol groups

- peroxygens: hydrogen peroxide

227
Q

What is chlorhexidine effective against

A

Prevents development of spores but doesn’t kill them; mycobacteriostatic, yeasts, low activity against viruses; high activity against Protozoa

228
Q

What is cadexomeer iodine

A

Reduces bacterial load while providing moist wound environment

229
Q

How do you debride a wound

A

Remove dead tissue, flush with NS,

230
Q

What is becplermin

A

Platelet derived growth factor that promotes cell proliferation and angiogenesis *only agent approved for treatment of chronic diabetic foot ulcers; **BLACK box warning - malignancy

231
Q

What should you use to keep wounds moist depending on stage

A

Debridement stage: hydrogels
Granulation stage: foam and low adherence dressings
Epithelialization stage: hydrocolloid and low adherence dressing

232
Q

What are the topical antibacterial agents

A
  • bacitracin: peptide abx; inhibits cell wall synthesis; active against gram +, neisseriae, tetanus, diptheria; often causes contact derm
  • neomycin: aminoglycoside abx; binds to 30S; gram neg; contact derm
  • polymyxin B: peptide abx; binds to phosphor-lipids to alter permeability; gram neg; rarely causes allergic reaction
233
Q

What are the topical antifungal imidazoles

A

Topical imidazoles: block ergosterol synth; miconazole (cream, vaginal cream), clotrimazole (cream, vaginal cream), efinaconazole (onychomycosis give for 48 weeks), ketoconazole (cream, shampoo)

234
Q

What is ciclopirox

A

Topical antifungal; activity against candida and malezzia

235
Q

What is terbinafine

A

Inhibits squalene epoxidase - neeed for syn of ergosterol; less active against yeast; cream can cause local irritation; avoid contact with mucous membranes

236
Q

What is tolnaftate

A

Antifungal; not effective against candida

237
Q

What is nystatin

A

Binds to fungal sterols and alters membrane permeability;; limited to topical treatments of cutaneous and mucosal candida

238
Q

What is amphotericin B

A

Binds fungal sterols; alters membrane perm; treatment of candida; may cause yellow staining of skin

239
Q

What are the oral antifungals for cutaneous infection.

A

Fluconazole, itraconazole: tinea versicolor
Terbinafine: onychomycosis
Griseofulvin:infections of scalp and non-hairy skin caused by epidermophyton, micro sprout and trichophyton; ineffective against candida and malassezia

240
Q

What can topical calcineurin inhibitors be used to treat

A

Anogenital pruritus

241
Q

What are the topical therapies for itching

A

Doxepin, menthol, capsaicin (neuropathic itch), salicylic acid, local anesthetics (lidocaine, pramoxine - face assoc with CKD)

242
Q

What kind of topical steroid potency should you use in diff areas

A

On face, genitals and skin folds use low potency; anywhere else start high potency then titrations down

243
Q

How does salicylic acid help with itching

A

Causes epidermal cells to shed more rapidly; need protection from sun

244
Q

What antidepressants are helpful in itching

A
  • mirtazapine: nocturnal pruritis
  • paroxetine
  • fluvoxamine
  • sertraline: cholestatic pruritis
245
Q

What mu opioid receptor antagonists are useful for itching

A

Naltrexone: cholestatic pruritis and CKD assoc

246
Q

What kappa opioid receptor agonists/mu antagonists are useful for itching

A

Butorphanol: nocturnal and intractable itching

247
Q

What anticonvulsants are used for itching

A

Gabapentin and pregabalin: neuropathic pruritis; can cause weight gain

248
Q

What substance P antagonist is used for itching

A

Aprepitant: used to control N/V of chemo but benefits in intractable pruritis

249
Q

What is used to get the red out of rosacea

A
  • brimonidine: alpha 2 agonist topical; vasoconstriction by stimulating post synaptic receptors
  • oxymetazoline: alpha1/2 agonist applied topically
250
Q

What is used for eye redness

A

Naphazoline, tetrahydrozoline, phenylephrine, oxymetazoline - all adrenergic agonists

