Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Musculoskeletal Diseases > Apex- Musculoskeletal diseases > Flashcards

Apex- Musculoskeletal diseases Flashcards

1
Q

Select the statement that BEST describes myasthenia gravis

A. Pregnancy reduces the severity of symptoms
B. Neonates of affected mothers are at risk for msucle weakenss
C. Edrophonium impairs muscle strength during symptom exacerbation
D. Acetylcholine production is decreased

A

B. Neonates of affected moms are at risk for muscle weakness

A - pregnancy exacerbates the sx of MG
B- yes - anti- AchR IgG antibodies cross placenta
C- doesnt fix the non-functioning post synaptic receptors
D- Ach is present in sufficient quantiy - post synaptic issue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Myasthenia gravis- are symptoms worse in the morning or worse as the day goes on

A

worse as the day goes on

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Early signs of Myasthenia gravis (2)

A

diplopia and ptosis

bublbar muscle weakenss - dysphagia, dysarthia, drooling
DOE
proximal muscle weakness (jsut think oral muscles affected, they are proximal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Thoughts about mom with myasthenia gravis

A

Her: preganancy and stress exacerbate sx
baby: 15-20% of neonates come out with weakness

Anti-AchR IgG antibodies cross placenta - can persist for up to 2-4 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What’s the Tensilon test and when would it be used? How much?

A

Edrophonium 1-2mg IV to somone with MG to differentiate between cholineric crisis from too much pyridostigmine or exacerbation of MG (myasthenic crisis)

Edrophonium = anticholinesterase

-if muscle strength improves, the pt has myasthenic crisis
> increasing the concnetration of ACH at the NMJ improved the pts muscle strengtrh
> if it doesnt > cholinergic crisis - give anticholinergic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Patient with MG will be (select 2):

-Sensitive to Vec
-Resistant to Roc
-Sensitive to Sux
-Resistant to Sux

A

Sensitive to Vec
Resistant to Roc

Sensitive to NDMR - less functioning receptors = less that need to be blocked
Resistant to SUX- sux requires functioning receptors to exert it’s effects

-neurotransmission is imparied, takes more sux (acts like ach) to depolarize the membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

If sux is indicated in a myasthenia gravis patient for RSI, how should you adjust the dose?

A

increase to 1.5-2mg/kg
(resistance to sux)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

identify the characteristics comon to Eaton-Lambert syndrome (select 3):

-destruction of voltage-gated calcium channels
-bulbar muscle weakness
-diagnosed with tensilon test
-destruction of the nicotinic recpetor
-increased sensitivity to sux
-small cell lung ca

A

-destruction of voltage-gated calcium channels
-bulbar muscle weakness
-diagnosed with tensilon test
-destruction of the nicotinic recpetor
-increased sensitivity to sux
-small cell lung ca

the other 3 are myasthenia gravis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How are eaton lambert and MG similar and how are they different

A

they both are disorders of the NMJ resulting in muscle weakness mediated by IgG destruction

Eaton Lambert = destruction of presynaptic voltage-gated calcium channels at the presynaptic nerve terminal

Myasthenia gravis = estruction of the post-synaptic nicotinic ach receptors on the motor endplate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is myasthenic syndrome

A

Eaton-Lambert Syndrome

IgG mediated destruction of the presynaptic voltage gated calcium channels that result in muscle weakness

AKA: Lambert- Eaton Myasthenic syndrome (LEMS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Common comorbidies with Eaton-Lambert Syndrome vs MG

A

EL = small cell lung ca (oat-cell)
MG = thymoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Muscle weakness in EA vs MG

proximal/distal muscles
which one better in the morning and which one worse

A

both proximal muscles

EA= worse in the AM and gets better throughout day
MG= best in the AM and gets worse throughout day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

T/F: Anticholinestereases can be helpful with eaton-lambert syndrome

A

false

tensilon test dont do shit either

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is 3,4-diaminopyridine (DAP) used to tx?

what does it do?

A

Eaton-Lambert Syndrome

increases Ach release from the presynaptic nerve terminal and improves strength of contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

which disease begins with an influenza-like illness that is followed by ascending paralysis?

A

Guillain-Barre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What describes a group of diseases characterized by intermittent attacks of skeletal muscle weakness that are associated with hypo- or hyperkalemia

A

Familial periodic paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What describes a group of diseases where the hallmark is prolonged muscle contracture (myotonia) after a voluntary skeletal muscle movement

A

Myotonic dystrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is myotonia

what is it associated with

A

prolonged muscle contracture

myotonic dystrophy

occuring after a voluntary skeletal muscle movement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is Charcot-Marie-Tooth disease?

