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TWU FHN 3 Test 1

Chronic illnesses are characterized by one or more of the following: duration > 6 months permanent or residual disability nonreversible pathological changes need for special rehabilitation long term medical and/or nursing care
Some chronic illnesses have acute exacerbations resulting in: loss of control of illness times of instability with need of medical/nursing assistance increased dependence on family members
Disability: a limited functional ability as the result of an impairment; it is the term preferred over “handicap”
Sequelae of chronic conditions: Limitation of functions; disfigurement Dependence on medications or special diet Current need for medical care/ related services Special ongoing treatments at home, work
Major Chronic Conditions Chronic sinusitis Allergic rhinitis Asthma Chronic bronchitis Heart disease Hypertension Diabetes Psoriasis Arthritis Orthopedic impairments Migraine headache Visual impairment Hearing impairment
What % of adults have 1 or more chronic diseases 50
Each chronically ill person has average of 2 chronic diseases Related--HTN and CHF Unrelated--HTN and arthritis
1/3 of those with chronic illness have limitations in performing ADL’s Arthritis Cancer Coronary artery disease Spinal cord injury Highest incidence in people > age 65
Exact number of children with chronic illness unknown; estimates differ by definition of chronic illness in children 31% of children under 18 years have chronic health condition Incidence of chronic conditions have not changed (CDC, 2008) Prevalence of children affected increased due to increasing survival and enhanced recognition
Maternal and Child Health Bureau Division of Services for Children With Special Needs created definition of “special health needs” for federal and state programs: Children who have or are at risk for a chronic physical, developmental, behavioral, or emotional condition and who also require health and related services of a type or amount beyond that required by children generally.
Children affected by large number of rare diseases , genetic, or prenatal conditions Not stable; subject to acute exacerbations
Adults affected by relatively small number of common diseases that increase in morbidity with age. Generally stable conditions
Any loss of physical/mental function has major impact on a person’s life Changes in family roles Drains major power sources (income, self esteem, autonomy) Taxes coping abilities of the person Grief over loss of normal function
Engel’s Theory of Loss Shock and disbelief over diagnosis Unable to accept facts of illness
Engel’s Theory of Loss Development of awareness Aware of lifelong implications of illness Depression
Engel’s Theory of Loss Restitution Family and patient provide mutual support in coping with reality of disease
Engel’s Theory of Loss Resolution Responds to loss with psychological coping Roles are adjusted to normalize activities of daily living
Individual Response to Chronic Illness Depends on: Pattern of coping strategies used in the past Pathophysiology causing the disease Visibility of disease Degree and type of limitations Relationship between the disease and person’s functioning in social roles family support Pain, fatigue, and fear
Societal Response to Chronic Illness Members of society tend to avoid persons with chronic disease Impact on patient: social isolation lack of social support
Living With Chronic Illness Managing a medical crisis Delegation of control to others Can result in damage to patient’s self concept and body image
Living With Chronic Illness Carrying out prescribed regimens Family and/or family must learn regimens of care Timing of interventions Coping with side effects Learning how to use equipment Pain management
Living With Chronic Illness Controlling symptoms Learning acceptance of limitations on lifestyle imposed by disease Redesigning/timing activities and hobbies
Living With Chronic Illness Dealing with lack of monetary resources for treatment Costly treatments Limitations on ability to work Worry, anxiety, depression
Living With Chronic Illness Managing the trajectory (disease pattern) Variable, depending on predictability of illness and ability of patient to cope
Living With Chronic Illness Preventing social isolation Dependent on patient response to his/her tendency to withdraw from friends and society Patient response to societal withdrawal from her/him
Living With Chronic Illness Normalizing Not focused on seven problems of the disease itself Involves working through above tasks Occurs when patient and family accept new, realistic identities and roles Achieves normalization-optimal level of functioning within the limits imposed by illness
Corbin & Strauss Trajectory Framework describes the experience of chronic illness
Further refinement of Strauss’s earlier theory is applicable to Cardiac illness Cancer Multiple sclerosis Diabetes Elderly with chronic illness
Corbin & Strauss Common phases Pre-trajectory prior to diagnosis emphasize prevention
Corbin & Strauss Common phases Trajectory onset signs and symptoms
Corbin & Strauss Common phases Crisis phase life threatening inpatient care
Corbin & Strauss Common phases Acute phase interventions carried out illness/complications
Corbin & Strauss Common phases Stable phase planned interventions
Corbin & Strauss Common phases Unstable phase plan not working managed out-patient
Corbin & Strauss Common phases Downward phase deterioration
Corbin & Strauss Common phases Dying phase terminal illness
Psychosocial adaptation to a chronic illness is optimally achieved by maximizing self-control and independence
General Management of chronically ill Evaluate the patient’s self-care abilities Help the patient adjust to limitations imposed by illness Help the patient adjust to changes in body image Work to increase self-esteem Assist the patient to express feelings
Assess coping & help the patient practice new coping mechanisms Facilitate the grieving process Promote social interaction Teach the family about the illness Participate with the health care team to devise a comprehensive plan of care General Management of chronically ill
Care at the End of Life Most persons will carry a chronic illness diagnosis at the end of life Role of the FNP: Pain management Facilitator of hope Explore patient expectations about the end of life Patient/family communication about care/prognosis Clarification of limits of care Caring for the family Follow-up and grieving for family
Confusion: Alteration in mental status Common term used to describe impaired cognition resulting in disturbed behavior and/or emotions Symptom of underlying condition Diagnostically challenging
Confusion: Alteration in mental status Important early sign in elderly of : Disease Of the brain itself Other organ systems Medication problems
Confusion: Alteration in mental status Need to determine How abruptly it started How long it has been going on If the situation is progressing, and if so, how fast
Delirium or acute confusional state is a syndrome of a disturbance in consciousness with reduced ability to focus, sustain, or shift attention that occurs over a short period of time and tends to fluctuate over the course of the day
Acute Delirium: A Medical Emergency Acute effect of physical illness on brain function Affects 10-52% of hospitalized elderly Of those with dementia, the incidence of delirium is 32-82% Often neglected as medical emergency no history available, best to assume confusion is of new onset
Acute Delirium: Brain maladaptive reaction to acute stressor Infection Hypoxia Hypoperfusion Trauma Surgeries
Acute Delirium: Pathogenesis: Metabolic changes Alter availability of amino acids from plasma to the brain Modify cerebral neurotransmission Increased secretion of cytokines Induces neurotransmission state of cholinergic deficiency and dopaminergic excess
Acute Delirium: DSM-IV Diagnostic Criteria not accounted for by a dementia Develops over hours to days Fluctuates during the course of the day Impaired ability to focus, sustain, or shift attention Cognition impaired or perceptual disturbance (misinterpretations, illusions, hallucinations)
Associated with sleep-wake cycle disturbance, disturbed psychomotor behavior, emotional disturbance,(EEG) abnormalities Evidence that disturbance is caused by a general medical condition, substance intoxication or withdrawal, or multiple etiologies Acute Delirium: DSM-IV Diagnostic Criteria
Acute Delirium: symptoms Acute change in mental status Sleep disturb Fluctuating course Attention disturb Memory disturb Orientation disturb Perceptual disturbance Thought disturbance Consciousness disturbance Speech disturbance Psychomotor activity disturbance
Main differentiating feature between Delirium and Dementia symptom fluctuation that occurs with delirium
Acute Delirium Mandatory search for underlying cause(s): Intracerebral disease More often due to acute illness or physiological change elsewhere Treatment of several interacting diseases (medication)
Acute Delirium Common causes Acute systemic infection Pneumonia, Urinary sepsis, Cholecystitis, Diverticulitis, Meningitis, Encephalitis Head injury, subdural hematoma Acute myocardial event Rarely is one single factor responsible for onset of delirium
Risk factors for acute delirium Predisposing or vulnerability factors (See Ham & Sloan Chap 16) Precipitating or trigger factors
Precipitating Factor for acute delirium use of anticholinergic drug Anticholinergics play a dual role Both a predisposing and a precipitating factor total anticholinergic burden Reflects cumulative anticholinergic (antimuscarinic) actions of all medications taken by an individual
Several methods used to determine anticholinergic action In-vitro affinity to muscarinic receptor Opinion of clinical expert regarding adverse effect Serum anticholinergic activity
Definite Central Anticholinergics Ipratropium Bromide Inhaler Meclizine Oxybutinin Meperidine Paroxetine Hydroxyzine Chlorpheniramine Amitriptyline
Diagnosis of Delirium Acute change in mental status Accompanying attention deficit Disorganized thinking or change in alertness status
Acute and Fluctuating Changes in Mental Status as demonstrated by one of the following Family member interview Nurse interview Chart review > 2 pts acute drop in MMSE during hospitalization Discrepancy between different examiners regarding pt’s mental status
Attention Deficit as demonstrated by one of the following Nurse interview Patient inability to spell first name backward Patient inability to repeat a phone number Patient inability to count backward from 20 to 1
Disorganized Thinking as demonstrated by one of the following Nurse interview Patient incoherent speech Patient illogical speech
Hypoalert or Hyperalert Status as demonstrated by one of the following Nurse interview Chart review Patient sleepiness Patient restlessness
Agitation Consider professional sitter Assess impact of agitation on patient safety and d/c Foley and other tethers if possible Consider trazodone po q 6hr PRN If h/o ETOH consider Lorazepam PO/IM/IV q 4-6 hr PRN
Decreasing burden of delirium requires implementation of specialized delirium programs Active screening to identify patients with high vulnerability (Delirium vulnerability scale) Educating clinicians on recognizing and diagnosing delirium and identifying triggers
Alzheimer’s Disease A progressive, neurodengerative condition characterized by memory loss and cognitive decline. Most common form of dementia in the older population Insidious onset Slow and progressive An array of behavioral and emotional behaviors Accounts for about $100 billion per year Approx. $27,000 per year per patient (Dunphy, 2011)
According to the American Psychiatric Association, AD is characterized by the impaired ability to learn new information or recall previous learned information and one or more additional cognitive disturbances: Language (aphasia) Function (apraxia) Perception (agnosia) Executive function-interpersonal relationships, ADL’s
Pathologic markers for AD have been identified; however, these features also occur in the brains of cognitively intact persons Affects in general about 1 in 10 person over the age of 65 Affects as many as half of those age 85 and older Estimated to be 16 million affected in 2050
AD affects the 3 processes that keep neurons healthy Communication, metabolism, and repair.
