01 July 2009

Endocrine Emergencies



Endocrine Emergencies
By:Bobby Oakes


Endocrine Emergencies
* Diabetic Ketoacidosis
* Thyroid Storm
* Adrenal Insufficiency
Diabetic Ketoacidosis (DKA)
Physiology
* Hyperglycemia
* Ketoacidemia
* Fluid and Electrolyte Depletion
Diabetic Ketoacidosis General Considerations
Diabetic Ketoacidosis
* Essentials of Diagnosis
Diabetic Ketoacidosis Clinical Findings
* Symptoms:
* Signs:
Diabetic Ketoacidosis Laboratory Findings
Diabetic Ketoacidosis Treatment
* Insulin Replacement
* Fluid Replacement
DKA vs HHS
* Diabetic Ketoacidosis
* Hyperglycemic Hyperosmolar State
Thyroid Storm
Thyroid Storm Treatment
Acute Adrenal Insufficiency
Acute Adrenal Insufficiency General Presentations
Adrenal Insufficiency Diagnosis
Adrenal Insufficiency Treatment

Endocrine Emergencies.ppt

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Urinary Tract Infections



Urinary Tract Infections
By: Charles S. Bryan, M.D.

Overview of UTI by age and sex
Terms
* Urinary tract infection
* Significant bacteriuria
* Asymptomatic bacteriuria
* Acute pyelonephritis
* Chronic pyelonephritis
* “Upper” versus “lower” UTI
* Urethral syndrome
* UTI: the finding of microorganisms in bladder urine with or without clinical symptoms and with or without renal disease
* Significant bacteriuria: the finding of > 105 cfu/ml of urine (but lower counts can be significant)
* Asymptomatic bacteriuria: Significant bacteriuria without clinical symptoms or other abnormal findings.
* Acute bacterial pyelonephritis: a clinical syndrome of fever, flank pain, and tenderness, often with constitutional symptoms, leukocyte casts in the urine, and bacteriuria; or histologic findings thereof
* Chronic bacterial pyelonephritis: Long-standing infection associated with active bacterial growth in the kidney; or the residuum of lesions caused by such infection in the past
* Chronic interstitial nephritis: renal disease with histologic findings resembling chronic bacterial pyelonephritis but without evidence of infection
* “Upper UTI”: infection above the level of the bladder
* “Lower UTI”: infection at or below the level of the bladder
* “Urethral syndrome”: clinical manifestations of lower UTI (dysuria, frequency, urgency) without significant bacteriuria
* Pyuria: the presence of pus (WBC’s [leukocytes] in urine, which may or may not be caused by UTI. The preferred method for quantitation is enumeration in unspun urine using a counting chamber. The leukocyte esterase nitrite test has a sensitivity of between 70% and 90% for symptomatic UTI

Asymptomatic bacteriuria
Frequency of significant bacteriuria
Screening for significant bacteriuria
Urinary tract bacteriology
Etiology of community-acquired UTI
Etiology of nosocomial UTI
Urease-producing microorganisms
UTI in children
UTI in adults
Role of bacterial virulence in UTI
The role of bacterial virulence (2)
Host defenses: antibacterial properties of urine
Host defenses: anti-adherence mechanisms
Host defenses: miscellaneous
Routes of urinary tract infection
Mechanisms of lower UTI
Mechanisms of upper UTI
Localization of upper versus lower UTI
Acute uncomplicated cystitis in young women
Acute uncomplicated pyelonephritis in young women
White blood cell casts
Recurrent UTIs in women
Complicated UTIs
Catheter-associated UTI
Long-term bladder catheterization
Prostatitis

Urinary Tract Infections.ppt

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Alterations of Renal and Urinary Tract Function



Alterations of Renal and Urinary Tract Function

Urinary Tract Obstruction
* Urinary tract obstruction is an interference with the flow of urine at any site along the urinary tract
* Severity based on:
o Location
o Completeness
o Involvement of one or both upper urinary tracts
o Duration
o Cause
* Hydroureter
* Hydronephrosis
* Compensatory hypertrophy
* Postobstructive diuresis
* Kidney stones
Kidney Stone Formation
Kidney Stones
* Treatment
Lower Urinary Tract Obstruction
Tumors
Urinary Tract Infection (UTI)
Chronic Pyelonephritis
Glomerular Disorders
Nephrotic Syndrome
Acute Renal Failure (ARF)
Chronic Renal Failure

Alterations of Renal and Urinary Tract Function.ppt

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Tubulointerstitial Diseases Terminology



Tubulointerstitial Diseases Terminology

* Tubulointerstitial nephritis:
Tubulointerstitial nephritis Causes
Tubulointerstitial nephritis Pathogenetic mechanisms
Tubulointerstitial nephritis with immune complexes
Cell-mediated mechanism
Pathology of renal failure
acute
chronic
Acute renal failure (ARF)
Causes of ARF
Acute tubular necrosis (ATN)
Acute tubular necrosis
Etiology & Pathogenesis
Gross pathology
Light microscopy
ATN- Prognosis
Chronic renal failure
TUBULO-INTERSTITIAL DISEASE
Pyelonephritis
Acute Pyelonephritis
Predisposing factors
Acute pyelonephritis
Chronic pyelonephritis

Tubulointerstitial Diseases Terminology.ppt

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Pyelonephritis due to S. aureus



Pyelonephritis due to
S. aureus: an unusual case of Toxic Shock Syndrome.
By: Maureen Shevlin Gutierrez, MD
Georgetown University Internal Medicine
Washington, D.C.

Toxic Shock Syndrome (TSS)
* A rare but life-threatening bacterial illness.
* Caused by Staphylococcus aureus or by Group A Streptococcus bacteria.
* Historically, TSS has been a well recognized entity in menstruating females using tampons.
* More recently, TSS has been associated with surgical cases, skin and soft tissue infections, and postpartum complications.
* TSS requires early diagnosis and treatment as the case-fatality ratio is approximately 3% in menstrual cases, and 5% in nonmenstrual cases.

