26 February 2010


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.

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.

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.

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

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

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.

• 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

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.


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


24 February 2010

Genetic Hearing Loss

Genetic Hearing Loss
By: Jing Shen M.D.
Ronald Deskin M.D.
UTMB Dept of Otolaryngology

Syndromic deafness
Alport syndrome
Branchio-oto-renal syndrome
Jervell and Lange-Nielsen syndrome
Norrie syndrome
Pendred Syndrome
Treacher-collins syndrome
Usher syndrome
Waardenburg syndrome
Non-syndromic deafness
Ion homeostasis
GJB2 (Gap Junction Beta 2)
Transcription factors
Cytoskeleton proteins
Extracellular matrix components
Unknown function genes
Mitochondrial disorders
Genetic screening
Genetic counseling
Cochlear gene therapy
Resources for hereditary hearing loss

* Hereditary hearing loss home page http://www.uia.ac.be/dnalab/hhh
* Online Mendelian Inheritance in Man www.ncbi.nlm.nih.gov/Omim

Genetic Hearing Loss.ppt


Drug Induced Dementia: Proceed with Caution

Drug Induced Dementia: Proceed with Caution
By:David M. Angaran, MS, FASHP, FCCP
Clinical Professor University Florida College of Pharmacy
Angaran Associates, LTD

Presentation Objectives
* Explain how and when this may happen.
* Present examples of drug caused conditions and symptoms that worsen dementia.
* Provide drug examples that can worsen dementia
* Describe how to reduce the chance of this happening.

* Mental condition which represents a deterioration from previous function in at least three of the following functions:
* Language, understand what you are seeing, memory/reasoning and emotion
* Includes:
o Alzheimer’s, Mild Cognitive Impairment, Lewy Body, and Vascular

But First a Reminder
“The SUNNY side”
Medications can be vital to a better life for the caregiver and patient

Drugs make Dementia Worse:
* Direct acting on the brain
o Delirium Dizziness
o Agitation Hallucinations
o Memory Loss Depression
* Indirect acting on the body
o Constipation Blood sugar
o Urinary retention Dehydration

How often does this happen?
* No ONE really knows
* Patients with mental changes
o 10-30% thought to be drug induced.
* Adverse drug effects emergency room visits for >65 yr. (Gurwitz JH et al. JAMA 2003;289:1107-1116)
o Dementia related
+ Neuropsychiatry 5%
+ Falls, dizzy, 8.5%
* If it happens to you or a loved one it is 100%.

Who is at greatest risk?
* Already demented or brain injury
* Frail elderly, the older the more susceptible.
* Has other disease states
* Taking more drugs
* Taking drugs unknown to physician or pharmacist
o Prescription (another Dr, another Pharmacy)
o Over the counter (OTC) eg. Sleep meds.
o Herbal

When can it happen?
* When a new drug is started.
o >65 yr. Go low and slow
* When the dose is changed.
* When another drug is added, stopped, or changed
* When a drug is stopped
o Treated condition can get worse
o Withdrawal side affects eg. Valium, antidepressants

What Can YOU Do To Help?
“Talk with your Dr. and RPh”
* Must know every drug the person is taking.
o OTC: Benadryl
o Herbal: St. Johns Wart
o Home remedy
o Nutritional supplements eg. Ephedrine
o Alcohol
* Must know HOW the drugs are being taken.
o How much
o How often
o How regular
o How long

What Can you Do to Help?
“Be Informed”
* Keep a Drug log. Name, Use, Directions.
* Do NOT stop, start or change drug regimen without consulting your Dr. or RPh.
* Know what trouble looks like and what to do.
o Side effects
o What action to take
* Ensure the drugs are taken as prescribed.
o What to do if you miss a dose.
* Ask for a “Medication Review” at regular intervals.

Drugs that MAY worsen Dementia
* Anti Cholinergic Alternative
o Elavil- antidepressant Paxil
o Benadry-allergy Claritin
o Demerol-pain Percocet
o Mellaril-antipsychotic Risperdal
* Anti anxiety
o Valium Xanax
* The list goes on and on……….

Nursing Home Do NOT use list
Pentazocine (Talwin): Confusion, hallucinations, dizziness, lightheadedness, euphoria, and sedation
Long-acting benzodiazepines(Librium): Sedation, drowsiness, ataxia, fatigue, confusion, weakness, dizziness, vertigo, syncope, psychological changes
Amitriptyline(Elavil) Anticholinergic and sedating properties, which can result in confusion, delirium, or hallucinations
Doxepin(Sinequan):Anticholinergic and sedating properties, which can result in confusion, delirium, or hallucinations
Meprobamate(Equanil): Highly addictive and sedating, which can result in drowsiness and ataxia
Lisi DM. Medscape Pharmacotherapy 2000;2 www.medscape.com adapted
Digoxin(Lanoxin): Toxic signs include headache, fatigue, malaise, drowsiness, and depression
Methyldopa(Aldomet) May exacerbate depression
Chlorpropamide(Diabenese) Hypoglycemia, which can result in altered mental state (confusion, amnesia, coma)
GI antispasmodics(Bentyl) Highly anticholinergic properties, which can result in confusion, delirium, or hallucinations
Barbiturates(Seconal) Highly addictive and sedative, resulting in drowsiness, lethargy, depression, severe CNS depression
Muscle relaxants(Robaxin): Anticholinergic properties, which can result in sedation, weakness, confusion, delirium, or hallucinations
Antihistamines(Chlortrimeton): Anticholinergic properties, which can result in confusion, delirium, or hallucinations
Reserpine: Depression, sedation
Diphenhydramine(Bendaryl) Highly anticholinergic, which can result in confusion, delirium, or hallucinations
Indomethacin(Indocin) Headache, dizziness, vertigo, somnolence, depression, fatigue
Disopyramide(Norpace): Strongly anticholinergic properties, which can result in confusion, delirium, and hallucinations
* What is IN that over the counter (OTC)?
o DON’T trust the name: Excedrin/Excedrin PM
o Unfamiliar contents: Ask and let them know why you are asking.
o Cautions on the labels are NOT enough.
+ Heavy machinery and driving cautions
+ Sedation and excitement

Mental status has suddenly gotten worse;what will your Dr. Do?
* Drug related questions:
o Could it be caused by a drug?
o What are ALL the drugs the patient is taking?
o Has any drug been started, stopped, or changed?
o How are they TAKING these drugs?
* Actions that may take place.
o Medication review
o Stop, substitute, increase/decrease dose

Getting Help
* Your Pharmacist
o Consultants for nursing homes and assisted living homes.
o Drug needs at ONE pharmacy
+ Complete drug profile
+ Get to know you and your situation
+ Rx medication information sheet NOT written for people suffering from dementia
* Web sites
o www.medscape.com Medscape
o www.intelihealth.com Harvard Medical School

* Medications can be VERY beneficial for you and your loved one.
* Keep all your healthcare providers informed about what and how drugs are used.
* Keep a record of all the drugs.
* Know what “trouble” looks like and what to do about it.