A

an inherited peripheral neutopathy presenting as skeletal muscle weakness and wasting

-usually confined to the lower third of the legs but can also affect the quads, hands and forearms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the most common cause of acute, generalized paralysis

A

GBS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Which diseae is characterized by an immunologic assault on the myelin in the peripheral nerves

A

GBS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

GBS time frames:
flu like illness:
symptoms persists for:
full recovery within:

A

1-3 weeks prior to symptoms
2 weeks
4 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe the paralysis associated with GBS

A

flaccid paralysis beginning distally and ascending proximally twoards the trunk and face

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Treatment for GBS (2)

A
  1. IV IgG
  2. Plasmapheresis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

T/F: steroids are useful in treatment of GBS

A

FALSE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

SUX vs NDMR for GBS

A

NO SUX!!

-reduce dose of NDMR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Can you use regional anesthesia for GBS?

A

controversial - inconclusive data

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

The peripheral nervous system includes all the nerves of the body where

A

outside of the brain and spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is acute idiopathic polyneuritis?

A

GBS

immunolgic attack on myelin in the peripheral nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

3 most common viruses associated with GBS

3 other things assoicated with it

A
  1. Campylobacter jejuni bateria
  2. Ebstein-Barr Virus
  3. Cytomegalovirus

  1. vaccines!
  2. surgery!
  3. lymphomatous diseaise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Which NMD will ephedrine result in an exaggerated response and why

A

GBS

peripheral desruction of mylin, impaired synaptic transmission, upregulation of postjuncitonal reeptors - acetycholine and adrenergic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is plasmapheresis and when would it be used?

A

it’s when blood is withdrawn from the body, blood and plasma are seperated into plasma and cells, and the cells are transfused back

-goal is to remove plasma which has antibodies that are causing issues in autoimmune diseases

like dialsysis but specifically removes antibodies from the plasma portion of hte blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

T/F: Interferon has shown to improve outcomes in GBS

A

False -MS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

T/F: Regional anesthesia is preferrred over GA in GBS

A

False

there is controversy with regional and GBS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Which agents are safe to administer to the patietn with hypokalemic periodic paralysis? (select 2):

-Roc
-terbutaline
-D5LR
-Acetazolamide

A

ROC & Acetazolamine

*acetazolamide is the treatment for both hyperand hypokalemic variants

-hypokalemia periodic paralysis can follow a glucose-insulin infusion. pt becomes weak when serum k decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Hypokalemic vs Hyperkalemic period paralysis

-which results in muscle weakenss following a glucose-insulin infusion vs potassium administration

A

hypokalmeic - glucose-insulin infusion
hyperkalemia- oral potassium administration

both result in skeletal mujscle weakenss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Treatment for Familial period paralysis - hypo vs hyperkalemic forms

A

Acetazolamide for both

-creates a non-anion gap acidosis (loss of bicarb)- protects agaisnt hypokalemia
+facilitates renal K excretion > guards agisnt hyperkalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Familial periodic paralysis - which is more important to avoid- hypo or hyperthermia

A

avoid hypothermia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Sux considerations with familial periodic paralysis: hyperkalemic vs hypokalemic

A

hyperkalemic- contraindicated for obvious reasons
hypokalemic- contraindicated bc it’s associated with MH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

T/F: Familial Periodic paralysis is a disease of the NMJ

A

FALSE- disorder of the skeletal muscle membrane

hypoklemic PP Is associated with a calcium channelopathy
hyperkalemic PP is associated with a sodium channelopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Which NMD is acetazolamide used for and why

A

Familial periodic paralysis- both varients hypo or hyperkalemia

it results in non-anion gap acidosis, protecting agaisnt hypokalemia
and facilitates renal potassium exretion - protecting agaisnt hyperkalemia

*FPP = skeletal muscle weakness resulting from either hypo or hyperkalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

T/F: LR has potassium in it

A

True

avoid in hyperkalemic periodic paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

MH isi primarily associated with the genetic mutation of the:
A. SERCA2 pump
B. ryanodine receptor
C. dihydropyridine receptor
D. actin myofilamint

A

B.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is an inheritied disease of skeletal muscle that’s characterized by disordered calcium homeostasis?