How is the diagnosis made?
* TSS is a clinical diagnosis with 6 criteria:
1. Fever
2. Hypotension
3. Rash
4. Desquamation (1-2 weeks after illness onset)
5. Abnormalities in 3 or more organ systems
6. Negative blood, throat, CSF cultures

Case Presentation
HPI
Physical Exam
Assist Control respiratory support
Laboratories
Imaging
The diagnosis
Staphylococcal Toxic Shock Syndrome
Staphylococcal TSS
Nonmenstrual cases
Literature search
Case fatality ratio
Why is it so virulent?
Virulence = Superantigens
Treatment of TSS
Patient Update
Take home points
* Toxic shock is no longer predominately a disease of menstruating females.
* Almost 50% of cases are nonmenstrual, which include post-surgical procedures, skin and soft tissue infections, and postpartum complications.
* Our literature search revealed that “unusual sites” have previously been reported.
* Our case, along with one other previously reported case, demonstrates that pyelonephritis should be added to this growing list of unusual sites of infection associated with S. aureus TSS.
* Recognition of the syndrome despite the site of infection is crucial to diagnosis and management.
Resources

Pyelonephritis.ppt

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Outpatient Management of Acute Pyelonephritis



Outpatient Management of Acute Pyelonephritis
Dx of Acute Pyelonephritis
* History/Physical exam
* Labs
* Imaging
* Unable to take PO
* Concerns about compliance
* Uncertain of diagnosis
* Sever illness with high fevers, pain, significant debility

Choice of antibiotics
Duration of therapy
Follow-up
Moyamoya Disease
Epidemiology
Clinical Features
* Ischemic events
* Hemorrhagic stroke
* Epilepsy

Outpatient Management of Acute Pyelonephritis.ppt

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Acne Vulgaris - known as blackheads



Acne Vulgaris
(Otherwise known as zits, pimples and blackheads)
By: Cynthia Salinas, M.D.

Conference Goals
* Review pathogenesis as a way to help us understand why we use certain meds
* Differentiate common types of acne
* Generate a quick differential diagnosis
* Apply a stepwise approach to treatment prior to referral to dermatology

Epidemiology
Onset?
Prevalence?
Causes?
Pathogenesis
HPI
Differential Diagnosis
Types of Acne
Comedonal Acne
Papulopustular Acne
Nodulocystic Acne
Management
Four Major Goals of Treatment
Take home points:
Retinoids
Topical Antibiotics
Other
Comedonal Acne
Papulopustular Acne
Oral antibiotics
Nodulocystic Acne
Education
Completing Therapy
Follow-up on Patient
Conclusions
Sources

Acne Vulgaris.ppt

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Cosmetic Dermatology in Primary Care



Cosmetic Dermatology in Primary Care
by: Jenifer Hammond MD

What is Skin?
* A protective, yet permeable barrier for the human body
* Body’s largest organ
* Most essential source of sensory stimulation

Three layers of skin
* Epidermis
* Dermis
* Subcutaneous fat (hypodermis)

Facts of Aging Skin
Clinical Signs of Aging Skin
Clinical Signs of Photoaging Skin
FACTS about PhotoAging
Photodamaged Skin
What is the treatment for Photoaging Skin?
You Are What You Eat!
What is Good Skin Care?
Exfoliate
Microdermabrasion
Hydrate
Protect
Skin Cancer Facts 2007
Topical C
Prevage MD
UVB Protection
Sun Protection Tips
UVA protection “What’s New”
Sunscreen
Retinoids
Rejuvenation Procedures
Peels
What are Chemical Peels?
Types of Peels
Glycolic Acid (AHA)
Jessnar’s Peel
TCA Peel
Facial Fillers
Collagen
Collagen Lip Augmentation
Hyaluronic Acids
Juvederm
Radiesse
Marionette before After 3 months
Nasolabial before After 3 months
Cheeks before After 3 months
Sculptra
Before Sculptra
Sculptra after 3 treatments
Lasers
IPL Photo-Facial
IPL with Levulan Therapy
Laser Hair Removal
“What’s New”
Ablative & Non-Ablative Skin Resurfacing
Mechanism of Light-induced Skin Rejuvenation
Light absorption by tissue water
Inflammatory response
Release of inflammatory mediators into dermal interstitium
Aesthetica Cosmetic & Laser Center
Non-ablative tissue tightening

Cosmetic Dermatology in Primary Care.ppt

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Acne



Acne
By: David M. Bracciano, D.O.

Acne Vulgaris
* Chronic inflammatory disease of the pilosebaceous follicles
* Comedones, papules, pustules, cysts, nodules, and often scars
* Face, neck, upper trunk, and upper arms
* Disease of the adolescent
* 90% of all teenagers
* May also begin in twenties
* Usually involution by 25
* Occurs primarily in oily{seborrheic} areas of the skin
* Face occurs; cheeks> nose>forehead>chin
* Ears; comedones in concha, cysts in lobules
* Retroauricular and nuchal cysts

Comedo
* Commonly known as the blackhead
* Basic lesion of acne
* Produced by hyperkeratosis of the lining of the follicles
* Retention of keratin and sebum
* Plugging produced by the comedo dilates the mouth of the follicle
* Papules are formed by inflammation around the comedones