Drug Induced Dementia: Proceed with Caution.ppt


Treatment Options for Dementia

Treatment Options for Dementia
By:Deb Bynum, MD
Division of Geriatric Medicine
University of North Carolina

* 1. Understand the use of cholinesterase inhibitors in the treatment of alzheimer type, vascular and mixed dementias
* 2. Review the current literature regarding the use of Memantine for severe dementia
* 3.Understand the appropriate use of nonpharmacologic strategies for behavioral problems with dementia
* 4. Review the appropriate use of antipsychotics for psychosis and behavioral symptoms in dementia
* 5. Discuss possible means of preventing dementia

* 1. Cholinesterase inhibitors in the treatment of AD, vascular and overlap dementias
* 2. Memantine
* 3. Treatment of behavioral symptoms
* 4. ?Prevention
* 5. Future Directions

The Cholinergic Hypothesis
* Depletion of acetylcholine and nicotinic receptors thought to occur early and relate to memory impairment with AD
* Focus on AD treatment with Acetylcholinesterase inhibitors: Recommended as first line treatment for patients with mild to moderate AD

Cholinesterase Inhibitors
* Trials in patients with mild to moderate disease (10-24 on MMSE)
* On average these drugs seem to stabilize cognitive function and activities of daily living and may have benefits with QOL and behavioral disturbances for at least one year
* Side Effects: GI

* Trials demonstrating delay of cognitive decline by 6 months
* Delayed time to nursing home placement: At 800 days, 45% in low dose or no tacrine underwent placement vs 21% in high dose tacrine group
* Evidence for long term cost effectiveness
* Reversible hepatotoxicity in 50%

Donepezil (Aricept)
Three large RCT demonstrate modest effectiveness in stabilizing cognitive function
Well tolerated (no difference in adverse events compared to placebo)
Not hepatoxic, no significant drug-drug interactions
Single bedtime dose: start 5 mg, increase to 10 mg after 4-6 weeks
Most common side effects: sleep disturbance, GI

* May have increased selectivity for hippocampus and neocortex (areas affected by AD)
* Modestly effective in treatment of mild to moderate AD (but only at high doses of 6-12 mg/day)
* Recommended starting dose: 1.5 mg BID with breakfast and dinner
* Minimize GI side effects with 4-6 week titration, increasing to 3 mg BID, 4.5 mg BID, 6 mg BID
* More GI side effects, weight loss (dose dependent)

* Potential second mechanism: modulator at nicotinic cholinergic receptor
* Three large RCTs indicate effectiveness in mild to moderate AD (same degree as other agents) at doses of 16, 24, 32 mg/day
* Open label 6 month extension of US trial: Possible disease modifying effect
* Starting dose: 4mg BID with meals, increase by 4mg BID every 4-6 weeks

Cholinesterase inhibitors in moderate to severe AD
* RCT of donepezil vs placebo: 24 week international trial of 290 patients (MMSE 5-18)
* 63 % of donepezil treated patients were stable/better vs 42% in placebo group

Comparison of Cholinesterase Inhibitors…
* Cochrane Dementia Group: 3 systematic reviews on efficacy of donepezil, rivastigmine, and galantamine
* Each drug seems to have similar treatment effect at 6 months on global and cognitive rating scales
* No double blind head to head trial

Cholinesterase Inhibitors and AD: Summary
* Approved for treatment of mild to moderate AD
* Probably effective in treatment of more severe AD
* Goal: stabilization (not miracle drugs)
* Delay in nursing home placement, decline in ADLS
* Probably benefits behavioral and functional status as well
* Data suggest no big difference in efficacy among the 3 agents, although donepezil is easier to titrate and better tolerated

Cholinesterase Inhibitors and Other Dementias…
* Vascular dementia and Dementia with Lewy Bodies each account for 10-15% cases
* Prominence of mixed pathology (especially vascular and AD in older population)

Galantamine: Vascular and AD/Vascular Dementia
* Placebo controlled trial, 6 months, 592 patients
* 50% in study had AD plus radiological evidence of CVD, 41% had probable vascular dementia, 9% indeterminant
* Results for the whole group were similar to previous trials in typical AD : 74% galantamine groupwere improved/stable vs 59% in placebo group
* AD-CVD subgroup similar effects to prior trials with AD patients

Summary of Galantamine and Vascular dementia
* Patients with typical features of AD mixed with features of CVD or evidence of CVD on radiological tests seem to respond similarly to patients with AD alone
* Subgroup with CVD alone does better over long term (even with placebo)
* Surprise: patients with what appears to be only CVD also seem to have some benefit (these patients not traditionally felt to have specific degeneration of cortical cholinergic pathways)

Cholinesterase Inhibitors and Other dementias
* Lewy Body Dementia: may respond even more than AD patients
* Frontal Lobe Dementia: often respond adversely to cholinesterase inhibitors with increased agitation and insomnia

* NMDA (glutamate) receptor activation thought to be involved in neurodegeneration
* Memantine: NMDA antagonist aimed at protecting neurons from glutamate mediated excitotoxicity
* Approved in Europe in 2002 for treatment of severe AD (MMSE 3-14)
* Randomized, double blind, placebo controlled study: 166 patients with severe dementia (AD and vascular, MMSE <10)
* Cognitive and Behavioral Rating Scale significantly better with treatment, regardless of dementia type
* Other European studies have looked at treatment for moderate-severe Vascular Dementia, demonstrating similar efficacy
* 28 week RCT of 252 patients with severe AD (MMSE 3-14) in NEJM: memantine associated with less deterioration in cognitive and functional measures than placebo
* Problem: small numbers, high drop out rate
* Preliminary study: 400 patients with severe AD, 6 months RCT of memantine plus donepezil vs placebo plus donepezil: memantine group had significant benefit in comparison

Memantine: Summary
* Approved for treatment of moderate-severe AD
* Likely of benefit also in severe vascular and mixed dementias as well
* Likely will be used in combination with donepezil or other cholinesterase inhibitors
* Cochrane Dementia Group: “memantine is a safe drug and may be useful for treating AD, vascular and mixed dementia, although most of the trials so far reported have been small and not long enough to detect clinically important benefit”

Behavioral Symptoms: Nonpharmacologic Treatment
* Depression, agitation, aggression, wandering, sleep disturbance, paranoia, anxiety
* Assess for/treat depression
* Assess cause for increased symptoms (caregiver, environmental changes, medications, infection)
* Assess for caregiver depression
* ID and avoid triggers of negative behavior
* Redirection
* Environmental modification for wandering
* Sleep hygiene

Use of Atypical Antipsychotics
* Older, “typical” agents such as haloperidol and thioridazine (mellaril) associated with significant extrapyramidal symptoms
* Theoretically combination of dopamine and serotonin effects of atypical agents allow treatment of positive and negative psychotic symptoms with less EPS

* Evidence demonstrates efficacy in treatment of psychotic and behavior symptoms in patients with dementia
* Exacerbates movement disorder in patients with Parkinson’s
* Start .25/day, average daily dose 1-1.5mg/day
* EPS in dose dependent manner (6mg/day)
* Insomnia, hypotension, weight gain
* Elevation of prolactin levels

* Evidence that it is effective in AD patients
* Increases motor symptoms in PD patients
* Recommended not to use with PD
* Start: 1.25-2.5/day, increase to 5/day (dosages of 10-15/day are not more effective!)
* More sedating than others (more anticholinergic effects)
* Sedation, weight gain, orthostatic hypotension, seizures, glucose intolerance
* Showing promise in patients with AD and PD
* Does not exacerbate movement disorder of PD
* May be first line for PD patients with psychosis
* 12.5 QHS, titrate every 3-5 days
* Sedation, HA, orthostatic hypotension
* ?Cataract formation