Brain Changes in Alzheimer’s Amyloid Plaques one of the hallmarks of AD protein fragments that the body produces normally Healthy brains are able to break down and eliminate the protein fragments. In AD the fragments accumulate for form hard insoluble plaques
Brain Changes in Alzheimer’s Neurofibrillary Tangles Insoluble twisted fibers found inside the brain’s microtubules in neurons. In a healthy brain these microtubules are a transport system in the brain. In AD, the tau protein is abnormal and the microtubule structures collapse.
Alzheimer’s Genetic Factors Less than 10% of cases are familial
Alzheimer’s Risk Factors Advancing age Family history of APOE genotype Obesity Insulin Resistance Dyslipidemia Hypertension Inflammatory Markers Traumatic Brain Injury
Trisomy 21 predisposes to Alzheimers in late life Down’s syndrome (late 40’s or 50’s) Chromosome 1, 14, and 19 implicated in both familial and sporadic forms
Mild Alzheimer disease Signs of mild AD can include the following: Memory loss Confusion of familiar places Taking longer for normal, daily tasks Trouble handling money and paying bills Compromised judgment, often leading to bad decisions Loss of spontaneity and sense of initiative increased anxiety
Moderate Alzheimer disease Increasing memory loss confusion Shortened attention span Problems recognizing friends and family members Diff with language; reading, writing,numbers diff organizing thoughts and thinking logically Inability to learn new things or situations
Restlessness, agitation, anxiety, tearfulness, wandering, especially in pm Repetitive statements or movement; Hallucinations, delusions, suspiciousness or paranoia, irritability Loss of impulse control: Perceptual-motor problems: Moderate Alzheimer disease
Patients with severe AD cannot recognize family or loved ones and cannot communicate in any way. They are completely dependent on others for care, and all sense of self seems to vanish. Other symptoms of severe AD can include the following: Weight loss Seizures, skin infections, difficulty swallowing Groaning, moaning, or grunting Increased sleeping Lack of bladder and bowel control
History for Dementia 5 areas that require assess/reassessment Ability to perform ADLs and Instrumental ADLs Cognitive functioning Comorbid medical and mood disorders Caregiver status
Functional Activities Questionnaire (FAQ) Bill paying Assembling records relating to business Shopping alone Playing a game of skill Performing multi-step task (writing letter, stamping, and mailing)
Preparing balanced meal Awareness of current events Understand/discuss TV program, book, article Remembering and keeping appointments Driving, taking bus, walking to familiar places Functional Activities Questionnaire (FAQ)
Screen for depression (US Preventive Services Task Force) Over the past 2 weeks have you felt down, depressed, or hopeless Over the past 2 weeks have you felt little interest or pleasure in doing things?
Identify primary caregiver and assess for adequacy of family support other support services availability
No true treatment for Alzheimer Disease cholinesterase-inhibiting drugs may improve function and slow decline, however in clinical trials these drugs benefits fewer than 50% of patients.
The glutamate antagonist memantine (Namenda) has been shown to prolong daily function in patients with moderate-to-advanced AD
Acetylcholinesterase inhibitors Reversibly bind and inactive the enzyme that degrades acetylcholine, which is involved in memory. Used as first line agents Most trials have found no difference in effectiveness among the agents in this class. The most common side effects are nausea, vomiting and diarrhea and dose related. Rivastgmine (Exelon) patches my be better tolerated
Used as first line agents Most trials have found no difference in effectiveness among the agents in this class. The most common side effects are nausea, vomiting and diarrhea and dose related. Rivastgmine (Exelon) patches my be better tolerated The most common side effects are nausea, vomiting and diarrhea and dose related. Rivastgmine (Exelon) patches my be better tolerated
Cholinestrase Inhibitors Donepezil (Aricept) Longer duration of inhibitory action; greater specificity for brain tissue Treatment of mild, moderate, and severe Second generation cholinesterase inhibitor Initially 5 mg/day--increase to 10 mg/day after 4-6 weeks May have initial increase of agitation; subsides in 2 weeks Side effects: Nausea, diarrhea Reduce by taking with food
Cholinestrase Inhibitors Rivastigmine (Exelon) Treatment of mild to moderate 1.5 mg twice daily Can increase by 1.5 mg twice daily (3 mg/day) every 4 weeks Max 6 mg bid Side effects: Nausea, vomiting, diarrhea, h/a, abdominal pain, fatigue, anxiety, agitation Reduce by taking with food
Cholinestrase Inhibitors Galantamine (Razadyne, previously Reminyl) Treatment of mild to moderate 4 mg bid taken with bid with meals for 4 weeks After 4 weeks, increase to 8 mg bid for 4 weeks Consider 12 mg bid if tolerated and benefit noted Advantage: no sleep disturbance Side effects: nausea vomiting, diarrhea Reduce by taking with food
NSAIDs should be avoided with cholinesterase inhibitors (additive effective for ulcer formation)
NMDA Receptor Antagonist Memantine (Namenda) New class of medications N-methyl-D-aspartate (NMDA) receptor antagonists Indicated for moderate to severe AD In AD, abnormal glutamatergic activity may cause neuronal toxicity and impair learning Namenda (memantine HCl) permits activation of NMDA receptor
Memantine (Namenda) May be used in conjunction with donepezil (Aricept) for additive effect Dosing— Use to be a gradual titration Now changing to extended tabs: Namendia XR 28mg once a day-same apporx. Cost $300/month May consider stopping in 3-6 months if no improvement-taper over 4 weeks to prevent rebounds
Monoamine oxidase type B inhibitor selegiline (Eldepryl 5 mg bid) In some studies some improvement seen for 4-6 wks, no improvement after 6 weeks. Rationale: slows progression of AD Possible association of free radicals and oxidative stress contribute to neural degeneration.
Anxiety in AD Buspirone 5-7.5 mg bid up to 30 mg/day
Depression in AD SSRIs are first line Zoloft (sertraline) less effect on metabolism of other meds Tricyclic antidepressents NOT recommended due to anticholinergic activity
Sleep disturbances and insomnia in AD Good sleep hygiene Pharmacologic as last resort
Treatment of Agitation In AD Warnings in the elderly: Older patients with dementia who are treated with atypical antipsychotics have a 2x higher mortality rate. Federal law states that if antipsychotics used in treatment in nursing homes, drug reduction efforts must be made every 6 months or less
Antipsychotics: Evidence suggests that olanapine (Zyprexa) and risperidone (Risperdal) reduce aggression and risperidone reductes psychosis in patients with AD.
AD Management: Behavioral Balance environmental stimulation Familiarize routines for security and predictability Art and expressive recreation can improve mood Exercise outdoors to improve mood and behavior
Ten Warning Signs of AD Memory loss affects job skills Difficulty with familiar tasks Problems with language Disorientation to time and place decreased judgment Problems with abstract thinking Misplacing things Changes in mood/behavior/personality Loss of initiative
SIMPLE LINEAR SKULL FRACTURES Small breaks in the skull that are not associated with depressed bone fragments and underlying brain injury.
CONCUSSION Trauma-induced alteration in mental status that may or may not involve loss of consciousness
CLASSIFICATION OF HEAD INJURIES Minimal No loss of consciousness or amnesia. Glasgow Coma Scale of 15. Normal alertness and memory. No focal neurological deficit. No palpable depressed skull fracture.
Classification of Head Injuries Mild Brief (<5 min.) loss of consciousness. Amnesia for the event. Glasgow Coma Scale score of 14. Impaired alertness and memory.
CLASSIFICATION OF HEAD INJURIES Moderate to severe Prolonged (>5 min.) loss of consciousness. Glasgow Coma Scale score < 14. Focal neurological deficit. Post traumatic seizure. Intra-cranial lesion detected on CT scan.
The Most Common Cause of Traumatic Head Injuries in All Ages is Falls
Head injuries in infants These head injuries are most often associated with falls and abuse. ALWAYS CONSIDER “shaken baby syndrome.
How long after a head injury should an unhospitalized patient be observed? 48 hours
What s/s are the hallmarks of a Concussion? Confusion, amnesia
normal BMI 18-24.9
overweight: 25-29.9
Class I: Obesity BMI 30-34.9
Class II: Obesity BMI 35-39.9
Class III Obesity BMI 40+
Distribution of fat differs in individuals Apple-shaped (upper body obesity) More common in men Associated with greater risk of most complications of obesity
Pear-shaped (lower body obesity) More common in women Tend to accumulate more fat in gluteofemoral region.
Visceral fat in abdominal cavity more hazardous to health than subcutaneous fat around abdomen
Health risks are increased when: Waist circumference Men: >102 cm (40 in) Females > 88 (35in)
Health risks are increased when: Waist : Hip ratio > 1.0 in men > .85 in women
Waist circumference and waist to hip ratio are both a better predictor than BMI for health risk Diabetes mellitus Stroke Coronary artery disease Early death
relative risk associated with obesity decreases with age Weight no longer risk factor in adults >75 years of age
Increased weight results in increased incidence of CVD Type 2 diabetes Degenerative joint disease (Osteoarthritis) Hypertension Hyperlipidemia Certain cancers: suppressed immune function Digestive tract disease Increased surgical and obstetric risks Endocrine abnormalities Proteinuria
40-70% of obesity explained by genetic influences
Obesity results from genetic predisposition, environmental factors, and psychological behaviors
Visceral abdominal adipose tissue associated with obesity appears to be act as an endocrine gland releasing several atherogenic, inflammatory, proteins associated with increase diabetes and CVD risk.