Severity of Acne
* Typical mild acne; comedones predominate
* More severe cases; pustules and papules predominate, heal with scar if deep
* Acne Conglobata; suppurating cystic lesions predominate, and severe scarring results
Types
* Acne comedo; mild case were eruption is composed almost entirely of comedones on an oily skin
* Papular acne; inflammatory papules, most common in young men with coarse, oily skin
* Atrophic acne; residual atrophic pits and scars
Etiology
* Keratin plug in lower infindibulum of hair follicle
* Androgenic stimulation of sebaceous, proliferation of propionbacterium acnes which metabolizes sebum to produce free fatty acids
Pathogenesis
* Disruption of the follicular epithelium permits discharge of the follicular contents into the dermis
* Causes the formation of inflammatory papules, pustules, and nodulocystic lesions
* FFA are chemotactic to components of inflammation
* Effects of tetracycline are obtained by the reduction of FFA
* Antibiotics do not produce involution of the inflammatory lesions present, but inhibit the formation of new lesions
* Topical retinoic acid acts on keratinization, causing horny cells to lose their stickiness
* Androgens enlarge the sebaceous glands
* In women consider hyperandrogenic state

Histology
Treatment
Antibacterials
Tetracyclines
Minocycline
Bacterial Resistance
Oral Contraceptives
Hormonal Therapy
Isotretinoin
Topical Treatment
Benzoyl Peroxide
Topical Retinoids
Topical Antibacterials
Other Topicals
Surgcial Treatment
Intralesional Corticosteroids
Complications of Acne
Acne Conglobata
Acne Fulminans
SAPHO Syndrome
Tropical Acne
Premenstrual Acne
Preadolescent Acne
Neonatal Acne
Infantile Acne
Acne Venenata
Acne Cosmetica
Acne Detergicans
Acne Aestivalis
Excoriated Acne
Acneiform Eruptions
Gram Negative Folliculitis
Acne Keloidalis
Hiradenitis Suppurativa
Perifolliculitis Capitis Abscedens
Acne vs. Rosacea
Ocular Rosacea
Granulomatous Rosacea
Rosacea Etiology
Differential Diagnosis Rosacea
Inflammatory rosacea
Rosacea Treatment
Rosacea Rhinophyma
Pyoderma Faciale
Perioral Dermatitis

Acne.ppt

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Dermatology



Dermatology
By: Katrice L. Herndon, MD
Internal Medicine/Pediatrics

Acne Vulgaris

* Acne is a self-limited disorder primarily of teenagers & young adults.
* Acne is a disease of pilosebaceous follicles.
* 4 factors are involved:
* External Factors that contribute to Acne
* Acne vulgaris typically affects those areas of the body that have the greatest number of sebaceous glands:
* In addition to the typical lesions of acne vulgaris, scarring and hyperpigmentation can also occur.
* Hyperpigmentation is most common in patients with dark complexions
* Classification of Acne

Acne Vulgaris What is this?

Acne Rosacea
* Rosacea is an acneiform disorder of middle-aged and older adults.
* Characterized by vascular dilation of the central face, including the nose, cheek, eyelids, and forehead.
* The cause of vascular dilatation in rosacea is unknown.
* The disease is chronic.
* rosacea is a chronic disorder characterized by periods of exacerbation and remission.
* Increased susceptibility to recurrent flushing reactions that may be provoked by a variety of stimuli including hot or spicy foods, drinking alcohol, temperature extremes, and emotional reactions.
* The earliest stage of rosacea is characterized by facial erythema and telangiectasias.
* Patients with rosacea may develop severe sebaceous gland growth that is accompanied by papules, pustules, cysts, and nodules.
Allergic Contact Dermatitis
Psoriasis
Psoriasis Treatment
Vitiligo
Pityriasis Rosea
Cellulitis
Erysipelas
Ecthyma
Treatment
Tinea Vesicolor
Cutaneous Warts
Differential Diagnosis
Secondary Syphilis
Treatment
Herpes Zoster
Treatment
Actinic Keratosis
References

Dermatology.ppt

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30 June 2009

Children and Adolescents with Bipolar Disorder



Children and Adolescents with Bipolar Disorder
By: Boris Birmaher MD
Department of Child Psychiatry
Western Psychiatric Institute and Clinic
University of Pittsburgh Medical Center

Do children and adolescents have Bipolar Disorder (BP)?
Bipolar Disorder in Youth
Clinical Manifestations
Bipolar Disorder – Classical Clinical Manifestations
DSM-IV Manic episode
DSM-IV Hypomanic episode
Bipolar Disorder Clinical Manifestations
DSM-IV Major depression episode
Subtypes of Bipolar Disorder
Bipolar I disorder
o Manic
o Depressed
o Mixed
o Rapid cycling
o Psychotic

Bipolar II disorder (hypomania and MDD episodes)
Cyclothymic disorder (hypomania and mild depressions)
Bipolar Not Otherwise Specified (NOS)
Difficulties Diagnosing Pediatric Bipolar Disorder
Developmental Manifestations of Manic Symptoms in Children
To clarify the diagnosis:
Retrospective Studies of Adults with BP-I
Frequent Prodromal Features Before Onset of BP-I
WPIC Child Mood & Anxiety Disorder Outpatient Clinic
Hamilton Depression Scores
Child & Adolescent Bipolar Services (CABS)
Course and Outcome of Bipolar Youth (COBY)
Demographics (COBY) (Cont’)
COBY Subjects – Lifetime Presence of Psychiatric Diagnoses
Prepubertal Bipolar Disorder
In General, BP in youth can presented as:
* Typical phenotype (DSM Bipolar I and II)
o Many have frequent episodes and mixed bipolar episodes
* Typical phenotype but for a short time (DSM-IV BP NOS or rapid cycling)
o Many have frequent episodes and mixed episodes
* Broad phenotype (DSM-IV BP NOS or rapid cycling)
Clinical Manifestations - Questions?
In addition to different subtypes of BP disorder, severity of symptoms, and rapid changes in symptomatology it is difficult to diagnose BP in children because:

