Learning Objectives
Understand the pathophysiology of TOS
Learn the provocative maneuvers to diagnose TOS
Understand treatment options for TOS

Case Presentation
EB is a 30 year old white female who presents with left upper extremity swelling and pain, which began while she was watching a movie in a theater. She says that when she left the movie, a couple of hours after the symptoms initially began, she noted that the swelling of her left arm was worse and there was pain in her shoulder region. She also could not get her ring off of her finger and her left hand was dusky. She did not have any shortness of breath or pleuritic chest pain. A few days before that the patient had been shoveling snow during a heavy snow storm and the day after that developed upper respiratory symptoms including sore throat, sharp chest pain, a sensation of her ears being plugged and swollen glands in her neck.
The patient had a Doppler evaluation which revealed clot in the subclavian and axillary veins. A CT scan of the chest revealed no evidence of pulmonary embolism. She had a hypercoagulable workup which was negative. She was treated with heparin and then started on Coumadin and consideration was given a couple of times to giving thrombolytics but this was not done. She was taken off her OCP.
Ultrasound of the left upper extremity was performed about 15 days after the onset of symptoms and revealed interval partial recanalization of the left subclavian vein and slight increase in flow within the left axillary vein in a patient with previous occlusive thrombus in these vessels.
MRI of the left upper extremity was performed to look for a compressive component to her vasculature in the left upper extremity as a cause for the DVT.

TOS – Differential Diagnosis
Cervical disc disease
Cervical facet disease
Malignancies (Pancoast/local tumors, spinal cord tumors)
Peripheral nerve entrapments (ulnar or median nerve)
Brachial plexitis
Rotator cuff injuries
Fibromyalgia, muscle spasm
Neurologic disorders (MS)
Chest pain, angina
Vasospastic disorder (Raynaud’s)
Neuropathic syndromes of upper extremity

Stroke:An Introduction

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What is a Stroke? (Brain Attack)
Disruption of blood flow to part of the brain caused by:
Occlusion of a blood vessel (ischemic stroke)
Rupture of a blood vessel (hemorrhagic stroke)

What happens with cutoff of blood supply?
Oxygen deprivation to nerve cells in the affected area of the brain -->
 Nerve cells injured and die -->
 The part of the body controlled by those nerve cells cannot function.

What happens with rupture of a blood vessel?
Oxygen deprivation to nerve cells in the affected area of the brain and local destruction of nerve cells-->
 Nerve cells injured and die -->
 The part of the body controlled by those nerve cells cannot function.

Stroke Impact
750,000 strokes per year
Third leading cause of death
(1st: heart disease, 2nd: all cancers)
Over 160,000 deaths per year
Over 4 million stroke survivors

Stroke Diagnosis
Symptoms of Stroke
Sudden numbness or weakness of face, arm or leg, especially on one side of the body
Sudden confusion, trouble speaking or understanding
Sudden trouble seeing from one or both eyes
Sudden unsteadiness, dizziness, loss of balance or coordination
Sudden severe headache with no known cause

Common Stroke Patterns
Left (Dominant) Hemisphere:
Right hemiparesis
Right hemisensory loss
Right visual field defect
Left gaze preference
Difficulty reading, writing, or calculating

Right (Nondominant) Hemisphere:
Left hemiparesis
Left hemisensory loss
Left neglect
Left visual field defect
Right gaze preference

Brainstem/Cerebellum/Posterior Circulation
Motor or sensory loss in all 4 limbs
Crossed signs (face vs. body)
Limb or gait ataxia
Dysconjugate gaze
Cortical blindness

Spinal Cord lesions

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Spinal cord lies within protective covering of vertebral column.
Begins just below foramen magnum of the skull.
Ends opposite 2nd lumbar vertebra.
Below L2 continue as a leash of nerve roots known as cauda equina.
Prolongation of the pia matter forms filum terminale.

