Brainscape's Knowledge GenomeTM

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


See full index

CMS200 > CMS midterm key > Flashcards

CMS midterm key Flashcards

1
Q

liver cirrhosis

A

irreversible, scar tissue replaces liver tissue

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

NASH is

A

> 5% hepatic steatosis PLUS hepatocellular injury and inflammation, with or without fibrosis

fat accumulation and ballooning degeneration

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

causes of NAFLD

A

obesity
T2D
dyslipidemia/hypertriglyceridemia

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

findings in liver disease

A

palpable liver edge, spider angioma, captut medusa, palmar erythema, gynceomastia, ascites, portal hypertesnion

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

bad AST/ALT ratio

A

> 1 in advanced fibrosis and cirrhosis

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

imaging for liver disease

A

ultrasonogrpahy

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

NASH can only be diagnosed by

A

liver biopsy and histology

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

obesity BMI, WC, Waist to hip

A

BMI >30

Waist circumference
females >35 inches
males >40 inches

Waist to hip
males >1
females >0.85

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

gold standard for assessing body fat

A

dual energy x ray absorptometry DXA

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

% obesity in north america

A

30%

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

primary vs secondary obesity

A

primary: increase calories and decrease activity [95% of cases]

secondary: genes, medications, medical conditions

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

gestational diabetes testing ; what and when

A

2 step oral glucose challenge at 24 weeks

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

pre eclampsia? at what week in gestation?

A

hypertension (140/90) and proteinuria and/ or end-organ dysfunction at 20 weeks gestation
(thrombocytopenia, increased ALT and AST, increased creatinine

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

if there is hypertension before 20 weeks gestation it is not pre eclampsia it is

A

chronic hypertension

need to be 20 weeks for pre eclampsia and have proteinuria

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

how much weight to gain in pregnancy if obese BMI >30

A

5-9kg/11-20lbs which is 0.2kg/0.5lbs per week

and gain in 2nd and 3rd trimester

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

menopause

A

non pathologic, estrogen deficient

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

obstructive sleep apnea and obesity

A

neck circumference> 40 cm

diagnose with polysomnography

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

NAFLD in obesity? how much weight loss?

A

NAFLD is 80-90% of obese adults

3-5% weight loss for steatosis
7-10% weight loss for NASH

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

lifestyle or meds or surgery for obesity?

A

BMI >30 or >25 with 2 risk factors= lifestyle modifications

BMI >35 or >27 with 2 risk factors = lifestyle and medications

BMI >40 or >35 with 2 risk factors= weight loss surgery (get lots of markers for vitamins and bones and what not every 6-12 months)

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

5 As of obesity

A

ask
assess
advise
agree
assist

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

idiopathic T1D

A

no pancreatic beta cell autoimmune… only like 5% of cases

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

screening for T1D

A

no

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

screening for T2D

A

yes- if asymptomatic with BMI >25 or risk factors (A1C>5.7, impaired fasting glucose, impaired glucose tolerance)

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

screen for T2d in kids

A

insufficient evidences; only if overweight and have 2 risk factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

screening in elders

A

no recommendations for routine screening, doesnt effect life expectancy possibly

pre diabetes is very common

stop screening at age 70 to avoid overdiagnosis

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

when to test for T2d if overweight or obese but have blood results in normal limits

A

every 3 years

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

annual screening if

A

> 45 years old
<45 with risk factors

normal is every 3 years

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

T2D: the leading cause of death is

A

myocardial infarction

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

inflammation and immune in T2d

A

adipocytes secrete adipokines and also TNF Alpha and IL-6 all contribute to impaired insulin signaling

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

gestation diabetes in % of pregnancies

A

8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

when to screen fro gestational diabetes

A

24-48 weeks

also check after 6-12 weeks postpartum

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

testing for gestational diabetes

A

2 step glucose tolerance test

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

T2D in kids complications

A

DKA and hyperglycemic hyperosmolar state

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

mature obset diabetes of the young (MODY) in how many % of cases

A

5% but often misdiagnosed as T1D OR T2D

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

what is MODY

A

non insulin dependent form of diabetes that has ok beta cell function

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

cause of MODY

A

genetic; autosomal dominant

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

weight in MODY

A

non obese

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

types of MODY; most common? least dangerous? what is like T1D or T2D symptoms?