A

MH

exposure to halogenated anesthetics or sux activates the defective ryanodine recpetor (RYR1) > stimulates the sarcoplasmic retriculum to release way to much calcium into the cell.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What happens with MH when the defective ryanodine receptor (RYR1) is exposed to triggering agents?

A

it stimulates sacroplasmic reticulum to release way too much calcium into the cell

> sustained skeletal muscle contraction
>hypermetabolic state
increased o2 consumption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

MH triggers -2

A

halogenated anesthetics and depolarizing NMBs (SUX)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

3 co-existing diseases that are definitely associated with MH

A
  1. King-Denborough syndrome
  2. Central core disease
  3. Multiminicore disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Is Duchenne’s muscular dystrophy associated with MH?

A

no

but its assoicated with rhabdo if sux is given

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

T/F: MH is not associated with Beker musuclar dystrophy

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Is myotonia congenitia a risk factor for MH?

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

T/F: myotonic dystrophy carries of risk of MH

A

False

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

T/F: osteogenesis imperfecta is not associated with MH

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

RyR1 receptor vs RyR2 receptor

A

RyR1 is located in skeletal muscle
RyR2 is located in the cardiac muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Word association game:

King-Denborough syndrome

A

MH

+central core disease
+multiminicore disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Word association game:

Central core disease

A

MH

+king-denborough syndrome
+mulitminicore disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Association b/t MH and Duchenne’s

A

halogenated agents and sux can initiate an MH-like syndrome but this is NOT MH, it’s due to rhabodmyolysis

lack of dystrophin (a structural protein) destablizes the sarcolemma during muscle contraction and increases membrane permeability

so giving SUX = muscle contraction = destabalized sarcolemma
>CA is free to enter the cell , increasing rate of metabolism
>intracellular K is free to exit > hyperkalemic cardiac arrest
>Myoglbin is free to exit the cell > renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

T/F: Duchenne’s pts have a normal RyR1 receptor and can safely get inhalationals and sux

A

False - they DO have a normal RyR1 reeptor but cant get inhalational and sux bc they cause a MH-like syndrome caused by rhabdo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

T/F: ANY pt with duchennes should get TIVA over GA

A

True

INH can induce rhabdo somehow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

ANY patient with ANY muscular dystrophy who sustains cardiac arrest on induction should immediately be treated with what

why

A

Calcium chloride

assume severe hyperkalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Incidence of MH

A

1:5,000 to
1:50,000

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

4 states that have a higher risk of MH

A

Wisconsin
Nebraska
West Virgina
Michigan

males > females

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Early vs Late signs of MH (3 each)

A

Early = masseter spasm, increased etco2, tachy
Late = hyperthermia, cola urine (rhabdo), DIC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is the most sensitive indicator for MH

A

EtCO2 that rises out of proportion to minute ventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

MH can occur as late as how many hours/days following exposure to a triggering agent

A

6 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Core temp can (but does not always) begin to rise within what time frame after exposure to a triggering agent

A

15 mins

but profound hyperthermia is usually a late sign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are the differences between trismus and masseter muscle rigidity

A

Trismus = tight jaw that an still be opened (normal response to sux)

Masseter muscle rigidity = tight jaw that cant be opened (NMB will not relax)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

T/F: true masseter muscle rigidity cannot be relaxed with a NMB

A

True -yikes then what lol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

T/F: if a patient experiences masseter muscle rigidity, assume MH until proven otherwise

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

4 differential diagnosis’s for MH

A
  1. thyroid storm
  2. pheo
  3. sepsis
  4. heatstroke
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Early/intermediate/late sign of MH:

warm soda lime

A

Early

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Early/intermediate/late sign of MH:
Irregular heart rhythm

A

can occur during any phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Early/Intermediate/late sign of MH:
musle rigidity

A

late

*masster spasm is early

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

T/F: masseter muscle rigidity can be a normal response to sux

can you proceed with surgery?

A

FALSE - Trismus (jaw tight but can still be opened) can be a normal response to sux

no for masseter muscle, yes for trismus

prob wise to convert to a non-triggering agent anyway they say

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Why won’t NMB work for masseter muscle rigidity?

A

bc the spasm is due to increased calcium in the myoplasm which is distal to the NMJ, so blocking it wont fix the problem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What is the caffeine-halothane contracture test the gold standard for diagnosing?

how is it done?

sensitivity/specificity?