Plasminogen Activating Inhibitor 1 (PAI-1) PAI-1 decreases with caloric restriction, exercise, weight loss and metformin treatment
Retinol-binding protein 4 (RBP-4) Reported to be associated with visceral-fat accumulation and parameters of the metabolic syndrome (MetS). Studies of bariatric surgery weight loss patients show marked decreases that correlate with loss of visceral fat
Adipokinases affect insulin action in obesity: Tumor Necrosis Factor alpha Secreted from adipose tissue proposed as a molecular link between obesity and insulin resistance. Inactivates insulin receptors Correlates with BMI, percentage of body fat and insulin resistance. Weight loss decreases TNF
Peptide resistin Interferes with insulin action on glucose metabolism Levels elevated in obese animal models
Leptin (1994) protein (leptin = Greek for thin) Leptin is released from fat cells in response to changes in body fat Crosses the blood brain barrier-receptors in the hypothalmus Increases sensitivity to insulin by increasing hepatic responsiveness Appears to affect appetite: decreased levels of leptin are associated with obesity
Leptin replacement has shown improved glycemic control, decrease in triglycerides, decrease in caloric intake
Adiponectin Also seems to increase sensitivity to insulin by increasing hepatic responsiveness
Angiotensinogen Major risk factor for CVD Associated with obesity---adipose tissue is the major extrahepatic source of AGE Appears to increase new adipose formation
Serotonin Regulates food selection Increases mood Increases carbohydrate cravings/food addiction
Thermogenesis alterations in obesity Normal process involves use of calories by converting food to heat In obese, energy is stored, not converted to heat Less sympathetic nervous system activity
60% of obese individuals have metabolic syndrome as defined by NCEP ATP III: Elevated abdominal circumference Men > 102cm (40 inches) Women >88cm (35 inches) Elevated blood pressure >130/85 Elevated blood triglycerides > 150 mg/dl Elevated fasting blood sugar >110 mg/dl (others >100mg/dl) Lo HDL cholesterol
WHO criteria for Metabolic Syndrome slightly different: High insulin levels Elevated FBS or post prandial glucose +2 Of the NCEP ATP III Guidelines
patients with Metabolic Syndrome have Decrease in tissue (liver, muscle, adipose) sensitivity to insulin or “insulin resistance” This produces an increase in circulating insulin levels Increased insulin produces more fat cells Fat and glucose metabolism impaired Desire to eat more
Most obesity is the result of overeating/decreased exercise with the accompanying cascade of metabolic changes
Major endocrine disorders that may manifest with obesity are: Pituitary and adrenal dysfunction Thyroid disease Polycystic ovary syndrome Hypothalamic disease
OBESITY IN CHILDREN Overweight before age 3 not prediction of future obesity, unless parents obese After 6, the chance that obesity will persist increases 50% Approximately 70% of obese adolescents will remain so as adults
Overweight in Children: defined as a sex and age specific BMI at or above the 95th percentile based on revised growth charts by the CDC
Obesity in Children defined as a mean weight above the 120th percentile for height. Some sources use the 125th percentile and some use 130th. BMI >85 percentile.
Obese children should be evaluated for presence of associated co-morbidities Cardiovascular disease Type 2 Diabetes- Weight related orthopedic problems Skin disorders Psychiatric problems Sleep apnea
Factors influencing weight in Children Heredity Overeating Emotional and Psychological Factors Body Changes and Puberty Medications/Medical Conditions Community Factors
What % of overweight children can achieve optimal weight with intervention 80-90
Childhood Obesity intervention Plans incorporate Modification of child and family’s diet Regular exercise Family-based behavior modification programs Establish treatment plan with the family
Obesity assessment required at every well child exam
Childhood Obesity Goals Normalize child’s weight within his genetic potential Reduce health risks through improved diet and activity Support treatment of underlying biological and psychosocial contributors. View obesity as a symptom with diverse contributors
Contraindications to weight loss Pregnancy Anorexia nervosa Terminal stages of illness Medical or psychiatric illnesses should be stable
MANAGEMENT OF OBESITY Goals of treatment: Lowest weight the patient can comfortably maintain- initial goal is 5-10% of total body weight Cosmetic goals should be discouraged Prevention of weight gain
Alternative goals for management of obesity: Improvement in comorbidities, mobility, and feelings of well-being, reduction in waist circumference and adherence to a diet and exercise regimen.
Weight loss requires creating a calorie deficit To lose 1 pound-must ingest 3,500 fewer calories than expended Most lose weight if ingest fewer than 1,500 calories per day and do aerobic exercise regularly
Fats: body uses only 3 calories to store 100 calories of fat.
Body uses 25-40 calories to convert 100 calories of protein into body fat
Daily fat intake should not exceed ____ of total caloric intake 30%
Fiber: Improves blood glucose levels through enhancing insulin effects and reduces number of calories absorbed by the body
EXERCISE Raises metabolic rate Helps keep weight down that was lost Walking briskly for 20-30 minutes a day
SUPPLEMENTS Not all that on market are safe and effective Herbal products still largely unregulated
Chromium: Mineral-key role in increasing cell sensitivity to insulin Lowers body wt, yet increases lean body mass Recommended dosage 400-600 mcg/day. no reported significant adverse effects Refined sugars, white flour, and lack of exercise deplete chromium
Thermogenic Formulas Ephedrine ( also ma huang) Data conflicting, weight loss rarely permanent, esp after drugs disc. SE: insomnia, irritability, jitters, elevated BP Products have been removed from the market 2004!!
Guggul: Herb used in ancient Indian system of medicine Increases HDL and lowers total cholesterol and trig. Dose for wt loss is 25 mg TID No adverse effects noted
Pantothenic Acid (vit B5) used in energy production of fats and carbohydrates 1 study demonstrated wt. loss in subjects on 10 gms/day followed by maint. 1-3 gm/day
Coenzyme Q10: Can improve energy production at cellular level, increasing thermogenic response to meals No serious SE Statins and beta blockers lower body’s CoQ10 levels Supplementation may be helpful in pts taking these
FORMULA DIETS Called supplemented fasts Optifast, HMR, and Medifast Provide superior weight loss and rapidly reduce severity of number complications of obesity Close medical supervision Must be used with support and behavior, nutrition, and exercise education.
Obesity PHARMACOTHERAPY May be used as adjunct Indications for use of FDA approved drugs: Patients with a BMI >30 Patients with BMI >27 in presence of concomitant obesity-related risk factors or diseases
Orlistat (Xenical) approved for long term use <2 years Prevents absorption of 30% of fat Reduces LDL and increases HDL, reduces BP, and fasting insulin levels Causes diarrhea, flatulence Encourage use of multiple vitamin 120 mg TID with meals No significant adverse reactions
Belviq: a serotonin 2C receptor agonist FDA approved 2012 Schedule IV 10 mg BID for up to 12 weeks Contraindicated in pregnancy Warnings Serotonin Syndrome/Neuroleptic Malignant Syndrome reaction Valvular heart disease Cognitive impairment Monitor for depression/suicidal thoughts Antidiabetic meds: Hypoglycemia with wt loss Priapism: seek treatment for erection > 4 hrs
Qsymia (ku-si-mia) is an extended release combination of two drugs (FDA approved 9/2013) Phentermine, a sympathomimetic: (Schedule IV) Appetite suppressant Topiramate, an antiepileptic Increases feelings of fullness, blunts taste, and increases calorie burning BEST USE BY BARIATRIC MD
Appetite suppressants-most controversial and less used today due to rebound weight gain & CVD risk Chemically related to amphetamines Schedule IV Short-term ( 3 month) use Rare side effect of pulmonary hypertension Phentermine HCL Adipex, Fastin, Ionamin, others Dosed differently
Both glucophage (Metformin) and Byetta (exenatide) have been shown to reduce weight in diabetics.
MAINTENANCE OF WEIGHT LOSS Successful strategies Consultation with health care provider or nutritionist or other support source Adhering to stable diet Monitoring weight Eating breakfast Regularly exercising
Consistent weight loss is limited by adherence to a consistent regimen
MAINTENANCE OF WEIGHT LOSS Behavioral factors associated with success Establish social support avoid disinhibited eating Avoid binge eating Avoid eating in response to negative emotions/stress Be accountable for one’s decisions Foster sense of autonomy, internal motivation and self-efficacy toward wt loss maintenance
Risk factors associated with weight regain Disinhibited eating Binge eating Periods of excessive hunger Eating in response to negtive emotions/stress Passive reactions to problems Less assumption of responsibility in life
SURGICAL TREATMENT According to National Institute of Diabetes and Digestive and Kidney Diseases GI surgery most effective treatment for severely obese persons who fail to lose weight through diet and exercise.
SURGICAL TREATMENT Option for weight reduction in limited number of patients with BMIs >40 or >35 with comorbid conditions Include: vertical-banded gastroplasty and gastric bypass
Malabsorptive operation decreases the amount of food that can be ingested, as well as calories and nutrients.
Restrictive operations reduce stomach size: adjustable gastric banding and vertical banded gastroplasty
Gastric bypass patients require nutritional supplementation at risk for vitamin B-12 deficiency may experience dumping syndrome (weakness, sweating, diarrhea
Anorexia Nervosa Definitions Refusal to maintain a reasonable body weight; divided into restricting and binge-eating/purging subtypes (Dambro, 2000). Symptomatic disturbance of eating behavior unique to the developed world (Uphold & Graham, 2003).