Spinal cord structure
The spinal cord consists of central core of grey matter containing nerve cell bodies, and outer layer of white matter of nerve fibers.
Within the grey matter, the dorsal horn contains sensory neurons, the ventral horn contains motor neurons and the lateral horn contains preganglionic sympathetic neurons.
Within the white matter run ascending and descending nerve fiber tracts, which link the spinal cord to the brain.
The principle ascending tracts are the spinothalamic tracts, spinocerebellar tracts and dorsal columns. The coticospinal tracts is an important descending tract.
The spinal cord receives information from, and controls the trunk and limbs.
This is achieved through 31 pairs of spinal nerves which join the cord at intervals along its length and contain afferent and efferent nerve fibers connecting with the structures at the periphery.

Causes of spinal cord lesions
congenital; spinal stenosis.
Infection; TB ,abscess.
Trauma; vertebral body fracture or facet joint dislocation.
Inflammatory; Rheumatoid arthritis.
Disc and vertebral lesion.
Vascular;  epidural and subdural hemorrhage.

Congenital spinal stenosis
The patient is born with a narrow spinal canal due to abnormally formed parts of the spine.
This condition is most common in patients with a short stature, such as achondroplastic dwarves.

Other causes of spinal stenosis
aging process (most common cause )
herniated discs
bone and joint enlargement
bone spurs

Spine surgery:
  used when conservative treatment failed.
 -laminectomy (removing bone behind the spinal cord).
 -foramenotomy (removing bone around the spinal nerve).
 -discectomy (removing the spinal disc to relieve pressure).

   Dural tears.
   Instability of the spine

“ the occurrence of menses on only five or fewer occasions per year”
2ry Amenorrhoea:
“ the absence of menses for 6 months ( or greater than three times the previous cycle intervals) in a woman who has menstruated before”

Hypo-estrogenic 2ry Am’rrhoea
Hypothalamic-pituitary dysfunction
Premature ovarian failure

Hypothalamic-pituitary dysfunction:
Eating disorders e.g, Anorexia nervosa, extensive dieting or exercise. A loss of >10 kg … a’hoea… estrogen lllow …osteoporosis
Hypothalamic lesions
Nonsecreting pituitary adenomas
Other CNS system neoplasms
Sheehan’s syndrome

Premature ovarian failure:
Chromosomal abnormalities. Amenorrhoea < 35 years of age
47 XXY ….. High risk of malignancy… gonadectomy
Turner’s syndrome mosaic (XX/XO)

Resistant ovarian syndrome. May be due to auto antibodies against ovaries or gonadotropin receptors. Could be part of disease involving thyroid, adrenal and acid receptors in stomach
If  present in younger age <35 years check auto antibodies

Premature menopause. < 45 mainly familial
High FSH & LH Low Estradiol, chromosomal analysis / ovarian biopsy

Prolactin secreting tumours. 40-50% of cases; most are “micro-adenomas” (,10mm diameter). Macro adenoma levels >2500-3000 mU/l
Idiopathic. 40% levels are usually <2500 mIU/L
Other tumours compressing the the pituitary stalk. Rare, e.g. cranio- pahryngioma.
Primary hypothyroidism (3-5%).
Drugs (1-2%).  Metochlopramide and phenothiazides are the commonest + cimetidine, haloperidol, methyl dopa and reserpine
Systemic problems.
Acute or chronic renal failure
Herpes zoster of the breast dermatomes

Slight to moderate elevation. Repeat the test, if still high, screen for gross abnormality by lateral skull X-ray. If it shows enlargement of the pituitary fossa or erosion of the clinoid process …. CT scan to detect macro-adenoma.
Marked elevation… repeat the test + arrange CT scan ASAP. Specially urgent when headache or visual field defect present

Insulin Resistance Syndrome

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ACE position statement
Clinical manifestations include CVD, hypertension, PCOS, and nonalcoholic steatohepatitis NASH, and the list continues to expand.
(AACE) championed the creation of the new ICD-9 Code 277.7 for the “Dysmetabolic Syndrome”
use the term Insulin Resistance Syndrome to describe the consequences of insulin resistance and compensatory hyperinsulinemia
absence of a straightforward diagnostic test or definitive clinical trials, identification and treatment of a syndrome