A

most common MODY 3

least dangerous MODY 2

like T1D and T2D is MODY 1 and MODY 3

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

diagnostic values of
-fasting plasma glucose
-oral glucose tolerance test
-HbA1C

A

> 126
126 or 200 @ 2 hours
6.5%

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

what test for DKA

A

urinalysis

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

diabetic nephopathy; markers in kidneys; how common is ESRD due to diabetes

A

1/3 of ESRD due to diabetes

albumin, urea, creatinine

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

diabetic neuropathy; most common type

A

distal symmetric polyneuropathy most common

autonomic neuropathies can affect GI, CVD, genitourinary

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

diabetic retinopathy

A

catacacts, glaucoma, dry eye syndrome, macular edema

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

diabetic foot ulcers? severe symptoms?

A

with osteomylitis (bone inflammation)

if severe infection; increases temperature, pulse, RR, WBC

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

DKA is primarily from what diabetes type

A

T1D

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

causes of DKA

A

infection, inadequate insulin treatment, CVD, etc

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

symptoms of DKA

A

N/V, coffee ground emesis

polyuria, polydipsia, kussmaul breathing, tachycardia, hypertension

cerebral edema (rare)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

labs of DKA

A

high plasma glucose (hyperglycemia), low pH, low bicarbonate (acidosis), ketones in urine

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

which is life threatening and which is emergent condition; DKA and hyperosmolar hyperglycaemic state (HHS)

A

DKA- life threatening
HHS- emergent

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

who Is hyperosmolar hyperglycaemic state (HHS) most often seen in

A

elders with T2D

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

causes of hyperosmolar hyperglycaemic state (HHS)

A

infections, medications, coexisting conditions etc

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

symptoms in hyperosmolar hyperglycaemic state (HHS)

A

thirst, hyperglycemia, polyuria, tachycardia, seizures, coma

rare; vascular occlusions, rhabdomyolysis

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

labs of hyperosmolar hyperglycaemic state (HHS)

A

increased plasma glucose, increase serum osmolarity, increased pH

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

difference between HHS and DKA

A

DKA has low pH and ketones in urine

HHS has high pH and no excessive ketonuria

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

what hypothryoid is most common

A

95% of cases are primary hypothyroid (and autoimmune)

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

central hypothryoid from what most commonly

A

pituitary adenoma

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

2 main mechanisms in hypothyroid

A
  1. slowed metabolism
  2. polysaccharides accumulate in interstitial space
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

goiter
commonly?
endemic?
physiologic?
testing?

A

usually euthyroid (can be hypo or hyper)

physiologic: pregnancy, adolescence

endemic: iodine deficiency

test: fine needle aspiration biopsy if nodules

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

what 2 NHPs affect thyroid

A

biotin and st johns wart

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

biotin effect on thyroid

A

falsely decreases TSH and increase T3,T4 making it look like hyperthyroid (or overmedicated hypo)

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

st johns wart effect on thyroid

A

transiently elevated TSH

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

hyperthyroid TSH and T4 values

A

low TSH, high T4

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

primary hypothyroid TSH and T4 values

A

high TSH, low T4

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

subclinical hypothyroid TSH and T4 values

A

High TSH, normal T4

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

central hypothyroid TSH and T4 values

A

low TSH, low T4

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

when to treat vs monitor subclinical hypothryoid? TSH values?

A

monitor if TSH 4-10, treat if TSH >10 or TPO antibodies

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

in asymptomatic and non pregnant individuals, what does Canada CTFPHC and USA USPSTF recommend for thyroid screening

A

Cad- recommends against screening

US- says evidence insufficient

68
Q

thyroid hormone changes in pregnancy

A

thyroid hormone requirement increases 20-40% in pregnancy (i.e. increase drug dose if were hypothryoid before pregnancy)

levothyroxine safe in pregnancy

69
Q

why not test thyroid antibodies in pregnancy?