Anorexia Nervosa Etiology Exact etiology is unknown; however, is thought to be largely emotional Co-morbid major depression and/or dysthymia in 50-75% of patients Obsessive-compulsive disorder in 10-13% of patients
Anorexia Nervosa Predispositions First degree female relatives Usually adolescents or young adults Female-to-male ratio: 10:1 Perfectionistic, rigid, inflexible, and conforming personalities Low self-esteem Acceptance of the culturally condoned ideal of slimness
Anorexia Nervosa Signs & Symptoms Insidious onset, or Stress-related onset Deny problem Claim to feel fat Elaborate eating rituals Preoccupation with body size/weight control Extensive exercising Stress fractures Cracked, dry skin Social isolation Sexual disinterest
Fine, downy lanugo hair on extremities, face, and trunk Amenorrhea Hypotension and bradycardia Hypothermia Cognitive decline Anorexia Nervosa Signs & Symptoms
Diagnostic Criteria for Anorexia Nervosa Refusal to maintain weight at or above a minimally normal weight for age and height Severe body-image disturbance in which wt has undue influence on feelings of self-worth; denial that current wt is problematic Intense fear of weight gain Amenorrhea
Types of Anorexia Nervosa Restricting type: not regularly engaged in binging or purging behaviors Binge-Eating/Purging type: regularly engaged in binging or purging behaviors
Anorexia Nervosa History Obtain weight history Establish absence of diagnostic criteria via appropriate questions Medication use to induce weight loss Inquire about other eating behaviors Careful diet history Exercise patterns
Anorexia Nervosa Initial lab should include CBC, UA Electrolytes Calcium, magnesium, phosphorous Liver function, BUN, Creatinine, TSH Serum amylase Elevated during active vomiting Return to normal within 72 h after vomiting stops May be useful in documenting presence of bulimia EKG
Anorexia Nervosa Hospitalize if weight <75% of normal for height and age if marked orthostatic hypotension, bradycardia <40, tachycardia >100, or inability to sustain core body temperature of 98.6° if patient is suicidal; or if there has been no response to outpatient therapy
Anorexia Nervosa Outpatient Treatment Imperative to build trust and treatment alliance Involve client in establishing target weight Achieve gradual weight gain Weigh weekly at first; monthly when progress is evident
Focus on overall indices of health, rather than wt gain alone Challenge fear of wt gain Family therapy for adolescents; couples therapy for older clients When conditioning is chronic, goal may be to achieve a safe wt rather than a healthy wt Anorexia Nervosa Outpatient Treatment
Anorexia Nervosa Medication Treatment Medications should not be used as sole or primary treatment of this disorder; however: SSRIs relieves symptoms, are considered safest antidepressants Helpful for patients with depression, anxiety, and obsessive-compulsive tendencies
Bulimia: Diagnosis Episodic binge eating At least 2x weekly for 3 months Sense of lack of control followed by recurrent inappropriate compensatory behavior to prevent weight gain Self-induced vomiting Diuretic or laxative use dieting or fasting excessive exercise
Types of Bulimia Nervosa Purging type: engaged in self-induced vomiting, laxative, diuretic or enema use on regular basis Nonpurging type: engages in fasting or excessive exercise, but not regularly engaged in above purging behaviors
bulimia affects predominantly Young, white, middle and upper class women More difficult to detect than anorexia due to the typically normal weight for age and height Some individuals may have above normal weight range however As high as 19% of college-age women
Binge eating Premeditated, secretive episodes of binging Consume large quantities of easily ingested high-calorie foods Fast eating with inability to slow down or stop Eat until painfully full Typically occurs separately from regular meals
Purging Self-induced vomiting Relieves pain and facilitated further binging Fingers, spoon, toothbrush used to trigger gag reflex Some can elicit vomiting reflex at will Cathartics, diuretics Syrup of ipecace, enema use
Bulemia Non purging type Binging, then use of compensatory mechanism to make up for calories consumed Fasting Excessive exercise Defined as taking precedence over other important activities Ritualistic Less secretive than other compensatory behaviors, so can serve as red flag to clinicians Strict dieting
Bulimia Nervosa Clinical findings History of premorbid obesity Greater incidence of cathartics and diuretics More impulsive or anti-social behavior Menstruation is usually preserved Symptoms usually related to mechanism of purging Abdominal pain
Bulimia Nervosa pt complain of Abdominal pain due to Gastroesophageal reflux due to loss of lower esophageal sphincter control due to repetitive vomiting Gastritis due to irritated mucosa from increased acid exposure Early satiety Involuntary vomiting Hematemesis or esophageal rupture
Physical exam of Bulimia Dehydration Orthostatic hypotension Enlargement of parotid glands Oral cavity Abdominal tenderness Abrasion of finger joints (PIPs) due to scraping of fingers against teeth to induce vomiting Tachycardia and hypertension
Bulimia Laboratory findings Vomiting Metabolic alkalosis Hypokalemia Hypochloremia
Bulimia Laboratory findings laxative overuse Metabolic acidosis Hypokalemia Hypochloremia
Bulimia Laboratory findings Elevated amylase due to chronic parotid stimulation
Complications of Bulimia Gastric dilatation Pancreatitis (check amylase) Poor dentition Pharyngitis Esophagitis and esophageal rupture Aspiration pneumonia Electrolyte imbalance and dehydration Severe constipation with withdrawal of laxatives Hemorrhoids
Diet pill side effects Insomnia Hypertension Tachycardia Seizure Sudden death
Bulimia Hospitalization If failure in outpatient management If medically unstable If K+ < 3.0 mEq/L inpatient admission Oral K+ supplementation IV K+ if <2.5
Chronic dehydration in bulimia Renin-angiotensin-aldosterone axis and antidiuretic hormone level elevate to compensate for chronic dehydration Fluid retention possible when dehydration corrected as levels take 7-10 days to normalize Patient at risk for CHF
Psychotherapy and nutrition counseling in Bulimia Cognitive-behavioral therapy (CBT) Understand disease Suggestions for stopping binge/purge cycle Interpersonal therapy (IPT) Understand the sources and reason for poor coping skills Family therapy Nutrition therapy Normalize eating patterns
Drug therapy For Bulimia SSRIs recommended (FDA approved in higher doses than for depression) Fluoxetine (Prozac) 60 mg/day Blackbox warning: risk of suicide in children and adolescents
Medical Therapy in Bulimia Electrolyte monitoring periodically Drug therapy Treatment for reflux and gastritis Parotid gland swelling and pain Sucking on tart candy Application of heat
Long-term psychiatric prognosis in severe bulimia is worse than that in anorexia nervosa Prognosis is better if younger age of onset and shorter duration of illness Prognosis worse if coexisting psychiatric conditions
Associated problems of eating disorders Depression and anxiety Obsessive-compulsive disorders Suicidal ideation and attempt
NP role is in recognizing, diagnosing, and appropriately referring cases of bulimia nervosa. Listen for physical complaints that may provide clues that patient is in denial; d Establishing a therapeutic alliance is essential Proceed in nonjudgmental manner assessment of healthy behaviors and nutritional habits to diffuse denial
Depression Definition: illnesses that affect mood and results in a range of feelings and symptoms. Diagnosis based on criteria in the Diagnosis and Statistical Manual of mental Disorders, 4th Edition (DSM-IV).
DSM-IV Criteria 1. Depressed mood/Sadness 2. loss of pleasure 3. Sleep changes 4. Appetite changes 5. Feelings of worthlessness 6. Fatigue or loss of energy 7. Trouble concentrating/making decisions 8. Low self-esteem 9. Recurrent thoughts of suicide (ideation)
Depression ETIOLOGY: Organic: can be a part of or presenting symptom of medical illness: Alzheimer’s End-stage renal failure Parkinson’s disease CVA Cancer Chronic fatigue, chronic pain+
Depression often occurs in individuals with family history of depression or related illnesses
Brain-based illness: changes in brain neurochemistry and function demonstrated by research, including sleep electroencephalographic studies, positron-emission tomography, single-photon-emission CT, or CSF catecholamine metabolite levels.
Medications that Cause Depression Antihypertensives Hormones Anticonvulsants Steroids Digitalis Antiparkinsonian agents Antineoplasstic agents Antibiotics
Mixtures of environmental/biologic factors underlying severe mood disorders. Elevated cortisol Blunted response to TSH Abnormal response of growth hormone to prolactin Neurotransmitter levels (norepinephrine/ serotonin 5-HT) may be altered.
Major Depressive Disorder: Est. that 1 out of every 10 people treated in primary care. > in females. Episodes can be single or recurrent. Can last up to 2 years. High co-morbidity with substance abuse disorders.
Dysthymic Disorder (Chronic Depression):Onset less discreet, symptoms less acute. Duration of symptoms must be in excess of 2 yrs. (1 year in children). Usually do not require hospitalization due to less acute symptoms. Talk psychotherapy needed along with pharmacotherapy. Pts. at risk for suicide and substance abuse.
Substance-Induced Depressive Disorder: Consider DX when symptoms emerge as result of use of illegal drugs, medications, or toxins. Symptoms exceed what is usually seen with intoxication and withdrawal syndromes or when symptoms are severe enough to warrant independent evaluation and treatment.
Adjustment Disorder (Situational depression): Symptoms associated with an identifiable stressor within the last 6 months. Symptoms > 6 months would indicate a major depression.
Seasonal Affective Disorder: Episodes of MDD emerge in fall and last through winter and cannot be attributed to other biologic or psychosocial stressors. Higher the latitude, more prevalent the incidence. Treatment with traditional therapy and medications along with exposure to intense light is effective.
Postpartum Depression: Onset occurs within 4 weeks after birth of infant. Symptoms similar to MDD, but in addition mother often has psychotic symptoms that involve delusional thoughts about the infant. Occurs in up to 1 in 500 births. Can result in infanticide. Mother needs emotional support and often separation from infant.
Premenstrual Dysphoric Disorder (PMDD): Depressive symptoms during the late luteal phase of the menstrual cycles may occur throughout the year.
Psychotic Depression: Exhibits all S&S of MDD as well as psychotic symptoms. May include delusions and/or hallucinations. Associated with high incidence of suicide and commonly warrants inpatient care. Meds include antidepressants and antipsychotics.
Bipolar Disorder: 1% of the general population Strong biological and genetic influence 10% of children with one parent who is bipolar will develop the illness Episodes of mania and depression, or extreme highs and lows. 4 or more episodes/yr are “rapid cyclers” Psychotic features may or may not be present during manic episodes. Generally manic phase is shorter than depression phase
Bipolar characterized by excesses: hyperactivity increased irritability/flight of ideas over indulges in activities that later regrets overspending/gambling sexually acting out hasty marriage, quitting a job
Treatment of Bipolar Disorder Mood stabilizers are the main foundation for maintenance therapy. Antidepressants are not used as first line and should be used only with a mood stabilizer. Electroconvulsive therapy may be used for nonresponsive to psychopharmacology
Depression - Any type First-must evaluate patient’s potential risk for self-harm and ensure patient safety.
Depression - Management Adjunctive psychotherapy should be considered . Treatment is usually effective> 90% Treatment 6-9 months for MDD Adults who exercise regularly report lower levels of depressive and anxiety disorders.
Antidepressants should be continued indefinitely at full dosage in persons with more than 2 episodes after age 40 or one episode after age 50.