1) Coexisting disorders
2) Overlap in symptoms with other disorders
Bipolar Disorder - Comorbidity
Bipolar Disorder - Differential Diagnoses
Diagnostic Overlap between Mania & ADHD
DSM-IV Criteria
Hyperactivity / goal-directed activity
DSM-IV Criteria
Distractibility
Inflated self-esteem / grandiosity Commonly associated
Epidemiology
BP-I Natural Course Multicenter
Pilot Study
BPD-I Natural Course
Course and Outcome of Bipolar Youth (COBY)
Diagnosis at Intake:
Bipolar Disorder - Natural Course
Natural Course General Conclusions
Sequela
Bipolar Disorder - Sequela
Pediatric Bipolar Disorder - WPIC Mood & Anxiety D/O Outpatients
Pediatric Bipolar Disorder Oregon Study
Predictors of Bipolar Disorder
Bipolar Disorder- Family Studies
Children of Parents with BP
NIMH-Bipolar Offspring Study (BIOS)
Bipolar Offspring Study (BIOS) Instruments
BIOS - SAMPLE
BIOS - Demographics – Offspring Preliminary Analyses
BIOS- Probands
Lifetime Disorders
BIOS- Offspring of BP parents-Lifetime Disorders- Definite/Probable
Any Substance/alcohol
Offspring of BP vs. Controls-CBCL Scores
Treatment
Bipolar Disorder - Psychoeducation
Pharmacological Treatment
Divalproex Treatment for Bipolar Disorder
Lithium for Adolescents with Acute Mania
Side Effects/Laboratory Tests Prior and During Psychopharmacological Treatment
Check for presence of “side effects” prior to starting treatment
Bipolar Depression - Treatment
Psychosocial Treatments
Family-Focused Treatment of Bipolar Disorder
Family-Focused Treatment for Adolescent Bipolar Patients
Interpersonal and Social Rhythms Therapy (IPSRT)
Bipolar Disorder – Treatment Other Considerations
Bipolar Disorder- Conclusions

Children and Adolescents with Bipolar Disorder.ppt

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Depression: A Brief Overview of the Disorder in Childhood



Depression: A Brief Overview of the Disorder in Childhood
By: James H. Johnson, Ph.D., ABPP
University of Florida

Case Examples
Childhood Depression:
History
Acceptance of Depression as a Child Disorder
Child Depression Lite
DSM IV CRITERIA: Major Depressive Episode
Major Depressive Episode
Major Depressive Disorder
Anxiety Versus Depression
Childhood Depression:
Prevalence
Comorbidity
Prognosis: Initial Recovery
Prognosis: Recurrence
Etiology: Conceptual Models of Depression
Psychoanalytic Views
The Role of Life Stress
Specific Life Stressors
Cognitive/Behavioral Views
Examples of Cognitive Distortions
Cognitive/Behavioral Views
Behavioral Views
Learned Helplessness and Depression
Learned Helplessness
Cognitive/Behavioral Views: Child Research Findings
Research Findings
Biological Perspectives
Genetic Factors
Other Biological Findings
Treatment of Childhood Depression
Interpersonal Therapy
Cognitive Behavior Therapy
Psychotropic Medications
Combination Therapies
Treatment: Final Comments

Depression: A Brief Overview of the Disorder in Childhood.ppt

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Mood Disorder



Mood Disorder
* Depressive disorders
Major depressive disorder (MDD)
Dysthymic disorder
* Biopolar Disorder
* Mood disorder due to a medical condition
* Substance-induced mood disorder

Psychopathology of Mood Disorders - Depression
* Not diagnosed or misdiagnosed - a lot
* Prevalence - 9-20% in general population
* Female - 10-20%; male - 5-12% (life time)
* Recurrence rate - 50% - 80%
* Seeking professional help - 16-23%
* Suicide rate

Assessment
* History of onset
* Comorbid substance - alcohol, med.
* Physical examination - senile, meta. dis.
* Non mood psychiatric disorders
* Stress level, coping & social support
* Presence and/or level of suicidal ideation
* Others - measurement scales, biological measures (cortisol, hormone, sleep pattern)

Measures of Depression (I)
Measures of Depression (II)
Diagnosis Criteria for Depression
Dysthymic Disorder
Diagnosis Criteria for Major Depression
Etiology of Depression
Genetic theory
Cultural, age, gender considerations
Depression in Children
Predisposing factors in Children and adolescents
Depression in Women
Depression in Men
Depression and the Elderly
Predictors for elderly suicide
Diagnostic Evaluation
Treatment of Depression
Nursing Diagnoses related to Mood Disorders
Assessment for Suicidal behavior
Suicide Prevention
Interventions
Interventions (II)
Monitor the side-effect of antidepressant
* Energy & motivation↑ -suicide tendency ↑
* Drug-drug & food-drug interactions
* Toxicity of the medications
* TCAs – drowsiness, agitation, tachycardia
* MAOIs – dizziness, fatigue, vertigo
* SSRIs – nausea, vomiting, tremor
* Lithium – diarrhea, muscle weakness, atxia; lag time 7-10 days
Biopolar Disorders
Young & Biopolar
Checklist for the Bioplar Child
Criteria for Bipolar Disorders - Manic episode
Manic Genius
Tendencies of Manic Patients
Etiology of Bipolar Disorders
Intervention - Bipolar Disorders
Interventions for suicidal pts
Self-help
Family and friends can help
Where to get help

Mood Disorder.ppt

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Bipolar Disorder in DSM-IV



Bipolar Disorder in DSM-IV
* Bipolar I disorder: manic episode(s)
or mixed episode(s) plus MDE(s)
* Bipolar II disorder: major depressive episode(s) plus hypomanic episode(s)
* Cyclothymia: hypomanic symptoms
plus depressive symptoms

