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BRAIN BATTACK > CH45: Muscle > Flashcards

CH45: Muscle Flashcards

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1
Q

Muscles make how many percent of body weight of human beings (p. 1405)

A

40%

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2
Q

interdigitating filaments
contractile proteins
structural proteins
regulatory proteins

(p. 1405)

A

myofilaments
actin and myosin
titin and nebulin
tropomyosin and troponin

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3
Q

Basic physiologic unit in all reflex, postural and voluntary activities (p. 1405)

A

Motor unit

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4
Q

Type I vs Type 2 Muscles (p. 1406)

A

Type 1: increase oxidation, decrease glycogen stores

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5
Q

percussion myotonia vs myoedema (p. 1410)

A

myoedema are electrically silent

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6
Q

brief fascicular contraction that is induced by tapping a anormal or partially denervated muscle (p. 1410)

A

idiomuscular contraction

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7
Q

In this type of contracture, the muscles remain shortened for many minutes because of failre of the metabolic mechanism necessary for relaxation (p. 1410)

A

trye physiologic contracture

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8
Q

There is fibrosis of muscle and surroinding tissues as a result of ischemic injury usually after a fracture of the elbow (p. 1410)

A

Volkmann contracture

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9
Q

Form of fibrous contracture that is found in newborns involving two features: fibrosis of muscle and neural or muscular apparatus that results in muscular weakness (p. 1410)

A

Arthrogryposis

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10
Q

Triad of Satayoshi syndrome (p. 1411)

A

pianful leg cramps
alopecia universalis
diarrhea

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11
Q

Puffy face and tender muscles
Biopsy: segmental necrosis, interstitial infilammatory infiltrates, predominance of eosinophils
EMG: profuse fibrillation potentials
(p. 1415)

A

Trichinosis

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12
Q

Treatment for Trichinosis

A

No treatment is required in most cases.

If with severe cases: thabendazole, predinisone or albendazole

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13
Q

Weakness, wasting, myalgia, failure of other organs, increased CK
focal infammation where parasitic pseudocyst ruptures

A

Toxoplasmosis

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14
Q

Treatment for Toxoplasmosis (p. 1415)

A

Sulfadiazine with Pyrimethamine or trisulfapyramide

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15
Q

Parasitic infection wherein there is dramatic pseudohypertrophy of calf muscles (p. 1415)

A

cystecircosis

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16
Q

HIV treatment with myopathy as side effect (p. 1416)

A

Zidovudine

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17
Q

Pattern of weakness in early HIV patients (p. 1416)

A

painless wekaness of girdle and proxima limb muscles
Elevated CK
EMG: fibrillations, brief polyphasic motor units, complex repetitive discharges

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18
Q

Pathologic findings in Zidovudine- induced myopathy (p. 1416)

A

Presence of ragged red fibers

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19
Q

representative example of inflammatory myopathy
painbless weakness of the proximal limb muscles
ocular muscles are rarely affected
muscles are not tender
dermatologic findings:localized or diffuse erythema, maculopapular eruption, scaling eczematoid dermatitis, exfoliative dermatitis (p. 1417)

A

Dermatomyositis

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20
Q

Dermatologic findings in dermatomyositis (p. 1417)

A

Gottron papules
- red, raised, papules on the elbows, knuckles and distal and proximal IPjoints

Heliotrope rash

Shawl sign

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21
Q

Other physical findings in dermatomyositis (p. 1418)

A

periarticular and subcutatneous calcifications

Reynaud phenomenon

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22
Q

Also check in patients with polymyositis (p. 1418)

A

Cardiac abnormalities
Interstitial lung disease with anti- Jo
Carcinoma (lung and colon in men; breast and ovarian in women)

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23
Q

Gait in pediatric patients with dermatomyositis (p. 1418)

A

tiptoe gait because of the contractures of flexors of the ankles

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24
Q

Specific antibodies in severe, necrotizing inflammatory myositis (p. 1419)

A

SRP (cytoplasmic ribonucleoprotein complex)

Mi-2 (nuclear helicase)

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25
Q

anti tRNA synthetase (p. 1419)

A

anti-Jo

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26
Q

EMG findings in DM and PM (p. 1420)

A

polyphasic units that simulate denervation- reinnervation changes, juxtaposed with myopathic motor units

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27
Q

DM vs PM pathological findings (p. 1420)

A

DM- perifascicular muscle fiber atrophy
PM- scattered

Inflammatory infiltrates
DM- perimysial connective tissue
PM- endomysium

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28
Q

Principal changes in idiopathic PM (p. 1420)

A

widespread destruction of segments of muscle fibers with an inflammatory reaction
phagocytosis of muscle fibers by mononuclear cells and infiltration with a varying number of lymphocytes and lesser numbers of other mononuclear and plasma cells