Treatment for Depressive Disorders Takes 4-6 weeks to yield significant reduction or remission of symptoms. Small percentage are unresponsive to existing treatments.
Depression Nonsedating medication: Tricyclic antidepressants and SSRIs are appropriate antidepressants prescribed by primary providers Both equally efficacious, but SE of SSRIs are less problematic and more frequently used.
Tricyclics For Depression Available since the 1950’s All have similar effects, dosing, & efficacy Major advantage over newer agents is sedation potential and cost Start at low doses and increase gradually
Side Effects of Tricyclic medications Anticholinergic effects: dry mouth, constipation, urinary retention, increased ocular pressure, confusion. Anti-adrenergic effects: postural hypotension, less with Nortriptyline Have quinidine-like effects increasing QT interval on the ECG.
Serotonin Reuptake Inhibitors Few side-effects Major reason for stopping is libido/ejaculatory problems Tolerated by elderly, but start at low doses Monitor for worsening of Parkinson’s symptoms SSRI’s inhibit various isoenzymes of the cytochrome P-450 system of the liver
SSRI and combinations have now been given a warning in pregnancy due to risk of congenital problems. SSRI and combinations have now been given a warning in pregnancy due to risk of congenital problems.
Fluoxetine (Prozac) 10-20 mg Long half-life Well tolerated Main reason for stopping: decreased libido/ejaculatory problems (true for all SSRIs) Stigma associated with Prozac Now available in generic-may be less cost
Zoloft (Sertraline) 50-100mg x 1 Similar to Prozac in action and side effect. SSRI for Depression
Celexa (Citalopram) 20 mg x 1 SSRI for Depression Less effect on libido
Paxil (Paroxetine) 10-20mg x 1 FDA approval for anxiety, panic, OCD
SSRI/norepinephrine, dopamine blocker Bupropion (Wellbutrin, Zyban) Wellbutrin, should use SR Less weight gain-warning with eating disorders. Low toxicity Lower risk of sexual dysfunction Useful with bipolar and ADHD Disadvantage-raises threshold for seizures
Norepinephrine/serotonin Reuptake Inhibitors work well with both depression and anxiety symptoms Different structure than any other antidepressant Can elevate B/P Need to titrate dose when starting and weaning off Effexor and Cymbalta, Headache, dizziness, body aches, with abrupt withdrawal.
St John’s Wart: more effective than placebo in mild to moderate depression. Warning: MAO derivative-drug interactions Interacts with oral contraceptives
Exercise combined or alone improves mild to moderate depression.
All antidepressants effective in acute treatment of all grades of depressive disorder in young adults
No clinical significance in effectiveness between different kinds of antidepressants. Did vary on tolerance of side effects.
ECT involves passing electrical current through brain to induce series of generalized seizures. Hypothesized that these seizures render changes in neurotransmitter receptors which are similar to those seen in pts who have been on long-term pharmacotherapy with antidepressants.
Current research suggests ECT is one of safest treatments for MDD and psychotic depression. Works quickly and proven useful for pts who are unresponsive to lengthy trials of medications. Causes short-term, temporary confusion and memory loss.
Consideration for Referral/Hospitalization At risk for suicide Inability to care for oneself Diagnosis of Bipolar Disorder Initiation of ECT Evaluation and treatment with psychotherapy and/or cognitive therapy Education and support for family members
Depression Treatment of children, adolescents, and elders. Children/adolescents do have depression, Counseling is an important component. SSRI’s frequently used. Children with severe symptoms should be referred.
Diagnosis of depression should be considered in all older persons who report somatic symptoms, particularly those having chronic symptoms that appear to have no definite organic basis. Elderly: Side effects more of an issue Start with 1/4 to 1/2 average dose At higher risk for suicide
Depression Follow-up initial follow-up visit within 1 week to evaluate medication SE and encouragement Weekly or biweekly visits for 6 weeks while medications are being adjusted and evaluated Then Monthly or bimonthly PT should be seen quarterly as long as on medication
ECT should be primary treatment for patients with psychotic or delusional depression or for patients who are actively suicidal or who will not eat or drink, but societal and legal prejudice limits its use.
A signed “contract” may be an option to utilize in a clinic setting for a patient that is waiting for appointment at a psychiatrist, especially if they have suicidal ideation. Should see these patients daily until stable or seen by specialist.
DEFINITION of ANXIETY: Common natural emotion: temporary sense of panic, fear, nervousness, or being overwhelmed-everyone experiences May be part of disorder in which symptoms are prominent, persistent and disruptive to daily living or to sense of well being
Anxiety - Second most common group of mental disorders in general population Women 2X than men Persons seek medical attention because attribute symptoms to serious physical problems Anxiety disorders frequently unrecognized
Types of Anxiety Disorders Panic disorder Generalized anxiety disorder (GAD) Adjustment disorder with anxious mood Post traumatic stress disorder (PTSD) Simple phobia Social phobia Obsessive-compulsive disorder (OCD)
Anxiety Associated with specific biological abnormalities in CNS; associated with receptor of neurotransmitter (GABA) and area in pons called locus ceruleus. Stimulation of locus ceruleus increases anxiety. Benzodiazepines stimulates GABA receptors and reduces anxiety symptoms. GABA receptors in cerebral cortex are inhibitory. May have a genetic component
Panic Disorder EPIDEMIOLOGY: Most commonly presents in young adulthood (24-26 years- mean) Increase in onset of panic attacks observed at ages 15-19. Onset of panic disorder after age of 40 is rare
Panic Disorders SYMPTOMS: Dyspnea, choking sensation, syncope, palpitations, tachycardia, chest pain, diaphoresis, nausea, trembling, paresthesias, hot flashes, and chills Fear that they are going crazy or doing something uncontrolled
Panic Disorders CLINICAL FINDINGS Initial attack-spontaneous, unexpected Attacks occasionally follow excitement, emotional trauma, or exertion and do not necessarily represent panic disorder Ingestion of caffeine, alcohol, or nicotine or drugs may precede attack
Panic disorders Typical attack: begins with 10-15 minute period of accelerating symptoms Entire attack lasts about 30 minutes Not unusual for patient to develop phobic avoidance of certain situations coincidental with panic attack Common feature-anticipatory anxiety Young, healthy adults frequently present to ER with cardiac and respiratory complaints
Panic Disorders DSM-IV diagnostic criteria: Recurrent unexpected panic attacks At least one of attacks has been followed by at least 1 month of one or more of following: Concern about additional attacks Worry about implications or consequences of an attack Significant change in behavior related to attacks not due to direct effects of a substance not better accounted for by another mental disorder
Panic Disorders LABORATORY TESTS: Basic tests and studies needed to rule out associated disease: thyroid studies, serum electrolytes, blood glucose, ECG, CXR. Other tests based on clinical judgment
Panic disorders TREATMENT: Psychological Relaxation training Exposure therapy in PD with agoraphobia Cognitive therapy
Panic disorders TREATMENT-PHARMACOLOGICAL Antidepressants-effective. Imipramine-improvement in symptoms in 70-90% of pts after 6 weeks of therapy. Tricyclics, SSRIs used in full therapeutic antidepressant doses
Benzodiazepines effective in reducing anticipatory anxiety. Xanax results in marked improvement in 50% of pts. Should be for short term use only.
Panic Disorders treatment Most effective form is combination of pharmacologic agent and cognitive behavioral therapy
Panic disorders Lifestyle Changes: DIET: Avoid caffeine, nicotine, and ETOH. Stress management !!!!!! Relaxation Techniques: Yoga! Exercise: 30 minutes aerobic exercise per day Desensitization to triggers
GENERALIZED ANXIETY DISORDER SYMPTOMS: Worry and anxiousness over multiple real or projected problems. Worry out of proportion to situation and out of control At least three of following Restlessness Fatigue Trouble concentrating Irritability Sleep disturbance Muscle tension
GENERALIZED ANXIETY DISORDER Frequently episodes of severe autonomic symptoms: Cardiac: chest pain, palpitations, tachycardia, tachypnea Pulmonary: hyperventilation, smothering sensations, dyspnea Gastrointestinal: indigestion, abdominal pains, flatulence, diarrhea, constipation
Obsessive Compulsive Disorder Recurring thoughts such as fear of exposure to germs. Anxiety may be alleviated by ritualistic performance-frequent hand washing, hair pulling, in severe forms may perform self mutilation-cutting May present with an eating disorder
SYMPTOMS COMMON TO ANXIETY AND DEPRESSION: Fatigue Tearfulness Eating disturbances Irritability Excessive worry Difficulty concentrating
SYMPTOMS ESPECIALLY CHARACTERISTIC OF ANXIETY Difficulty falling asleep or staying asleep Pain syndrome-tends to be acute, sharp Complaints of nervousness-want help Mood may be elevated Autonomic symptoms prominent
SYMPTOMS ESPECIALLY CHARACTERISTIC OF DEPRESSION: Early morning awakening Pain syndromes-chronic, dull Pts unaware of their illness, want to be left alone Mood may be depressed Anhedonia Suicidal thoughts
Depression combined with Anxiety TREATMENT: Psychotherapy Stressors should be sought and patient’s coping mechanisms explored Supportive counseling, cognitive therapy, psychodynamic psychotherapy, family therapy, or various behavior therapies most frequently used Other: exercise, medication, etc
Depression/Anxiety TREATMENT- Pharmacotherapy(agents) SSRI frequently used in Primary Care Azipirones: 1 approved-Buspirone (BuSpar). Benzodiazepines: grouped according to duration of action: Tricyclic antidepressants: Often used with antianxiety agents. Occasionally effective alone for GAD
Approaches to Pharmacologic Treatment/Insomnia Hypnotics: Scheduled drugs CIV CYP 34A inhibitors
Ambien-warnings for abnormal sleep activity-sleep walking/driving behavior Zolpidem (Ambien) CR version is delayed release Eszopiclone (Lunesta)
Sedating antidepressant for sleep disorders: Elavil 10-50 mg at hs Trazedone 50-100 mg at hs Pamelar (Nortriptyline 50-100mg
5.2 Million with CHF in the United States 400,000 cases CHF diagnosed per year
200,000 patients die from CHF per year 870,000 hospitalizations (estimates in 2013 approach 1 Million) 1. Re-hospitalization rate within 30 days approaches 20%
5. CHF costs 1. Accounts for 5-10% of all hospital admissions 2. Annual U.S. Cost: $38.1 billion ($44.6 billion by 2015)
1. Heart Failure is a syndrome, not a disease 1. Heart Failure is a final common pathway 2. Maximize treatment of the underlying causes 3. Control the causes and prevent end organ damage
Heart failure (cardiac insufficiency, ventricular failure) is the inability of the heart to pump adequate amounts of blood into the systemic circulation to meet tissue metabolic demands.