A

bc they become very low

70
Q

postpartum thyroiditis

A

abnormal TSH 12 months postpartum (no nodules or TPO antibodies)

71
Q

which autoimmune condition is most common with hypothyroid

A

Addisons (adrenal insufficicieny, decreased cortisol)

72
Q

symptoms of Addisons? if have Addisons and hypothryoid how to treat?

A

weight loss, tachycardia, N/V, ab pain, hypotension, low Na+, high K+

treat Addisons 1st and hypothryoid might go away

73
Q

celiac and hypothyroid

A

increase thyroid medicine dose or do gluten free diet

74
Q

hypothyroid and it increasing coronary artery disease? symptoms?

A

decrease cardiac output, decrease HR, increase atherosclerosis, diastolic hypertesnion

levothyroxine can increase heart rate and precipitate acute coronary syndrome or arrhythmia

75
Q

TSH changes with age

A

increases in elderly; reduce dose of meds

76
Q

what meds and food interact with levothyroxine

A

meds like antidepressants, antipsychotics etc

soybean flour, walnuts, grapefruit

77
Q

myxoedema coma symptoms 911!!!

A

hypothermia, hypotension, bradycardia, hypoglycemia, hyponatremia, edema

78
Q

fatigue can come from

A

overexertion, URTI, anemia, depression, medications, sleep apnea…

79
Q

75% of fatigue is from

A

psychiatric illness

80
Q

acute, subacute, and chronic fatigue

A

acute is less than 1 month and better with rest

chronic is more than 6 months and not relieved by rest

81
Q

physiologic vs secondary fatigue

A

physiologic: lifestyle imbalance, better with rest

secondary: underlying medical condition

82
Q

3 criteria for fatigue

A
  1. generalized weakness
  2. easy fatiguability
  3. mental fatigue
83
Q

2 main causes of chronic fatigue

A

70% depression and anxiety
25% medical condition

84
Q

systemic exertion intolerance disease (SEID) affects what systems in the body

A

a biological (not psychological) disorder

autonomic, neuroendocrine, and immune dysfunction (hormones, inefctions, oxidative stress)

85
Q

physical exams for fatigeu

A

vitals, lymph, oropharyngeal

86
Q

lab work for fatigue; how does it affect management?

A

affects management 5% of time

CBC, ESR, thyroid, urinalysis, pregnancy, chemistry panel (include liver and kidney)

87
Q

fatigue criteria

A
  1. > 6 month decrease in ability to do activities, not better with rest
  2. post exertion malaise > 24 hours
  3. unrefreshing sleep

1/2 of the following

  1. cognitive impairment
  2. orthostatic intolerance
88
Q

major criteria, minor criteria and physical criteria for chronic fatigue/ SEID

A

major:
- >6 months
- not better with rest
- decrease activity to < 50%
- exclude other conditions

minor:
- sore throat, myalgia, headache, sleep disturbance, arthralgia etc.

physical:
-low grade fever
-lymphadenopathy
-non exudative pharyngitis

89
Q

intrinsic vs extrinsic shoulder pain

A

intrinsic = shoulde
extrinsic i.e. neurological disorders or visceral conditions with referring pain

90
Q

most common extrinsic cause of shoulder pain

A

cervical spine disease

91
Q

how does arm movement affect pain in extrinsic vs intrinsic causes

A

arm movement increases pain in intrinsic causes

pain unrelated to movement in extrinsic cause

92
Q

if pain only occurs on active ROM then what to consider

A

muscle, tendon and ligament so thinks about soft tissue disorders

such as rotator cuff or biceps tendonitis, rotator cuff tendinopathy/tears, or subacromial bursitis.

93
Q

if trauma to the shoulder what conditions to consider

A

fracture, dislocation then tears of the rotator cuff or labrum

94
Q

if pain occurs with active and passive ROM what to consider

A

JOINTS

involvement of the glenohumeral joint (eg, osteoarthritis, frozen shoulder, gout, osteonecrosis) or AC joint disease (eg, separation or osteoarthritis).