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29
Q

DM vs PM re etiology and pathogenesis (p. 1421)

A

PM- large number of activated T cells, mainly CD8 class whereas B cells are sparse

DM- the percentage of B cells at all sites is significantly higher than it is in PM

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30
Q

Treatment for DM or PM (p. 1421)

A

prednisone 1mg/kg

acute or severe cases: MPPT 1g IV each day for 3 -5 days

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31
Q

Prognosis of DM or PM (p. 1422)

A

Good

extent of recovery depends on acuteness and severity of the disease

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32
Q

steadily progressive, painless, muscular weakness and modest atrophy usually distal in the arms and both proximal in the legs (p. 1422)

A

Inclusion Body Myositis

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33
Q

Contrast DM and IBM (p. 1422)

A

The deltoids are spared and the thumb flexors are weak in IBM (opposite to PM and and DM)

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34
Q

IBM vs ALS (p. 14223)

A

the EMG changes are restricted to the weakend muscles

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35
Q

Denominative finding in IBM (p. 1423)

A

intracytoplasmic, subsarcolemmal vacuoles, eosinophilic inclusions

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36
Q

Cystosolic antibodies found 2/3 of patietns with IBM (p. 1423)

A

anti-cN1

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37
Q

Treatment of IBM (p. 1423)

A

difficult; not responded in any consistent fashion to treatment with corticosteroids

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38
Q

Antibody directed to the signaling of TGF-b has shown the improvement of muscle mass; but no definitive clinical effect yet.

A

Bimagrumab

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39
Q

Features that virtually exclude myositis (p. 1424)

A
  1. lack of reduced peak power of contraction

2. normal EMG, serum enzymes and muscle biopsy

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40
Q

In eosinophilia-myalgia syndrome, severe eosinophilia and myalgia were found following the ingestion of which amino acid? (p. 1425)

A

L- tryptophan

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41
Q 
dystrophy with rapid progressive course
X linked recessive
almost exclusively in amles
symptoms show before learning to walk
greatly elevated CK 
waddling gait
A

Duchenne muscular dystrophy

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42
Q

Muscles that are large in DMD (p. 1427)

A

gastrocnemii
lateral vasti
deltoids

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43
Q

Waddling gait in DMD is due to (p. 1427)

A

weakness of gluteus medius

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44
Q

Posture of DMD (p. 1427)

A

lumbar lordosis
hip flexion and abduction
knee flexion
plantar flexion

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45
Q

ECG findings in DMD (p. 1427)

A

prominent Rwaves in R prevordial leads and deep Q waves in L precordial and limb leads

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46
Q

EMG findings in DMD (p. 1427)

A

fibrillations, positive wavesw, low- amplitude and brief polyphasic MUP, high frequency discharges

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47
Q

MD onset is later
patient can walk into adult life
retain their ability to raise the head fully off the bed (p. 1428)

A

Becker Muscular Dystrophy

48
Q

most distinctive features of DMD and BMD (p. 1428)

A

prominent segmental degeneration and phagocytosis of single muscle fibers or groups of fibers and evidence of regeneerative activity
necrosis excites a regenerative or restorative process which explains the forking of fibers and clustering of small fibers with prominent nuclei
hyalinization of sarcoplasm
contraction bands, expressive of the irritability of dystrophic muscle

49
Q

Hypertrophy of muscle in DMD and BMD due to (p. 1428)

A

work-induced enlargement of the remainign sound fibers in the face of adjacent fiber injury

50
Q

largest gene known to human, spanning more than 2Mb of DNA (p. 1428)

A

Dystrophin

51
Q

X-linked muscular dystrophy
special feature is muscle contractures
early appearance of contractures in the flexors of the elbow, extensors of the neck and posterior calf muscles
(p. 1429)

A

Emery-Dreifuss Muscular Dystrophy

52
Q

Constituent of the nuclear membrane, encoded by EMD on the X chromosome (p. 1429)

A

emerin

53
Q

slowly progressive dystrophy, with periods of complete arrest
age of osnet 6-20 years old
Weakness and atrophy are major physical findings
present with difficulty raising the arms
deltoids may seem to be unusually large and strong
amyoplasia is associated
(p .1430)

A

Fasciohumeral Muscular Dystrophy

54
Q

Biceps waste less than the triceps and the brachioradialis muscles even less. Hence, upper arm may be thinner than fore arm. (p. 1430)

A

Popeye effect

55
Q

FSHD1 gene (p. 1431)

A

DUX4, on tip of chromosome 4q

56
Q

Early onset, relatively rapid progression of FSH
Facial diplegia
sensorineural deafness
exudative retinal detachment (p. 1431)