Left-sided failure (congestive heart failure [CHF]) Results from failure of the left ventricle to maintain adequate output. Blood backs up into the left atrium and into the pulmonary veins. Increasing pressure in the pulmonary capillary bed causes congestion, result in respiratory distress. Increasing pulmonary pressure results in increased pressure on right side of heart.
Right-sided failure (cor pulmonale). Results from failure of the right ventricle to maintain adequate output. Blood backs up into the systemic circulation and causes peripheral edema. 3. Most common cause is secondary to left-sided failure and chronic pulmonary disease
Each side of the heart is dependent on the other for adequate function. 1. Left-sided failure results in pulmonary congestion; precipitates right-sided failure. the majority of clinical situations involve failure on both sides. However, right-sided failure may occur alone for an extended period of time. Frequently associated with chronic lung problems.
The heart will attempt to maintain the body requirements for cardiac output (increasing cardiac rate, vasoconstriction) when these mechanisms become in- effective, cardiac decompensation or failure will occur.
In children, HF occurs most often as the result of a congenital defect of the heart.
Edema development in heart failure. Decreased cardiac output leads to decrease in renal perfusion, the kidneys respond by increasing the retention of sodium and water. Resulting in pitting dependent edma
Pulmonary congestion (left-sided failure). Dyspnea and cough on exertion Orthopnea, tachypnea Paroxysmal nocturnal dyspnea respiratory distress and hypoxia Hemoptysis. Congested breath sounds. Feeding difficulties in infants due to dyspnea and decreased tolerance of activity.
Systemic congestion (right-sided failure). Hepatomegaly early sign in children. Peripheral edema and weight gain. Dependent edema or generalized edema in infants; evaluate by weight gain. Ascites. Increase in (CVP). Jugular vein distention (JVD) with head elevated 30 degrees
1. Systolic Dysfunction (60-70% of Heart Failure cases) 1. Decreased contractility 2. Decreased Left Ventricular Ejection Fraction
2. Diastolic Dysfunction (30-40% of Heart Failure cases) 1. Decreased compliance 2. Decreased filling 3. Variable Left Ventricular Ejection Fraction
All CHF patients should undergo Echocardiogram
NYHA Classification Class I Symptoms with more than ordinary activity
NYHA Classification Class III Symptoms with minimal activity 1. Class IIIa: No Dyspnea at rest 2. Class IIIb: Recent Dyspnea at rest
NYHA Classification Class II Symptoms with ordinary activity
NYHA Classification Class IV Symptoms at rest
Stroke or brain attack is the disruption of the blood supply to an area of the brain, resulting in tissue necrosis and sudden loss of brain function. It is the leading cause of adult disability in the United States.
Atherosclerosis, resulting in cerebro- vascular disease, frequently precedes the development of a stroke
Ischemic stroke Thrombotic stroke: formation of a clot that results in the narrowing of a vessel lumen and eventual occlusion; most common stroke. Embolic stroke: occlusion of a cerebral artery by an embolus.
Thrombotic stroke: formation of a clot that results in the narrowing of a vessel lumen and eventual occlusion; most common stroke. Associated with hypertension and diabetes. (2) Produces ischemia of the cerebral tissue.
Embolic stroke: occlusion of a cerebral artery by an embolus. ) Common site of origin is the endocardium. (2) May affect any age group
Hemorrhagic stroke. Rupture of a cerebral artery caused by hyperten- sion, trauma, or aneurysm. b. Bleeding compresses the brain and causes inflammation. C. The area of edema resulting from tissue damage may precipitate more damage than the vascular damage itself.
Transient ischemic attack (TIA, silent stroke). a. Brief episode, less than 24 hours, of neurologic dysfunction; usually resolves within 30-60 minutes. Should be considered a warning sign of an impending stroke. c. Neurologic dysfunction is present for minutes to hours, but no permanent neurologic deficit remains.
Reversible ischemic neurologic deficit (RIND). Symptoms similar to TIA. b. Neurologic symptoms last longer than 24 hours, but less than a week.
Stroke: client has neurologic deficits related to mobility, sensation, and cognition.
PVD • Symptoms 1. Presentations 1. Classic Claudication: 10% of cases 2. Atypical Leg Pain: 50% of cases 3. Asymptomatic: 40% of cases
2. Classic Claudication1. Cramp-like leg muscle pain with Exercise, better with rest 1. Calf pain typical (pain may occur in thigh, buttock) 2. Pain worse with exertion 3. Pain relieved within 10 minutes rest 4. Pain relieved with rest and dependent position
3. Critical Limb Ischemia (1% of presentations) 1. Tissue loss or gangrene 2. Chronic rest pain
PVD 1. Timing of symptoms related to degree of stenosis 1. Exertional pain: 70% arterial pain 2. Nocturnal pain: 70 to 90% arterial stenosis 3. Ischemic rest pain: 90% arterial stenosis
PVD 1. Vascular Exam (Arterial Bruits or diminished pulses) 1. Abdominal aorta bruit 2. Femoral artery pulse 3. Dorsalis pedis pulse (absent in up to 3% of normal patients) 4. Posterior tibial pulse 5. Carotid Artery pulse and bruit (for comorbid Carotid Stenosis)
PVD 2. Neurologic Exam 1. Critical in determining Acute Limb Ischemia degree (see Rutherford Classification) 2. Extremity Motor Exam 3. Extremity Sensory Exam
1. Most reliable signs of Peripheral Vascular Disease 1. Posterior tibial artery doppler Ultrasound 2. Dorsalis pedis AND posterior tibial pulse absent 3. Femoral artery bruit 4. Atypical Skin Color (pale, red, blue) of extremity
1. Posterior tibial artery doppler Ultrasound 1. All 3 components present rules-out Peripheral Arterial Disease 2. Only 1 of 3 components present is strongly suggestive of PAD (Positive Likelihood Ratio = 7.0)
2. Dorsalis pedis AND posterior tibial pulse absent test for PAD 1. Test Sensitivity: 63% 2. Test Specificity: 99%
3. Femoral artery bruit test for PAD 1. Test Sensitivity: 29% 2. Test Specificity: 95%
4. Atypical Skin Color (pale, red, blue) of extremity test for Pad 1. Test Sensitivity: 35% 2. Test Specificity: 87%
2. Local Signs of Peripheral Vascular Disease Dry, scaly, shiny atrophic skin Skin hairless over lower extremity Dystrophic, brittle Toenails Non-healing ulcers or other wounds on legs or feet Decreased skin Temperature Decreased Capillary Refill Time Distal extremity color change with position
PVD Sign 7. Distal extremity color change with position 1. Skin rubor when leg dependent 2. Skin pallor when leg elevated >1 minute 1. Color returns within 15 seconds in mild cases 2. Delay >40 seconds suggests severe ischemia
Signs: Acute Limb Ischemia (5 P's) 1. Early finding 1. Pain 2. Late findings 1. Pulselessness 2. Pallor 3. Paresthesias 4. Paralysis
FOUR HEART LAYERS Pericardium Epicardium Myocardium Endocardium
PERICARDIUM Outermost layer Known as parietal pericardium Holds the heart in a fixed position Provides a physical barrier against infection.
EPICARDIUM Covers the surface of the heart. Known as visceral pericardium Together with the pericardium form a sac around the heart Space between the pericardium and epicardium contains 10-30 cc serous fluid.
MYOCARDIUM Middle layer Thick and muscular Contains all of atrial and ventricular muscle fibers Responsible for the movement of blood in and out of the heart.
ENDOCARDIUM Innermost layer Thin layer of endothelium is continuous with blood vessels Lines inner chambers of heart and valves. Disruption can lead to infection
RIGHT ATRIUM (RA) Thin walled receiving chamber, 2mm thick. Receives blood from SVC, IVC and coronary sinus. Atrial contraction (atrial kick) contributes 30 % to ventricular filling. O2 Sat about 75%
RIGHT VENTRICLE (RV) Most anterior chamber Lies directly below the sternum 3-5mm thick Blood enters via tricuspid valve during diastole, (resting phase). Ejected into the pulmonary circulation through pulmonic valve
LEFT ATRIUM (LA) Most posterior chamber Receives oxygenated blood from the lungs via R/L pulmonary veins. 3mm thick O2 Sat about 98%
LEFT VENTRICLE (LV) 2-3 times thicker than the RV, 13-15 mm in size, necessary to generate enough pressure to move blood into the circulation. Apex is the tip of the LV PMI – is the movement of the apex during ventricular contraction.
CARDIAC VALVES Prevent regurgitation from one chamber to another – blood flows in ONE direction. Flexible, fibrous tissue, covered with endocardium Open/Close in response to pressure gradients 4 valves- tricuspid, pulmonic, mitral, aortic.
ATRIOVENTRICULAR VALVES Mitral – 2 cusps Tricuspid – 3 cusps Separates atriums from ventricles. Cusps are attached by the chordae tendinae and papillary muscles. These are at risk for damage with an anterior MI.
SEMILUNAR VALVES Aortic and pulmonic Separates the ventricles from their outflow arteries. Smaller than the AV valves Aortic cusps are thicker than the pulmonic Composed of fibrous supporting ring – ANNULUS.
CORONARY ARTERIES RCA RCA – supplies posterior septum, left papillary muscle, sinus and AV nodes.
CORONARY ARTERIES LCA LCA – divides into LAD and LCX. Supplies anterior ventricular wall, anterior septum, papillary muscle and apex.