Ziprasidone (Geodon)
* New, clinical data lacking
* Non dose-dependent QT prolongation

* Very effective in treating psychosis in PD patients
* The most effective agent in treatment of drug induced psychosis in PD
* Some efficacy with AD patients
* Start: 6.5mg/day
* Agranulocytosis, frequent monitoring limits use

Antipsychotics in Dementia: Summary
* Start very low, monitor for hypotension, P450 effects, sedation, EPS
* Monitor and avoid use as “chemical restraint”
* Avoid if at all possible in Dementia with Lewy Bodies

Prevention of Dementia
* HTN and Hyperlipidemia
o Observational studies show less risk of AD in patients on statin agents (RCTs do not show effect)
o Original HTN in Elderly studies: patients initially on placebo with systolic HTN had persistent elevation in risk of dementia
* Vascular risk factors seem to play role even for AD!
* Evidence lacking for Vit E, Estrogen, NSAIDS

Future Directions
* Amyloid B peptide (plaque component) vaccination
* Amyloid modulators
* ?Anti-inflammatory drugs
* Treatment with statins
* ?Low flow VP shunting

Take Home Points
* Cholinesterase Inhibitors are MODESTLY effective in treatment of mild to moderate AD
* Cholinesterase Inhibitors are probably effective in more severe AD
* No large difference in efficacy between agents, but Donepezil more easily titrated and tolerated
* Evidence to support use of cholinesterase inhibitors for vascular and vascular/AD dementia
* Memantine looks to be effective for more severe AD and vascular dementia, will likely be used in combination with cholinesterase inhibitors
* Behavioral symptoms common, first line of treatment is nonpharmacologic
* Atypical antipsychotics can be effective, but use in low doses and watch carefully for problems (especially EPS, hypotension)
* For PD, quetiapine (seroquel) may be first line for psychotic symptoms
* Avoid antipsychotics with Lewy Body Disease!

Treatment Options for Dementia.ppt


Palliative care of advanced dementia

Palliative care of advanced dementia A patient centered approach
By:VJ Periyakoil, MD
Director, Palliative Care Fellowship Program
Stanford University General Internal Medicine &
VA Palo Alto Health Care System

Main Message
* Currently, patients with dementia do not get access to quality palliative care
* Access to quality palliative care can be facilitated only if we take an inter-disciplinary approach to care

Talk Agenda
* Current state of palliative care for dementia
* Key challenges in providing palliative care for dementia patients
+ Prognostication
+ Decision making
+ Advance care plan
+ Symptom management
+ Caregiver stress

Prognostication questions in dementia
* Patient’s question: “How long do I have before my mind is shot?”
* Health professional’s question: “ Is s/he eligible for palliative care?”
* Family’s question: “How long does s/he have to live ?”
* Caregiver’s question: “ I am exhausted. How much longer can I do this?”

Is dementia a terminal illness? If so, when do they start dying?

Dementia hospice eligibility
* Stage 7 or beyond according to the FAST scale
* Unable to ambulate without assistance
* Unable to dress without assistance
* Unable to bathe without assistance
* Urinary or fecal incontinence, intermittent or constant
* No meaningful verbal communication, stereotypical phrases only, or ability to speak limited to six or fewer intelligible words
* Plus one of the following within the past 12 months:
o Aspiration pneumonia
o Pyelonephritis or other upper UTI
o Septicemia
o Multiple stage 3 or 4 decubitus ulcers
o Fever that recurs after antibiotic therapy
o Inability to maintain sufficient fluid and calorie intake, with 10 percent weight loss during the previous six months or serum albumin level less than 2.5 g per dL (25 g per L)

Schonwetter RS, Han B, Small BJ, Martin B, Tope K, Haley WE. Predictors of six-month survival among patients with dementia: an evaluation of hospice Medicare guidelines. Am J Hosp Palliat Care 2003;20:105-13.

Decision making in dementia
* Hierarchy of decision making
* Competence v. capacity
* Special circumstances

Special circumstances
Case 1: Incapacitated pt with no proxy and unknown preferences
Case 2: Chronically mentally ill pts with no capacity
Case 3: Chronically mentally ill pts with fluctuating capacity

Intact decision making prior to death in the elderly
Alzheimer’s Disease
Diseases other than Alzheimer’s
Lentzer HR et al “ The quality of life in the year before death”. Am J Public Health 82: 1093-1098, 1992
Interface between palliative care and dementia

* Clarity of decision making
o Soft balls ( relatively speaking):
o Hard balls

The decisions themselves are never easy.
Advance care planning
Shades of Gray
Possible levels of care:
Heroic life prolonging measures
* “Whopper no veggie*”
* Artificial nutrition
* Artificial hydration
* Antibiotics

What are the goals of care?

Tube feed or not tube feed?
That’s the question
* The facts:
Palliative care symptoms and cognitive impairment
Presentation of these symptoms is skewed
What does dying look like?

* Decline in functional status
* Lack of desire to eat or drink
* Withdrawn
* Sleep- wake state
* Mottling of limbs
* Jaw movement
* Death rattle
* Co-morbid symptoms
* Unpaid
* Overworked
* On-call 24/7
* Sleep deprived
* No social life
* Poor support system

Palliative care of advanced dementia A patient centered approach.ppt


Geropsychiatry: Delirium and Dementia

Geropsychiatry: Delirium and Dementia
By:Robert Averbuch, MD
Assistant Professor
Department of Psychiatry

Disorders of Cognition
* DSM-IV devotes an entire section to a subset of “organic” disorders that primarily affect cognition: “Delirium, Dementia, and Amnestic and other Cognitive Disorders”

What is “organic”?
* Previous differentiation between mental disorders with a clear “physical or biological” etiology (Organic) and those without (“Functional” or “Primary”)
* Falsely implied that Functional (or primary) disorders have no underlying pathophysiological basis
* Primary mental disorder- not due to a GMC or substance

Disorders of Cognition
* Delirium-disturbance in consciousness and cognition that develops rapidly
* Dementia- multiple cognitive deficits that include memory disturbance
* Amnestic Disorder- primarily memory impairment

Delirium: defined
* Disturbance of consciousness (awareness of the environment) and attention,
o Changes in cognition (ie, “thinking”-memory, orientation, language, etc) OR
o Perceptual disturbances

The Course of Delirium
* Evolves rapidly (hrs to days)
* Usually resolves rapidly as well:
o May be self-limited, persist for weeks, or progress to death
* Degree of impairment fluctuates

Delirium: Associated Features
* Disturbance in sleep-wake cycle
* Easily distracted by irrelevant stimuli
* Changes in activity level
o Restlessness, hyperactivity
o Picking at clothes, getting out of bed
o OR hypoactivity (lethargy)
* Emotional disturbances- mood lability, anger, irritability, euphoria, apathy

Delirium: Associated Features
* Speech or language disturbances
* Perceptual abnormalities- common:
o Illusions, hallucinations, delusions
* Neurological deficits/dysfunction