A

MH

live muscle biopsy sample

high sensitivity and low specificity
(think MH is HIGHLY SENSITIVE to SUX)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Which drug is contraindicated in the management of MH?
A. Verapimil
B. Mannitol
C. Calcium chloride
D. Insulin

A

A. Verapamil

due to life-threatening hyperkalemkia that can resoult when a CCB is co-administered with dantrolene

-mannitol is in each vial of dantroline so rule that out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

T/F: data suggests dantrolene prophylaxis is MH precaution patients

A

false

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

MH Precautions: 3 things you want to do

A
  1. Flush with high flow o2 for 20-100minutes dependeing on vent
  2. remove and replace all external parts
    > CO2 absorbent, circuit, breathing bag
  3. Remove vaporizers
79
Q

T/F: if pt doesnt present with s/s MH within the ifrst hour, it’s very unlikely that it will occur later

A

True

80
Q

How do you use charcoal filters

A

put one on each port (I&E) of anesthesia machine and flush the machine with high FGF > 10LPM for 90 seconds prior to using machine on pt

81
Q

Dantrolene - what are the 2 MOAs

A
  1. reduces calcium release from the RyR1 recpetor in the skeletal myocyte
  2. prevents calcium entry into the myocyte , which reduces the stimulus for calcium-induced release
82
Q

Dantrolene vial:
How many mg dantrolene
What else is in it
How much to reconsitute with and what

A

20mg
3g of manitol
60mL of preservative-free water

83
Q

T/F: you should diute dantrolene with NS

A

false- introduces additional solute, prolonging the time it takes for it to dissolve

60mls of perservative-free water

84
Q

T/F: dantrolene is classified as a muscle relaxant

A

true

85
Q

First 3 steps in treating MH

A

4 is giving dantrolene or ryanodex

  1. Discontinue triggering agent
  2. Call for help (notify suregon to terminate)
    3-A. hyperventilate with 100% fio2 at a minimum of 10L/min
    3-B charcoal filters and new circuit and bag

*dont waste time changing the soda lime

86
Q

How often do charcol filters need to be replaced?

A

every hour

87
Q

Dose of Dantrolene

when to stop

A

2.5mg/kg IV every 5 -10 mins

stop when symptoms of hypermetabolism subside

88
Q

If pt requires more than how much dantrolene should you then reconsider a diganosis of MH

A

> 20mg/kg - no more than 8 doses

89
Q

Ryanodex vial contains how much dantrolene

how much to dilute

A

250mg

5mL of sterile water

90
Q

MH pt…your giving dantrolene, cooling them, correcting acidosis, treating hyperkalemia….how should you protect agaisnt dysrhythmias?

A

Class 1 antidysrhythmics

Procainamide 15mg/kg IV
Lidocaine 2mg/kg IV

91
Q

MH- urine output should be maintained greater than what

why

how can you facilitae this

A

> 2ml/kg/hr

protects agaisnt renal injury from free myoglobin

IV hydration
Mannitol 0.25mg/kg IV
Fureosemide 1mg/kg IV

92
Q

MH can reoccur up to how many hours post stabalization

A

36 hrs

93
Q

MH- when to stop cooling pt

A

when temp drops below 38

94
Q

Can you give calcium with MH ?

A

Yes calcium chloride 5-10mg/kg IV for hyperkalemia

insulin 0.15units/kg + 1ml/kg D50

95
Q

Insulin and D50 dosing for MH hyperkalemia

A

0.1units/kg + 1ml/kg D50

96
Q

10 Steps in treating MH

A
  1. D/C agent
  2. call for help
  3. A- hyperentilate 100%/10L
  4. B- charcoal filter and change circuit
  5. Dantrolene 2.5mg/kg q 5 mins w 60mls water
  6. cool pt
  7. correct acidosis
  8. treat hyperkalemia
  9. protect agaisnt dysrhythmias
  10. maintain uop > 2ml/kg/hr
  11. coags to check for DIC (impending demise)
97
Q

Preop findings in the patient with Duchenne muscular dystrophy include: (select 2):

-mitral stenosis
-pulmonary fibrosis
-increased creat kinase
-deep q waves in limb leads

A

-increased creat kinase
-deep q waves in limb leads

  • dystrohin stablizes cell membrane - DMD has none so sarcolemma becomes unstable during contraction and increases membrane permeability.