Bipolar Disorders: DSM-IV Nosology
Criteria
Mania
Hypomania
Major depression
Mixed state
BPD I
BPD II
Manic Episode: Diagnostic Criteria
Manic Episode: Differential Diagnoses
Hypomanic episode
Mixed episode
History of treatment for depression
Differential diagnosis
* Physical
* Psychological
Mixed Episode: Diagnostic Criteria
Characteristics BPD I BPD II
Ethnic/racial differential
Gender differential M = F F›M (?)
Bipolar Disorders: Epidemiology
Characteristics BPD I BPD II
Bipolar Disorders: Epidemiology
Epidemiology
Diagnostic Dilemmas:
Unipolar Versus Bipolar
Unipolar
Etiology
Heritability
ADOPTION STUDIES
Cognitive Deficits
* Working memory
* Sustained attention
* Abstract reasoning
* Visuomotor skills
* Verbal memory
* Verbal fluency
* Cognitive flexibility
* General cognitive functioning
Potential Explanations for Cognitive Deficits
* Iatrogenic or Alcohol use
* Temporary functional changes
* Degenerative brain changes
* Permanent structural lesions
* Permanent functional alterations of neural networks underlying affect and cognition

Alcohol Use
Iatrogenic
Temporal Functional Deficits
Summary

Bipolar Disorder in DSM-IV.ppt

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Psychiatric disorders



Psychiatric disorders
By: * Peter Liddle * Chris Rorden

Disorders of Mind & Brain
* Mind and brain are two sides of one coin; disorders of the mind are disorders of the brain.
* Particular clusters of symptoms (syndromes) tend to occur together in various different mental illnesses
* The ways in which symptoms cluster together tells us something about the structure of the human mind and brain

Anatomy of psychiatric disorders
* Contemporary psychiatry implicates neurotransmitters rather than anatomy.
o Schizophrenia :: dopamine
o Depression :: serotonin
* To some degree, this may reflect the popular treatments – neurotransmitters specific to brain regions.

Major symptom clusters
* Reality distortion
* Disorganization
* Psychomotor poverty
* Psychomotor excitation
* Depression
* Euphoria
* Anxiety

Reality distortion

* Mismatch between representation of reality in individual’s mind and representation supported by objective evidence
* Hallucinations and delusions
* Hallucination: perception with quality of a sensory perception but nor derived form stimulation of a sense organ
* Delusion: fixed belief derived by erroneous inference or unjustified assumption that cannot be accounted for by culture or religion

Delusions
* Delusions usually false but the key issue is lack of rational grounds and fixity.
* Ability to engage in logical deduction about other issues is usually intact; certain ideas seem exempted from the need for logic.
* Non-psychotic distortions of reality (eg in OCD or in non-psychotic depression) reflect biased thinking but are less resistant to debate

Psychotic Reality Distortion
* Can occur in schizophrenia, mania, psychotic depression, brain injury or degeneration
* Themes: persecution; alien control, religion, grandiosity, guilt
* Influenced by culture, but some themes are common across cultures

Reality distortion in schizophrenia
* Characteristic forms (but not present in every case)
* Less specific but common forms:

Affective psychosis
* Mood disorder with psychotic features is diagnosed if psychotic illness is dominated by mood symptoms unless there is reality distortion without substantial mood symptoms for at least two weeks
* Delusions and hallucinations are usually mood congruent (eg guilt, worthlessness, critical voices with depressed mood; grandiose delusions and self-reinforcing halluciations in mania)
* Reality distortion shows similar response to antipsychotic medication irrespective of diagnosis

Neuropsychological correlates of reality distortion
* Reality Distortion can occur in absence of general defect in reasoning.
* Defective internal monitoring of self-generated mental activity (Frith & Done 1989; Mlakar et al, 1994)
* Jumping to conclusions – the bead test (Huq et al, 1988)
* Patients with persecutory delusions tend to attribute negative outcomes to external causes (Bentall, 1994)

Regional cerebral activity and reality distortion
Neurochemistry and pharmacology of reality distortion
Pharmacology of reality distortion
Hypothesis for generation of reality distortion
Disorganization syndrome
Neuropsychological correlates of disorganization
Regional cerebral activity and disorganization
Psychomotor poverty and excitation
Neuropsychological correlates of psychomotor poverty
Psychomotor poverty and brain structure
Neurochemistry & pharmacology of psychomotor poverty
Neurochemistry & pharmacology of psychomotor excitation
Depression & Elation
Mood disorders
Neuropsychological correlates of depression
Brain structure and mood disorders
Regional cerebral activity and depression
Regional cerebral activity associated with elation
Regional cerebral metabolism in bipolar disorder
Neurochemistry and pharmacology of mood disorders
Bipolar affective disorder
Anxiety
Regional cerebral activity associated with anxiety
Pharmacology of anxiety
Concepts of schizophrenia
Reality distortion
Characteristic time course
ICD 10 diagnostic criteria
Aetiology : predisposing factors
Brain structure in schizophrenia
Cognitive deficits in schizophrenia
Pharmacology
Bipolar mood disorder
Genetics
Aetiology of bipolar disorder
Ventricular enlargement
Anatomy of bipolar disorder
Pharmacology of bipolar disorder
Psychopathy
Aetiology of psychopathy
Cognition and information processing in psychopathy

Psychiatric disorders.ppt

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Rett’s Disorder



Rett’s Disorder
By:By: Natalie Sten

An Overview of Rett Syndrome for Professionals
Possibly the leading cause of mental retardation and neurodevelopmental impairment in females.

After this seminar you will be able to:

* List the warning signs and symptoms of Rett Syndrome.
* Describe how to cope with children with Rett Syndrome and what the most important aspects of treatment are.
* State how school dynamics can play a critical role in the development of children with Rett Syndrome.