A

Coats disease

57
Q

Patients that dont fit to DMD, BMD, GSH; lack hypertrophy of calves

A

LGMD
LGMD1- dominant 6
LGMD2- recessive 19

58
Q

Achilles tendon contracture
Very high serum CK levels
Dysferlin

A

Calpainopathy

59
Q

Problems of levators of the eyelids
Simultaneous invlvement of all EOM permits the eye to remain in a central position hence diplopia is uncommon
Hutchinsonian facies (p. 1433)

A

Kearns Sayre Syndrome

60
Q

Kearns Sayre mutations (p. 1434)

A

twinkle
ANT1
POLG

61
Q

Oculopharyngeal Dystrophy gene (p. 1434)

A

PABN1

62
Q

Unstable nucleotide sequence in Myotonic Dystrophy (p. 1434)

A

CTG

63
Q

Myotonia +distal weakness
Cardiac arrthythmias
Small muscles of the hands along with extensor muscles of forearms atrophy
hatchet facies
Swan neck
Progressive frontal alopecia, testicular atrophy, gynecomastia(p. 1434)

A

Myotonic Dystrophy 1

64
Q

Myotonic dystrophy vs Myotonia congentia (p. 1434)

A

In myotonic dystrophy, the characteristic hypertrophy in myotonia congenita is absent

65
Q

Pathologic feature in Myotonic Dystrophy (p. 1436)

A

peripherally placed sarcoplasmic masses and circular bundles of myofibrils (ringbiden)

66
Q

Most prominent features of congenital myotonic dystrophy (p. 1436)

A

profound hypotonia

facial diplegia at birth

67
Q

T/F Like the expanded CTG repeat in myotonic dystrophy, the CCTG expansion in PROMMis assocaited with intranuclear accumulation of the expanded RNAtranscript and like the CTG repeat of myotonic dystrophy, the CCTG segments do not code for a protein (p. 1436)

A

T

68
Q

adult life onset
weakness and atrophy of the leg muscles most prominent in the peroneal or the gastroneius and soleus muscles
dysferlin

A

Miyoshi Myopathy

69
Q

The major congenital muscular dystrophies share an improtant biologic attriubte: (p. 1439)

A
  1. abnormality of a protein that binds to the dystrophin complex (laminin or merosin)
  2. abnormality of a protein in the Golgi apparatus taht is important in processing proteins
70
Q

Predominant isoform of alpha-laminin (p. 1439)

A

Merosin

71
Q

Treatment of Myscular Dystrophies (p. 1440)

A

Prednisone 0.75mg/kg daily

72
Q

This drug is shown to reduce myotonia (p. 1441)

A

Mexiletine

73
Q

Enzyme that initiates the metabolism of glycogen (p. 1442)

A

Myophosphorylase

74
Q

T/F All the glycogenoses are inherited as autosomal recessive traits (p. 1442)

A

T

75
Q

Skeletal muscles are weak and hypotonic
Tongue is enlarged giving the infant a cretinoid appearance
Pompe Disease (p. 1442)

A

Acid maltase deficiency

76
Q

Treatment for Acid Maltase deficiency (p. 1443)

A

Enzyme replacement therapy

77
Q

Primary deficiency of myophophyrylase (which prevents the conversion glycogen to glucose 6-phosphate)

Primary deficiency of phosphofructokinase deficiency (which converts glucose 6 phosphate to glucose 1 phosphate)

p. 1443

A

McArdle disease

Tarui disease

78
Q

Test for McArdle disease and Trui disease (p. 1443)

A

forearm ischemic exercise test

lactate fails to rise

79
Q

Treatment for McArdle and Tarui (p. 1444)

A

Sucrose 75g in a beverage

80
Q

Carnitine is derived from (p. 1445)

A

lysine and methionine

81
Q

Progressive lipid storage myopathy and cardiomyopathy
No dicarboxylic aciduria
(p. 1447)

A

Primary systemic carnitine deficiency

TX: L carnitine 2 to 6 g/d

82
Q

Differentiate the Carnitine Palmitoyltransferase Deficiency (p. 1447)

A

I necrosis of muscle fiers; between attacks normal muscles
IIA lipid bodies in liver
IIB lipid bodies in liver, heart, kidneys, skeletal muscle

83
Q

Recently, this drug has been helpful in patients with mild CPTII (p. 1447)

A

Bezafibrate

84
Q

Muscle of the pelvic girdle and thigh are weakend more than others in thyroid myopathies (p. 1448)

A

Basedow paraplegia

85
Q

EOM affected in thyroid myopathy (p. 1449)

A

inferior and medial recti

86
Q

T/F pupillary and ciliary muscles are always spared (p. 1449)

A

T

87
Q

How many percent of patients with MG have hyperthyroidism (p. 1449)

A

5%

88
Q

Cretinism +muscle abnormalities (p. 1450)