-CK leaks through muscle membrane > elevated plasma concentration

-like skeletal muscle, cardiac muscle is also at risk for degeneration, leading to MR (not stenosis, cardiomyopathy, and conduction defects

-scarring of the posterobasal aspect of hte lv manifests as R wave amplitude increase in lead I and deep Q waves in limb leads

98
Q

EKG changes in DMD (2)

A

deep q waves in limb leads
increased R wave in lead I

from scarring of hte posterobasal aspect of the left ventricle … great

-found something that says when calcium freely inters the cell, it activates proteases that destroy contactile elements and cause inflammation, fibrosis , and cell death

-while that somewhat suports this scarring - why is it only the posterobasal aspect of the LV?

99
Q

T/F: DMD just affects skeletal muscle

A

false

cardiac muscle is also at risk for degeneration leading to MR, cardiomyopathy, and conduction defects

100
Q

What is the most common skeletal muscle myopathy?

A

Duchenne’s muscular dystrophy

absence of dystrophin protein

101
Q

T/F: DMD results in a restrictive lung disease

A

True - from kyophoscoliosis

102
Q

DMD is an x-linked autosomal (recessive/dominate) disease

A

x-lined recessive

103
Q

What is the critical structural component of the skeletal and cardiac myocytes that helps anchor actin and myosin to the cell membrane

A

Dystrophin

104
Q

Why does are DMD pts at risk of hyperkalemia following sux?

A

bc the absence of dystrophin allows extrajunctional reeptors to populate the sarcolemma

105
Q

3 signs of cardiomyopathy

A
  1. resting tachycardia
  2. JVD
  3. S3/S4 gallop
  4. displacement of PMI
106
Q

What angle describes the magnitude of spinal curvature in pts with scoliosis

what angle is an indication for surgery

A

Cobb

> 40-50 degrees

107
Q

Scoliosis surgery 6 considerations

A
  1. VC < 40% predicted correlates with requirement for post-op ventilation
  2. cervical scoliosis may cause difficult intubation
  3. thoracic correction higher than T8 may require one-lung ventilation
  4. prepare for significant blood loss
  5. monitor end-organ perfusoin with serial ABGs ( risk of metabolic acidosis) and urine output
  6. risk of VAE
108
Q

Pt’s undergoing scoliosis correction…. VC < what would indicate need for post op ventilation

A

< 40%

109
Q

thoracic scolioisis correction higher than what may require one-lung ventilation

A

> T 8

110
Q

T/F: VAE is a risk with scoliois correction surgery

A

true

111
Q

5 causes of scoliosis

which has the highest incidence

A
  1. idopathic*
  2. Congential
  3. myopathic
  4. neuropathic
  5. traumatic

idopathic = 80% of caes

112
Q

2 myopathic caues of scolioisis

A

muscular dystrophy
amytonia congenita

113
Q

Cobb angle of what is associated with decreased pulmonary reserve

what angle would pulm symptoms be seen

A

60

70

thats why they suggest you get it corrected when its 40-50

114
Q

Goal of spinal fusion with instrumentation fo scolioisis is what

A

to stop the progression of hte curvature and prevent further deterioation of cardiopulmonary function

115
Q

cardiac complications associated with scoliosis mostly affect the right or left heart

A

right - due to increased PVR

RV hypertrophy
RV strain
RA enlargement

but also may have MVP, MR, and coarctation of aorta

116
Q

T/F: MVP is the most common co-exisiting cardiac condition in those with scoliosis

A

True

MR & coarcaation too

117
Q

Which is superior for the pt in the prone position to reduce IAP and improve pulm compliance… jackson frame or wilson

A

Jackson better

118
Q

T/F: Nitrous oxide increases PVR

A

True

119
Q

VAE would result in (select 2):
-increaed etco2
-decreased etco2
-increased PacO2-Etco2 gradient
-decreased Paco2 - etco2 gradient

A

-decreased etco2
-increased paco2-etco2 gradient

increased dead space (air no blood), VAE

120
Q
A

Dens

AKA: Odontoid process

superior boney projection off the axis (C2)
provides a pivot point that faciltates head rotation

121
Q

RA impacts the airway in what 3 places

A
  1. TMJ
  2. Cricoarytenoid joint
  3. Cervical spine
122
Q

T/F: RA decreases mouth opening and size of the glottic opening

A

True

*use smaller ETT to minimize laryngeal trauma
*risk of post-extubation airway obstruction

123
Q

atlantoaxial subluxation and seperation of the atlanto-odontoid articulation is the most common airway complication of which disease?

what does this increase the risk for (2)

A

RA

quadriparesis or paralysis

124
Q

You see your pt has RA… so you appropriately downsize your tube, your preceptor asks why

A

bc they have RA which affects the cricoarytenoid joints and they can have decreased glottic opening diameter

125
Q

RA pts are at risk for quadriparesis or paalysis due to c-spine immobility, is flexion or extension worse?