GLOSSARY
* Rett Syndrome (RS): A neurodevelopmental disorder that is classified as a pervasive developmental disorder
* Pervasive Development Disorders (PDD): Refers to a group of five disorders characterized by delays in the development of multiple basic functions including socialization and communication.
* Apraxia: A neurological disorder characterized by loss of the ability to execute or carry out learned purposeful movements, despite having the desire and the physical ability to perform the movements.
* Respite Care: The provision of short-term, temporary relief to those who are caring for family members who might otherwise require permanent placement in a facility outside the home.

What is diagnostic criteria for Rett Syndrome?
* Diagnostic Criteria for 299.80 Rett's Disorder
All of the following:
o apparently normal prenatal and perinatal development
o apparently normal psychomotor development through the first 5 months after birth
o normal head circumference at birth
o deceleration of head growth between ages 5 and 48 months
o loss of previously acquired purposeful hand skills between 5 and 30 months with the subsequent development of stereotyped hand movements (e.g., hand-wringing or hand washing)
o loss of social engagement early in the course ( although often social interaction develops later)
o appearance of poorly coordinated gait or trunk movements
o severely impaired expressive and receptive language development with severe psychomotor retardation

RS is Associated with PDDs or Autistic Spectrum Disorder
* Autism, also called autistic disorder, is a complex developmental disability that appears in early childhood, usually before age 3.
* Autism prevents children and adolescents from interacting normally with other people and affects almost every aspect of their social and psychological development.

How is Rett Syndrome Associated with Autism?
* Girls with RS often have autistic-like characteristics (speech & emotional contact impairment/ repetitive hand gestures) at an early age but differences begin to occur as the child continues to grow.

* The critical difference is the gene mutation that is defining of RS. However, females meeting criteria for RS do not meet the symptoms for autism.

Symptoms seen in RS that are NOT seen in Autism are:
* Deceleration of the rate of head growth
* Loss of purposeful hand skills
* Mobility or the irregular breathing patterns
* Repertoire of purposeless hand stereotypes
* Children with RS almost always prefer people to objects
* Children with RS often enjoy affection

Who is affected by RS?
Warning Signs and Symptoms:
There are 4 stages in the child’s development:
* Stage 1: Early Onset (6-18 months)
* Stage 2: Rapid Destructive (1-4 yrs old)
* Stage 3: Plateau (2-10 yrs. old)
* Stage 4: Late Motor Deterioration (Usually after age 10)

Do biological factors play a role?
Rett Syndrome:
Is a neurodevelopmental disorder that is quite rare. It causes a genetic mutation, linked to the X chromosome, which affects the production of a vital protein that controls brain development.
School dynamics associated with students with RS:
* A secure emotional environment is the first, most important aspect of a teaching environment so that children feel safe.
* Children with RS could be placed in a variety of classrooms from special education units to full inclusion according to their own individual needs and abilities.
* Structured, stimulating, restrictive-free classroom environments with direction and organization are necessary.
Interventions must be created based on the individualized needs of the child!

What can families do?
Stimulating environments at home:
Can you think of some emotionally motivating movements that could occur automatically?
It’s the Law in Pennsylvania

How you can help:
Parents and professionals can expect difficulties. What can help you cope?
* Talk about it.
* Be gentle with yourself.
* Learn how to ask for help.
* Trust your instincts.
* Learn to let go and to accept what can’t be changed.
TREATMENT
Therapies Include:
* Aquatic Rehabilitation
* Hydrotherapy
* Love Therapy
* Music Therapy
* Physical Therapy
* Therapist's Role
* Behaviors
* Hippotherapy
* Motor Development
* Occupational Therapy
* Speech Therapy

Where to go for more info?
1) International Rett Syndrome Association www.rettsyndrome.org
2) NIH/National Institute of Neurological Disorders and Stroke
www.ninds.nih.gov
3) National Institute of Child Health and Human Development (NICHD)
www.nichd.nih.gov
References

Rett’s Disorder.ppt

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28 June 2009

Chronic Kidney Disease



Chronic Kidney Disease
By:Justin A. Glass, MD
Emory Family Medicine

Objectives
* CKD o Definition
o Epidemiology
o Management

Literature sources
Normal Kidney Function
* Regulation of fluid / electrolyte balance
* Regulation of blood pressure
* Regulation of red cell mass
* Regulation of calcium / phosphate metabolism
* Renal hormones
o Renin
o Bradykinin
o Prostaglandins (PGE2 / PGI2)
o Erythropoietin
o Calcitriol

Definition of CKD
* Chronic Kidney Disease (CKD)
* Kidney Damage
o Proteinuria
o Abnormal urine sediment
o Abnormal serum or urine chemistries
o Abnormal imaging study

Proteinuria
Abnormal Sediment
Definition: Chronic Kidney Disease
Renal Function Measurement
Classification of CKD
* Stage 0: At risk patients
* Stage 1: Kidney damage w/ normal GFR
* Stage 2: GFR 60-89
* Stage 3: GFR 30-59
* Stage 4: GFR 15-29
* Stage 5: GFR <15 or dialysis
CKD: Burden of disease
* Definitions (expanded)
Risk Factor Modification
CKD: Cause
Prevention of progression
Complications of CKD
Anemia due to CKD
Anemia in CKD
Anemia in CKD: Treatment
Bone Disease in CKD
Hypertension in CKD
Cardiovascular Disease in CKD
CVD Prevention in CKD
When to refer?

Chronic Kidney Disease.ppt

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GOUT



GOUT
By:
Wayne Blount, MD, MPH
Professor, Emory Univ. S.O.M.