95
Q

pain with elevation above arm

A

impingement syndrome

96
Q

Pain on lifting items with the biceps or pain with wrist supination

A

biceps tendinitis

97
Q

most common intrinsic shoulder pain

A

Impingement syndrome/rotator cuff tendinitis(includes full and partial rotator cuff tears): 48%-85% prevalence

98
Q

tendinopathy vs tendonitis

A

tendinopathy= degeneration

tendonitis= inflammation

99
Q

progression of tendinotpathy

A

peritendinitis and focal thickness

leads to mucoid degeneration, chondral metaplasia, and amyloid deposition together with reparative changes and inflammation such as an increase of fibroblastic cells and neovascularization

leads to tendon tears

100
Q

what test is associated with a complete tear

A

drop arm test

101
Q

most frequent articular surface to tear

A

supraspinatous

PASTA (partial articular supraspinatus tendon avulsion)

102
Q

fat atrophy affecting shoulder tears

A

higher rate of recurrence after surgical repair if atrophy >50% of muscle

103
Q

massive rotator cuff tear

A

involvement of two or more tendons or a retraction greater than 5 cm

104
Q

how to isolate glenohumeral joint

A

first 20-30 degrees of abduction

105
Q

what tests for shoulder pain/ rotator cuff tear

1 provocation test
3 strength tests
1 composite test

A

provocation:
-painful arc test (AC joint at 60-120 and impingement at 180 degrees)

strength:
-internal rotation lag test (subscapularis)
-external rotation lag test (supraspinatous and infraspinatous)
-drop arm test (supraspinatous)

composite:
-external rotation resistance test (infraspinatous)

106
Q

1st line imaging for rotator cuff disease

A

x ray/ radiograph

107
Q

what imaging for soft tissue of shoulder

A

MRI

the rotator cuff, tendons, biceps muscle, subacromial and subdeltoid bursae.

108
Q

what imaging for fracture or dislocation

A

CT scan

109
Q

imaging for full thickness rotator cuff tear

A

ultrasound or MRI

110
Q

imaging for partial thickness rotator cuff tear

A

ultrasound

111
Q

assess shoulder joints via

A

MRI

112
Q

gold standard in evaluating a suspected labral tear or shoulder instability.

A

MR arthrography, or MRA

113
Q

how to fix shoulder impingment

A

self limiting; rest, analgesic, exercises

114
Q

what shoulder thing can be asymptomatic

A

rotator cuff tear

115
Q

treatment of partial rotator cuff tear

A

physical therapy and scapular and rotator cuff muscle strengthening.

However, research suggests that 40% of the partial thickness tears progress to full thickness tears in 2 years.

116
Q

negative prognostic factor for successful surgical treatment in full thickness rotator cuff tear

A

fatty infiltration

117
Q

what does untreated full thickness subscapularis tendon tears lead to

A

premature osteoarthritis

118
Q

calcified tendinopathy

A

deposits of CPPD might migrate to the subacromial bursa causing bursitis

119
Q

which ROM is most inhibited by adhesive capsultis

A

external rotation

120
Q

MRI shows what findings in adhesive capusultis

A

*In the acute inflammatory phase, MRI can show axillary capsular thickening and capsular edema

  • Progressively hypervascularization and fibrosis occur, which may be reflected on MRI images by thickening of the coracohumeral ligament, subcoracoid fibrosis, and capsular thickening.
121
Q

2 main origins of nerve denervation syndromes

A

viral inflammation and overuse [athletes with overhead activities]

122
Q

supra scapular neuropathy from

A

related to compression of an associated paralabral cyst in a superior labrum injury

123
Q

axillary nerve denervation from what other shoulder problem

A

anterior inferior shoulder dislocation

124
Q

shoulder impingement from narrowing of what space

A

subacromial space

125
Q

internal shoulder impingement is from

A

repetitive overhead throw or manual labour

126
Q

what articular side does internal impingement involve

A

articular-sided rotator cuff pathology

127
Q

neer’s 3 stages of shoulder impingement

A
  • In stage I, impingement primarily results from edema,
    hemorrhage, or both.
  • Stage II is characterized by greater fibrosis and
    irreversible tendon changes.
  • Stage III shoulder impingement syndrome is characterized
    tendon degeneration of the rotator cuff as well as the long head of biceps, bony changes and tendon rupture.
128
Q

extrinsic risk factors of shoulder impingement

A

repetitive overhead activities

bearing heavy loads, infection, smoking, and fluoroquinolone antibiotics.