A

flexion

RA= no flex ZONE

126
Q

If you see pt has hx RA- try and pay attention to their voice quiality- why

A

bc if they are hoarse, stridorus, or dyspneic, theres an increased risk of airway obstruction (cricoarytenoid arthritis)

127
Q

T/F: the thoracolumbar spine is generally not affected by RA

A

true

128
Q

Anesthetic considerations for the patient with RA include (select 3):

-Aortic regurg
-obstructive ventilatory pattern
-hypercoagulability
-hypoglycemia
-anemia
-pulmonary effusion

A

Anemia
Aortic regurgitation
Pulmonary effusion

aortic regurg from dilation of hte aortic root

-restritive pulm defect due to intersistal fibrosis, costrochondral involevment and pleural effusions
-NSADS = first line tx of RA; asa inhibits plaetet functio nand increases risk of bleeding
-glucocortioids are used to reduce inflammation. this ncreases (not decreases blood sugar)

129
Q

What is the most common hematologic complication of RA?

A

Anemia

130
Q

T/F: pleural effusion is hte most common pulmonary complication of RA

A

True

131
Q

RA patients - increased or decreased risk of bleeding

A

increased - NSAIDS = first line tx

132
Q

RA patients - increased or decreased blood sugar

A

increased due to glucocorticoids to reduce inflmmation

133
Q

First line tx for RA

A

NSAIDS

134
Q

What is RA?

A

an autoimmune disease targeting synovial joints

there is also widespread systemic involvement leading to vasculitis

135
Q

Hallmark of RA

A

morning stiffness that generally improves with activity

pain, swollen, warm joints
weakness, fatigue, anorexia

136
Q

T/F: RA typicallly affects proximal interphalangeal and metacarpophalngeal jointsi n the heads and feet and not weight-bearing joints

A

True

OA affects weight bearing joints

137
Q

medical mangement of RA aims at reducing inflammation by which 3 methods

A
  1. antirheumatics
  2. glucocorticoids
  3. nsaids

antirheumatics = methotrexate, cyclosporine, and etarercept
*immune suppression (autoimmune disease) - increases risk of infection and cancer

138
Q

3 antirheumatic drugs used for RA

risk?

A

1 Methotrexate
2. cyclosporine
3. Etanercept

infecftion and cancer

  • Methotrexate associated with liver dysfunction and bone marrow suppresion
  • Cyclosporine prolongs duration of sux
139
Q

T/F: RA is more common in men

A

False - women (2-3x more common)

140
Q

What is Sjorgen’s syndrome associated with (2)

A

RA and corenal abrasion

141
Q

What is Rheumatoid factor ?

A

it’s an anti-immunoglobin antibody that is increased in 90% of pts with RA

142
Q

T/F: CRP and sed rate are both increased in RA pts

A

True

143
Q

How do antirheumatic drugs work

A

They inhibit:
Tumor necrosis factor (TNF)
Interleukin-1 & 6
T cells and B lymphocytes

144
Q

Risk with methotrexate

A

liver dysfunction and bone marrow supression

145
Q

Which antirheumatic drug can prolong the duration of sux

A

Cyclosporine

146
Q

Durgs that are MOST likely to induce systemic lupus rythematosus include: (select 2):

-cyclophosphamide
-hydralazine
-isoniazid
-hydrocortisone

A

Hydralazine and isoniazid

cylophosphamide and hydrocortisone are treatements for SLE

147
Q

What is Lupus?

A

an autoimmune disease affecting nearly every organ system

sx result from antibody-induced vasculitis and tissue destruction

148
Q

2 most common problems with lupus

A

polyarthritis and dermatitis

149
Q

T/F- 75% of lupus pts develop the classic butterfly rash

A

False

30-50%

150
Q

4 drug groups for tx of SLE

A
  1. NSAIDS
  2. corticosteroids
  3. immunosupressants (methotrexate, cyclophosphamide)
  4. antimalarials (hydroxychloroquine)
151
Q

T/F- pts with SLE are at higher risk for hypercoagulability and thrombosis

A

True- if they develop antiphospholipid antibodies

152
Q

Is SLE a disease that targets older or younger women

A

younger

153
Q

Drug induced lupus generally persists for how long

symptoms? (4)

A

several weeks to months

mild symptoms of arthralgia, anemia, leukopenia, fever

154
Q

What is PISSED CHIMP a mneumonic for what what does it stand for ?