A

Kocher Debre Semelaigne syndrome

89
Q

Myxedema + muscle hypertrophy (p. 1450)

A

Hoffman syndrome

90
Q

Speed of contractile process is related to __
Speed of relaxation depends on ___

(p. 1450)

A

myosin adenosine triphosphatase

release and reaccumulation of calcium

91
Q

EMG findings of corticosteroid myopathy (p. 1450)

A

mildly myopathic– small and abundant action potentials but no fibrillations

92
Q

Noted to be related in the incidence of critical illness myopathy (p. 1450)

A

intake of neuromuscular blockade

93
Q

Identifying histologic feature in patients with critical illness myopathy (p. 1451)

A

striking loss of thick myosin filaments. Sevvere degrees of muscle necrosis; accompanied by elevated CK levels and myoglobinuria with renal failure

94
Q

In hypoparathyroidism, this is prominent.

In hypo and hyperparathyroidism, this is prominent. (p. 1451)

A

Muscle cramping

Tetany

95
Q

Biopsy findings in weakness in acromegaly (p. 1452)

A

atrophy and reduced numbers of type 2 fibers; necrosis of only a few fibers

96
Q

statin myopathy noted to be worse when this drug was added (p. 1453)

A

gemfibrozil

97
Q

gene carrying risk fo statin myopathy (p. 1453)

A

SLCO1B1

98
Q

Pathologic finding in Colchicine neuromyopathy (p. 1454)

A

rimmed vacuoles on Gomori trichrome strain more central in the muscle fibers than those seen with IBM

99
Q

Manifestation of acute alcohol myopathy (p. 1454)

A

severe pain, tenderness, edema of the muscles of the limbs and trunk

100
Q

Muscles noted to be absent in amyoplasia (p. 1455)

A 
Palmaris longus
Pectoralis
Trapezius
Serratus anterior
Quadriceps femoris
101
Q

Agenesis of the pectoral muscle with scoliosis, webbed fingers, underdevelopment of ipsilateral arm and hand (p. 1455)

A

Poland syndrome

102
Q

Gene associated with floppy infant and risk for malignant hyperthermia (p. 1457)

A

RYR1 Mutation of Central Core myopathy

103
Q

EMG findings of central core myopathy (p. 1457)

A

brief, small- amplitude motor unit potentials with normal interference pattern

104
Q

Unique feature of central core myopathy (p. 1457)

A

central portion of each musce fiber of a dense, amorphous condensation of myofibrils or myofibrillar material

105
Q

Unlike the central core myopathy, the muscles of the trunk and limbs (proximal > distal) as well as the facial, lingual, and pharyngeal muscles are strikingly thin and hypoplastic. (p. 1457)

A

Nemaline (Rod-Body) Myopathy

106
Q

Nemaline Rod Myopathy are genetically heterogenous but 20% are due to mutations in (p. 1458)

A

ACTA1

107
Q

Myopathy with hypotonia, weakness. Limbs remain flexic throughout life. Motor development is slowed. Cerebral abnormality with seizures is noted. (p. 1458)

A

Centronuclear Myopathy

108
Q

EMG findings in muscle cramps (p. 1460)

A

high frequency, high voltage action potentials and precramp phase with runs of activity in motor units

109
Q

Mechanism of cramping is obscure but this enzyme is controversially included (p. 1460)

A

myoadenylate

110
Q

Treatment for cramps (p. 1460)

A

Quinin sulfate but no longer recommended due to ventricular arrhythmia

Diphenhydramine hydrochloride
Phenytoin
Carbamazepine

111
Q 
Universal alopecia
Amenorrhea
Intestinal malabsorption- diarrhea
Epiphyseal destruction
Retarded growth (p. 1460)
A

Stayoshi syndrome

112
Q

Proximal muscle pain, sometimes asymmetrical
Common in middle age
Every movement reported is stiff and painful
(p. 1461)

A

Polymyalgia rheumatica

113
Q

Widespread pain

Focal areas produced by 4kg digital pressure in 11/18 typical locations over muscles, tendon and bones (p. 1461)

A

Fibromyalgia

114
Q

Deposition of bone within substance of muscle (p. 1463)

A

Myositis ossificans

115
Q

First symptom of myositis ossificans (p. 1463)

A

firm swelling and tenderness in a paracertebral or cervical muscle

116
Q

Myositis ossificans vs calcinosis universalis (p. 1463)

A

Calcinosis universalis usually occurs in relation to scleroderma or polymyositis and is characterized by calcium deposits in the skin, SC tissues, and connective tissue sheaths round the muscles.

In myositis ossificans, there is actual bone in the muscles.

117
Q

Treatment for myositis ossificans (p. 1463)

A

Diphosphanate (inhibits deposition of calcium phosphate)

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