What Are the Causes?
* DIRECT: Brain pathology: head injury, seizures (during and after), strokes, infections
* INDIRECT: Systemic Illness: electrolyte abnormalities, dehydration, uremia, hepatic encephalopathy, cardiovascular compromise

More Causes of Delirium
* Sensory deprivation
* After surgery (post-operative state)- ie. “ICU Psychosis”
* Side effects of medications or toxins or with abused recreational drugs:
“Substance-Induced Delirium”
o Ex. NMS (Neuroleptic Malignant Syndrome)
o Ex. Serotonin Syndrome

Treating Delirium
* Considered a Medical Emergency
* Supportive care in an ICU setting
* Safety- close monitoring
* Remove offending agent, treat underlying cause

Hallmark is Memory Impairment
* Memory problems usually evident early
* Memory impairment alone is not enough to make the diagnosis…

Dementia- defined
* Memory problems AND at least one additional cognitive deficit:
o Aphasia
o Apraxia
o Agnosia
o Problems with “executive functioning”

Details, Details: Aphasia
* Aphasia is a drop off in language function that shows up in a variety of ways

* “impaired ability to pantomime the use of known objects or to execute known motor acts”

* Trouble recognizing or identifying things despite intact sensations (ex. You can see fine, but you can’t recognize a stop sign)
* May include difficulty recognizing family members or even themselves in the mirror

Disturbances in Executive Functioning
* Abstract thinking
* Planning, initiating, sequencing, and stopping behaviors
* May manifest as trouble with novel tasks or new situations

Associated Features
* Spatial disorientation
* Poor insight and judgment means…they get themselves in trouble by overestimating their abilities and underestimating risks
* Perceptual Abnormalities:
o Delusions- especially persecution
o Hallucinations- especially visual

More associated features
* Personality Changes:
o Disinhibition
o Neglect of personal hygiene
o Apathy and withdrawal

Course of Dementia
* Course may be progressive, static, or remitting
* Small percentage of cases are reversible

What causes Dementia?
* Alzheimer’s is by far the most common type
* Cerebrovascular Disease
* Degenerative Diseases: Parkinson’s, Huntington’s, CJD (Mad Cow Disease)

More causes:
* Autoimmune Illness
o Lupus
o Multiple Sclerosis
* B12, Folate Deficiencies
* Head Trauma, Brain Tumors
* Infections- like HIV and Syphilis

Dementia of the Alzheimer’s Type (DAT)
* Diagnosis of exclusion
* Hallmark: gradual onset of recent memory problems
* Onset may be early (65 y/o or younger) or Late (over 65)

* Slowly progressive (8-10 years from diagnosis to death)
* Many show personality changes
* Often with associated behavioral disturbances (wandering, agitation, etc.)

Vascular Dementia
Aka Multi-Infarct Dementia
Vascular Dementia
* Evidence of cerebrovascular disease on physical exam and head scans
* Usually caused by several strokes over time
* Onset abrupt, followed by stepwise, fluctuating course with “patchy” deficits

Treatment of Dementia
* Search for a reversible cause and treat (ex. B12 deficiency, Normal Pressure Hydrocephalus, Syphilis, etc)
* Rule out Pseudodementia (change in cognition associated with depression)
* Environmental/behavioral interventions- ex. no fail environment
* Medications

* Cholinesterase Inhibitors:
o Aricept (donepezil)
o Reminyl (galantamine)
o Exelon (rivastigmine)

* NMDA-receptor antagonists
o Namenda (memantine)
o Neuroprotective by blocking excessive glutamate stimulation of the NMDA (N-methyl-D-aspartate) receptor

Geropsychiatry: Delirium and Dementia.ppt


23 February 2010

Warts Diagnosis and Treatment

Warts Diagnosis and Treatment
By:Rick Lin, DO MPH
Texas Division of KCOM Dermatology Residency Program

Background Information
* Warts are small harmless lesions of the skin
* caused by a virus: the human papilloma virus.
* The appearance of warts can differ based on the type of wart and where it is located on the body.
* Warts are common in children. Most cases occur between ages 12-16 years.
* Up to 30% of warts disappear by themselves within 6 months. Most will disappear without any treatment within 3 years.
* Warts are caused by the DNA-containing human papillomavirus (HPV). There are at least 63 genetically different types of HPVs.
* The virus enters the skin after direct contact with recently shed viruses kept alive in warm, moist environments such as a locker room, or by direct contact with an infected person.
* The entry site is often an area of recent injury. The incubation time—from when the virus is contracted until a wart appears—can be 1-8 months.
* Contrary to popular mythology, touching a frog will not give you warts.

Types of warts
* Common warts (verrucae vulgaris): These common warts typically develop on the hand, especially around the nail. They are gray to flesh colored, raised from the skin surface, and covered with rough, hornlike projections.
* Plantar warts (verrucae plantaris): Plantar warts, by definition, occur on the plantar surface, or bottom, of the foot.
* They usually occur in high pressure areas such as the heel and the metatarsal heads (just behind the toes).
* They usually grow into the skin, not outward like common warts.
* This growing into the skin makes them more difficult to treat.
* Flat warts (verrucae plana): Flat warts are most commonly seen on the face, the back of the hands, and lower legs.
* They usually appear as small individual bumps about 1/4 inch across.
* Flat warts may spread rapidly on the face and lower legs from the activities involved in shaving.

* Verruca vulgaris (common wart) is caused by varous strains of human papilloma virus (HPV 1, 2, 4, 7, 26-29).
* Macroscopically verruca vulgaris may present as hard, rough surfaced papule
2 – 20 mm (solitary or multiple).
* Microscopically, this is an exophytic, symmetric, papillomatous lesion with large keratohyaline granules and characteristic inturning of the rete ridges.

* Parakeratotic columnar tiers of stratum corneum overlie the papillomatous surface.
* Small amounts of hemorrhage may be present within the columns of parakeratosis.
* Other characteristic features include koilocytosis, hypergranulosis and presence of multinucleated cells.

* Home care is effective in making the wart or warts go away. No matter what technique you use, warts will disappear 60-70% of the time.
* Techniques may be done with and without medication.
* The ultimate goal of the medical therapies (not the surgical treatments) is to get your body to recognize the wart as something foreign and to destroy it, much like the body destroys a cold virus.

Adhesive tape therapy
* Place several layers of waterproof adhesive tape over the wart region (even duct tape).
* Do not remove the tape for 6-1/2 days. Then take off the tape and open the area to the air for 12 hours.
* Reapply tape for another 6-1/2 days.
* The tape works best in the region around the fingernail.
* Tape works because the air-tight, moist environment under the tape does not allow the virus to grow and reproduce

Salicylic acid therapy
* Salicylic acid is available by many different trade names at the drug store.
o Dual Film
o Wart-Off
o Dr. Scholl’s Wart Medication
o Medi-Plast
* It comes either as a liquid to paint on the wart or as a plaster to be cut out and placed on the wart tissue.
* The area with the wart should be soaked in warm water for 5-10 minutes.
* The wart should then be pared down with a razor. A simple razor works fine for this, then throw it away.
* Do not shave far enough to make the wart bleed.
* Apply the salicylic acid preparation to the wart tissue.
* Do not apply it to other skin because of salicylic acid's potential to injure normal tissue.
* Follow directions on the package for how long to apply the acid.