251
Q

What drugs are used to kill ectoparasites

A
  • malathion: topical; organophosphate cholinesterase inhibitor
  • permethrin: topical; binds to insect Na channels and blocks repolarization
  • ivermectin:oral; binds glutamate gated Cl channels and hyperpolarizes it
  • lindane: topical;disrupts GABA transmission in insects but toxic so used last
252
Q

What is the treatment for mild acne

A

Topical retinoid

253
Q

What is the treatment for moderate acne

A

Oral abx + topical retinoid + BPO

If female, can try hormonal therapy + topical retinoid + topical abx

254
Q

What is the treatment for severe acne

A

Oral isotretinoin

255
Q

What is tretinoin

A

Topical retinoid; once daily at bedtime; can cause dryness; fish allergy

Similar: Adapalene, tazarotene (cant use in pregnancy)

256
Q

What are the topical antimicrobials

A
  • benzoyl peroxide: can bleach hair or clothing
  • clindamycin
  • erythromycin
  • dapsone
  • sulfacetamide
257
Q

What is azaleic acid

A

Dicarboxylic acid; white powder found in plants; it kills acne bacteria and decreases production of keratin; used to treat mild to moderate acne and post inflammatory hyperpigmentation

258
Q

What oral abx can you give for acne

A
  • tetracycline
  • doxycycline
  • minocycline - drug induced lupus
  • erythromycin
  • azithromycin
  • TMP-SMX - Steve Johnson
259
Q

What kind of acne is spironolactone usd to treat

A

Adults women with menstrual cycle related breakouts; contraindicated in pregnancy

260
Q

What are the adverse effects of isotretinoin

A

Teratogenic, mucocutaneous effects, hypertriglyceridemia

261
Q

What is the initial choice for mild to moderate psoriasis

A

Emollients and corticosteroids

262
Q

What are the other topical therapies for psoriasis

A

Topical vit D (calcipotriene, calcitriol), tar, tazarotene, calcineurin inhibitors, anthralin, salt water bath

263
Q

What is a good initial choice for moderate to severe psoriasis

A

UVB; photochemo (PUVA) - patients typically ingest plant photosensitizer psoralen before; increases risk of melanoma

264
Q

What are the systemic therapies for psoriasis

A

Methotrexate, apremilast (PDE4 inhibitor), retinoids, systemic calcineurin inhibitors, biological (ustekinumab - IL12 and 23, secukimab and ixekuzumab - IL17)

265
Q

What are the effects of apremilast

A

Decreases NO synthase, TNF alpha and IL23; increase IL 10; oral; HA most common complaint

Crisaborole is topical

266
Q

How is ustekinumab given

A

SQ; increases risk of infections and SCC

267
Q

What is the treament for actinic keratoses

A

Liquid nitrogen cryotherapy, surgery, pharm (5FU, imiquimod, ingenol mebutate - derived from plants, diclofenac, retinoids), red light therapy, dermabrasion, chemical peels

268
Q

What does 5FU do

A

Inhibits thymidylate synthetase - causes destruction of lesion with blistering, necrosis, and then re-epithelialization

269
Q

What is used to treat advanced BCC

A

Vismodegib or sonidegib: oral hedgehog inhibitors

270
Q

What chemo is used for melanoma

A

Dacarbazine

271
Q

What MAPK inhibitors are used for melanoma

A

Used if BRAF mutation; vemurafenib

272
Q

What are treatments for male pattern baldness

A
  • minoxidil: vasodilator due to K opening;increases growth phase and shortens rest phase
  • finasteride: oral inhibitor of dihydrotestosterone production; can cause sex dysfunction; increases hair count
273
Q

What is the treatment for female pattern hair loss

A

Minoxidil is first line

Anti-androgens second line: spironolactone, finasteride, flutamide

274
Q

What is the treatment for alopecia areata

A

Corticosteroid (topical), topical immunotherapy(diphenylcyclopropenone) - used to cause contact derm which increases hair growht

MSK II (2 decks)

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