OBJECTIVES

* Identify diagnostic criteria for gout
* Identify 3 treatment goals for gout
* Name the agents used to treat the acute flares of gout and the chronic disease of gout


Why Worry About Gout ?
* Prevalence increasing
* May be signal for unrecognized comorbidities : ( Not to point of searching)
Obesity (Duh!)
Metabolic syndrome
DM
HTN
CV disease
Renal disease

URATE, HYPERURICEMIA & GOUT
* Urate: end product of purine metabolism
* Hyperuricemia: serum urate > urate solubility (> 6.8 mg/dl)
* Gout: deposition of monosodium urate crystals in tissues

HYPERURICEMIA & GOUT
* Hyperuricemia caused by
Overproduction
Underexcretion
* No Gout w/o crystal deposition
THE GOUT CASCADE
* Urate
* Oevrproduction Underexcretion
* Silent Gout Renal Associated
* Tissue manifestations CV events &
* Deposition mortality

GOUT: A Chronic Disease of 4 stages
* Asymptomatic hyperuricemia
* Acute Flares of crystallization
* Intervals between flares
* Advanced Gout & Complications

ACUTE GOUTY FLARES
SITES OF ACUTE FLARES
INTERVALS SANS FLARES
FLARE INTERVALS
ADVANCED GOUT
* Chronic Arthritis
* X-ray Changes
* Tophi Develop
* Acute Flares continue
* Chronic Arthritis
* Polyarticular acute flares with upper extremities more involved

TOPHI
TOPHI RISK FACTORS
RADIOLOGIC SIGNS
X-RAYS
DIAGNOSING GOUT
SERUM URATE LEVELS
GOUT RISK FACTORS
DIFFERENTIAL DIAGNOSIS
* Pseudogout: Chondrocalcinosis, CPPD
* Psoriatic Arthritis
* Osteoarthritis
* Rheumatoid arthritis
* Septic arthritis
* Cellulitis
Gout vs. CPPD
RA vs Gout
REDNECK MEDICAL TERMS
TREATMENT GOALS
ENDING ACUTE FLARES
Acute Flare Med Choices
MED Considerations
PROTECTION VS. FUTURE FLARES
PREVENT DISEASE PROGRESSION
URICOSURIC AGENTS
XANTHINE OXIDASE INHIBITOR
WHICH AGENT ?
NEW AGENTS
URICASE ENZYMES
CASE STUDIES
WHAT ARE J.F.’s RISK FACTORS FOR GOUT ?
HOW WOULD YOU DX GOUT ?
NEXT STEP FOR J.F. ?
IN WHAT STAGE OF GOUT IS M.B. ?
WOULD YOU CHANGE MD’S RX ?
WHAT OTHER ISSUES WOULD YOU CONSIDER ?
CONCLUSIONS

GOUT.ppt

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Celiac Disease



Celiac Disease
By:Lianne Beck, MD
Assistant Professor
Emory Family Medicine

Celiac disease
* Autoimmune disorder with a prevalence of approximately 0.5 to 1 percent in the United States. (1 in every 100-200 persons)
* Inappropriate immune response to the dietary protein gluten, which is found in rye, wheat, and barley.
* After absorption in the small intestine these proteins interact with the antigen-presenting cells in the lamina propria causing an inflammatory reaction that targets the mucosa of the small intestine.
* Manifestations range from no symptoms to overt malabsorption with involvement of multiple organ systems and an increased risk of some malignancies.
* Most all patients with celiac disease express human leukocyte antigen (HLA)-DQ2 or HLA-DQ8, which facilitate the immune response against gluten proteins
* Concordance rates of 70 to 75 % among monozygotic twins and 5 to 22 % among first-degree relatives.

Risk Factors for Celiac Disease
Dermatitis Herpetiformis
Signs and Symptoms
* Common
o Diarrhea
o Fatigue
o Borborygmus
o Abdominal pain
o Weight loss
o Abdominal distention
o Flatulence
* Uncommon
o Osteopenia/ osteoporosis
o Abnormal liver function
o Vomiting
o Iron-deficiency anemia
o Neurologic dysfunction
o Constipation
o Nausea

Differential Diagnosis of Celiac Disease
* Anorexia nervosa
* Autoimmune enteropathy
* Bacterial overgrowth
* Collagenous sprue
* Crohn's disease
* Giardiasis
* Human immunodeficiency
virus enteropathy
* Hypogammaglobulinemia
* Infective gastroenteritis
* Intestinal lymphoma
* Irritable bowel syndrome
* Ischemic enteritis
* Lactose intolerance
* Pancreatic insufficiency
* Soy protein intolerance
* Tropical sprue
* Tuberculosis
* Whipple's disease
* Zollinger-Ellison syndrome

* Consider testing in symptomatic patients at high risk for celiac disease with any of the following conditions:
o Autoimmune hepatitis
o Down syndrome
o Premature onset of osteoporosis
o Primary biliary cirrhosis
o Unexplained elevations in liver transaminase levels
o Unexplained iron deficiency anemia

Test selectively as part of the medical evaluation when symptoms could be secondary to celiac disease:
o Autoimmune thyroid disease
o Cerebellar ataxia
o First- or second-degree relative with celiac disease
o Irritable bowel syndrome
o Peripheral neuropathy
o Recurrent migraine
o Selective immunoglobulin A deficiency
o Short stature (in children)
o Sjögren's syndrome
o Turner's syndrome
o Type 1 diabetes mellitus
o Unexplained delayed puberty
o Unexplained recurrent fetal loss

SEROLOGY
* Serum immunoglobulin A (IgA) endomysial antibodies and IgA tissue transglutaminase (tTG) antibodies. Sensitivity and specificity > 95%.
* Testing for gliadin antibodies is no longer recommended because of the low sensitivity and specificity for celiac disease.
* The tTG antibody test is less costly because it uses an enzyme-linked immunosorbent assay; it is the recommended single serologic test for celiac disease screening in the primary care setting.
* When the prevalence is low, as in the general U.S. population, the risk of a false-positive result is high even with an accurate test . PPV 49.7%, NPV 99.9%
* Confirmatory testing, including small bowel biopsy, is advised.

SMALL BOWEL BIOPSY
Normal small intestine
Villous atrophy
Normal villi
Patient presents with symptoms of celiac disease
Perform serologic IgA tTG antibody testing
High clinical suspicion?
Low probability of celiac
Evaluation for Celiac Disease
Treatment
COMORBIDITIES
Follow-up
Screening
SORT: KEY RECOMMENDATIONS FOR PRACTICE
Key clinical recommendation Evidence rating
Quiz
Reference

Celiac Disease.ppt

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Hyponatremia



Hyponatremia
By:James Yost, MD, MS, MBA
Emory Family Medicine

Hyponatremia
* Definition
* Epidemiology
* Physiology
* Pathophysiology
* Types
* Clinical Manifestations
* Diagnosis
* Treatment

* Definition:
o Commonly defined as a serum sodium concentration 135 meq/L
o Hyponatremia represents a relative excess of water in relation to sodium.
* Epidemiology:
* Physiology
o Serum sodium concentration regulation:
+ stimulation of thirst
+ secretion of ADH
+ feedback mechanisms of the renin-angiotensin-aldosterone system
+ renal handling of filtered sodium
+ Aldosterone

* Pathophysiology
Hypovolemic hyponatremia
* Nonrenal loss
* Renal Loss
Euvolemic hyponatremia
Redistributive hyponatremia
* Pseudohyponatremia
* Clinical Manifestations
* Diagnosis
* Laboratory tests
* Treatment
* Symptomatic or Acute
* IV Fluids
* Example:
* Asymptomatic or Chronic

Hyponatremia.ppt

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Endometrial Biopsy



Endometrial Biopsy
By:Lianne Beck, MD
Assistant Professor
Emory Family Medicine

Indications
* Abnormal uterine bleeding: postmenopausal bleeding, malignancy/hyperplasia, ovulation/anovulation, HRT
* Evaluation of patient with one year of presumed menopausal amenorrhea
* Assessment of enlarged utereus (combined with US and neg HCG)
* Monitoring adjuvant hormonal tx (tamoxifen)
* Evaluation of infertility
* Abnormal Pap smear with atypical cells favoring endometrial origin (AGUS)
* Follow-up of previously diagnosed endometrial hyperplasia
* Cancer screening (e.g., hereditary nonpolyposis colorectal cancer)
* Inappropriately thick endometrial stripe found on US
* Endometrial dating


Contraindications
* Pregnancy
* Acute PID
* Clotting disorders (coagulopathy)
* Acute cervical or vaginal infections
* Cervical cancer

Conditions Possibly Prohibiting Endometrial Biopsy
* Morbid obesity
* Severe pelvic relaxation with uterine descensus
* Severe cervical stenosis

Equipment
* Non-sterile Tray (Examination for Uterine Position)
o Nonsterile gloves
o Lubricating jelly
o Absorbent pad to place beneath the patient on the examination table
o Formalin container (for endometrial sample) with the patient's name and the date recorded on the label
o 20 percent benzocaine (Hurricaine) spray with the extended application nozzle *
* Optional Equipment
* Sterile Tray for the Procedure
o Sterile gloves
o Sterile vaginal speculum
o Uterine sound
o Sterile metal basin containing sterile cotton balls soaked in povidone-iodine solution
o Endometrial suction catheter
o Cervical tenaculum
o Ring forceps (for wiping the cervix with the cotton balls)
o Sterile 4 x 4 gauze (to wipe off gloves or equipment)

Procedure
* Patient in lithotomy position, bimanual exam to determine uterine size, position, uterocervical angulation.
* Insert sterile speculum.
* Clean cervix with povidone-iodine solution.
* Sound the uterus. If needed, use tenaculum, grasping the anterior lip of cervix, for counter-traction.
* Pull outward with tenaculum to straighten the uterocervical angle.
* Insert sound to the fundus, using steady moderate pressure. Usually measure 6-8 cm.

* May need cervical dilators if sound will not pass through internal os.
* Insert sterile endometrial biopsy catheter tip into cervix to the fundus, or until resistance is felt, avoiding contamination from nearby tissues.
* Fully withdraw the internal piston on the catheter, creating suction at the catheter tip.
* Obtain tissue by moving with an in-and-out motion and using a 360-degree twisting motion. Allowing tip to exit endometrial cavity will lose suction.
* Once the catheter fills with tissue, withdraw it, and place sample in the formalin container, by pushing piston back into the catheter tip. Make a second pass if necessary.
* Remove tenaculum, apply pressure to any bleeding, then remove speculum.
Follow Up
* Normal endometrial
o Proliferative (estrogen effect or preovulatory)
o Secretory (progesterone effect or postovulatory)
* Atrophic endometrium
o Hormonal therapy
* Cystic or simple hyperplasia w/o atypia
o Progress to cancer is < 5%
o Hormonal manipulation (medroxyprogesterone [Provera], 10 mg daily for five days to three months)
o Close follow-up w/ repeat EBx in 3-12 months
* Atypical complex hyperplasia
o Progresses to cancer in 30 to 45 %
o D&C to exclude endometrial cancer
o Consider hysterectomy for complex or high-grade hyperplasia.
* Endometrial carcinoma
o Referral to a gynecologic oncologist for definitive surgical therapy.

Pitfalls/Complications
References

Endometrial Biopsy.ppt

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ACC Heart Failure Guideline



ACC Heart Failure Guideline
Prepared by:
Hitinder S. Gurm, MBBS, FACC
Kim Eagle, MD, FACC

Twenty Points to Remember from the
2007 UA/NSTEMI Guideline Update

Based on the ACC/AHA Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction

A Report of the ACC/AHA Task Force on Practice Guidelines Writing Committee to Revise the 2002 Guidelines for the Management of Patients with Unstable Angina/Non-ST-Elevation Myocardial Infarction

ACC Heart Failure Guideline

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