* Liquid nitrogen or cryotherapy is used to deep freeze the wart tissue.
* With liquid nitrogen applied to the wart, the water in the cells expands, thus exploding the infected tissue.
* The exploded cells can no longer hide the human papillomavirus from the body's immune system.
* The immune system then works to destroy the virus particles.
* Periungual area may scar if cryotherapy with liquid nitrogen is used improperly.
* Scarring could lead to permanent nail disfiguration.

Laser Therapy
* Laser therapy: Lasers are simply very intense light sources.
* This light has an enormous amount of energy that heats the tissue enough that it vaporizes.

Shave Removal
* Shave removal and electrodessication of the base may be necessary when other treatment methods fail.
* This would involve numbing the region around the wart and shaving the wart flat with the surface and light electrodessication of the base.

* Most warts will disappear without treatment anywhere from 6 months to 3 years.
* Warts may recur after treatment and require additional treatments.
* Avoid touching warts on others or touching them on yourself (refrain from rubbing a warty finger across your face).
* Children needs to avoid biting or chewing warts.
* Wear shower shoes in the gym locker room to lower your risk of picking up the virus that causes plantar warts from the moist environment.

When to Refer
* If you feel uncomfortable treating warts.
* Warts that are resistant to your treatment
* Unsure of diagnosis

Warts Diagnosis and Treatment.ppt


Dermal and Subcutaneous Tumors

Dermal and Subcutaneous Tumors

Urticaria pigmentosa
* Local and systemic accumulations of mast cells
* Persistent pigmented itchy skin lesions
* Urticate on mechanical or chemical irritation
* c-KIT mutation
* Birth to middle age, ½ < 6 mo
* Macules, papules, nodules, plaques, vesicles
* Lesions persist and gradually become chamois- or slate-colored
* Darier’s sign, pruritis
* Severe symptoms may result from massive liberation of histamine from mast cells after ingestion of known mast cell degranulators
* Spontaneous resolution is likely in those pts whose disease began in childhood

Solitary mastocytoma
* May be present at birth, may develop during the first weeks of life
* Brown macule that urticates upon stroking
* Smooth or peau d’ orange
* Dorsum of the hand near the wrist
* Edema, urtication, vesiculation may be observed
* Generalized eruption, childhood type
* Pseudoxanthomatous mastocytosis
* Diffuse cutaneous mastocytosis
* Generalized eruption, adult type
* Erythrodermic mastocytosis
* Telangiectasia macularis erupta perstans
* Systemic mastocytosis
* Familial urticaria pigmentosa
* Giemsa, azure A, or polychrome toluidine blue
* Local anesthetic adjacent to the lesion, without epi
* Dx is bx confirmed
* Histamine metabolites methylhistamine and methylimidazole acetic acid

Prognosis and treatment
* In all forms without systemic involvement the prognosis is good
* Solitary lesions usually involute within 3 years
* H1 and H2 blockers
* Intralesional and topical steroids
* Avoid physical stimuli

Abnormalities of neural tissue
Solitary neurofibroma
* Soft, flaccid, pinkish white, 2-20 mm
* Invaginates on pressure, “buttonholing”
* Solitary or multiple
* Distinctive histopathologic findings, fibrils, cellular proliferation, and degenerative changes
* Sx excision

Granular cell tumor
* Well-circumscribed, solitary firm nodule, with a brownish red or flesh tint
* Usually solitary, 10-15 % multiple
* 1/3 of cases have occurred on the tongue
* May occur anywhere on the body
* Grows slowly
* Cells stain positively with vimentin, neuron-specific enolase, S-100, and myelin protein
* Malignant granular cell tumor is rare

Neuroma cutis
* Three true neuromas exist in the skin and mucous membranes: traumatic neuroma, multiple mucosal neuromas, and solitary palisaded encapsulated neuromas
* Traumatic neuromas occur commonly on the fingers, tender and painful
* Multiple mucosal neuromas occur as part of multiple mucosal neuroma syndrome
* solitary palisaded encapsulated neuromas occur commonly on the face, resembles BCC

* Nerve sheath myxoma
* Benign tumor of nerve sheath
* Mitotic figures and nuclear atypia are sometimes observed
* Intradermal or subcutaneous
* Histologically are divided into two subtypes: myxoid and more common cellular variant

* neurilemmoma
* Usually a solitary nerve sheath tumor
* Most often seen in women
* Occur almost exclusively along the main nerve trunks of the extremities
* Soft or firm nodules, may be painful
* May be multiple
* May be assoc. with NF-1 or NF-2
* Occur in many other organs
* excision

Infantile neuroblastoma
* The most common malignant tumor of childhood
* Cutaneous nodule are most often seen in the younger patients
* Blue nodules the when rubbed form a halo of erythema
* Periorbital ecchymoses and heterechromia
* Good prognosis for patients with skin involvement, spontaneous remission

* Rarely described in the skin as an isolated entity
* Arise most often in von Recklinghausen’s neurofibromatosis
* Occur in childhood

Nasal glioma
* Cephalic brainlike heterotopias
* Rare, benign congenital tumors
* Easily confused with hemangiomas
* Firm, reddish blue lesion on the nasal bridge
* No connection with the subarachnoid space
* Radiography and neurosurgical consultation
* Does not involute spontaneously

Cutaneous memingioma
* Psammoma
* Results from the presence of meningocytes outside the calvarium
* Small, hard, fibrous, calcified nodules occurring along the spine, in the scalp, and on the forehead
* Usually seen within the first year
* No distinctive appearance, dx by histo

Encephalocele and Meningocele
* Primary defect in the neural tube
* Present in infancy along the midline
* Compressible masses that may transilluminate or enlarge with crying
* Midline masses require intensive radiologic and neurosurgical evaluation before biopsy

* Slow-growing, locally invasive
* Firm, smooth nodules in the sacralcoccygeal region or at the base of the skull
* Arise from notochord remnants
* May metastasize late in their course
* Wide excision and postoperative radiation therapy

Abnormalities of Fat Tissue
* Subcutaneous tumors composed of fat tissue
* Most commonly found on the trunk
* Also neck, forearms and axillae
* Soft, single or multiple, lobulated and compressible
* Growth to size and remain stationary
* again be careful of sacrococcygeal lipomas
* Lesion may be left untreated or excised
* Solitary lesions reaching greater than 10 cm should be investigated for malignancy
* Multiple lesion may be painful if growing rapidly
* Madelung’s disease, benign symmetric lipomatosis
* Dercum’s disease, assoc with weakness and psychiatric disturbances
* Familial multiple lipomatosis, AD inheritance
* Bannayan-Riley-Ruvalcaba syndrome
* MEN 1
* Frohlich’s syndrome
* Gardner’s syndrome

* A painful subcutaneous nodule just slightly above the level of the skin
* Has all other typical features of a lipoma
* Seen in young adults who have multiple painful lumps in the skin
* Multiple subcutaneous angiolipomas have no invasive or metastatic potential

Neural fibrolipoma
* Overgrowth of fibro-fatty tissue
* Occurs along a nerve trunk and often leads to compression
* Slowly enlarging subcutaneous mass with tenderness and decreased sensation or parasthesia
* Median nerve is most commonly involved
* MRI, no effective treatment