129
Q

tests for shoulder impingement syndrome

A

include the Hawkins test, Neer sign, Jobe/Empty can test, and a painful arc of motion. Individually, these tests have Likelihood Ratios (LR), but when combined, they can help complete the picture of shoulder impingement syndrome.

130
Q

critical shoulder angle (CSA) greater than ___ increased likelihood that a rotator cuff is contributing to impingement syndrome.

A

35 degrees

131
Q

acromiohumeral distance (AHD) can help to detect rotator cuff pathologies and defects. if it is ____ than the normal range is approximately 7 to 14 mm in men and 7 to 12 mm in women = bad

A

lower

132
Q

how to treat shoulder impingement

A

physical therapy, NSAIDs, corticosteroid injections, and other means of conservative therapy yield

might have torn rotator cuff… and could image?

133
Q

complications in a shoulder impingement

A

complications that may arise predominantly result from structural damage within the subacromial space, altered biomechanics, or avoidance of use with subsequent atrophy

134
Q

who is frozen shoulder/adhesive capsulitis most seen in

A

40-65ys, women esp perimenopausal

or endocrine disorders, such as diabetes mellitus or thyroid disease.

incidence of adhesive capsulitis following shoulder trauma or breast cancer care (pro infalmmatory)

135
Q

time course of frozen shoulder/adhesive capsulitis

A

self-limiting condition of approximately 1–3 years’ duration, it can be extremely painful and debilitating.

136
Q

phases of frozen shoulder

A
  • phase 1: Progressive stiffening, loss of motion in the shoulder with increasing pain on movement, which may be worse at night (months 2–9), usually referred to as the painful phase.
  • phase 2: Gradual decrease in pain but stiffness remains and there is considerable restriction in the range of movement (months 4–12), usually referred to as the stiffening or ‘freezing’ phase
  • phase 3: Improvement in range of movement (months 12– 42), usually referred to as the resolution phase.
137
Q

primary (idiopathic) vs secondary frozen shoulder

A

primary= unknown

secondary= causes ; diabetes, trauma, cardiovascular disease and hemiparesis

138
Q

useful clinical sign for frozen shoulder

A

limitation of movement of external rotation with the elbow by the side of the trunk.

139
Q

key alerting feature is restriction in _____ for frozen shoulder

A

restriction of passive and active shoulder movement in all directions.

140
Q

imaging for frozen shoudler

A

usually clinical diagnosis (no imaging) but arthrographt can help therapeutically

141
Q

what is needed to stabilize the shoulder

A

elies on rotator cuff muscle strength, scapular control and the integrity of the fibrocartilaginous glenoid labrum

142
Q

which direction do 95% of the shoulder dislocations/ instability occur in?

A

anterior direction (outstretched and abducted arm)

143
Q

future dislocation?

A
  • Patients 21 years or younger have a 70–90% risk of future dislocation
  • Patients 40 years or older have a much lower rate (20– 30%).
  • After a second dislocation, the recurrence rate is extremely high, up to 95%, regardless of age.
144
Q

what to look for in shoulder dislocation

A

bankart lesions

hill Sachs lesion

145
Q

what are atraumatic shoulder dislocations usually cause by

A

by intrinsic ligament laxity or repetitive microtrauma leading to joint instability; often seen in athletes involved in overhead and throwing sports (eg, in swimmers, gymnasts, and pitchers).

146
Q

tests for shoulder instability

A

apprehension test, the load and shift test, and the O’Brien test.

147
Q

bankart lesion from

A

damage to labrum and glenoid rim in an anterior shoulder dislocation

148
Q

imaging for shoulder dislocation

A

xray/ radiograph

149
Q

dislocation/instability treatment

A

manual reductions are usually performed in the emergency department then sling immobilization, early physical therapy to maintain range of motion and strengthening of rotator cuff muscles

150
Q

bicipital tendinitis is usually primary or secondary (what’s more common)? what a common secondary cause?