A

Things that can exacerbate SLE symptoms
Pregnancy
Infection
Surgery
Stress
Enalapril
D-penicillamine
Captopril
Hydralazine
Isosonazid
Methylodpa
Procainamide

155
Q

Match each disease with its defining characterisitic:
-Osteogenesis imperfecta
-Ehlerhs-Danlos syndrome
-Marfan syndrome

Aortic insufficinecy, bleeding into joints, blue sclera

A

-Osteogenesis imperfecta + Blue sclera
-Ehlerhs-Danlos syndrome + Bleeding into joints
-Marfan syndrome + aortic insufficency

156
Q

Connective tissue disorder associated with AI, aortic dissection, pectus excavatum, kyphoscoliosis and hyperflexible joints

A

Marfans

*careful with positioning

157
Q

What is an inherited isorder of collagen and is associated with arterial aneurysm and increased bleeding tendency

what 2 things should be avoided

A

Ehlers-Danlos syndrome

avoid regional and IM injections

158
Q

What disorder is characteristized by “brittle bones” iand is a connective tissue disorder with a high risk of fractures with airway managment and BP cuff

A

osteogenesis imperfecta

159
Q

which disorder is associated with spontaenous bleeding into joints

what else is a big association with it

A

Ehlers-Danlos Syndrome

Bleeding into joints + AAA

*increased bleeding risk - avoid regional and IM injections

160
Q

T/F: Increased bleeding tendency with ehlers-Danlos syndrome is a result of coagulopathy

A

False - poor vessel integrity

*collegen disorder

161
Q

Which disease can result in fractures due to fasiculations from sux?

A

Osteogenesis imperfecta

brittle bones

high risk for fractures
-careful airway mgmt - cspine

162
Q

Blue sclera is unique to which disease

A

osteogenesis imperfecta

brittle bones

sclera can actually fracture

163
Q

B/t- marfan, ehlers Danlos syndrome (EDS) and osterogensis imperfecta (OI) which one is associated with:

Spontaneous ptx

A

Marfans

keep pips low

164
Q

B/t- marfan, ehlers Danlos syndrome (EDS) and osterogensis imperfecta (OI) which one is associated with:

AI

A

Marfans

AI & AAA

165
Q

B/t- marfan, ehlers Danlos syndrome (EDS) and osterogensis imperfecta (OI) which one is associated with:

Frequent fractures

A

OI

166
Q

B/t- marfan, ehlers Danlos syndrome (EDS) and osterogensis imperfecta (OI) which one is associated with:

increased bleeding tendency

A

EDS

bleeding into jints and AAA

avoid IM injections and regional

167
Q

B/t- marfan, ehlers Danlos syndrome (EDS) and osterogensis imperfecta (OI) which one is associated with:

Tall stature

A

Marfans

Abe lincoln

168
Q

B/t- marfan, ehlers Danlos syndrome (EDS) and osterogensis imperfecta (OI) which one is associated with:

Increased serum thyroxine

A

OI

169
Q
A
170
Q

What is Multiple sclerosis?

A

a demylinating diesase of the CNS (brain and spinal cord)

171
Q

Do we need to avoid hyperthermia or hypothermia in Ms pts

A

avoid hyperthermia

increases risk of demylination

172
Q

Are MS pts at risk for aspiration?

A

yes- bulbar muscle dysfunction

173
Q

MS patients - which is safe vs questionable - epidural vs spinal

A

epidural = safe
spinal = questionable - m ay exacerbate sx

174
Q

T/F: pts with myotonic dystrophy may safely receive a halogenated anesthetic

A

True

no risk of MH
may be more sensitive to them though

175
Q

3 things that increase the risk of contractures with myotonic dystrophy

A
  1. Sux
  2. anticholinesterase (use sugammadex)
  3. Hypothermia (shivering > contractions
176
Q

symptoms pts may have with MS

A

-so it’s demylination of brain and spinal cord so:

-senosry and motor deficits and autonomic instability
-aspiration risk due to cranial nerve involvement

177
Q

3 things used to treat MS

A

corticosteroids
interferon
azathioprine

178
Q

MS can be exacerbated by stress and increased body temp as small as what

A

1 degree C

179
Q

MS - can you give sux?