CORONARY ARTERIES CX CX – supplies inferior and posterior portions of LV in some people (left coronary dominance)
stroke volume. Systole – ventricles depolarized, blood ejected from the ventricles Amount of blood ejected with each heart beat. Comprised of; Preload Afterload Contractility
Ejection Fraction- ratio of blood ejected to blood present in ventricle (N = 50-100%)
FRANK-STARLING LAW “The more the heart muscle is stretched, the greater the force of contraction”.
CARDIAC OUTPUT (CO) Amount of blood expressed in liters or per minute. Determined by heart rate and stroke volume. “Heart rate X Stroke volume = CO Normal 4-8 liters /minute.
DETERMINANTS OF CARDIAC OUTPUT Heart Rate Stroke Volume Preload Afterload Contractility
HEART RATE Chronotropic SA node – N=60-100 Influenced by neural, (PNS –SNS) hormonal, (catacholamines) chemical (acid-base disturbances) and pharmacological means (medications).
PRELOAD Pressure (load) generated in cardiac chambers prior (pre) to ejection. (pressure in the ventricles at the end of diastole). Determined by the end diastolic volume, (the amount of blood left in the ventricles during rest)
AFTERLOAD Resistance (load) to ejection (after) of blood from the ventricles (the amount of pressure the ventricles must push against). Clinical indicators; systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR)
CONTRACTILITY Inotropic The force of ejection . Can be positive or negative. Clinical indicators; cardiac output, and cardiac index.
CARDIAC INDEX Relationship between cardiac output and body surface area. Decrease indicates heart failure. Increase indicates decreased SVR, (common in sepsis). Calculate by dividing CO into body surface area. Normal; 2.5 – 4.0 liters/min.
CHF Most common cause of in-hospital mortality. 1/3 rd of patients with AMI die of CHF. 2nd most common complication after an MI Men are affected more than women. 5 yr mortality rate for men is 60 %, women 45%.
CHF DEFINITION Inability of the heart to pump enough blood to meet the body’s metabolic requirements leading to discrepancies between myocardial oxygen supply and demand.
CHF PATHOPHYSIOLOGY Malfunction of the contractile properties of the heart leading to decrease CO. Heart rate Stroke volume
Damaged heart is unable to pump extra volume = decreased CO, (decreased CO=^ HR = short diastolic filling time and ^myocardial O2 demand.
STROKE VOLUME Preload Volume of blood in ventricles at end of systole. Volume causes maximal stretch. Greater the stretch = greater SV up to a certain point. Past this point = overstretch of muscle = a non-compliant ventricle, needs extra volume = heart failure.
CHF Causes Primary: cardiomyopathies, CAD or valvular disorders. Aortic stenosis; narrow valve = hypertrophy, non-compliant ventricle. Aortic regurgitation: back flow of blood = hypertrophy. Mitral regurgitation; pulmonary congestion = RV failure.
PRECIPITATING FACTORS FOR CHF Cessation of cardiac drugs. Dysrythmias – tachycardia, atrial dysrythmias. Viral and/or bacterial infections Environmental, emotional or physical stress
Right-sided failure: CHF ineffective (R) ventricular contraction or total (R) sided failure, ie; PE, right-sided MI, or blood backing up into the left ventricle.
Left-sided failure: inability of the (L) ventricle to produce adequate SV = decreased CO. ie; (L) ventricular MI, HTN and/or valvular disease.
Systolic vs. diastolic failure Systolic ; inability of ventricles to eject adequate volume. Diastolic failure; inability of ventricles to relax and fill.
High vs. low output failure; High-conditions that increase CO i.e.; fever, thyrotoxicosis Low: insufficient ejection that results in inadequate CO.
Forward Failure: inability of the ventricles to pump blood into the systemic and pulmonary circulation. (afterload)
Backward Failure: Inadequacy of the ventricles to empty the blood into the arterial circulation.
Acute CHF ; heart overwhelmed by abrupt alteration in cardiac function; unable to bring compensatory mechanisms into play.
Chronic CHF compensatory mechanisms have time to partially/completely restore cardiac function.
IMPROVE CONTRACTILITY Positive inotropic agents. Dopamine Dobutamine Primacor Digoxin Natrecor
DECREASE Cardiac PRELOAD AND AFTERLOAD Loop/potassium sparing diuretics - prevents reabsorption of NA. Nitrates- increases CO and reduces ventricular filling pressures. (not effective in chronic therapy) ACE inhibitors- vasodilatation by blocking the renin-angiotensin-aldosterone system.
Carvedilol (Coreg) Beta-1 and alpha-1 blocker Reduce afterload HF classes II, III and IV Symptomatic hypotension, start low and increase to 25 mg BID. Use caution in asthmatics
Amiodarone Reduces the possibility of sudden death in patients with LV dysfunction from AMI. Effective in atrial fibrillatio Anti-ischemic effects Does not increase mortality Half life – 40-50 days.
Some of the causes of heart failure include: coronary artery disease (CAD), damage after a heart attack (which stems from coronary artery disease), high blood pressure, diabetes, obesity, heart valve disease, viruses,  chemotherapy agents, chronic alcohol use and abuse, & drug abuse.
There are two major underlying causes of the symptoms in heart failure: excess fluid accumulation that may occur in the lungs and symptoms associated with reduced cardiac output that worsens with exertion.
Shortness of breath (dyspnea). In CHF This is one of the earliest symptoms of heart failure. The patient gets winded and fatigued more quickly than before, just by doing regular daily activities or even lying in bed.
The normal pumping ability of our left ventricle is 50-75%
BNP is very helpful in diagnosing CHF. A normal BNP level is about 98% accurate in ruling out the diagnosis.
BNP is very helpful in guiding the treatment of CHF. Effective therapy reduces the backup of blood in the heart. The heart chambers get smaller, and as the muscle cells recover from being stretched, they produce less BNP
Right Heart Catheterization (RHC). A catheter is passed through the jugular vein in your right neck into the right side of your heart. This catheter is used to measure right and left pressures, as well as, pulmonary wedge pressures.
Left Heart Catheterization (angiogram) is performed to determine if you have coronary artery disease. A catheter is inserted in your right groin and guided to your heart. blockages in the coronary arteries are shown on x-ray.
Heart failure is usually a chronic condition that has taken years to develop and worsen. Treatment for heart failure is generally designed for three purposes: 1. to improve any symptoms 2. to slow progression of the heart failure, and 3. to prolong survival.
CHF lifestyle changes include limiting salt intake and reduced fat diet to achieve or maintain a healthy weight. Other lifestyle modifications include stress management, limiting caffeine and alcohol, stop smoking, and getting regular exercise
What would be a key education point to make with patients about low salt diets and salt substitutes? Salt substitutes vary in their composition, but their main ingredient is always potassium chloride.
Patient education specific to CHF that should be included: Keep a daily weight diary and call for an increase in >3lbs in a single week Staying as active as possible once cleared for activity Take frequent breaks and rest periods throughout the day Limit salt intake Avoid excess fluid intake
Agonist drugs that bind to a receptor site to CAUSE a response
Antagonist drugs that block a receptor site from a response or to keep other drugs from binding
Inotropic Action- myocardial contraction (positive increases contraction, negative decreases contraction)
Chronotropic Action- heart rate (positive increases HR, negative decreases HR)
Alpha Receptors- Alpha 1- generalized vasoconstriction and mediates positive inotropic and negative chronotropic effects Alpha 2- mediates arteriolar and venous vasoconstriction
Beta Receptors- Beta 1- increases heart rate, cardiac contractility, conduction and irritability Beta 2- vasodilation in skeletal and smooth cardiac muscle and bronchodilation
Dopaminergic Receptors vasodilation of renal and mesenteric arteris
The diuretics most commonly used for heart failure are loop diuretics. These diuretics are usually taken by mouth on a long-term basis Loop diuretics are preferred for moderate to severe heart failure.
Thiazide diuretics, which have milder effects and can lower blood pressure, may be prescribed particularly for people who also have high blood pressure For people with severe heart failure due to systolic dysfunction, Spironolactone is the preferred potassium-sparing diuretic
The mainstay of heart failure treatment is a group of drugs called ACE inhibitors. These drugs not only reduce symptoms and the need for hospitalization but also prolong life.
Beta-blockers are often used with ACE inhibitors to treat heart failure. By blocking the action of the hormone norepinephrine (which causes the heart to pump faster and more forcefully), these drugs produce long-term improvement in heart function and survival.
Beta-blockers may significantly reduce the force of the heart's contractions initially, so they are usually introduced after heart failure has first been stabilized with other drugs. In people with heart failure due to diastolic dysfunction, beta-blockers are used to slow the heart rate and relax the stiff or thickened muscle allowing for complete filling.
Digoxin is the only oral inotrope available. It has been used to treat heart failure since the 1700's. However, modern science recommends the treatment of heart failure should now begin with the prescribing of ACE inhibitors or carvedilol before digoxin.
Digoxin does NOT reduce mortality rates, but it improves symptoms and seems to decrease hospitalizations.
Lacunar Infarction Seen more in the elderly and diabetic patients Small lesions usually < 5 mm in diameter that occur in the basal ganglia, pons, cerebellum, usually associated with poorly controlled HTN. The neurologic symptoms progress over 24-36 hrs before stabilizing
Klippel-Trenaunay syndrome Triad of of varicose veins, limb hypertrophy, and a cutaneous birthmark (port wine stain or venous malformation)-Tierney pg 451
“Tracheal tug” is palpable pull from midline with breathing pull with inspiration (Adam’s apple (trachea) moves up and down) is a diagnostic sign for emphysema (also pull with pulsation is diagnostic sign for aneurysm of the arch of the aorta)
Digital clubbing does not normally accompany asthma or COPD-IF PRESENT SUSPECT CONCOMITANT LUNG CANCER
Chronic bronchitis Blue Bloater due to obstruction-term not used today
Emphysema Pink Puffers (term not used today)- No obstruction with adequate oxygen intake, puff to blow off extra co2 Differentiated from acute asthma (asthma remits between episodes
Pulmonary Function Tests will determine severity of both obstructive and restrictive pulmonary dysfunction Defines severity Helps in determining prognosis Measures response to therapy Measures disease progression
COPD Treatment Smoking cessation most important intervention- must be documented
Supplemental oxygen COPD only other drug therapy that is documented to alter natural history of COPD in pts with resting hypoxemia Prolongs life and improves quality
Ipratropium bromide (Atrovent) Superior in achieving bronchodilation in pts with mod to severe COPD Slower onset but longer duration Advantage Low incidence of SE’s; no tachyphylaxis
Tiotropium (Spiriva) capsule activated inhaler once a day dosing-a significant improvement for compliance issues some studies show greater efficacy over ipratropium over 1 year but may be a compliance issue used with short acting bronchodilator
Narcotics are contraindicated in COPD
Oxygen Criteria Prescribe O2 at 0.5-4 L/min to produce Pao2 >65 mm or SaO2>90% at rest and with activity Specify in L/min and hours per day used Reevaluate in 1-3 months as 30-45% will not need long-term therapy
Consider COPD, and perform spirometry, if any of these indicators are present in an individual over age 40. Spirometry is required to establish a diagnosis of COPD Dyspnea that is Progressive Characteristically worse with exercise. Persistent. Chronic cough: Chronic sputum production: Any pattern of chronic sputum production History of exposure to risk factors: Tobacco smoke Family History
Spirometry is required to make a clinical diagnosis of COPD; the presence of a postbronchodilator FEV 1 /FVC < 0.70 confirms the presence of persistent airflow limitation and thus of COPD.