A

secondary to other injuries (from rotator cuff tendinopathy or impingement syndrome)

primary if baseball, volleyball, etc (5% of time)

151
Q

pathophysiological changes in long head biceps tendinitis

A

there is LHB sheath thickening, fibrosis, and vascular compromise.

  • The LHB tendon undergoes degenerative changes, and associated scarring, fibrosis, and adhesions eventually compromise LHB tendon mobility. In effect, the tendon becomes pathologically “anchored” in the groove,

end-stage conditions, the LHB tendon can eventually rupture

152
Q

what characteristic deformity is seem in proximal biceps tendinitis complete rupture

A

Popeye deformity

153
Q

provocative testing for proximal biceps tendinitis

A

bicipital groove palpation

speed test

uppercut test

yergason test

**examine for possible associated labral and/or rotator cuff pathologies.

154
Q

imagining for proximal biceps tendinitis

A

ultrasound

MRI

MRA

155
Q

surgery for proximal biceps tendon tear

A

biceps tenotomy or tenodesis

cut an attach tendons…

156
Q

distal biceps rupture from

A

excessive eccentric force as the arm is brought into extension from flexion. (while proximal biceps rupture is usually correlated with rotator cuff disease)

Risk factors include age, smoking, obesity, use of corticosteroids, and overus

157
Q

distal biceps tendon rupture evaluation

A

-history of single traumatic event
-painful pop
-palpable and visible retraction of biceps muscle belly (reverse Popeye deformity)
-weakness

158
Q

acromioclavicular joint injury causes? what part of the acromion is hurt? what position is arm in?

A

sports, falling, car accidents

The most common mechanism of injury is direct trauma to the lateral aspect of the shoulder or acromion process with the arm in adduction. Falling on an outstretched hand or elbow may also lead to AC joint separation

159
Q

___ aspect of shoulder or acromion process with arm in ___ for AC joint injury is most common

A

lateral ; adduction

160
Q

the ___ sign is when the clavicle is elevated and rebounds after inferior compression;; seen in acromioclavicular joint injury

A

piano key sign

161
Q

imaging fro AC joint injury

A

x ray

162
Q

6 types of AC joint injuries (get progressively worse)

A
  • Type I is referred to as a sprain of the acromioclavicular ligaments only and demonstrates no displacement.
  • Type II involves tearing of the acromioclavicular ligament and sprain of the coracoclavicular ligament with less than 25% increase in the coracoclavicular interspace or with the clavicle elevated but not superior to the border of the acromion.
  • Type I and II sprains are managed non-operatively with a sling, analgesia, ice, and physical therapy.
  • Type III AC joint separation involves tearing of both the acromioclavicular ligament and coracoclavicular ligaments resulting in clavicle elevation above the border of the acromion with a 25 to 100% increased coracoclavicular distance on x-ray compared to the contralateral side.
  • Type III injuries are frequently managed non-operatively similar to type I and II; however, if the displacement is greater than 75%; the patient is a laborer, elite athlete, or concerned about cosmesis; or is not improving with conservative management, then surgical intervention may be considered.
  • Posterior displacement of the distal clavicle into the trapezius defines type IV injuries. Type V injuries have a superior displacement by more than 100% compared to the contralateral side.
  • Type VI is rare and is an inferolateral displacement in a subacromial or subcoracoid displacement behind the coracobrachialis or biceps tendon.
  • Type IV through VI injuries are typically managed surgically, and warrants referral to an orthopedic surgeon.
163
Q

test for AC joint integrity

A

cross-body adduction test

164
Q

alarm symptoms in shoulder pain

A

visible swelling or deformity, fever or chills, constant and progressive pain, axillary pain, night pain, numbness or tingling, weight loss, dyspnea

think infection,tumor, neuropathy, heart disease etc

165
Q

when to refer in shoulder pain

A

Failure of conservative treatment over 3 months.

full RC tears, bad partial tears

at risk for second dislocation

etc

CMS200 (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions