Showing posts with label General Medicine. Show all posts
Showing posts with label General Medicine. Show all posts

02 June 2012

Dyslipidemia



Dyslipidemia: High blood cholesterol levels.
Lipid disorders; Hyperlipoproteinemia; Hyperlipidemia; Dyslipidemia; Hypercholesterolemia

Dyslipidemia
Dyslipidemia .ppt

Diabetes Is a CHD Risk Equivalent
Diabetes Is a CHD Risk Equivalent.ppt

New Concepts in the Evaluation and Treatment of Dyslipidemia
Nathan D. Wong, PhD, FACC
New Concepts in the Evaluation and Treatment of Dyslipidemia.ppt
Epidemiology Clinical Trials Mgm.ppt

Approaches To Dyslipidemia Treatment in Children and Adolescents
Lorenzo Iughetti; Barbara Predieri; Patrizia Bruzzi; Fiorella Balli
Dyslipidemia_Treatment_Children_Adolescents2011.ppt

Hypertriglyceridemia
Jenny Gordon
Tryglycerides.ppt

Diabetes Mellitus and Hypertension: Diagnosis and Management
T. Villela, M.D.
Diabetes.ppt

Awareness, Treatment and Control of Hypertension among Filipino Americans
Mariano Rey, M.D.
Awareness_Tx_Control_HTN.ppt

Treatment of Dyslipidemia
Treatment of Dyslipidemia.ppt

Lipid droplet proteins in the control of cellular lipid metabolism
Perry Bickel
Lipid droplet proteins in the control of cellular lipid metabolism.ppt

Interactive Case Presentation
Doug Kutz MD
Interactive Case Presentation.ppt

Hypertension: New Trials – Best Treatments
Karen Moncher, MD
Hypertension: New Trials – Best Treatments.ppt

CHD is the single largest killer
CHD is the single largest killer.ppt

Hyperlipidemia
Hyperlipidemia.ppt

Linked Metabolic Abnormalities
http://www.pitt.edu/~super4/33011-34001/33711.ppt

Cardiometabolic Syndrome
Nabil Sulaiman
http://www.pitt.edu/~super4/33011-34001/33751.ppt
http://www.pitt.edu/~super7/5011-6001/5311.ppt

Atherosclerotic Vascular Disease Risk Factors, Screening to Prevent
David R. Rudy, M.D., M.P.H.
Atherosclerotic Vascular Disease Risk Factors, Screening to Prevent.ppt

Diabetes Guidelines and Treatment
Diabetes Guidelines and Treatment.ppt

Primary Biliary Cirrhosis (PBC)
Thomas W. Faust, M.D., M.B.E.
Primary Biliary Cirrhosis.ppt

Diabetes: Guideline-Based Management
Eric L. Johnson, M.D.
DiabetesGuidelinemanagement5-12-11.ppt

Dyslipidemia
Stanford Massie M.D.
Hyperlipidemia.ppt

The Relationship of Weight and Obstructive Sleep Apnea
Mia Zaharna, MD, MPH
The Relationship of Weight and Obstructive Sleep Apnea.ppt
536 free full text articles

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28 May 2012

Insufficient sleep syndrome



Sleep Loss and Fatigue – Addressing the Issue
SAFER_Presenation.ppt

Sleep Trajectories in Infancy: Predictors and Consequents
Sleep Trajectories in Infancy.ppt

Fatigue and Resident Education
Fatigue and Resident Education.ppt

The Gift of Sleep: Promoting Healthy Sleep Habits for Infants and Toddlers
Jean Twomey, PhD
The Gift of Sleep.ppt

Sleep, sleep loss, sleep disorders, and metabolism
Orfeu M. Buxton, Ph.D.
Sleep, sleep loss, sleep disorders, and metabolism.ppt

Thalamic Stroke and Disordered Sleep
Kenneth C. Sassower, M.D.
Thalamic_Stroke_and_Disordered_Sleep_guest_lecture.ppt

An Overview of Puberty 
Betsy Pfeffer MD
PubertyOverview.ppt

Sleep Health and Safety for Railroaders
Janis L Anderson, Ph.D.
Sleep Health and Safety for Railroaders.ppt

MOOD FLIPS and BAD TRIPS
MOOD FLIPS and BAD TRIPS.ppt

Sleep and Our Health DO YOU OR A LOVED ONE SNORE?
DR. TERRI PRODOEHL
DO YOU OR A LOVED ONE SNORE.ppt

Basic Human Needs Sleep
Basic Human Needs Sleep.ppt

Eating and Sleep Disorders
Eating and Sleep Disorders.ppt

Health and Wellness: What everyone should know
Pat Duncan
Health and Wellness.ppt

leep Disturbances and Weight Gain: Examining the Evidence
Eileen Chasens, DSN, RN
leep Disturbances and Weight Gain.ppt

Perinatal Mood and Anxiety Disorders
Cort A. Pedersen, M.D.
Perinatal Mood and Anxiety Disorders.ppt

Psychiatric Sequalae of Sleep Disorders
Mark Brown, M.D.
Sleep Disorders.ppt

Why sleep? The origins and development of Sleep Medicine
HistoryOfSleepMed.ppt

Sleep When a cup of warm milk is not enough
K. Van Gundy, M.D.
sleep_disorders.ppt

SLEEP, ALERTNESS, and FATIGUE EDUCATION
SAFER.ppt

Sleep Basics for Health Promotion
Barbara B. Richardson, PhD
Sleep Basics for Health Promotion.ppt

Sleep and Relaxation
Bob Whitman, Ph.D.
Sleep_and_Relaxation_Wellness.ppt

Physician Sleep Deprivation: To Sleep or Not to Sleep?
Don Hayes, Jr., MD
Physician Sleep Deprivation.ppt

Published scholarly articles

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22 May 2012

Intraosseous Infusion



Intravenous Access, Blood Sampling, and Intraosseous Infusion
Intravenous Access.ppt

The 5 Rights of Intraosseous Vascular Access
Intraosseous Vascular Access.ppt

Intraosseous Procedure Update
Intraosseous Procedure Update.PPT

Infusion Therapy
Infusion Therapy.ppt

Double-blind Clinical Trials
Double-blind Clinical Trials.ppt

Redesign of an Intraosseous Needle
Jonathan Hughes, Michael Audette, Christopher Sullivan
Redesign of an Intraosseous Needle.ppt

Shock: rapid intravenous or intraosseous infusion
Shock: rapid intravenous or intraosseous infusion.ppt

ECG and Arrhythmia Assessment
Bryan Cannon, M.D.
ECG and Arrhythmia Assessment.ppt

Intraosseous Cannulation
Intraosseous Cannulation.ppt

Principles and Routes of Medication Administration
Principles and Routes of Medication Administration.ppt

Fluid and Electrolytes
Jan Bazner-Chandler
Fluid and Electrolytes.ppt

Pediatric Trauma
PediTrauma.ppt

Placement of an intraosseous line
Placement of an intraosseous line.ppt

Intraosseous
Intraosseous.ppt
108 full text articles list:

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12 April 2012

Physical Examination Videos



Physical Examination Videos from The University of Wisconsin School of Medicine and Public Health in Madison



Presentation

Picture from Physical Exam: Introduction and Vital Signs video
L. Zakowski

Picture from Physical Exam: Head and Neck video
L. Zakowski

Picture from Physical Exam: Axilla, Pulmonary, Cardiac video
L. Zakowski

Picture from Physical Exam: Abdominal Exam video
L. Zakowski

Picture from Physical Exam: Upper Extremities video
L. Zakowski

Picture from Physical Exam: Lower Extremities video
L. Zakowski

Picture from Physical Exam: Quality of Physical Exam and Closure video
L. Zakowski

Picture from Physical Exam: Advanced Abdominal Exam video
L. Zakowski

Picture from Physical Exam: Advanced Cardiovascular Exam video
L. Zakowski

Picture from Physical Exam: Advanced ENT Testing video
L. Zakowski

Picture from Physical Exam: Advanced Pulmonary Exam video
L. Zakowski

Picture from Controversies in  Preparticipation Sports Screening video
D. Bernhardt

Picture from Physical Exam: Anterior and Posterior Thorax and Axilla Exam video
C. Seibert

Picture from Musculoskeletal Exam: Spine video
F. Salvi

Picture from Musculoskeletal Exam: Hip video
F. Salvi

Read more...

Techniques of the Physical Examination



Techniques of the Physical Examination
PtAssessment/Technique1.ppt
PtAssessment/Technique2.ppt

The History of the Physical Exam and Diagnostic Techniques
Hughes Evans, MD, PhD
Physical Exam and Diagnostic Techniques.ppt

Patient Assessment Process Goals of the Focused History and Physical Exam
Patient Assessment Process.ppt

Physical Examination of the Chest
PhysicalExamination.ppt

Health History and Physical Assessment
Rachel S. Natividad, RN, MSN, NP
Health History and Physical Assessment.ppt

Physical Assessment
Wanda Dooley, MSN, RN, CS, FNP
Physical Assessment.ppt

The Demise of the Physical Exam
Cam Hebson, MS IV
The Demise of the Physical Exam.ppt

Principles of The Physical Examination
Principles of The Physical Examination.ppt

Clinical assessment
Clinical assessmentPower_Point.ppt

Health history Physical exam
Health history Physical exam.ppt

Physical Exam
Physical Exam.ppt

Osteopathic Abdominal Exam
Osteopathic Abdominal Exam.ppt

Obtaining and Documenting Audit Evidence
Obtaining and Documenting Audit Evidence.PPT

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26 February 2010

PEGylation



Mr. Sanju Patel a visitor of this blog asked me to post detail information on pegylation.

According to medical dictionary -
Oeginterferon alfa-2a,
a covalent conjugate of recombinant interferon alfa-2a and polyethylene glycol, used in the treatment of chronic infection by hepatitis C virus. It is administered subcutaneously. - Mosby's Medical Dictionary, 8th edition.

Pegasys
Pharmacologic class: Interferon
Therapeutic class: Biological response modifier
Pregnancy risk category C
FDA Boxed Warning

• Drug may cause or aggravate fatal or life-threatening neuropsychiatric, autoimmune, ischemic, and infectious disorders. Monitor patient closely with periodic clinical and laboratory evaluations. Withdraw drug in patients who have persistently severe or worsening signs or symptoms of these conditions. In most cases, these disorders resolve once therapy ends.
• Concurrent use with ribavirin may cause birth defects or fetal death. Use extreme care to avoid pregnancy in female patients and female partners of male patients.
Action

Unclear. Thought to bind to specific cell-surface receptors, suppressing cell proliferation and viral replication. Also increases effector protein levels and reduces white blood cell (WBC) and platelet counts.
Availability

Injection: 180-mcg/ml vial

⊘Indications and dosages

➣ Chronic hepatitis C virus infection

Adults: 180 mcg subcutaneously q week for 48 weeks. If poorly tolerated, reduce to 135 mcg weekly; some patients may need reduction to 90 mcg.
Dosage adjustment

• Neutrophil count less than 750 cells/mm3 or platelet count less than 50,000 cells/mm3
• Hepatic disease
• End-stage renal disease requiring dialysis
• Serious adverse reactions
Off-label uses

• Renal cell carcinoma
Contraindications

• Hypersensitivity to drug
• Autoimmune hepatitis
• Decompensated hepatic disease
• Infants and neonates (due to benzyl alcohol content)
Precautions

Use cautiously in:
• thyroid disorders; bone marrow depression; hepatic, renal, or cardiac disease; pancreatitis; autoimmune disorders; pulmonary disorders; colitis; ophthalmic disorders; depression
• elderly patients
• pregnant or breastfeeding patients
• children younger than age 18.
Administration

• Keep refrigerated. Before giving, roll vial between palms for 1 minute to warm; don't shake. Protect solution from light.
• Don't use if solution is cloudy or contains visible particles.
• Administer undiluted in abdomen or thigh by subcutaneous injection.
• Know that drug may be used alone or with ribavirin.

Adverse reactions

CNS: dizziness, vertigo, insomnia, fatigue, rigors, poor memory and concentration, asthenia, depression, irritability, anxiety, peripheral neuropathy, mood changes, suicidal ideation

CV: hypertension, chest pain, supraventricular arrhythmias, myocardial infarction

EENT: vision loss, blurred vision, retinal artery or vein thrombosis, retinal hemorrhage, optic neuritis, retinopathy, papilledema

GI: nausea, vomiting, diarrhea, abdominal pain, dry mouth, anorexia, GI tract bleeding, ulcerative and hemorrhagic colitis, pancreatitis

Hematologic: anemia, leukopenia, thrombocytopenia, neutropenia

Metabolic: diabetes mellitus, aggravated hypothyroidism or hyperthyroidism

Musculoskeletal: myalgia, back pain, joint pain

Respiratory: pneumonia, interstitial pneumonitis, bronchoconstriction, respiratory failure

Skin: alopecia, pruritus, diaphoresis, rash, dermatitis, dry skin, eczema

Other: weight loss, flulike symptoms, injection-site reaction, pain, autoimmune phenomena, severe and possibly fatal bacterial infections, severe hypersensitivity reactions including angioedema and anaphylaxis
Interactions

Drug-drug. Theophylline: increased theophylline blood level

Drug-diagnostic tests. Absolute neutrophil count, hematocrit, hemoglobin, platelets, WBCs: decreased values

Alanine aminotransferase: transient increase

Glucose, thyroid function tests: decreased or increased levels

Triglycerides: increased levels
Patient monitoring

Assess cardiac and pulmonary status closely. Watch for evidence of infections and hypersensitivity reactions, including anaphylaxis.
• Before therapy begins, assess CBC (including platelet count), blood glucose level, and thyroid, kidney, and liver function tests. Continue to monitor at 1, 2, 4, 6, and 8 weeks and then every 4 weeks during therapy (more often if abnormalities occur). Monitor thyroid function tests every 12 weeks.
Monitor for development of diabetes mellitus, hypothyroidism, and hyperthyroidism.
If serious adverse reaction occurs, discontinue drug or adjust dosage until reaction abates, as prescribed. If reaction persists or recurs despite adequate dosage adjustment, discontinue drug.
Patient teaching

• Teach patient or caregiver how to administer injection subcutaneously in thigh or abdomen and how to dispose of equipment properly, if appropriate.
Advise patient to promptly report rash, bleeding, bloody stools, infection symptoms (such as fever), decreased vision, chest pain, severe stomach or lower back pain, shortness of breath, depression, or suicidal thoughts.
• Instruct patient to administer drug exactly as prescribed. If he misses a dose but remembers it within 2 days, tell him to take missed dose as soon as possible; if more than 2 days have elapsed, tell him to contact prescriber.
• Caution patient not to switch brands without prescriber's approval.
• Instruct patient to have periodic eye exams.
• Advise female patient of childbearing age to avoid pregnancy and use two birth control methods before, during, and up to 6 months after therapy. Instruct male patient to use condoms.
• As appropriate, review all other significant and life-threatening adverse reactions and interactions, especially those related to the drugs and tests mentioned above.

Nursing Spectrum Drug Handbook 2009. © 2009 by The McGraw-Hill Companies, Inc.

Interferons

PEGylation: A successful Approach to Drug Delivery

Pegylated Liposomal Doxorubicin (Doxil) in metastatic breast cancer

PEG protocol

Current and Future Treatment of Chronic Hepatitis C

Treatment of Chronic Hepatitis C

Read more...

13 February 2010

Gallstone Disease



Gallstone Disease
By:Tad Kim, M.D.

Overview
* Gallstone pathogenesis
* Definitions
* Differential Diagnosis of RUQ pain
* 7 Cases

Gallstone Pathogenesis
* Bile = bile salts, phospholipids, cholesterol
o Also bilirubin which is conjugated b4 excretion
* Gallstones due to imbalance rendering cholesterol & calcium salts insoluble
* Pathogenesis involves 3 stages:
o 1. cholesterol supersaturation in bile
o 2. crystal nucleation
o 3. stone growth

Definitions
Infection within bile ducts usu due to obstrux of CBD. Charcot triad: RUQ pain, jaundice, fever (seen in 70% of pts), can lead to septic shock

Cholangitis
Gallstone in the common bile duct (primary means originated there, secondary = from GB)

Choledocho-lithiasis
GB inflammation due to biliary stasis(5% of time) and not stones(95%). Seen in critically ill pts

Acalculous cholecystitis
Recurrent bouts of colic/acute chol’y leading to chronic GB wall inflamm/fibrosis. No fever/WBC.

Chronic cholecystitis
Acute GB inflammation due to cystic duct obstruction. Persistent RUQ pain +/- fever, ↑WBC, ↑LFT, +Murphy’s = inspiratory arrest

Acute cholecystitis
Wax/waning postprandial epigastric/RUQ pain due to transient cystic duct obstruction by stone, no fever/WBC, normal LFT

Symptomatic cholelithiasis
Differential Diagnosis of RUQ pain

* Biliary disease
o Acute chol’y, chronic chol’y, CBD stone, cholangitis
* Inflamed or perforated duodenal ulcer
* Hepatitis
* Also need to rule out:
o Appendicitis, renal colic, pneumonia or pleurisy, pancreatitis
Case 1

* 46yo F w RUQ pain x4hr, after a fatty meal, radiating to the R scapula, also w nausea. Pt is pain-free now.
* No prior episodes
* Minimal RUQ tenderness, no Murphy’s
* WBC 8, LFT normal
* RUQ U/S reveals cholelithiasis without GB wall thickening or pericholecystic fluid
* Diagnosis: ?

Symptomatic cholelithiasis

* aka “biliary colic”
* The pain occurs due to a stone obstructing the cystic duct, causing wall tension; pain resolves when stone passes
* Pain usually lasts 1-5 hrs, rarely > 24hrs
* Ultrasound reveals evidence at the crime scene of the likely etiology: gallstones
* Exam, WBC, and LFT normal in this case
* Treatment: Laparoscopic cholecystectomy

Spectrum of Gallstone Disease
Cholelithiasis
Asymptomatic
cholelithiasis
Symptomatic
cholelithiasis
Chronic
calculous
cholecystitis
Acute
calculous
cholecystitis
* Symptomatic cholelithiasis can be a herald to:
o an attack of acute cholecystitis
o or ongoing chronic cholecystitis
* May also resolve

Case 2
* Same case, except pt has had multiple prior attacks of similar RUQ pain
* No fever or WBC
* Ultrasound reveals gallstones, thickened GB wall, no pericholecystic fluid
* Diagnosis: ?
Chronic calculous cholecystitis

* Recurrent inflammatory process due to recurrent cystic duct obstruction, 90% of the time due to gallstones
* Overtime, leads to scarring/wall thickening
* Treatment: laparoscopic cholecystectomy

Case 3
* Same pt, now > 24hrs of RUQ pain radiating to the R scapula, started after fatty meal, a/w nausea, vomiting, fever
* Exam: Palpable, tender gallbladder, guarding, +Murphy’s = inspiratory arrest
* WBC 13, Mild LFT
* U/S: gallstones, wall thickening (>4mm), GB distension, pericholecystic fluid, sonographic Murphy’s sign (very specific)
* Diagnosis: ?
* Curved arrow
o Two small stones at GB neck
* Straight arrow
o Thickened GB wall
* GB also appears distended

Acute calculous cholecystitis
* Persistent cystic duct obstruction leads to GB distension, wall inflammation & edema
* Can lead to: empyema, gangrene, rupture
* Pain usu. persists >24hrs & a/w N/V/Fever
* Palpable/tender or even visible RUQ mass
* Nuclear HIDA scan shows nonfilling of GB
o If U/S non-diagnostic, obtain HIDA
* Tx: NPO, IVF, Abx (GNR & enterococcus)
* Sg: Cholecystectomy usu within 48hrs
* 87yo M critically ill, on long-term TPN w RUQ pain, fever, WBC
* Ultrasound: GB wall thickening, pericholecystic fluid, no gallstones

Acute acalculous cholecystitis
* In 5-10% of cases of acute cholecystitis
* Seen in critically ill pts or prolonged TPN
* More likely to progress to gangrene, empyema, perforation due to ischemia
* Caused by gallbladder stasis from lack of enteral stimulation by cholecystokinin
* Tx: Emergent cholecystectomy usu open
* If pt is too sick, perc cholecystostomy tube and interval cholecystectomy later on

Complications of acute cholecystitis
Less commonly, perforates into adjacent viscus = cholecystoenteric fistula & the stone can cause SBO (gallstone ileus)
Occurs in 10% of acute chol’y, usually becomes a contained abscess in RUQ
Perforated gallbladder
More commonly in men and diabetics. Severe RUQ pain, generalized sepsis. Imaging shows air in GB wall or lumen
Emphysematous cholecystitis
Pus-filled GB due to bacterial proliferation in obstructed GB. Usu. more toxic, high fever
Empyema of gallbladder

Case 5
* 46yo F p/w RUQ pain, jaundice, acholic stools, dark tea-colored urine, no fevers
* Known history of cholelithiasis
* Exam: unremarkable
* WBC 8, T.Bili 8, AST/ALT NL, HepB/C neg
* Ultrasound: Gallstones, CBD stone, dilated CBD > 1cm

Choledocholithiasis
* Can present similarly to cholelithiasis, except with the addition of jaundice
* DDx: cholelithiasis, hepatitis, sclerosing cholangitis, less likely CA with pain
* Tx: Endoscopic retrograde cholangiopancreatography (ERCP)
o Stone extraction and sphincterotomy
* Interval cholecystectomy after recovery from ERCP

Case 6
* 46yo F p/w fever, RUQ pain, jaundice (Charcot’s triad)
* If also altered mental status and signs of shock = Raynaud’s pentad
* VS tachycardic, hypotensive
* ABC’s, Resuscitate
o 2 large bore IV, Foley, Continuous monitor
o 1-2L fluid bolus, repeat until resuscitated
* Diagnosis: ?

Cholangitis
* Infection of the bile ducts due to CBD obstruction 2ndary to stones, strictures
* Charcot’s triad seen in 70% of pts
* May lead to life-threatening sepsis and septic shock (Raynaud’s pentad)
* Tx: NPO, IVF, IV Abx
* Emergent decompression via ERCP or perc transhepatic cholangiogram (PTC)
* Used to require emergency laparotomy

Case 7
* 46yo F p/w persistent epigastric & back pain
* Known history of symptomatic gallstones
* No EtOH abuse
* Exam: Tender epigastrum
* Amylase 2000, ALT 150
* Ultrasound: Gallstones
* Diagnosis: ?

Gallstone pancreatitis
* 35% of acute pancreatitis 2ndary to stones
* Pathophysiology
o Reflux of bile into pancreatic duct and/or obstruction of ampulla by stone
* ALT > 150 (3-fold elevation) has 95% PPV for diagnosing gallstone pancreatitis
* Tx: ABC, resuscitate, NPO/IVF, pain meds
* Once pancreatitis resolving, ERCP w stone extraction/sphincterotomy
* Cholecystectomy before hospital discharge

Take Home Points
* As always, ABC & Resuscitate before Dx
* Understanding the definitions is key
* Is this acute cholecystitis? (fever, WBC, tender on exam with positive Murphy’s)
* Or simply cholelithiasis vs ongoing chronic cholecystitis? (no fever/WBC)
* Is patient sick or toxic-appearing, to suspect empyema, gangrene or even perforation?
* Elicit h/o jaundice, acholic stools, tea-colored urine
* Rule out cholangitis, because this will kill the patient unless dx & tx early

Gallstones Disease.ppt

Read more...

17 January 2010

Morbidity and Mortality



Morbidity and Mortality
by:Randy Hoover MD

Eponyms: Livedo reticularis associated with stroke-like episodes is known as?
* Sly’s Syndrome
* Sneddon’s Syndrome
* Riley-Day Syndrome
* Shwachman’s Syndrome
* Richter’s Syndrome
73 year old woman presents to an outside acute care clinic with a chief complaint of back pain.
* Upper-thoracic region
* Described as a “bunch,” mild in severity
* Constant, no radiation or change with position, not respirophasic
* Similar to recent transient episodes

History of Present Illness
* Associated with fatigue and malaise
* Night prior to presentation, unable to get comfortable; sweats and nausea
* Recent nose bleeds
* No fevers or rigors
* No chest pain, SOB or abdominal pain
* No bowel or bladder symptoms

Past Medical History
* Chronic A.Fib
o Anticoagulated on warfarin
* H/O Atypical Chest Pain
o Cath 12/00, normal
* Chronic Low Back Pain
* HTN
* CRI
o Baseline Creatinine 1.5
* COPD
* Chronic Diarrhea
* Temporal Lobe epilepsy
* S/P Appendectomy, herniated bowel repair

Medications
* Diltiazem CD 360 mg po qd
* Losartan 50 mg po qd
* Triamterene 50 mg po qd
* Warfarin 5 mg po qhs
* Metoprolol XL 50 mg po qd
* Amlodipine 5 mg po qd

ADR’s: Morphine, ACE Inhibitors
Social History
* Widowed mother of 2
* Consumes a glass of sherry and of cognac daily
* Current 2 ppd smoker
o Approx 100 pk year history
* Lives alone and functions independently

Physical Exam
Gen: 73 yowf, pleasant, NAD, who appeared older than her stated age
T=97.9 P=89 R=18 BP=126/90
Heent: EOMI, PERLA, OP pink and moist. Sclera anicteric
Neck: Supple, JVP =6 cm
Lungs: Poor air movement but otherwise clear
CV: Irreg Irreg no MRG and variable S1
AB: + Bs, soft, non-tender, non-distended, no masses, no hepatosplenomegaly
Back: Tender in the mid-dorsal region. Pain could be reproduced. No paravertebral or bony tenderness. No muscular spasm
Ext: No c/c/e
Labs
Initial Radiology
* RUQ Ultrasound: Multiple gallstones, no
wall thickening, no free fluid or dilated ducts
* CT Abdomen: Gallbladder is distended, no gallstones, slightly enlarged common hepatic and common bile ducts

Further Evaluation
* 2 weeks later: Seen by general surgery at DHMC for possible symptomatic cholelithiasis
o Pt extremely reluctant to undergo surgery
o “ I’ve not been significantly bothered by this”
o Referred to GI for possible ERCP
* 1 month later: Seen by GI
o Persisently elevated alk phos and amylase
o Thought secondary to etoh vs stone passage

-Management Options-
What would you do next?
* Ursodeoxycholic acid
* HIDA scan
* MRCP
* ERCP
* Recommend Surgery
* Watchful waiting

-Test Characteristics-
Magnetic Resonance Cholangiopancreatography (MRCP)
MRCP (Thin Slab)
* ERCP
o Could only cannulate pancreatic duct
o Dye injected into pancreatic duct showed local dilatation
o Brushings of pancreatic duct
o Sent to IR for transhepatic cholangiogram
* Percutaneous Transhepatic Cholangiogram
o Mildly distended intra/extrahepatic ducts
o Narrowing of distal common bile duct
o No dye spilling into duodenum, cholecystostomy tube placed

Admitted for monitoring
Physical Exam
Labs
Assessment and Plan
* Hypertensive urgency
o EKG without signs of ischemia. Pt with lethargy and + proteinuria
o IV Labetalol PRN until SBP decreased < 180
o Restart oral antihypertensive agents: diltiazem, losartan, metoprolol, and amlodipine
* Ductal dilatation s/p ERCP and PTC
o Hydrate
o Monitor LFTs and for signs of post-ERCP pancreatitis
o Cefotetan for prophylaxis
o F/U on Brushings
Post-ERCP Pancreatitis
* Serum amylase elevated in 75% of patients
* 5% have clinical pancreatitis
* MOST mild/moderate, rarely (0.4%) severe
* Usually with therapeutic (versus diagnostic)
* Prediction rules
o Amylase < 276, lipase < 1000 @ 2 hours
* Prevention
o Technical, stents, pharmacologic
+ Antibiotics, calcitonin, glucagon, nifedipine, C1-inhibitors, secretin, anticoagulation, corticosteroids, somatostatin, octreotide, gabexate mesilate, IL-10
Hospital Days 2-4
* Hypertension/A.fib
o Improved with oral agents
* Post ERCP pancreatitis
o Amylase 600
o Lipase 3780
o NPO, pain control, continue IV Hydration
* Cholecystostomy tube falls out
o IR contacted: recommend monitoring LFTs
* Day 4
o Feeling much better, tolerating clear liquids, LFTs stable at baseline
Hospital Day 5
* C/o Increasing RUQ pain, worsening abdominal distention, and nausea
* Labs:
* Plan: NPO, adequate pain management, follow LFTs, place PICC line and begin TPN
Hospital Day 6
* Worsened abdominal pain and distention.
* New rhonchi bilateral lung bases
* Labs:
* CT Abdomen and Pelvis

Hospital Day 7
* Worsening abdominal pain and distention
* Return to IR
o Attempted to drain bile pool around liver, but unable to do so
o Replace cholecystostomy tube
* Somnolent and short of breath
o ABG: 7.25/50/77 on 2 L, oxygen increased to 4 liters
o CXR: CHF
o Lasix 20 mg IV
o Appeared to stabilize

Hospital Day 8
* Somnolent and unarousable
* Acute Abdomen
o Absent bowel sounds, + guarding and rebound
o Urgent surgical consultation
* Exploratory Laparatomy
o Bile Leak from right medial lobe of liver at previous puncture site, cultures sent
o Cholecystectomy: gallbladder full of stones, signs of chronic cholecystitis
o T-Tube inserted
o No masses noted
* Transferred to ICU on ventilator

Hospital Day 9-13
* Fever spikes
o Peritoneal fluid growing Enterococci
o Hospital acquired pneumonia
* Brushings Returned:
Bile Duct: negative for malignancy, + inflammation
Pancreatic Duct: ATYPICAL; atypical ductal epithelial cells. Metaplastic and benign mucosal cells present
Hospital Day 14
* Defervesced
* Oliguric, rising BUN/CR
* Increased ventilatory requirements
* Increasing LFTs
Family Meeting
* Family Meeting
o Daughter indicated that her mother would not want her life prolonged by aggressive measures
o Family requested to withdraw support
o Pt made DNR/DNI
* Support withdrawn
o Pt died peacefully 3 hours later
* Family refused autopsy
Haunting Questions
At what point did this go wrong?
What was her diagnosis?

Morbidity and Mortality.ppt

Read more...

25 December 2009

Pregnancy and the Inflammatory Bowel Disease



Pregnancy and the Inflammatory Bowel Disease
By:David G. Binion, M.D.
Director, IBD Center
Associate Professor of Medicine
Medical College of Wisconsin
Milwaukee, WI

Case 1: Pregnancy and IBD
Case 2: Pregnancy and IBD

Introduction: Pregnancy and IBD

* Highest age adjusted incidence rates of IBD (15 – 30) overlap peak reproductive years.
* Improved medical and surgical treatment of IBD has allowed patients with more significant illness to consider pregnancy and having children.
* Optimal treatment algorithms for IBD patients during pregnancy have not been defined, including issues regarding high risk pregnancy.
* Optimal management of reproductive heath in IBD patients is a challenge to gastroenterologists, obstetricians, IBD surgeons.

Goals: Pregnancy and IBD

* Fertility – becoming pregnant.
* Having an uneventful term pregnancy:
o Avoiding preterm delivery
o Avoiding severe flare r- isk for preterm delivery
* Use of safe medications to maintain remission in mother during pregnancy.
* Use of safe medications during post-partum and breast feeding to help mother maintain remission.

Overview

* Fertility/Fecundity Rates
* Pregnancy Outcomes
* Effects of Medications on Pregnancy
* Special situations - IBD Surgery during pregnancy

Infertility: UC

Pregnancy and ileoanal pouch - I
Olsen KO, et al. Gastroenterology 2002;122:15-19

IPAA: Cumulative Incidence of Pregnancy

Cumulative Incidence of Pregnancy

Time to Pregnancy (months)

After surgery

Before diagnosis

Reference

Before surgery

Female Infertility After IPAA for UC

Johnson P, et al. Dis Colon Rectum. 2004;47:1119-1126.

Success Rate in Becoming Pregnant (%)

Infertility Rate

UC Patients Managed
Nonoperatively
IPAA Patients
After surgery
After diagnosis
IPAA Patients
UC Patients Managed
Nonoperatively
Before surgery
Before diagnosis
Pregnancy and ileoanal pouch - II
Infertility: Crohn’s Disease
Summary: Female Fertility

* Ulcerative Colitis
o Similar to the general population prior to colectomy
o Significantly decreased after IPAA

* Crohn’s Disease
o Studies vary
o Infertility partly voluntary
+ (dyspareunia, illness, MD advise)
o Surgery: decreased fertility

Pregnancy Outcomes in IBD
IBD pregnancy complications and outcomes MCW 1998 - 2004

* Pregnancies in 37 of 416 women (CD 316;UC 110)
* 51 total pregnancies reviewed (CD 81%;UC 19%)
* Mean pregnancy age 28 y/o
* Obstetric and IBD related complications in 57% of pregnancies
* 6 pregnancies required hospitalization (12%)
* Spontaneous abortion in 11.8% (mean age 30.6 years
* Term pregnancy in 70% CD and 80% UC (all children reported healthy)

Beaulieau DB, et al. Gastroenterology 128: A316, 2005.

MCW IBD Center’s Pregnancies
Numbers of IBD pregnancies
Pregnancy trimester
Beaulieau DB, et al. Gastroenterology 128: A316, 2005.
Norgard et al, Am J Gastroenterol 2003;98:2006-10.

Outcomes: Crohn’s Disease
Predictors of Poor Outcome

Pregnancy outcomes in women with inflammatory bowel disease: population based cohort study
U Mahdevan, WJ Sandborn, S Azmi, S Kane, DK Li,D Corley

* Cohort study among members of the Northern California Kaiser Permanente population
* Identified 493 pregnant women with a pre-birth diagnosis of IBD and frequency matched 493 non-pregnant women for age and hospital of pregnancy
* Univariate analyses included chi-square and t-test; multivariate analyses used unconditional logistic regression. All analyses were two tailed.

Patient Characteristics

* N=324 non-IBD vs 305 IBD (preliminary)
* Mean Age at Conception: 30.1 vs 30.8
* Smokers 61 (19%) vs 51 (17%) [p = 0.46]
* 203 UC and 96 CD
o IBD Duration: 6.1 years
o Immunosuppressant Use: 12 (4%)
o Aminosalicylate Use: 142 (47%)
o Corticosteroid Use: 57 (19%)
IBD Pregnancy Outcomes
IBD
Non-IBD
Summary
IBD Pregnancy Outcomes
* Preliminary Analysis
* IBD pts are more likely to have an adverse pregnancy outcome and complicated labor than women without IBD
* Adverse neonatal outcome not increased in IBD
* Impact of immunosuppressant medications is limited by a small sample size in available data

Medical Therapy in Conception and Pregnancy
Drugs in Pregnancy
* Limited data - Pharmaceutical trials almost never performed in pregnant women.
* PDRâ medicolegal disclaimer: use in pregnancy
is not recommended unless benefits justify risk to
the fetus.
* Half of all pregnancies are unplanned.
* FDA classification (A, B, C, D, X)
o Ambiguous
o Difficult to interpret and use in counseling

Koren G et al. N Engl J Med. 1998;338:1128.
FDA Teratogenicity Classification for Drugs during Pregnancy

* Category A: Controlled studies show no risk
o No IBD medications in Category A
* Category B: No evidence of risk in humans
* Category C:
o Animal reproduction studies show adverse effect
o No adequate studies in humans
o Drug’s benefits in pregnant women may be acceptable despite its potential risk
* Category D: Positive Evidence of Risk
* Category X: Contraindicated in Pregnancy

Nutritional Therapy

* Elemental Diet
o Case reports of effectiveness in acute flares during pregnancy [Teahon, Gut 1991]
o Important to maintain nutrition to the fetus
* Total Parenteral Nutrition
o Less desirable, but case reports of effectiveness [Gatenby, Human Nutrition 1987]

Fish Oil

* Essential Fatty acids (EFA) and Docosahexaenoic acid (DHA)
o Potential antithrombotic effect
o Prolong gestation
o No evidence of prevention of proteinuric pregnancy
* Mild benefit in Crohn’s disease
* Concern regarding risk of metal toxicity – USDA recommendation 8/03 to limit fish consumption during pregnancy

Pharmaceutical Therapy
Aminosalicylates - I

* Aminosalicylates – Category B
o Only controlled trial (Diav-Citrin 1998 Gastroenterology)
+ 165 pts. Prospectively followed, controls with smoking/Etoh NOT IBD: Mean daily dose 2 gm
+ No teratogenicity
+ Maternal weight gain significantly lower on 5ASA
+ preterm delivery, LBW
o Ludvigson (2002) LBW if mother treated with mesalamine or steroids during pregnancy

o Sulfasalazine should be given with folic acid 1 mg BID
+ Folic acid: neural tube defects, CV, urinary tract, cleft palate
+ Case reports of congenital malformation
o Placental and Breast Milk Transfer Occurs
+ Potential of allergic reaction in newborn with watery diarrhea
+ SAS not associated with kernicterus or displacement of bilirubin form albumin


Pharmaceutical Therapy
Aminosalicylates - II

Corticosteroids
* No evidence of teratogenicity in humans
o Poorer outcomes likely due to worse disease
* Theoretical concern of adrenal suppression in newborn
o Cross placenta
o 10-12% of maternal concentration
* Safe in breast feeding

Antibiotics
* Metronidazol/Ciprofloxacin
o Low risk of teratogenicity
+ Metronidazole: case-control study and meta-analysis
+ Ciprofloxacin: prospective controlled study
o Growing cartilage may be a target for cipro toxicity’
o Breast feeding is not advised
o Minimal benefit in Crohn’s and UC
o No data on long-term safety

Azathioprine/6-MP
* Purine analogues
* Interfere with synthesis of adenine and guanine ribonucleosides, precursors of DNA and RNA
* Act predominantly on rapidly dividing cells
* Incorporation of TGN nucleotides into cellular nucleic acids (cytotoxicity)
* Controversy - Class D label for pregnancy but commonly used in IBD, RA and transplant

Teratogenicity of 6MP/AZA
* Teratogenic in animals (mice, rabbits, rats)
o Given IV/IP at supratherapeutic doses (low oral bioavailability: 47% AZA, 16% 6MP)
o Increased cleft palate, ocular, skeletal, urogenital anomalies, hydrocephalus
o Poor oral bioavailability may produce levels too low to have substantial teratogenic effect
* No consistent increase in human teratogenicity
* Fetal liver in early pregnancy lacks inosinate pyrophosphorylase to convert AZA to active metabolites

o Polifka and Friedman (Teratology 65:240-261. 2002)

Human Studies: 6MP/AZA
* Transplantation Experience
o Frequency of congenital anomalies in renal tx 0.0-11.8% in 27 clinical series
o No recurrent pattern of anomalies seen
o No increase in anomalies in NTPR (Armenti 1994) in kidney transplant recipients on AZA
o Immunosuppression is never stopped in setting of organ tranplant
* No congenital anomalies in rheumatic disease, SLE

Norgard (Aliment Pharm Ther 2003)

* Population based prescription registry, Denmark
o 9 pregnancies (30d before concept/1st trimester)
o 10 pregnancies (exposed entire pregnancy)
o Outcomes vs (1) 19,418 pregnancies no drugs (2) any drug (3) 6MP/AZA >3 mos before pregnancy
* 11 pts: 55% IBD, 45% other disease
o Congenital malform OR = 6.7 (95%CI 1.4-32.4)
o Mortality OR = 20 (2.5-161.4)
o Preterm Birth OR = 6.6 (1.7-25.9)
o LBW OR = 3.8 (0.4-33.3)
* After exclusion of most ill pt (AIH), no statistical significance in OR

AZA/6-MP

* Experience in IBD

Cyclosporine
* Teratogenicity
o Not in animals, probably not in humans
o One case in humans, administered at 29 weeks.
o Healthy fetus at 34 weeks
o Used in fulminant colitis, better than emergent colectomy
* Breast feeding not advised
* Reserved for fulminant disease vs colectomy

Infliximab and pregnancy (Category B)
* Katz JA et al. (Am Journal Gastroenterol 2004)
* Infliximab Safety Database
o 146 identified pregnancies
o 82 CD, 1 UC, 10 RA, 3 unknown
* Outcome 96 pregnancies, n = 100 births
o Live birth 64 (67%)
+ 1 preterm 24 wks (died), 1 tetrology Fallot, 1 sepsis survived, 1 intestinal malrotation in twin
o Miscarriage 14(15%) (1 stillbirth on MTX)
o Therapeutic termination 18 (19%) (pts. choice)
* Data similar to expected for UC/CD note exposed to INF

Infliximab in Pregnancy: Outcomes of Women Exposed to Infliximab During Pregnancy

Therapeutic termination

Miscarriages
Intentional Infliximab in Pregnancy
10 Crohn’s disease patients intentionally exposed to
infliximab during pregnancy
Mahadevan U, et al. Aliment Pharmacol Ther. 2005;21:733-738.
Parenteral iron therapy

* Oral iron may be poorly tolerated, abdominal pain
* Patients with obstructive symptoms may not tolerate prenatal vitamin. Consider for gastroduodenal CD.
* Hyperemesis gravidarum – poor oral tolerance
* Intravenous iron sucrose 100 mg dosage
* FDA class B

Contraindicated Medications
* Methotrexate
o Known abortifacient
o Teratogenic (skeletal defects, cleft palate)
o 3 month “washout” in females and males prior to planned pregnancy
* Thalidomide
o 20-30% Rate of Birth defects or fetal death
o limb malformation (phocomelia)

Special Consideration
* Perianal Crohn’s Disease
* Fulminant Ulcerative Colitis
* Patients with IPAA

Perianal Crohn’s Disease

* Active perianal disease: Caesarean section recommended
o No history (1/39) or inactive (0/11) perianal disease at birth, risk of relapse very low post-vaginal delivery
o 4/4 with active perianal disease worsened post-vaginal delivery [Ilnycky 1999 AJG Manitoba database]
* Episiotomy may predispose to perineal disease (17.9%) without prior history of disease

Fulminant Ulcerative Colitis

* 2005 – look for C. Difficile infection
* Nutrition
* Intravenous corticosteroids
o 75% successful
* Infliximab
* Heparin compounds
* Cyclosporine
o 1 case report. IV CSA 10 days, 34th wk delivery
* Colectomy
o 50-60% fetal mortality reported
o Rare to have fulminant colitis in pregnancy
o Surgery in 2nd trimester is preferable
o Tocolytic therapy – high risk obstetrics in OR

Pouch Function and Pregnancy

* Reversible deterioration of pouch function during pregnancy
* No long-term detriment to pouch function
* Mode of delivery determined by obstetric indications
* Ravid Dis Col Rec 2002

Summary: IBD and pregnancy

* Fertility
o IPAA Surgery clearly reduces fertility rates in women
o Role of medications in fertility unclear
* Pregnancy Outcomes
o Complicated pregnancies occur in majority of patients
o Increased rates Preterm birth, SGA LBW
o No increase in congenital anomalies
o Aggressive management of IBD flare during pregnancy with medications is warranted
* Medications

Pregnancy and the Inflammatory Bowel Disease

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28 September 2009

Work Related Musculoskeletal Disorders



Work Related Musculoskeletal Disorders

Upper Extremity Disorders
* Carpel tunnel syndrome
* Cubital tunnel syndrome
* Thoracic outlet syndrome
* Raynaud’s syndrome (white finger)
* Rotator cuff syndrome
* DeQuervain’s disease
* Tendinitis
* Tenosynovitis
* Trigger finger
* Ganglion cyst

Neurovascular Disorders
* Carpal Tunnel Syndrome
o Impingement of the median nerve caused by irritation and swelling of the tendons in the carpal tunnel
* Cubital Tunnel Syndrome
o Pressure on the ulnar nerve when the elbows are exposed to hard surfaces

Neurovascular Disorders
* Thoracic Outlet Syndrome
o Compression of the blood vessels between the neck and shoulder caused by reaching above shoulder level or carrying heavy objects

* Raynaud’s Syndrome
o Also known as Vibration White Finger ; Blood vessels of the hand are damaged (narrowed) from repeated exposure to vibration for long periods of time

Tendon Disorders
* Rotator Cuff Syndrome
* DeQuervain’s Disease
o Combination of tendinitis and tenosynovitis
* Tendinitis
o Irritation of the tendon
* Tenosynovitis
o Irritation of the synovial sheath
* Ganglion Cyst
o Accumulation of fluid within the tendon sheaths

Tendinitis
Hand and Wrist
Common Occupational CTDs of the Upper Extremities

Carpal Tunnel Syndrome occurs from chronic swelling of the flexor tendons in the wrist.

The median nerve, which feeds the first three fingers and the thumb, can become impaired from pressure in the carpal tunnel in the wrist.

Symptoms include:

# pain in the first three fingers and the thumb
# numbness in these areas
# tingling in these areas

Carpal Tunnel Syndrome
Common Occupational CTDs of the Upper Extremities

Raynaud’s Syndrome is when blood vessels of the hand are damaged (narrowed) from repeated exposure to vibration for long periods of time

This is connected with use of vibrating tools, such as hair clippers and jack hammers.

Raynaud’s Syndrome
Symptoms

o Numbness and tingling in the fingers during vibration exposure; may continue after exposure has been discontinued
o Blanching (whitening) of one fingertip because of a temporary constriction of blood flow
o Other fingers also blanch
o Intensity of pain & frequency of attacks increase in time

Common Occupational CTDs of the Upper Extremities

Cubital Tunnel Syndrome is caused by resting the elbows on hard surfaces such as unpadded tables or armrests.

The ulnar nerve, which feeds the ring and little fingers, can become impaired from pressure near the elbows.

Symptoms include:
+ pain in the ring and little fingers
+ tingling in these areas
+ numbness in these areas


Cubital Tunnel Syndrome
Common Occupational CTDs of the Upper Extremities
Thoracic Outlet Syndrome is caused by frequent reaching above shoulder level, by carrying heavy objects, or poor posture involving a forward head tilt.

A Neurovascular bundle called the brachial plexus, which passes between the collar bone and the top rib, can become impaired from pressure associated with movements that causes these two bones to be positioned close together.

Symptoms include:
+ the arms “falling asleep”
+ weakened pulse
+ numbness in the fingers

Thoracic Outlet Syndrome
Common Occupational CTDs of the Upper Extremities
Rotator cuff syndrome is a disorder involving swelling and pain of tendons comprising the rotator cuff muscle group:

subscapularis, supraspinatus, infraspinatus, & teres minor

Symptoms include:

o Pain when you bend the arm and rotate it outwards against resistance
o Pain on the outside of the shoulder possibly radiating down into the arm
o Pain in the shoulder, which is worse at night
o Stiffness in the shoulder joint.

Rotator Cuff Syndrome Anterior View Posterior View
Common Occupational CTDs of the Upper Extremities

Tendinitis is a common CTD for the wrist, elbow, and shoulder. It occurs when we continually stress the tendon cables, causing them to become irritable and sore.

Lateral Epicondylitis - “Tennis elbow”

Medial Epicondylitis - “Golfer’s elbow”

Symptoms include:

# point tenderness
# swelling
# tennis elbow, pain radiates down to back of hand
# golfer’s elbow, pain radiates down to back of hand

Tendinitis

Tenosynovitis is swelling of the sheath that covers the tendon from constant rubbing against the tendon.

Symptoms include:
swelling
pain
loss of motion
loss of strength
Tenosynovitis
Trigger Finger is a tendon disorder that occurs when there is a groove in the flexing tendon of the finger

If the tendon becomes locked in the sheath, attempts to move the finger cause snapping or jerking movements

Usually associated with using tools that have handles with hard or sharp edges.

Trigger Finger
Ganglion Cyst is a bump under the skin caused by an accumulation of fluid within the tendon sheath. It is commonly found at the hand and wrist.

Ganglion Cyst

De Quervain’s Disease is an inflammation of the tendon sheath of the thumb attributed to excessive friction between two thumb tendons and their common sheath.

It’s a combination of Tendonitis and Tenosynovitis.

May be caused by twisting and forceful gripping

Symptoms include:

* swelling
* pain at the base of the thumb.

De Quervain’s Disease
Prospective Study of Computer Users
Fredric Gerr, et. al., 2002, “A Prospective Study of Computer Users: 1. Study Design and Incidence of Musculoskeletal Symptoms and Disorders”.

o 632 individuals
o Newly hired into jobs requiring  15 hr/week of computer use
o Were followed for up to 3 years

Primary Results
* Hand/Arm (H/A) & Neck/Shoulder (N/S) MSS and MSD were common among computer users
* More than 50% of users reported MSS during the 1st year after starting a new job
* Most common H/A disorder was DeQuervain’s tendonitis
* Most common N/S disorder was somatic pain syndrome

Common Occupational Injuries of the Back

Strains and sprains are damage to the tendons and ligaments caused by one time exertions such as lifting or carrying heavy objects.

These can lead to very noticeable back pain, but the pain usually begins to subside within a few days

Facet joint pain results from irritation of the area where the ribs meet the spinal column.

Typically, there is muscle swelling in the affected area and it can become very painful to sit or stand up straight. In some cases it may also be difficult to breath deeply.

Disk erosion occurs from prolonged pressure on the spinal disks, which causes them to become permanently compressed.

The space between the vertebrae becomes smaller, which can lead to impingement of the nerve roots leading out from the spine.

Sitting puts more pressure on the spinal disks than standing, and sitting with the back unsupported can lead to high levels of disk pressure.

Disc Erosion

Sciatic nerve impingement, also called sciatica, is common for people who sit for prolonged periods of time.

The sciatic nerve runs from your lower back down the back of your leg and into to your feet.
Swelling in certain muscles in the buttocks can put pressure on the sciatic nerve, causing pain down the leg.

Herniated discs occur when the inner portion of the disc protrudes, putting pressure on the nerve roots leading from the spine.

Pain or numbness in the legs is a common symptom of herniated discs in the lower back.

Herniated/Bulging Disc
QUESTIONS?

Work Related Musculoskeletal Disorders.ppt

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16 July 2009

General Internal Medicine Lectures



General Internal Medicine Lectures in ppt format from
Texas Tech University Health Sciences Centre School of Medicine

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12 May 2009

Evaluation and Management of Drooling



Evaluation and Management of Drooling
Presentation by:Karen Stierman, M.D. & Ronald Deskin, M.D.

* Drooling - serious medical and social problem
o maceration, infection, soiling of clothes and belongings, effects on caregiver
* Sialorrhea - increase in salivary flow
* Drooling - ineffective saliva management

Anatomy and Physiology of Drooling
* Three pairs of major salivary glands - parotid, submandibular, and lingual
* 70% of saliva comes from the submandibular glands at the resting state
* Ingestion of food causes parotid gland to secrete a higher percentage of saliva

Submandibular and Sublingual gland innervation
Parotid innervation
Salivary gland innervation
Functions of saliva
* Protective
* Swallowing
* Digestion
* Speaking

Etiology of Drooling
* Acute vs. Chronic
* Direct vs. Indirect

Pathophysiology of Drooling
* Multifactorial
* Primarily a defect in the oral phase of swallowing caused by:
o poor head control, inability to close the mouth, abnormal tongue mobility, reduced intra-oral sensation
* Sialorrhea can lead to drooling caused by:
o medications and poor fitting dentures

Diagnosis of Drooling
* History - severity, peak time, influencing factors, associated conditions, parental expectations, age and mental status of the patient
* Physical - Head posture, dental abnormalities, nasal and oral cavities, decreased intraoral sensitivity
* Other - lateral neck x-ray, audio, barium sw.

Treatment Options
* Pharmacological therapy
* Speech therapy
* Behavioral therapy
* Radiation therapy
* Surgery
* Initial approach is usually nonsurgical and reversible

Pharmacological therapy
Speech therapy
Behavioral therapy
Radiotherapy
Surgical options
* Submandibular duct rerouting
* Submandibular duct excision
* Parotid duct ligation
* Transtympanic neurectomy

Surgical indications
* Age 5-6
* Assess ability to interact with peers
* Failed nonsurgical management
* Stable neurological status

Rerouting of submandibular duct
* Success rate of 80-100%
* Cuff of mucosa dissected around duct and marked medially and laterally
* Duct dissected 3-4 cm or until gland reached
* Tonsil used to create a tunnel just posterior to anterior tonsillar pillar and sutures passed with duct
* Tonsillectomy performed if obstructive tonsils
* Sublingual adenectomy(Crysdale) versus ligating sublingual ductules(Cotton)
* Advantages: Decreased xerostomia, problems with taste and dysphagia
* Disadv: Ranula, FOM swelling, sialoadenitis, sialolithiasis, aspiration

Studies on submandibular duct rerouting
Submandibular Gland Excision
Parotid duct ligation
Transtympanic neurectomies

Summary

* Goal: decrease drooling and provide healthy oral cavity
* Order of management controversial
o Nonsurgical management first
o Submandibular duct rerouting
o Submandibular gland excision +/- parotid duct ligation
o Tympanic neurectomy

Drooling.ppt

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08 May 2009

Post-Operative Fever



Post-Operative Fever
Presentation lecture by: Jennifer Caffey, D.O.

HPI
* CC: Fever x 2 days
* HPI: 19 months old female with 2 days history of fever, max. 102F. Emesis x2, described as non-bilious, non-bloody. Appetite decreased but tolerating oral fluids. Good urine output. No sick contacts. Status-post Open Reduction, Internal Fixation 5 days prior to admission for developmental dysplasia of the left hip.

Review of Systems
* No URI symptoms
* No pain in extremities
* No dyspnea
* No chest pain
* No diarrhea, no constipation
* No rashes

Past History

* PMH: developmental dysplasia of left hip
* PSH: 2 prior corrective surgeries on left hip, 1st on May 6, 2nd on May 20, 2004
* Birth: term AGA female born via C-section secondary to hand presentation. Pregnancy complicated by transient episodes of maternal hypotension. Normal nursery stay.
* Previous Hospitalizations: 9 mos for febrile illness. Twice in May 2004 for hip surgery.
* Meds: Tylenol prn fever
* Allergies: NKDA
* Immunizations: UTD by history
* Diet: well rounded, age-appropriate
* Family Hx: Maternal grandmother with Type II DM
* Social Hx: Lives with mom, dad, 5y/o brother and 2m/o brother. Dad is a smoker. + Cats outside. No daycare.
* Developmental: Speaks Spanish only, multiple single words

Physical Exam

* V/S: T 37.3 (ax) HR 145 RR 24 BP: 103/53 Wt: 15kg (>95th)
* Gen: Lying on back in SPICA cast
* HEENT: normocephalic, PERRL, red reflex intact, nares patent, TM’s clear Bilaterally, moist mucosa, oropharynx with mild erythema, no cervical lymphadenopathy
* Heart: regular rhythm, no murmurs
* Lungs: Limited exam secondary to cast, upper lobes clear to auscultation bilaterally
* Abd: Limited secondary to cast, + bowel sounds, lower abdomen soft, not tender
* Ext: lower extremities in cast, lower extremity pulses 2+ and symmetrical
* Neuro: Limited exam, no focal deficits
* GU: normal female genitalia, left hip wound dressed and without drainage.

LABS (initial)
* CBC: WBC 15.6 H/H 8.6/27.2
G 69.5 L 19.6 M 10.4 E 0.2 B 0.2
Platelets 459,000
* Blood Culture -- drawn
* CXR: Lungs are clear except for some increased opacity behind the heart that may represent atelectasis.

Labs during Hospital Stay

* ESR 98 (5/26), repeat 78 (5/28)
* CRP 10.2 (5/26), repeat 2.1 (5/28)
* Blood Culture negative at 73 hours

Differential Diagnosis
* UTI
* Wound infection/abscess
* Pneumonia
* Vascular/venous catheters
* Deep vein thrombophlebitis
* Others…?

Postoperative Fever
* Fever > 38° is common in 1st few days after major surgery
* Most early post-op fever caused by inflammatory stimulus of surgery and resolves spontaneously

* Pathophysiology of fever:
- Fever is manifestation of cytokine release in response to stressful stimuli
- Cytokines released include interleukin-1, TNF-alpha, IFN gamma
- Fever-associated cytokines released by tissue trauma and do not necessarily signal infection
* Timing of fever after surgery is important in establishing differential diagnosis:
- Immediate - onset in operating suite or within hours after surgery
- Acute- onset within 1st week after surgery
- Subacute - onset from 1 to 4 weeks after surgery
- Delayed – onset >1 month after surgery

Post-op Fever- Immediate
Differential Diagnosis:
* Medications or blood products,
* Immune mediated reactions to transfused blood products and antimicrobials, and
* malignant hyperthermia
Fever due to trauma of surgery resolves within 2-3 days (fever due to severe head trauma may be persistent and not resolve for days to weeks)

Post-op Fever- Acute
Differential Diagnosis:
* Nosocomial infections
* Community acquired infections
* Surgical site infection
* Intravascular catheters
* Pneumonia
* UTI

Post-Op Fever- Subacute
Differential Diagnosis:
* Surgical site infection
* Central venous catheter related infections
* Thrombophlebitis
* Antibiotic associated diarrhea
* Drug Fever
* Deep Vein Thrombophlebitis
* Pulmonary Embolism

Post-Op Fever- Delayed
Differential Diagnosis:
* Infection
* Viral infections from blood products
* Surgical site infections

Causes of Post-op Fever
* Infectious:
Surgical site infections
Pneumonia
UTI
Catheter infection
Sinusitis
Meningitis
Parotitis
TSS
* Non-Infectious:
Stress of surgery
Medications
Malignant hyperthermia
Deep vein thrombosis
Fat embolism
Transfusion reactions
Atelectasis?

Orthopedic Procedures
Complications:
Spontaneously resolving fever is the rule after major orthopedic surgery
Differential Diagnosis:
* Surgical Site Infections
* Hematoma
* Deep Vein Thrombosis/Thrombophlebitis

Approach to Patient
* Evaluate patient systemically taking into account timing of onset of fever and the various possible causes
* Initial screen:
* Wind: consider pulmonary causes including pneumonia, aspiration, embolism
* Water: consider UTI
* Wound: consider surgical site infection
* What did we do ?: consider treatment interventions including medications, blood product transfusions, and intravascular, urethral, nasal and abdominal
Treatment

* Remove unnecessary treatments including medications and catheters
* Suppress fever with tylenol
* Antibiotics per clinical judgment/culture results

Post-Operative Fever.ppt

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06 May 2009

Medicine Grand Rounds Clinical Vignette ppt



Department of Medicine Grand Rounds Clinical Vignette ppt
from med.nyu.edu

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03 May 2009

Focus on Headache



Focus on Headache

Headache

* Probably the most common type of pain experienced by humans
* Majority of people have functional headaches
o Migraine or tension-type headaches
* Not all cranium tissues are sensitive to pain
* Pain-sensitive structures include venous sinuses, dura, cranial blood vessels, divisions of the trigeminal nerve, facial nerve, glossopharyngeal nerve, vagus nerve, and the first three cervical nerves
* Classification from the International Headache Society diagnostic criteria
* Primary classifications
o Tension-type
o Migraine
o Cluster


Tension-Type Headache

* Most common type
* Bilateral, band-like feeling of pressure around the head
* Constant, squeezing tightness
* Not aggravated by physical activity
* Usually mild or moderate
* Often subcategorized into
o Infrequent episodic
o Frequent episodic
o Chronic

Tension-Type Headache Etiology and Pathophysiology

* Mechanism in all patients with tension-type headaches has neurovascular factors similar to those involved in migraine headaches

Tension-Type Headache Clinical Manifestations
* No nausea or vomiting
* May involve sensitivity to light and sound
* May occur intermittently
* Can have combination of migraine and tension-type headaches
* Careful history taking
* Electromyography may be performed
o May reveal sustained contraction of neck, scalp, or facial muscles
o May not show increased tension even when test is done during headache

Tension-Type Headache Diagnostic Studies

Migraine Headache
* Recurring
* Characterized by unilateral or bilateral throbbing pain
* Triggering event or factor
* Strong family history
* Manifestations associated with neurologic and autoimmune nervous system function
* More common in females than males
* In United States, prevalence highest in those of lower socioeconomic status

Migraine Headache Etiology and Pathophysiology

* Evidence suggests vascular, muscular, and biochemical factors are involved
* Exact cause is unknown
* Can be preceded by an aura and prodrome
o May precede by days or hours
o Aura associated with wave of oligemia beginning at occipital lobe and spreading forward
* May be precipitated or triggered by
o Food
o Hormonal fluctuations
o Head trauma
o Physical exertion
o Fatigue
o Stress
o Pharmacologic agents

Migraine Headache Clinical Manifestations
Migraine Headache Diagnostic Studies
Cluster Headache Etiology and Pathophysiology
Cluster Headache Diagnostic Studies
Headache Other Types
Headache Collaborative Care
Headache Nursing Management

Focus on Headache.ppt
from South Texas College
(Relates to Chapter 59,“Nursing Management: Chronic Neurologic Problems,” in the textbook Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved. )

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02 May 2009

Intersexuality



Intersexuality

* Understanding Intersex
* Gender Identity: Nature vs. Nurture
* The Ethical Questions
* Discussion
* Papers


An advance warning

* For anyone who has done the reading, this will not come as a shock, but we will be discussing sex and gender today.
* Some of the video clips depict surgeries and genitals (sometimes blurred, sometimes not).
Understanding Intersex

* Simplest definition: intersex is a congenital anomaly of the reproductive and sexual system.
* There are many differences between those who are intersexed. It is difficult to point to any set of characteristics of intersexuality, though the most common characteristic is ambiguous genitalia.

A word on language…

* Hermaphrodite vs. Intersex
* “true hermaphrodites” in a medical context

Ambiguous Genitalia

* Generally, this is what tips off medical staff to the possibility of a newborn being intersexed.
* Quite simply, this is when the reproductive organs do not present themselves as they usually do. This can be because of the size or shape of the genitals.

Androgen-Insensitivity syndrome (AIS)

* Also known as “testicular feminization.”
* Though the genes read as XY, the androgen receptors in the body cannot “read” the masculinizing hormones the testes produce. Because of this, these “male” children's anatomy both in utero and after birth develop in a “feminized” manner.
* Often not discovered until puberty, when menstruation does not occur.

Progestin Induced Virilization

* Progestin was a drug administered to women in the 1950s and 60s to help prevent miscarriages.
* The drug would be converted to androgen by the prenatal XX child, which could result in the “masculinization” of the child. Possible side effects are enlarged clitoris, development of a phallus, and/or the fusing of the labia.

Progestin Induced Virilization

* In every case, ovaries and the uterus develop, though in some cases the vagina and cervix do not develop.
* After birth, a normal female puberty occurs.
* While Progestin is no longer used to prevent miscarriages (it was not effective), it along with estrogen is the primary components of birth control pills. Some take progestin-only birth control.

Congenital Adrenal Hyperplasia (CAH)

* An anomaly of adrenal function causes the synthesis and excretion of an androgen precursor, which begins the “masculinization” of an XX person.
* Since this process is metabolic in nature, the masculinizing effects continue after birth.
* Phenotype varies along the whole spectrum.

Klinefelter's syndrome

* Most men inherit a single X chromosome from their mother, and a single Y chromosome from their father.
* Men with Klinefelter syndrome inherit an extra X chromosomes from either father or mother.

A Little on Genetics

* Your DNA is a combination of the DNA of your parents.
* Generally, women receive an “X” chromosome from each parent; this is known as “46 XX”
* Most men receive an “X” from their mother and a “Y” from their father. This is known as “46 XY”

A Little More on Genetics

* Men with Klinefelter, with their “extra” “X” has what is known as “47 XXY.”
* Other variants are “45 XO” (“blank”), “47 XXX” (super-female) and “47 XYY” (super-male)

Hypospadias
For those who wonder if they are intersexed…
The Phall-o-meter
Common Treatments

* Most of the attention in the intersex debate is focused on cases of AIS and CAH.
* Traditionally, the treatment of these forms of intersex was to “correct” the genitals.
* Those with a “micropenis” would be surgically reassigned as females, while those with enlarged clitorises would have a cliterectomy.
* These surgical treatments would really occur in stages. Generally one operation would not be enough to make genitals that appeared normal, so procedures would occur for years.
* Anecdotal evidence supports that most with ambiguous genitals were assigned as females because it is easier to “dig a hole than build a pole.”

Components of a treatment

* Surgery on the genitals (can occur many times) and possibly other body parts (such as breasts after puberty)
* Hormone cocktails
* “Psychosocial” rearing according to norms for the assigned gender.

Gender Identity

* The Case of John/Joan & John Money in general
* Nature vs. Nurture
* What is at stake?

The Ethical Questions

* Involves paternalism, informed consent, and deception
* Also includes societal questions about the nature of gender. Raises issues about our understanding of sexual matters, as well as social conventions such as marriage.

The Readings
Fausto-Sterling

* What is her thesis?
* What do you think about it?

Letters

* Bird’s objection: How would you respond?

Intersexuality.ppt

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