Classification of Severity of Airflow Limitation in COPD (Based on Post-Bronchodilator FEV1) Gold 1 Mild FEV1≥ 80% predicted
Classification of Severity of Airflow Limitation in COPD (Based on Post-Bronchodilator FEV1) Gold 2 Moderate 50%≤FEV1< 80% predicted
Classification of Severity of Airflow Limitation in COPD (Based on Post-Bronchodilator FEV 1)Gold 3 severe 30% ≤ FEV1< 50% predicted
Classification of Severity of Airflow Limitation in COPD (Based on Post-Bronchodilator FEV 1)Gold 4 Very Severe FEV1< 30% predicted
FVC (Forced Vital Capacity): maximum volume of air that can be exhaled during a forced maneuver
FEV1 (Forced Expired Volume in one second): volume expired in the first second of maximal expiration after a maximal inspiration. This is a measure of how quickly the lungs can be emptied.
FEV1/FVC: expressed as a proportion of the FVC, gives a clinically useful index of airflow limitation. The ratio FEV 1 /FVC is between 0.70 and 0.80 in normal adults; avalue less than 0.70 indicates airflow limitation and thus of COPD.
Screening for Lung Cancer Screening for lung cancer has not been recommended by any major advisory groups
Low dose helical (spiral) computed tomography (LDCT) evaluated in randomized clinical trial by NLST* First validated screening test that reduces mortality from lung cancer 20% lower mortality from lung cancer vs. serial chest radiography
Bronchogenic carcinoma 4 types account for more than 90% of lung cancers Squamous cell carcinoma (25-35%) Adenocarcinoma (35-40%) Large cell carcinoma (5-10%) Small cell carcinoma (15-20%)
Small cell lung cancer (SCLC) Early hematogenous spread Agressive course Untreated survival of 6-18 weeks Not amenable to surgical resection
Non-small cell lung cancer (NSCLC) Includes other 3 types Spread more slowly Cure in early stages following resection Respond similarly to chemotherapy
Squamous Cell Carcinoma Originates from the respiratory epithelium. Typically x-rays show atelectasis or pneumonitis.
Adenocarcinoma Probably arise from the goblet cells in the major bronchi. Most often found in nonsmokers. Bronchoalveolar cell carcinoma: subset of adenocarcinoma can mimic an infectious or inflammatory pneumonia.
Large-Cell Carcinoma Tend to appear as large peripheral mass lesions. 50% develop brain metastases. Giant-cell carcinoma subset of large-cell carcinoma aggressive, highly malignant tumor
Horner’s Syndrome Ipsilateral symptoms (same side) Ptosis (drooping of eyelid) Miosis (pupilary constriction) Anhidrosis (absent sweating)
Horner’s Syndrome Cause: paralysis of paravertebral sympathetic nerve trunk due to compression by a tumor Most frequently caused by Pancoast tumor of either upper lung
TNM international staging Physical description of neoplasm T --size and location of primary tumor N --presence and location of nodal metastases M --presence or absence of distant metastases
Solitary Pulmonary Nodule (SPN) Unexpected finding, usually incidental on chest radiograph Referred to as a “coin lesion” Isolated , round opacity,< 3 cm No mediastinal adenopathy No associated infiltrate or atelectasis Important because carries significant chance of malignancy
Hodgkin’s Disease Peak incidence 3rd decade Fatigue, fever, weight loss, anemia Peripheral lymphadenopathy May involve the thorax Radiation and chemotherapy
Non-Hodgkin’s Peak incidence over 50 Involves mediastinum and lungs Fever, anorexia, weight loss Treatment with chemotherapy and radiation Response to treatment/prognosis less favorable than for Hodgkin’s
Sarcoidosis is a type of interstitial lung disease (diffuse parenchymal lung disease) Large group of disorders Share common response of lung to injury alveolitis or inflammation fibrosis of interalveolar septum
Sarcoidosis Epidemiology 1 per 10,000 per year Age 20-40 North American blacks Women > men Blacks have 3-4 times incidence of whites Northern European whites
Sarcoidosis Etiology Unknown Granulomatous inflammation of lungs Resolves in 2/3 15-20% lung damage 5% will die
Sarcoidosis Pathophysiology Hyperimmune response to unknown agent Lesions in any organ Lungs and intrathoracic lymph nodes affected in 90% Alveolitis Interstitial pneumonitis Granuloma formation
Children with chronic illnesses in general are affected by a ________ number of common diseases. large
In differentiating delirium from dementia, which of the following questions posed to a family member is most important? How long have the symptoms been present?
The most common cause of progressive dementia is: Alzheimer's disease
The most common type of Parkinson's Disease is: Idiopathic
Carbidopa is added to levodopa for which of the following reasons: Carbidopa inhibits breakdown of levodopa, increases CNS concentrations, and increases half-life of levodopa.
Serum amylase is often checked in patients with anorexia nervosa or bulimia. Elevated results would indicate: active vomiting and associated pancreatitis.
What should be the practitioner's initial goal in the treatment of anorexic clients? Establishing trust and a treatment alliance
Which of the two conditions anorexia nervosa and bulimia nervosa carry the poorest long-term psychiatric prognosis? bulimia nervosa
The regional distribution of body fat is helpful in determining risk for complications of obesity. Which of the following body shapes is associated with the highest risk: Apple-shaped.
A female patient presents with severe depressive symptoms that occur nearly monthly around her menstrual cycle. You suspect: Premenstrual Dysphoric Disorder
A person with chronic depressive symptoms of sadness, loss of interest, and withdrawal from activities over a period of 2 or more years with a relatively persistent course is MOST likely diagnosed with: Dysthymia
Which of the following would not routinely be ordered in the initial work-up to rule out medical causes of depression? CT brain scan.
In the management of depressive disorders the plan always includes: Evaluation of the patient's potential risk for self harm.
Symptoms especially characteristic of depression do not include Acute-sharp pain syndromes.
Symptoms of mania and depression that may show psychotic features is most consistant with the diagnosis of: Bipolar Disorder
Symptoms of palpitations, tachycardia, chest pain, hot flashes, & chills in an otherwise healthy 21 year old is most consistent with the diagnosis of: Panic Attack.
Which of the following statements concerning Panic Disorders is true? Onset of Panic Disorder is rare after age of 40.
DSM-IV criterion for major depressive episode? Persistence of symptoms for a period of at least 2 weeks
Calcium channel blockers should be used with extreme caution to treat angina or hypertension in a patient with congestive heart failure for the following reason: Calcium channel blockers can accelerate progression of congestive heart failure.
Clinical trials dealing with beta-blocker use in congestive heart failure have led to a strong recommendation that: Stable patients with congestive heart failure should be treated with beta blockers unless there is a noncardiac contraindication.
Inhibition of what system is important in preventing progression of congestive heart failure? renin-angiotensin-aldosterone system
A patient with peripheral arterial occlusive disease is also at risk for: Coronary artery disease.
Bruits heard with decreased pulse distally indicate: Significant obstruction.
The decline in stroke incidence over the last four decades has been MAINLY attributed to the management of which of the following risk factors for stroke. Hypertension
Immediate treatment for stroke due to ischemic infarction is: Thrombolytic therapy.
Chronic bronchitis is: Defined as excessive secretion of bronchial mucous and productive cough 3 month or more in at least 2 consecutive years.
A client with a long history of chronic airflow limitation has noticed an increased cough and a change in sputum over the past few days (increased amount of thick, yellow-green mucus, congestion). Appropriate therapy is: Augmentin 500 mg PO tid X 10 days.
In prescribing medications for your patient with COPD, you understand which of the following to be true: Bronchodilators are not as effective in emphysema as in asthma.
One of the most common complications of an acute exacerbation of chronic bronchitis is: Left sided heart failure
When assessing the pulmonary function studies of a client, which assessment finding is seen in chronic obstructive pulmonary disease? FEV1/FVC ratio is < 70%.
Your 76 year old male patient is complaining of increased dyspnea at rest. You note his SaO2 is 86% while sitting in your office. You know that the only drug therapy that is documented to alter this patient's hypoxemia is: Oxygen
Screening for lung cancer: has not been recommended by any major advisory groups.
The most aggressive type of lung cancer is: Small cell carcinoma
Upon consultation with the radiologist and pulmonologist, a Single Pulmonary Nodule is gauged as having a low probability of malignancy. The nurse practitioner's management plan will most likely consist of: Watchful waiting with serial radiographs every 3 months for a year then every 6 months for a second year.
A benign neoplasm that is thought to be congenital and comprises about 5% of all lung neoplasms is: Hamartoma
A patient states that he has noted his left pupil is smaller than his right and complains of a slight droop to the same eyelid. The practitioner upon noting this sign should check for Horner's syndrome by checking for absence of: sweating of the ipsilateral (same side) of the forehead
Hodgkin's disease typically: presents in the 3rd decade of life (20's)
Which of the following TNM stages represents the worst prognosis? Stage IV
Created by: kcorkinsnctc
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