Obesity and Insulin Resistance Syndrome
Obesity is a physiological variable that decreases insulin-mediated glucose disposal
BMI rather than abdominal circumference, be used to identify individuals at increased risk
Abdominal circumference are neither routinely performed nor is its quantification as well standardized
European Group for the Study of IR was not increased when abdominal circumference replaced BMI as the marker of obesity
BMI and abdominal circumference were closely related r=0.9 in 15,271 participants in NHANES III

Plasma insulin concentration and the IRS
Plasma insulin concentrations are useful surrogate marker of IR
Highly statistically significant correlations between measures of insulin-mediated glucose disposal and both fasting (r=0.6) and post-glucose challenge (r=0.8) plasma insulin concentrations
Methods to quantify plasma insulin concentrations are not standardized
Difficult to compare values measured in different clinical laboratories
Has not been established that an increase in plasma insulin concentration, by itself, in the absence of any of changes listed in Table 3, can predict the development of CVD
A research, not a clinical tool

Factors that increase the likelihood of IRS
include having CVD
polycystic ovarian syndrome
acanthosis nigricans
a family history of type 2 diabetes, hypertension, or CVD
a history of gestational diabetes or glucose intolerance
non-Caucasian ethnicity
sedentary lifestyle

Table of content
Determinants of insulin sensitivity
Mechanisms of insulin resistance
Endothelial dysfunction and insulin resistance
Nonalcoholic fatty liver disease
Lifestyle approaches for the IRS
Low-carbohydrate diet for atherogenic dyslipidemia
Relationship between obesity and the IRS
Adipocyte hormones and insulin action
Inflammation and the IRS

Mechanisms of insulin resistance
Carbon NMR studies with a profound defect in muscle glycogen synthesis in persons with type 2 diabetes
Phosphorus NMR studies suggest transport defects at the level of hexokinase or GLUT4 to be primary 
offspring of persons with type 2 diabetes suggest this abnormality to precede the onset of the disease
Further 13C NMR spectroscopy has suggested that the defect is at the level of GLUT4.
The abnormality in GLUT4 is strongly predicted by the free fatty acid (FFA) level and, even more strongly, by intramyocellular triglyceride levels
A potential mechanism by which fatty acid metabolites inhibit glucose transport activity appears to involve the insulin signaling cascade, with decreased phosphatidylinositol 3-kinase caused by activation of a serine kinase cascade via protein kinase C-[theta] decreasing the translocation of GLUT4 to the cell membrane.
peroxisome proliferator-activated receptor [gamma] agonists act by increasing adipose tissue fat stores and preventing the increase in fatty acid metabolites in liver and muscle.

Treat Pediatric Eye Conditions

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Differential Diagnosis Red Eye
Ophthalmia Neonatorum
Conjunctivitis (bacterial, Viral Or Allergic)
Traumatic Injury (e.g., Corneal Abrasion)
Corneal Infection/keratitis
Foreign Body
Uveitis (iritis)( Anterior)
Preseptal And  Orbital Cellulitis

Danger Features- Red Eye
Severe Pain (unilateral)
Reduced Visual Acuity/ Persistent Blurring
Reduced Ocular Movement
Ciliary Flush
Irregular Corneal Light Reflection

Ophthalmia Neonatorum
Moderate -severe Bacterial Conjunctivitis In Newborns <28 Days Of Age
This Condition Must Be Differentiated From The More Common Mild Conjunctivitis
- Generally Acquired From The Maternal Genital Tract
- Bacterial Organisms Include Chlamydia And Neisseria Gonorrhea
- Chlamydial Infection Is The More Common Cause Of Neonatal Conjunctivitis
- Less Commonly, Hemophilus Strains, Staphylococcus Aureus, Streptococcus Pneumoniae And Other Gram-negative Organisms May Be Involved

Nasolacrimal Ductobstruction –dacryostenosis
A Congenital Disorder Of The Lacrimal System Characterized By Blockage Of The Nasolacrimal Duct
Results In Excessive Tearing And Mucopurulent Discharge From The Affected Eye
The Condition Occurs In Approximately 2% To 6% Of Newborns
Onset Is Usually Within The First Few Weeks Of Life

An Abnormality In The Alignment Of The Eyes
The Classification Of Strabismus Is Complex
On An Etiologic Basis, It May Be Paralytic Or Non-paralytic
It Can Also Be Classified As Congenital Or Acquired, Intermittent Or Constant, Or Convergent Or Divergent

-when The Eyes Are Positioned So That An Image Falls On The Fovea (the Area Of Best Visual Acuity) Of One Eye, But Not The Other, The Second Eye Will Deviate So That The Image Falls On It’s Fovea As Well
-this Deviation May Be Up, Down, In Or Out And Results In Strabismus.

Causes  Of Strabismus
-weakness Or Paralysis Of One Or More Ocular Muscles
-deviation Is Asymmetric
-congenital: Secondary To Developmental Defect In Muscle Or Nerves Or To Congenital Infection
-acquired: Due To Extraocular Nerve Palsies; Indicates A Serious Underlying Problem (e.g., Fracture Of Facial Bone, Cns Tumor, Neurodegenerative Disease, Myasthenia Gravis, Cns Infection)

-most Common Type Of Strabismus
-extraocular Muscles And The Nerves That Control Them Are Normal
-occasionally, This Form May Be Secondary To Underlying Ocular Or Visual Defects Such As Cataracts Or Refraction Errors
-overall, Seen In 3% Of Children

Eye Injuries
Non Accidental Trauma/shaken Baby Syndrome
-hallmark Of Diagnosis Is Retinal Hemorrhage
-presence And Severity Of Hemorrhages Correlates Well With Level Of Brain Injury
-history Of Injury Often Vague And Not Well Correlated With Extent Of Injuries
-other Findings Associated With Non- Accidental Injury Include Ecchymosis Of Lids, Sub-conjunctival Hemorrhages, And Hyphema

Stable Angina, Guidelines & RACPC

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Promoting Assessment & Treatment which is
Structured, Systematic, Objective
In keeping with the patient’s wishes

Risk stratification
At presentation (“pre-test”)
After non-invasive assessment (“post-test”)
After Coronary Angiography

Angina : NSF Standards
Standard 8
    People with symptoms of angina or suspected angina should receive appropriate investigation and treatment to relieve their pain and reduce their risk of coronary events.
Standard 9
    People with angina that is increasing in frequency or severity should be referred to a cardiologist urgently or, for those at greatest risk, as an emergency.

Standard 10
    NHS Trusts should put in place hospital-wide systems of care so that patients with suspected or confirmed coronary heart disease receive timely and appropriate investigation and treatment to relieve their symptoms and reduce their risk of subsequent coronary events.

Evaluation and Diagnosis
In patients presenting with chest pain
detailed symptom history
focused physical examination
directed risk-factor assessment
Estimate the probability of significant CHD
if intermediate or high: refer to RACPC
Objective assessment (eg ExECG) is for:
Diagnosis of myocardial ischaemia
Assessment of severity & pathophysiology
Assessment of prognosis

Rapid Access Chest Pain Clinics
One-stop” assessment of stable patients
Recent (<6 months) onset of exertional chest pain, intermediate-high risk of angina
Known CHD which was stable (eg after PTCA or CABG) now symptomatic again
< 2 week wait to clinic

Classification of Chest Pain
Estimating the Probability of CHD from History of Chest Pain
Precipitated by exercise
Brief duration (<15 minutes)
Relieved promptly by rest or GTN
Central chest location
Radiates to Jaw, Throat, or L Arm
Absence of other causes for pain

Cholelithiasis and Cholecystitis
a. Cholelithiasis: formation of stones (calculi) within the gallbladder or biliary duct system
b. Cholecystitis: inflammation of gall bladder
c. Cholangitis:  inflammation of the biliary ducts
a.Gallstones form due to
  1.Abnormal bile composition
  2.Biliary stasis
  3.Inflammation of gallbladder
b.Most gallstones are composed primarily of bile (80%); remainder are composed of a mixture of bile components
c.Excess cholesterol in bile is associated with obesity, high-cholesterol diet and drugs that lower cholesterol levels
d.If stones from gallbladder lodge in the cystic duct
  1. There can be reflux of bile into the gallbladder and liver
  2. Gallbladder has increased pressure leading to ischemia and inflammation
  3. Severe ischemia can lead to necrosis of the gall bladder
  4. If the common bile duct is obstructed, pancreatitis can develop

Risk factors for cholelithiasis
b.Family history, also Native Americans and persons of northern European heritage
c.Obesity, hyperlipidemia
d.Females, use of oral contraceptives
e.Conditions which lead to biliary stasis:  pregnancy, fasting, prolonged parenteral nutrition
f.Diseases including cirrhosis, ileal disease or resection, sickle-cell anemia, glucose intolerance

Manifestations of cholelithiasis
a.Many persons are asymptomatic
b.Early symptoms are epigastic fullness after meals or mild distress after eating a fatty meal
c.Biliary colic (if stone is blocking cystic or common bile duct): steady pain in epigastric or RUQ of abdomen lasting up to 5 hours with nausea and vomiting
d.Jaundice may occur if there is obstruction of common bile duct

Manifestations of acute cholecystitis
a.Episode of biliary colic involving RUQ pain radiating to back, right scapula, or shoulder; the pain may be aggravated by movement, or deep breathing and may last 12 – 18 hours
b.Anorexia, nausea, and vomiting
c.Fever with chills

Complications of cholecystitis
a.Chronic cholecystitis occurs after repeated attacks of acute cholecystitis; often asymptomatic
b.Empyema:  collection of infected fluid within gallbladder
c.Gangrene of gall bladder with perforation leading to peritonitis, abscess formation
d.Pancreatitis, liver damage, intestinal obstruction

Autoimmune Pancreatitis

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AUTOIMMUNE PANCREATITIS - chronic pancreatitis with distinct clinical, serological, histological and imaging features and it is involved in hyper- IgG4 group of diseases.

1. Diagnostic (any one):
    a) Pancreatic histology showing periductal lymphoplasmacytic
        infiltrate with obliterative hlebitis (LPSP)
    b) Lymphoplasmacytic infiltrate with abundant (>10 cells/hpf) IgG4
        positive cells in the pancreas
2. Supportive (any one)
    a) Lymphoplasmacytic infiltrate with abundant (>10 cells/hpf) IgG4
        positive cells in involved extra-pancreatic organ
    b) Lymphoplasmacytic infiltrate with fibrosis in the pancreas

Typical imaging features:
1. CT/MR: diffusely enlarged gland with delayed (rim) endhancement
2. ERCP: Diffusely irregular, attenuated main pancreatic duct
Atypical Imaging Features: Pancreatitis, focal pancreatic mass, focal pancreatic duct stricture, pancreatic atrophy, pancreatic calcification

Elevated serum IgG4 level (normal 8-140 mg/dl)

Other Organ involvement
Hilar/intrahepatic biliary strictures, persistent distal biliary stricture, Parotid/lacrimal gland involvement, Mediastinal lymphadenopathy, Retroperitoneal fibrosis

Response to steroid therapy
Resolution/marked improvement of pancreatic/extrapancreatic manifestation with steroid therapy

     Diffuse or segmental narrowing of the MPD with irregular wall and diffuse or localized enlargement of the pancreas by imaging studies, such as abdominal US, CT, and magnetic resonance
     High serum γ-globulin, IgG, or IgG4, or the presence of autoantibodies such as antinuclear antibodies and rheumatoid factor
     Marked interlobular fibrosis and prominent infiltration of lymphocytes and plasma cells in the periductal area,     occasionally with lymphoid follicles in the pancreas

Diagnosis of AIP is established when criterion 1 and criterion 2 and/or 3 are fulfilled. However, it is necessary to exclude malignant diseases

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