Spindle-cell lipoma
* Asymptomatic, slow growing subcutaeneous tumor
* Predilection for the back and neck and shoulders of older men
* Consists of lobulated masses of mature adipose tissue

Painful Piezogenic pedal papules
* Transitory, soft, sometimes painful papules on the sides of the heels
* Elicited by weight-bearing and disappearing when this is stopped
* Occur in at least 75 % of normal individuals
* Suitable supportive shoes may alleviate discomfort
* May occur on the wrist

Nevus lipomatosus superficialis
* Soft, yellowish papule or ceribriform plaques, usually of the buttock or thigh, less often the ear or scalp
* A wrinkled surface characterizes this tumor
* Onset prior to age of 20
* Nevus lipomatosus superficialis

Folded skin with scarring
* Rare, aka Michelin Tire Baby Syndrome
* There are numerous deep, conspicuous, symmetrical, ringed creases around the extremities
* The underlying skin may manifest a smooth muscle hamartoma, a nevus lipomatosis, or elastic tissue abnormalities
* AD, sporadic or an isolated finding assoc with congenital facial and limb abnormalities

Diffuse lipomatosis
* Characterized by an early age of onset, by the age of 2, diffuse infiltration of muscle by and encapsulated mass of mature lipocytes
* Progressive enlargement and extension
* Usually involves a large portion of the trunk or extremity

(lipoma of brown fat)
* A form of lipoma composed of finely vacuolated fat cells of embryonic type
* Have a distinctive brownish color and a firm consistency
* Benign and usually occur singly
* Chiefly in the mediastinum and the interscapular region
* Onset usually in adult life

Pleomorphic lipoma
* Occur for the most part on the backs and necks of elderly men
* Occasional lipoblast-like cells and atypical mitotic figures may require differentiation from a liposarcoma
* Behave in a perfectly benign manner`

Benign lipoblastomatosis
* Frequently confused with a liposarcoma
* Affects exclusively infants and young children, 90% < age 3
* Commonly involves the soft tissues of the upper or lower extremity
* A circumscribed and a diffuse form can be distinguished
* TOC- complete local excision

* One of the less common mesenchymal neoplasms of the soft tissue
* Usually arise from intermuscular fascia
* Do not arise from preexisting lipomas
* Usual course is an inconspicuous swelling of the soft tissue with gradual enlargement
* When a fatty tumor becomes greater than 10 cm DX should be considered
* Upper thigh is the most common site
* Adult males are mostly affected
* May be well or poorly differentiated
* Tx is adequate radical excision
* For metastatic liposarcomas, radiation therapy may be effective

Abnormalities of smooth muscle
* Smooth muscle tumors
* Characterized by painful nodules
* Singly or multiple
* Benign
* Treatment is directed toward the removal of the pain source
* Simple excision is best
* Solitary cutaneous leiomyoma
* Multiple cutaneous leiomyomas
* Solitary genital leiomyoma
* angioleiomyoma

Grouped leiomyomata of the back
Congenital smooth muscle hamartoma
* Typically a skin colored or slightly pigmented patch or plaque with hypertrichosis
* Often present at birth
* Usually seen on the trunk, lumbosacral area in 2/3
* Michelin tire baby syndrome may result from a diffuse smooth muscle hamartoma
* Clinically may mimic a mastocytoma, pseudo-Darier’s sign is seen in 80%
* No treatment is necessary

* Of soft tissue origin are extremely rare
* May occur as metastasis from internal source
* Appears in the dermis as a solitary nodule, good prognosis
* Subcutaneous lesions have a guarded prognosis, with fatal hematogenous metastases in 1/3
* WLE or Mohs

Miscellaneous tumors and tumor-associated conditions
Cutaneous endometriosis
* Brownish papules in the umbilicus or lower abdominal scars after gynecologic surgery
* Tender or painful lesions
* Bluish black from cyclic bleeding
* Usually misdiagnosed as malignant metastases
* Surgical excision
* Preoperative tx with danazol or leuprolide may reduce size

* May develop in the skin but are most common in the ovaries or testes
* No characteristic clinical features
* Tissue representing all three germ layers are present
* Occasionally malignancy may occur

Metastatic carcinoma
* 5 to 10% of patients with cancer develop skin metastases
* Usually present as numerous firm, hard, or rubbery masses
* Predilection for chest, abdomen or scalp
* Sister Mary Joseph nodule, metastatic tumor localized to the umbilicus, most common primary sites include the stomach, large bowel, ovary and pancreas
* A poor prognosis is usually the rule
* The involvement of the skin is likely to be near the area of the primary tumor
* Breast cancer is the type most commonly metastatic to the skin in women and melanoma followed by lung cancer in men
* Metastatic lesions are uncommon in children

Paraneoplastic syndromes
* Some cancers produce findings in the skin that indicate to the clinician that an underlying internal malignancy may be present
* Bazex’s syndrome, characterized by violaceous erythema and scaling of the fingers, toes, nose, and aural helices.
* Secondary to a primary malignant neoplasm of the upper aerodigestive tract

Bazex’s syndrome
* Necrolytic migratory erythema, seen with glucagon-secreting tumors of the pancreas
* Erythema gyratum repens, erythema with characteristic wood-grain-pattern scales, is almost always associated with and underlying malignancy
* Hypertrichosis lanuginosa aquisata, most common with lung and colon ca
Hypertrichosis lanuginosa
* The sign of Lesser-Trelat, the sudden appearance of multiple pruritic seborrheic keratosis, associated with and internal malignancy
* Trousseau’s sign, migratory thrombophlebitis, pancreatic ca
* Pityriasis rotunda
* Tripe palms
* Several others with less frequency

* Characterized by distinctive involvement of the lungs, heart, gastrointestinal tract and the skin
* Cutaneous flushing lasting 5-10 minutes
* Involves the head and neck producing a scarlet color
* Cyanosis may be present
* Episodic flushing continues for months or years
* The release of excessive amounts of serotonin and bradykinen into circulation produces attacks of flushing of the skin, weakness, abdominal pain, nausea and vomiting, sweating, palpitation, diarrhea and collapse
* Tumor arises from the argentaffin Kulchitsky chromaffin cells of the appendix or terminal ileum (gi, lungs, ovaries, testes)
* The diagnosis may be established by finding high levels of 5-hydroxyindolacetic acid (5-HIAA) in the urine
* Tx- primary tumor should be removed, and excision of metastatic lesion should be considered
* Chemotherapy

Dermal and Subcutaneous Tumors.ppt


22 February 2010

Female Genital Cutting

Female Genital Cutting
By:Safa Magid

Female Genital Cutting(FGC)
* Also known as: female circumcision & female genital mutilation
* Female circumcision is the term preferred by cultures who practice this custom

FGC -Definition
* Procedure involving partial or total removal of the external female genitalia or other injury to the female genital organs whether for cultural, religious, or other non-therapeutic reasons.

WHO Classification of FGC
* Type 1: Excision of prepuce w/ or w/o excision of all of the clitoris
* Type 2: Clitoridectomy and partial or total excision of labia minora
* Type 3: Infibulation, includes removing all or part of ext. genitalia and re-approximation of remnant labia majora, leaving a small interoitus for passage of urine and menstrual blood

* Type 1 and Type 2 are the most common forms
* Type 1 and Type 2 account for 80% of the cases
* Infibulation accounts for 15% of the cases

* Currently ~ 130 million women and girls have had the procedure
* An estimated 2 million girls worldwide are at risk per year

FGC in the US

* Data from 2000 census suggests:
228,000 women and girls are with or at risk for FGC in the United States
* CA, NY, and MD have the most female immigrants and refugees from countries where FGC is prevalent.
* Occurs mostly in 28 sub-Saharan African countries
* FGC is practiced by Christians, Muslims, and adherents to traditional African religions
* Also practiced in Middle East and Asia

Origins and History
* Origins remain unclear
* FGC practiced in Pre-Islamic Arabia, ancient Rome, and Tsarist Russia
* Female circumcision was discovered in ancient Egyptian mummies in 200 B.C.
* Practiced in the United States until the 1970’s to tx hysteria, lesbianism, and erotomania

FGC and Religion
* Christianity:
FGC is not an obligatory religious requirement
* Islam:
FGC is not an obligatory religious requirement

* Performed between the ages of 5-10, or prior to marriage
* Performed by a member of community who is not a healthcare worker
* Often performed w/o anesthesia
* However in metropolitan areas the use of anesthesia is more common

FGC Procedure
* Performed w/o surgical instruments. Razor blades or other instruments which may or may not be sterile are used
* Depending on socio-economic factors FGC may also be performed in a health care facility by qualified health personnel
* WHO is opposed to medicalization of all types of female genital mutilation.
* Reasons currently practiced:
o Rite of passage to womanhood
o Maintains chastity
o Ensure marriageablity
o Belief that it improves hygiene
o Social pressure to adhere to custom
o Belief that it is a religious requirement

* Prevalence of complications is unknown
* Rate of complications increase with severity of procedure( i.e. women with type III have > complications that women w/type I)
* A study of 120 Somalian women suggests rate of complications are inversely proportional to the age of the child when FGC was performed
* Women who had FGC btwn the ages of 5-8, had more complications than their 9-12 y.o counterparts
* Long and short term complications
* Some women with FGC do not experience complications

Short term complications
* Hemorrhage
* Severe pain
* Shock
* Infection
* Urine retention
* Ulceration of genital region injury to adjacent tissue
* HIV?-Possibly transmitted due to use of unsterilized equipment

Long Term Complications
* Cysts and abscesses
* Post-partum fistulaes: vesico-vaginal
* Keloid scar formation
* Damage to the urethra resulting in urinary incontinence
* Dyspareunia and sexual dysfunction
* Infertility
* Difficulties with labor.

Case Report

* 16 y.o female presents w/severe dysmenorrhea
* PE revealed the absence of a clitoris and fused labia majora with a 1cm opening
* Physicians initially thought pt had corrective surgery for ambiguous genitalia
* Later determined that while visiting Africa with her mother she had FGC performed
* Perinealography revealed:
o Filling of the vagina,urethra, and bladder simulating a urogenital sinus.
o Dilated vagina suggested obstruction

Case Report
* Defibulation procedure was performed
* The patients symptoms of dysmenorrhea eventually resolved

FGC and Obstetric outcomes
* WHO Study

FGC & Length of maternal hospital stay
* FGC and length of maternal hospital stay
o FGC Type I- RR: 1.15
o FGC Type II-RR:1.51
o FGC Type III-RR:1.98

FGC and Mental Health
* Anxiety
* Depression
* Feeling of incompleteness

* Corrective procedure
* Involves division of the fused labia majora with suturing of each labia for hemostasis
* Thus the infibulated scar, which is a flap obstructing the introitus and urethra, is removed
* WHO Indications for defibulation:
* Urinary retention
* Recurrent UTI’s or kidney infections
* Dysmenorrhea
* Dyspareunia or apareunia
* Prior to coitus
* Prior to labor
* It is also reasonable that defibulation can be performed to alleviate any mental health consequences for women who do not meet the WHO indications

Approach to patients with FGC
* Some physicians remain unfamiliar w/FGC & have expressed their shock during PE
* Some women report being reprimanded by physicians for having the procedure done
* Despite the fact the majority had FGC while they were children and were not given a choice

Patients perspective of FGC
* Many pts w/FGC who have immigrated to the West do not feel as if they abused
* Some feel that FGC was done “for them” and not an attack against them

Patients perspective of FGC
* 1st generation pts born in the West who had FGC while traveling abroad often have very different views than their foreign born counterparts
* HC workers may need to modify their approach depending on the pts perspective

Legality of FGC
* U. S. passed a law in March 1997:
* Made performing any medically unnecessary surgery on the genitalia of a girl younger than 18 years of age a federal crime.
* Reinfibulation was not included as a federal crime, so it may be performed with absorbable sutures in a running fashion if a woman chooses the procedure

Resources for pts and HC providers
* African’s Women’s Health Center
o Established in 1999 by Dr. Nawal Nour a Sudanese-American OB/GYN
o Goal of clinic is to provide culturally appropriate holistic care to African women who are refugees who may or may not have undergone FGC
o Defibulation is performed at this clinic

Resources for pts and HC providers
* Website with information about FGC
* Includes fact sheet about FGC and guidelines for healthcare workers
* http://www.who.int/topics/female_genital_mutilation/en/
* http://www.who.int/reproductive-health/publications/rhr_01_18_fgm_policy_guidelines/index.html

Dedicated to all of my sisters who have had FGC.
To those who have suffered physical or mental consequences, I am inspired by your courage and strength.

Female Genital Cutting.ppt


Wound Healing, Dressing, and Drains

Wound Healing, Dressing, and Drains
By: Dr. Aidah Abu Elsoud Alkaissi

Wound healing
* Etiology of wounds:
o Surgical: caused by an incision or excision
o Traumatic: caused by an injury (mechanical, thermal, or chemical)
o Chronic:caused by an underlying pathophysiology, such as pressure sores, or venous leg ulcers, over time

Exact biologic process that takes place in orderly sequence
* An exudate containing blood, lymph, and fibrin begins clotting and loosely binds the cut edges together
* Blood supply to the area is increased, and the basic process of inflammation is set in motion
* Leukocytes increase in number to fight bacteria in the wound area and by phagocytosis help to remove damaged tissues
* The served tissue is quickly glued together by strands of fibrin and a thin layer of clotted blood, forming a scab

Wound Healing
* Plasma seeps to the surface to form a dry protective crust
* This seal helps to prevent fluid loss and bacterial invasion
* During the first few days of wound healing, the seal has little tensile (The resistance of a material to a force tending to tear it apart) strength
* After 3-4 days , connective tissue cells (fibroblasts)rapidly proliferate and give strength to the wound by producing collagen, a tough fibrous protein responsible for the structural integrity of the skin
* At the same time small blood vessels regenerate and build new blood channels, granulation tissue (fibrous connective tissue)includes blood vessels and lymphatics that proliferate from the base of the woind
* Rapidly growing and multiple epithelial cells begin to restore the epithelial continuity of the skin
* At this stage the wound appears healed, healing is not complete until the granulation tissue organizes into scar tissue
* By the ninth or tenth day, the wound is moderately well healed and then becomes progressively stronger
* The whole process of repair takes 2 weeks or more depending on factors such as physical condition of the patient, size and location of the wound, and stresses put on the incisional area
* During this time the scar (cicatrix)strengthens as the connective tissue shrinks
* The amount of tissue loss, the existence of contamination or infection and damage to tissue are all factors that determine the type of wound healing that will occur
* Process of healing takes place in one of three ways
o Healing by primary (first) intention
o Healinh by secondary infection (granulation)
o Healing by delayed primary closure (third intention)

Healing by primary (first) intention
* Edges of an incised wound in a healthy person are promptly and accurately approximated
* Contmination is held to a minimum by impeccable (without fault or error) aseptic technique
* Trauma to the wound is minimal
* After suturing , no dead space is left to become site of infection
* Drainage is minimal

Healing by secondary intention (granulation)
* When surgical wounds are characterized by tissue loss with inability to approximate wound edges, healing occurs through secondary intention
* This type of wound is left open and allowed to heal from the inside towaed the outer surface
* In infected wound this process allows the proper cleansing and dressing of the wound as healthy tissue builds up from the inside
* The area of tissue loss gradually fills with granulation tissue (fibroblasts and capillaries)
* Scar tissue is extensive because of the size of the tissue gap that must be closed. Contraction of surrounding tissue also takes place
* Consequently this healing process takes longer than primary intention healing

Healing by delayed primary closure (third intention)
* This healing process takes place when approximation of wound edges is delyed by 3-5 days or more after injury or surgery
* The condition contribute to a decision for a dalyed closure are:
o 1. Removal of an inflamed organ
o 2. Heavy contamination of wound

Factors influencing wound healing
* The patient´s nutritional status and overall recuperative (To return to health or strength; recover) power
* Especially significant is an adequate supply of protein, which is necessary for the growth of new tissues, the regulation of the osmotic pressure of blood and other body fluids and the formation of prothrombin, enzymes, hormones and antibodies
* Vit C which aids connective tissue production and strong scar formation
* Scrupulous aseptic technique must be used to prevent any wound infection-the most common cause of delayed wound healing
* Theories abound as to the genesis of wound infection. Cross – contamination from operating room, post anesthesia care unit and unit personel is believed to be a primary source
* Aseptic principles and maintenance of operating room environmental conditions are significant factors
* Length of time that the wound is open in the operating room has also been mentioned
* The pat own endogenous flora
* Rough handling of tissue causes trauma that cal lead to bleeding and other conditions conducive to the infection
* Other factors pat age, stress level, presxisting condition as diabete, anemia, malnutriion, cancer , obesity, advanced age, cardiovascular, respiratory impairments. Overall physiacal and psychological condition


* Keloid
* Proud flesh
* Gangrene
* Adhesions
* Dehiscence
* Evisceration

Wound Classification
* Clean wound
* Clean contaminated wound
* Contaminated wound
* Dirty or infected wound

Wound Healing, Dressing, and Drains.ppt


Management of Keloids

Management of Keloids
By: Thad Riley
Advisor: Bill Grimes

What is a Keloid?
* Non-cancerous fibrous proliferations that occur in the dermis after trauma or injury to the skin
* Keloids grow beyond the boundaries of the original wound site (vs. hypertrophic scar)
* Etiological factors that determine how a scar becomes a keloid remain unknown

Who and Why?
* Individuals with darker-pigmented skin or who freckle are more predisposed
* Seen largely in Africans, African-Americans, Hispanics, and Asians
* Can be a familial/genetic predisposition
* Can be due to immunological causes
* Bottom line… No one knows!

How? (Pathophysiology)
* A result of an overactive inflammatory response and fibroblast proliferation
* A result of an abnormal collagen deposition in healing skin wounds
* Skin wound tension is a contributing factor in keloid formation
* Individuals with an inflammatory or infectious element are at a predisposition for keloids

* Anterior Chest
* Mandibular angle
* Shoulder
* Earlobes
* Upper Arms & Upper Back
* Posterior Neck
* Lateral Neck

So…What’s the Problem?

The Problem
* The pathophysiology of these scars is so poorly understood that it is basically unknown
* Surgery is the only approved treatment
* A successful surgical protocol for removal of these types of scars is greatly lacking
* Surgical treatments available today only provide temporary relief
* Often grow back and do so in an aggressive manner

Possible Solutions
* Surgical excision alone
* Post-surgical treatment agents:
o Mitomycin C solution
o The dietary compound quercetin
o Imiquimod 5% topical cream
o Intralesional corticosteroid injection
o Topical silicone gel sheets

How they work…
* Mitomycin C solution (MC)
o An anti-neoplastic agent
o Has anti-proliferative effects on fibroblasts, stopping keloid formation
o MC effectively blocks angiogenesis during the healing process of the wound, thus inhibiting keloid development
o MC is widely available and relatively cheap
* The dietary compound quercetin
o most common sources: apples, onions, red wine, and ginkgo biloba.
o has strong anticancer, antioxidant, antiviral, anti-inflammatory, and antimicrobial characteristics
o Inhibit keloid fibroblast proliferation, collagen production, and contraction of keloid derived fibroblasts
* Imiquimod 5% topical cream
o Induces apoptosis in keloidal tissue
* Intralesional corticosteroid injection
o Inhibit fibroblast growth and break down collagen deposition
o postoperative steroid injection is the most common form of keloid treatment
o corticosteroids commonly used include hydrocortisone and dexamethasone.
* Topical silicone gel sheets
o Impermeable to water, reduces hemostasis and therefore, decreases the hyperemia and fibrosis often associated with keloids
o have been used for more than twenty years to help reduce the size of scarring
o efficacy and safety of the silicone gel sheets is well established.

And the Winner is…
* Imiquimod 5% topical cream
* 13 keloids from 12 patients were surgically removed
* All keloids were present for at least 1 year and free of any treatment for the past 2 months
* A thin layer of imiquimod 5% cream was applied topically each night for 8 weeks
* 4 week asessments
* At 24 weeks, no keloids had recurred

Pilot study of the effect of postoperative imiquimod 5% cream on the recurrence rate of excised keloids (Berman and Kaufman, 2002 )
* 2 cases of irritation and superficial erosion were reported; resolved with cessation of the cream
* At the 24 week assessment, RECURRENCE RATES of keloids treated with imiquimod 5% cream were LOWER than any previously reported in the literature
* Study did not control for the effects of vehicle application or other potential variables
* Further comparative studies with longer follow-up periods are needed
* Additional studies needed to determine dosing frequency and duration

Pilot study of the effect of postoperative imiquimod 5% cream on the recurrence rate of excised keloids (Berman and Kaufman, 2002 )

* To develop a successful treatment plan for the keloid, two things have to be done:
o 1. Further research to better understand the causes behind keloid formation
o 2. Establish a standard surgical protocol
* In short, the topic of keloids is greatly under-exposed.


Management of Keloids.ppt

All links posted here are collected from various websites. No video or powerpoint files are uploaded on this blog. If you are the original author and do not wish to display your content on this blog please Email me anandkumarreddy at gmail dot com I will remove it. The contents of this blog are meant for educational purpose and not for commercial use. If you use any content give due credit to the original author.

This site uses cookies from Google to deliver its services, to personalise ads and to analyse traffic. Information about your use of this site is shared with Google. By using this site, you agree to its use of cookies.

  © Blogger templates Newspaper III by Ourblogtemplates.com 2008

Back to TOP