CMS midterm key Flashcards
liver cirrhosis
irreversible, scar tissue replaces liver tissue
NASH is
> 5% hepatic steatosis PLUS hepatocellular injury and inflammation, with or without fibrosis
fat accumulation and ballooning degeneration
causes of NAFLD
obesity
T2D
dyslipidemia/hypertriglyceridemia
findings in liver disease
palpable liver edge, spider angioma, captut medusa, palmar erythema, gynceomastia, ascites, portal hypertesnion
bad AST/ALT ratio
> 1 in advanced fibrosis and cirrhosis
imaging for liver disease
ultrasonogrpahy
NASH can only be diagnosed by
liver biopsy and histology
obesity BMI, WC, Waist to hip
BMI >30
Waist circumference
females >35 inches
males >40 inches
Waist to hip
males >1
females >0.85
gold standard for assessing body fat
dual energy x ray absorptometry DXA
% obesity in north america
30%
primary vs secondary obesity
primary: increase calories and decrease activity [95% of cases]
secondary: genes, medications, medical conditions
gestational diabetes testing ; what and when
2 step oral glucose challenge at 24 weeks
pre eclampsia? at what week in gestation?
hypertension (140/90) and proteinuria and/ or end-organ dysfunction at 20 weeks gestation
(thrombocytopenia, increased ALT and AST, increased creatinine
if there is hypertension before 20 weeks gestation it is not pre eclampsia it is
chronic hypertension
need to be 20 weeks for pre eclampsia and have proteinuria
how much weight to gain in pregnancy if obese BMI >30
5-9kg/11-20lbs which is 0.2kg/0.5lbs per week
and gain in 2nd and 3rd trimester
menopause
non pathologic, estrogen deficient
obstructive sleep apnea and obesity
neck circumference> 40 cm
diagnose with polysomnography
NAFLD in obesity? how much weight loss?
NAFLD is 80-90% of obese adults
3-5% weight loss for steatosis
7-10% weight loss for NASH
lifestyle or meds or surgery for obesity?
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)
5 As of obesity
ask
assess
advise
agree
assist
idiopathic T1D
no pancreatic beta cell autoimmune… only like 5% of cases
screening for T1D
no
screening for T2D
yes- if asymptomatic with BMI >25 or risk factors (A1C>5.7, impaired fasting glucose, impaired glucose tolerance)
screen for T2d in kids
insufficient evidences; only if overweight and have 2 risk factors
screening in elders
no recommendations for routine screening, doesnt effect life expectancy possibly
pre diabetes is very common
stop screening at age 70 to avoid overdiagnosis
when to test for T2d if overweight or obese but have blood results in normal limits
every 3 years
annual screening if
> 45 years old
<45 with risk factors
normal is every 3 years
T2D: the leading cause of death is
myocardial infarction
inflammation and immune in T2d
adipocytes secrete adipokines and also TNF Alpha and IL-6 all contribute to impaired insulin signaling
gestation diabetes in % of pregnancies
8
when to screen fro gestational diabetes
24-48 weeks
also check after 6-12 weeks postpartum
testing for gestational diabetes
2 step glucose tolerance test
T2D in kids complications
DKA and hyperglycemic hyperosmolar state
mature obset diabetes of the young (MODY) in how many % of cases
5% but often misdiagnosed as T1D OR T2D
what is MODY
non insulin dependent form of diabetes that has ok beta cell function
cause of MODY
genetic; autosomal dominant
weight in MODY
non obese
types of MODY; most common? least dangerous? what is like T1D or T2D symptoms?
most common MODY 3
least dangerous MODY 2
like T1D and T2D is MODY 1 and MODY 3
diagnostic values of
-fasting plasma glucose
-oral glucose tolerance test
-HbA1C
> 126
126 or 200 @ 2 hours
6.5%
what test for DKA
urinalysis
diabetic nephopathy; markers in kidneys; how common is ESRD due to diabetes
1/3 of ESRD due to diabetes
albumin, urea, creatinine
diabetic neuropathy; most common type
distal symmetric polyneuropathy most common
autonomic neuropathies can affect GI, CVD, genitourinary
diabetic retinopathy
catacacts, glaucoma, dry eye syndrome, macular edema
diabetic foot ulcers? severe symptoms?
with osteomylitis (bone inflammation)
if severe infection; increases temperature, pulse, RR, WBC
DKA is primarily from what diabetes type
T1D
causes of DKA
infection, inadequate insulin treatment, CVD, etc
symptoms of DKA
N/V, coffee ground emesis
polyuria, polydipsia, kussmaul breathing, tachycardia, hypertension
cerebral edema (rare)
labs of DKA
high plasma glucose (hyperglycemia), low pH, low bicarbonate (acidosis), ketones in urine
which is life threatening and which is emergent condition; DKA and hyperosmolar hyperglycaemic state (HHS)
DKA- life threatening
HHS- emergent
who Is hyperosmolar hyperglycaemic state (HHS) most often seen in
elders with T2D
causes of hyperosmolar hyperglycaemic state (HHS)
infections, medications, coexisting conditions etc
symptoms in hyperosmolar hyperglycaemic state (HHS)
thirst, hyperglycemia, polyuria, tachycardia, seizures, coma
rare; vascular occlusions, rhabdomyolysis
labs of hyperosmolar hyperglycaemic state (HHS)
increased plasma glucose, increase serum osmolarity, increased pH
difference between HHS and DKA
DKA has low pH and ketones in urine
HHS has high pH and no excessive ketonuria
what hypothryoid is most common
95% of cases are primary hypothyroid (and autoimmune)
central hypothryoid from what most commonly
pituitary adenoma
2 main mechanisms in hypothyroid
- slowed metabolism
- polysaccharides accumulate in interstitial space
goiter
commonly?
endemic?
physiologic?
testing?
usually euthyroid (can be hypo or hyper)
physiologic: pregnancy, adolescence
endemic: iodine deficiency
test: fine needle aspiration biopsy if nodules
what 2 NHPs affect thyroid
biotin and st johns wart
biotin effect on thyroid
falsely decreases TSH and increase T3,T4 making it look like hyperthyroid (or overmedicated hypo)
st johns wart effect on thyroid
transiently elevated TSH
hyperthyroid TSH and T4 values
low TSH, high T4
primary hypothyroid TSH and T4 values
high TSH, low T4
subclinical hypothyroid TSH and T4 values
High TSH, normal T4
central hypothyroid TSH and T4 values
low TSH, low T4
when to treat vs monitor subclinical hypothryoid? TSH values?
monitor if TSH 4-10, treat if TSH >10 or TPO antibodies
in asymptomatic and non pregnant individuals, what does Canada CTFPHC and USA USPSTF recommend for thyroid screening
Cad- recommends against screening
US- says evidence insufficient
thyroid hormone changes in pregnancy
thyroid hormone requirement increases 20-40% in pregnancy (i.e. increase drug dose if were hypothryoid before pregnancy)
levothyroxine safe in pregnancy
why not test thyroid antibodies in pregnancy?
bc they become very low
postpartum thyroiditis
abnormal TSH 12 months postpartum (no nodules or TPO antibodies)
which autoimmune condition is most common with hypothyroid
Addisons (adrenal insufficicieny, decreased cortisol)
symptoms of Addisons? if have Addisons and hypothryoid how to treat?
weight loss, tachycardia, N/V, ab pain, hypotension, low Na+, high K+
treat Addisons 1st and hypothryoid might go away
celiac and hypothyroid
increase thyroid medicine dose or do gluten free diet
hypothyroid and it increasing coronary artery disease? symptoms?
decrease cardiac output, decrease HR, increase atherosclerosis, diastolic hypertesnion
levothyroxine can increase heart rate and precipitate acute coronary syndrome or arrhythmia
TSH changes with age
increases in elderly; reduce dose of meds
what meds and food interact with levothyroxine
meds like antidepressants, antipsychotics etc
soybean flour, walnuts, grapefruit
myxoedema coma symptoms 911!!!
hypothermia, hypotension, bradycardia, hypoglycemia, hyponatremia, edema
fatigue can come from
overexertion, URTI, anemia, depression, medications, sleep apnea…
75% of fatigue is from
psychiatric illness
acute, subacute, and chronic fatigue
acute is less than 1 month and better with rest
chronic is more than 6 months and not relieved by rest
physiologic vs secondary fatigue
physiologic: lifestyle imbalance, better with rest
secondary: underlying medical condition
3 criteria for fatigue
- generalized weakness
- easy fatiguability
- mental fatigue
2 main causes of chronic fatigue
70% depression and anxiety
25% medical condition
systemic exertion intolerance disease (SEID) affects what systems in the body
a biological (not psychological) disorder
autonomic, neuroendocrine, and immune dysfunction (hormones, inefctions, oxidative stress)
physical exams for fatigeu
vitals, lymph, oropharyngeal
lab work for fatigue; how does it affect management?
affects management 5% of time
CBC, ESR, thyroid, urinalysis, pregnancy, chemistry panel (include liver and kidney)
fatigue criteria
- > 6 month decrease in ability to do activities, not better with rest
- post exertion malaise > 24 hours
- unrefreshing sleep
1/2 of the following
- cognitive impairment
- orthostatic intolerance
major criteria, minor criteria and physical criteria for chronic fatigue/ SEID
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
intrinsic vs extrinsic shoulder pain
intrinsic = shoulde
extrinsic i.e. neurological disorders or visceral conditions with referring pain
most common extrinsic cause of shoulder pain
cervical spine disease
how does arm movement affect pain in extrinsic vs intrinsic causes
arm movement increases pain in intrinsic causes
pain unrelated to movement in extrinsic cause
if pain only occurs on active ROM then what to consider
muscle, tendon and ligament so thinks about soft tissue disorders
such as rotator cuff or biceps tendonitis, rotator cuff tendinopathy/tears, or subacromial bursitis.
if trauma to the shoulder what conditions to consider
fracture, dislocation then tears of the rotator cuff or labrum
if pain occurs with active and passive ROM what to consider
JOINTS
involvement of the glenohumeral joint (eg, osteoarthritis, frozen shoulder, gout, osteonecrosis) or AC joint disease (eg, separation or osteoarthritis).
pain with elevation above arm
impingement syndrome
Pain on lifting items with the biceps or pain with wrist supination
biceps tendinitis
most common intrinsic shoulder pain
Impingement syndrome/rotator cuff tendinitis(includes full and partial rotator cuff tears): 48%-85% prevalence
tendinopathy vs tendonitis
tendinopathy= degeneration
tendonitis= inflammation
progression of tendinotpathy
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
what test is associated with a complete tear
drop arm test
most frequent articular surface to tear
supraspinatous
PASTA (partial articular supraspinatus tendon avulsion)
fat atrophy affecting shoulder tears
higher rate of recurrence after surgical repair if atrophy >50% of muscle
massive rotator cuff tear
involvement of two or more tendons or a retraction greater than 5 cm
how to isolate glenohumeral joint
first 20-30 degrees of abduction
what tests for shoulder pain/ rotator cuff tear
1 provocation test
3 strength tests
1 composite test
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)
1st line imaging for rotator cuff disease
x ray/ radiograph
what imaging for soft tissue of shoulder
MRI
the rotator cuff, tendons, biceps muscle, subacromial and subdeltoid bursae.
what imaging for fracture or dislocation
CT scan
imaging for full thickness rotator cuff tear
ultrasound or MRI
imaging for partial thickness rotator cuff tear
ultrasound
assess shoulder joints via
MRI
gold standard in evaluating a suspected labral tear or shoulder instability.
MR arthrography, or MRA
how to fix shoulder impingment
self limiting; rest, analgesic, exercises
what shoulder thing can be asymptomatic
rotator cuff tear
treatment of partial rotator cuff tear
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.
negative prognostic factor for successful surgical treatment in full thickness rotator cuff tear
fatty infiltration
what does untreated full thickness subscapularis tendon tears lead to
premature osteoarthritis
calcified tendinopathy
deposits of CPPD might migrate to the subacromial bursa causing bursitis
which ROM is most inhibited by adhesive capsultis
external rotation
MRI shows what findings in adhesive capusultis
*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.
2 main origins of nerve denervation syndromes
viral inflammation and overuse [athletes with overhead activities]
supra scapular neuropathy from
related to compression of an associated paralabral cyst in a superior labrum injury
axillary nerve denervation from what other shoulder problem
anterior inferior shoulder dislocation
shoulder impingement from narrowing of what space
subacromial space
internal shoulder impingement is from
repetitive overhead throw or manual labour
what articular side does internal impingement involve
articular-sided rotator cuff pathology
neer’s 3 stages of shoulder impingement
- 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.
extrinsic risk factors of shoulder impingement
repetitive overhead activities
bearing heavy loads, infection, smoking, and fluoroquinolone antibiotics.
tests for shoulder impingement syndrome
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.
critical shoulder angle (CSA) greater than ___ increased likelihood that a rotator cuff is contributing to impingement syndrome.
35 degrees
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
lower
how to treat shoulder impingement
physical therapy, NSAIDs, corticosteroid injections, and other means of conservative therapy yield
might have torn rotator cuff… and could image?
complications in a shoulder impingement
complications that may arise predominantly result from structural damage within the subacromial space, altered biomechanics, or avoidance of use with subsequent atrophy
who is frozen shoulder/adhesive capsulitis most seen in
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)
time course of frozen shoulder/adhesive capsulitis
self-limiting condition of approximately 1–3 years’ duration, it can be extremely painful and debilitating.
phases of frozen shoulder
- 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.
primary (idiopathic) vs secondary frozen shoulder
primary= unknown
secondary= causes ; diabetes, trauma, cardiovascular disease and hemiparesis
useful clinical sign for frozen shoulder
limitation of movement of external rotation with the elbow by the side of the trunk.
key alerting feature is restriction in _____ for frozen shoulder
restriction of passive and active shoulder movement in all directions.
imaging for frozen shoudler
usually clinical diagnosis (no imaging) but arthrographt can help therapeutically
what is needed to stabilize the shoulder
elies on rotator cuff muscle strength, scapular control and the integrity of the fibrocartilaginous glenoid labrum
which direction do 95% of the shoulder dislocations/ instability occur in?
anterior direction (outstretched and abducted arm)
future dislocation?
- 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.
what to look for in shoulder dislocation
bankart lesions
hill Sachs lesion
what are atraumatic shoulder dislocations usually cause by
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).
tests for shoulder instability
apprehension test, the load and shift test, and the O’Brien test.
bankart lesion from
damage to labrum and glenoid rim in an anterior shoulder dislocation
imaging for shoulder dislocation
xray/ radiograph
dislocation/instability treatment
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
bicipital tendinitis is usually primary or secondary (what’s more common)? what a common secondary cause?
secondary to other injuries (from rotator cuff tendinopathy or impingement syndrome)
primary if baseball, volleyball, etc (5% of time)
pathophysiological changes in long head biceps tendinitis
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
what characteristic deformity is seem in proximal biceps tendinitis complete rupture
Popeye deformity
provocative testing for proximal biceps tendinitis
bicipital groove palpation
speed test
uppercut test
yergason test
**examine for possible associated labral and/or rotator cuff pathologies.
imagining for proximal biceps tendinitis
ultrasound
MRI
MRA
surgery for proximal biceps tendon tear
biceps tenotomy or tenodesis
cut an attach tendons…
distal biceps rupture from
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
distal biceps tendon rupture evaluation
-history of single traumatic event
-painful pop
-palpable and visible retraction of biceps muscle belly (reverse Popeye deformity)
-weakness
acromioclavicular joint injury causes? what part of the acromion is hurt? what position is arm in?
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
___ aspect of shoulder or acromion process with arm in ___ for AC joint injury is most common
lateral ; adduction
the ___ sign is when the clavicle is elevated and rebounds after inferior compression;; seen in acromioclavicular joint injury
piano key sign
imaging fro AC joint injury
x ray
6 types of AC joint injuries (get progressively worse)
- 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.
test for AC joint integrity
cross-body adduction test
alarm symptoms in shoulder pain
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
when to refer in shoulder pain
Failure of conservative treatment over 3 months.
full RC tears, bad partial tears
at risk for second dislocation
etc