A

no- life threatening hyperkalemia

-demylination of CNS , upregulation of receptors bc they arent getting as much ACH as they should be (i think)

180
Q

What does scleroderma cause?

A

excessive fibrosis in the skin and organs, espeically in the microvasculature

Airway - skin fibrosis limits mouth opening and mandibular mobility
lungs - pulmonary fibrosis and pulmonary htn
heart- dysrhythmias and CHF
vesels - decreased compliance > HTN
kidneys- renal failure and RAS > HTN
peripheral and cranial nerves - entrapment by tight connective tissue > neuroapthy
eyes - dryness - risk of corneal abrasion

181
Q

Which disease is associated with Telangiectasia

what is it

problem?

A

those with CREST syndrome - a type of sclerodoma

spider veins

increase risk of mucosal bleeding which can become problematic during airway manipulation (particularly during nasal intubation); concerning bc pts with scleroderma often have liited mouth oppening which may necesitate nasal fiberoptic intubation

182
Q

What disease is associated with excess osteoblastic and osteoclastic activity that causes abnormally thick, but weak, bone deposits

what 2 things can cause it

A

Paget’s disease

excessive PTH or decreased calcitonin

183
Q

2 most common porblems with paget’s disease

A

pain and fractures

neuropathy can occur too

184
Q

T/F- there is no vascular involvement with paget’s disease

A

True

just excess osteoblasts and osteoclasts activity > big weak bones
>pain and fractures
»nereve entrapment peripherally - neuropathy

185
Q

Which IVF is MOST likely to exacerbate skeletal muscle weakness in a patient with hypokalemic periodic paralysis?

A. D5W
B. LR
C. NS
D. Albumin

A

A. D5W

glucose load from D5W spikes insulin which shifts K into the cells

186
Q

SUX is MOST likely to impede airway management in a patient with which condition:

A. Guillain-Barre
B. Osteogenesis imperfecta
C. Myasthenia gravis
D. Myotonic dystrophy

A

D. Myotonic dystrophy

its characterized by a prolonged contracture after a voluntary contraction from dysfunctional calcium sequestration by the SR

-contractions can be so severe that they interfere with ventilation and intubation

-sux with GB - hyperkalemia
-sux with OI = fracture risk
-sux with MG - n/a - dose is increasesd

187
Q

FDA black box warning , sux to kids may cause :
MH or Rhabdo

A

Rhabdo

188
Q

What statements are true regarding acute idiopathic polyneuritis ? (select 3):

-exaggerated response to ephedrine
-sux should be avodied
-epstein bar is common etiology
-steroids improve symptoms
-no risk of aspiration
-paralysis starts with bulbar muscles

A

-exaggerated response to ephedrine
-sux should be avodied
-epstein bar is common etiology
-steroids improve symptoms
-no risk of aspiration
-paralysis starts with bulbar muscles

* Guillian barre*

189
Q

Airway complications of RA include all of the following except:

A. limited TMJ mobiity
B. AO subluxation
C. RLN palsy
D. Cricoarytenoid joint dislocation

A

C.

RLN palsy is a complication of SLE

190
Q

T/F: RLN palsy is a complication of SLE

A

True

191
Q

Which diseases are assoicated with vasculitis? (select 2)

-paget’s
-RA
-SLE
-OA

A

RA and SLE

192
Q

T/F: marfans syndrome is an acquired disease

A

false- autosomal dominant trait

193
Q

A pt with Marfans presents with AI and acute dissection of hte ascendign aorta; select the MOST accurate statement :

A. Spontaneous ptx is a rate complication
B. increased risk of cardiac tamponade
C. Esmolol infusion should be initiated
D. Marfan syndrome is an aquired disease

A

B. increased risk of tamponade

first line therapy for aortic dissection is an esmolol infusion to decrease wall stress, however, a slower HR increases the regurgitant fraction in the pt with AI

dissection of the ascending aorta can extend into the periocardium and this increases the risk of tamponade (JVD, hypotension, mujffled heart tones = becks triad)

*high risk for spontaenous PTX
*autosomal dominant trait (not acquired)

Musculoskeletal Diseases (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions