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AGACNP Test -2 Questions and Answers

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AGACNP Test -2 Questions and Answers COPD a common preventable and treatable disease characterized by persistent airflow limitation, usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. Small Airways Disease Airway inflammation Airway fibrosis, luminal plugs Increased airway resistance Parenchymal Destruction Loss of alveolar attachments Decrease of elastic recoil Airflow limitation Small airways disease and parenchymal destruction Modified British Medical Research Council (mMRC) Questionnaire 0. Not troubled with breathlessness except with strenuous exercise. 1. Troubled by shortness of breath when hurrying or walking up a slight hill. 2. Walks slower than people of the same age due to breathlessness or has to stop for breath when walking at own pace on the level. 3. Stops for breath after walking ~100 m or after a few minutes on the level. 4. Too breathless to leave the house or breathless when dressing or undressing. GOLD 1: Mild FEV1 80% predicted GOLD 2: Moderate 50% FEV1 80% predicted GOLD 3: Severe 30% FEV1 50% predicted GOLD 4: Very Severe FEV1 30% predicted PFT classification of COPD In patients with FEV1/FVC 0.70: Albuterol Short-acting beta2-agonists Salmeterol, andacaterol Long-acting beta2-agonists Ipratropium Short-acting anticholinergics Tiotropium, aclidinium Long-acting anticholinergics theophylline Methylxanthines beclomethasone Inhaled corticosteroids Milquetoast Phosphodiesterase-4 inhibitors The most common causes of COPD exacerbations viral upper respiratory tract infections and infection of the tracheobronchial tree. The goal of COPD treatment to minimize the impact of the current exacerbation and to prevent the development of subsequent exacerbations. indicates respiratory failure in COPD ABGs: PaO2 60 mm Hg with or without PaCO2 50 mm Hg when breathing room air Asthma Chronic inflammatory disorder of the airways leading to airflow limitation.Changes that occur within the airway 2nd to inflammation: Bronchoconstriction; Airway hyperresponsiveness; and Airway edema. Partially reversible Asthma treatment step 1 asthma education, environmental control, and as needed rapid acting beta2-agonists Asthma treatment step 2 asthma education, environmental control, and as needed rapid acting beta2-agonists and low dose inhaled corticosteroids or leukotreine modifer Asthma treatment step 3 asthma education, environmental control, and as needed rapid acting beta2-agonists and low dose inhaled corticosteroids plus long acting beta2-agonist or low dose inhaled corticosteroids plus leukotreine modifer or low dose inhaled corticosteroids plus sustained released theophylline or medium/high dose inhaled corticosteriods Asthma treatment step 4 asthma education, environmental control, as needed rapid acting beta2-agonists and add two of the following: low dose inhaled corticosteroids plus long acting beta2-agonist or low dose inhaled corticosteroids plus leukotreine modifer or low dose inhaled corticosteroids plus sustained released theophylline or medium/high dose inhaled corticosteriods. Asthma treatment step 5 asthma education, environmental control, as needed rapid acting beta2-agonists and add two of the following: low dose inhaled corticosteroids plus long acting beta2-agonist or low dose inhaled corticosteroids plus leukotreine modifer or low dose inhaled corticosteroids plus sustained released theophylline or medium/high dose inhaled corticosteriods. and add low dose oral glucocorticosteriod or anti IgE treament Exacerbations of asthma episodes of progressive increase in shortness of breath, cough, wheezing, or chest tightness Community Acquired Pneumonia (CAP) an acute infection of the pulmonary parenchyma in a patient who has acquired the infection in the communitycan be caused by a variety of pathogens with bacteria being the most common. Streptococcus pneumoniae is predominant Pathogens in pts with CAP that require admission to the ICU S. pneumonaie, legionella, GNB, staph aureus, and influenza. CURB-65 Confusion, BUN 19.6, Resp. rate 30, BP 90/60, age /= 65 The Pneumonia Severity Index used to determine a patient's risk of death. The total score is obtained by adding to the patient's age (in years for men or in years - 10 for women) the points assigned for each additional applicable characteristic. Risk score of IV or above, should be admitted Inpatient non-ICU treatment for pneumonia a respiratory fluoroquinolone (Avelox) or beta lactam (ceftriaxone) plus macrolide (arithromycin) Inpatient ICU treatment for pneumonia beta lactam (ceftriaxone) plus macrolide (arithromycin) or a respiratory fluoroquinolone (Avelox) Hospital Acquired Pneumonia (HAP) defined as PNA that occurs 48 hours or more after admission and that was not incubating at time of admission Ventilator Acquired Pneumonia (VAP) defined as PNA that occurs 48-72 hours after endotracheal intubation HCAP includes patients with PNA who are hospitalized in an acute care hospital for more than 2 days within 90 days of the PNA, those who reside in long term care, those who received recent IV antimicrobial therapy, chemotherapy, or wound care within 30 days of PNA, or those who received treatment in a dialysis center/hospital criteria for empiric ATB therapy Fever greater than 38 degrees C, purulent sputum, leukocytosis or leukopenia, decline in oxygenation (2 of 3) + new or worsening radiographic infiltrate Pleural effusion Abnormal Collection of fluid in the pleural space resulting from excess fluid production or decreased absorption. Results from disruption in hydrostatic and oncotic forces in the visceral and parietal pleural or impaired lymphatic drainage.Multiple etiologies but primarily caused by CHF, pneumonia, malignancy, or PE Transudates usually ultra filtrates of plasma in the pleura due to imbalance of hydrostatic and oncotic forces in the chest. Generally occurs in the absence of pleural ds. Exudates produced by inflammatory conditions or impaired lymph drainage and often require more extensive evaluation and treatments Light's Criteria If at least one of the following is present: Pleural fluid to serum protein 0.5; Pleural fluid to serum LDH than 0.6; Pleural fluid LDH 2/3 of the upper limits of normal serum value Acute Respiratory Failure Relatively rapid respiratory dysfunction leading to acute hypoxemia and/or acute hypercapnea leading to compromise of other organ functions Hypoxemic failure (PaO2 ≤50-60 mm Hg) an alteration in diffusion across the alveolar-capillary membrane treatment is to oxygenate Hypercapneic failure (PaCO2 ≥ 50 mm Hg) inadequate minute ventilation (movement of air) treatment is to ventilate Ventilation/perfusion (V/Q) ratio is defined as alveolar ventilation (~4 L/min)over pulmonary blood flow (~5 L/min); average = 0.8 Shunt defined as blood that flows past the alveoli with little or no gas exchange calculated by PaO2/FiO2 acute lung injury PaO2/FiO2 ratio = 300 ARDS PaO2/FiO2 ratio = 200 treat the cause, low tidal volume, PEEP usage with FiO2 needs Average Ventilation/Perfusion (VQ) ratio 0.8 VQ ratio increases in dead space (pneumothorax, pulmonary embolism) VQ ratio decreases in shunting (obstructive diseases, pneumonia, pulmonary edema, and ARDS) Shift to the left (bind O2) alkalosis, hypocarbia, DKA, hypothermia Shift to the right (release O2) acidosis, hypercarbia, COPD, hyperthermia, anemia Continuous Mandatory Ventilation (CMV) All breaths are mandatory and can be volume or pressure targeted. Controlled Ventilation when mandatory breaths are time triggered Mandatory breath - ventilator determines the start time (time triggered) and/or the volume or pressure target Assist/Control Ventilation A timed or patient triggered CMV mode in which the clinician sets a minimum rate, sensitivity level, type of breath (volume or pressure) Patient can trigger breaths at a faster rate than the set minimum, but only the set volume or pressure is delivered with each breath Pressure Controlled - CMV Time or patient triggered, pressure targeted (limited), time cycled ventilation. The clinician sets the length of inspiration (Ti), the pressure level, and the backup rate of ventilation. VT is based on the compliance and resistance of the patient's lungs, patient effort, and the set pressure and therefore a dependent variable Intermittent Mandatory Ventilation - IMV Periodic volume or pressure targeted breaths occur at set interval (time triggering). Between mandatory breaths, the patient breathes spontaneously at any desired pressure/volume without receiving a mandatory breath Spontaneous breathing Patients can breathe spontaneously through a ventilator circuit which allows for back-up rate to be set in case of apnea Disconnected and oxygen supplied per T-piece CPAP/PEEP for spontaneously breathing patients; used in conjunction with ventilator breath. Assists oxygenation in patients with refractory hypoxemia and a low FRC Pressure Support Ventilation - PSV Patient triggered, pressure targeted, flow cycled mode of ventilation Requires a patient with a consistent spontaneous respiratory pattern if not used in conjunction with another mode The ventilator provides a constant pressure during inspiration once it senses that the patient has made an inspiratory effort Non Invasive Positive Pressure Ventilation Deliver PS and CPAP via tight fitting mask (BiPAP: bi-level positive airway pressure) Can set "back up" rate May still need sedation Patient must be able to protect their airway! BiPAP The operator sets two pressure levels IPAP (Inspiratory Positive Airway Pressure) IPAP is always set higher than EPAP Augments VT and improves ventilation EPAP (Expiratory Positive Airway Pressure) Prevents early airway closure and alveolar collapse at the end of expiration by increasing (and normalizing) the functional residual capacity (FRC) of the lungs Facilitates better oxygenation To affect oxygenation, adjust: FiO2; PEEP; I time; PIP To affect ventilation adjust: Respiratory Rate; Tidal Volume ABCDE bundle Awake Breathing coordination Choice of sedative Delerium screening Exercise Gram Positive (stain blue) Staphylococcus; Streptococcus; Enterococcus Peptostreptococcus; Clostridium; Actinomyces Gram Negative (stain red) Neisseria; Moraxella; E.Coli, Proteus, Klebsiella, Serratia, Enterobacter, Shigella, Salmonella, Yersinia, Pneudomonas, Strenotrophomonas, Bacteroides Coagulase test enyzyme produced by some bacteria converts fibrinogen to fibrin. Used to differentiate species of staphylococcus Coagulase Positive staph aureus & some S. intermedius Coagulase Negative most other Staph spp. (eg S. epidermidis, S. capitis, S. lugdunensis, S. Saprophyticus). Usually contaminants Alpha Hemolytic Strep (partial hemolysis)- oxidizes the iron in hGb molecule to create met-Hgb: S. pneumoniae, Viridans strep. Beta Hemolytic Strep (complete hemolysis)- complete clearing of blood around bacteria: S. pyogenes, S. agalactiae Gamma Hemolytic Strep (no hemolysis): S. bovis, enterococcus(was considered a type of strep until 1980`s Anaerobes Include all bacteria which grow and only reproduce in absence of oxygen. Predominately found in GI tract (oral cavity) Generally stainable via gram stain, rarely referred to as Gm+ or Gm - in clinical practice. Examples: Clostridium, Bacteroides, Peptostreptococcus, Actinomyces Positive Nitrite Test suggest responsible organism produces nitrate reductase-(reduces nitrates normally occurring in the urine to nitrites). Occurs with anything but Enterococcus & S. saprophyticus Urine pH 6.5 in absence of alkalemia, suggest the organism produces enzyme urease, which catalyzes the hydralasis of urea into CO2 and ammonia. Limited to Proteus, Klebsiella, S. saprophyticus. Antibiotic any compound (natural or synthetic) that inhibits the growth of, or actively kills, microorganisms. Bacteriostatic inhibits bacteria from reproducing, but doesn't otherwise kill them Bactericidal actively kills bacteria Interferes with cell wall synthesis or maintenance Beta Lactams; Penicillins; Cephalosporins; Carbapenemsl; Monobactams; Vancomycin; Daptomycin; Polypeptides (bacitracin & colistin) Inhibit Nucleic Acid Synthesis or Function Quinolones; Trimethoprim/Sulfamethoxazole; Metronidazole, Nitrofurantoin Interferes with protein synthesis Macrolides; Clindamycin; Linezolid; Streptogramins; Chloramphenicol; Aminoglycosides; Tetracyclines; Tigecycline Beta-Lactams First, most diverse and most commonly used class of antibiotics Work by irreversibly inhibiting enzymes responsible for the final step in the synthesis of the peptidoglycan layer of bacterial cell walls Generally bactericidal Quinolones Bactericidal; Excellent absorption & bioavailability; Most are available IV and PO forms; Widely distributed, except: All quinolones have poor CNS penetration Aminoglycosides Bacteriocidal; Most commonly used for serious infections caused by aerobic GNR (include pseudomonas- but not as monotherapy) Not used as monotherapy for Gm positive infections, but are sometimes used in combination with a beta-lactam or vancomycin, especially for endocarditis; Development of resistance is uncommon; Use limited by relatively serious toxicities (nephrotoxicity, ototoxicity, neuromuscular blockade). TIA A transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction Stroke is evidenced by infarction on MRI ABCD2 Scale Age 60 years = 1 point Blood Pressure Systolic BP 140 mmHg OR diastolic BP 90 mm Hg = 1 point Clinical Features Unilateral weakness with or without speech impairment = 2 points Speech impairment without unilateral weakness = 1 point Duration 60 minutes = 2 points 10 - 59 minutes = 1 point Diabetes = 1 point 2 day stroke risk: 0 - 3: low risk 4 - 5: moderate risk 6 - 7: high risk Left hemisphere syndrome Aphasia, agraphia, acalculia, apraxia, left lateral gaze, preference, right visual field deficit, right hemiparesis, right hemisensory loss Right hemisphere syndrome Extinction, right gaze preference, left visual field deficit, flat affect, constructional apraxia, dressing apraxia, left hemiparesis, left hemisensory neglect Brainstem/cerebellar syndrome Hemiparesis, quadriparesis, hemisensory or 4 extremity loss, eye movement abnormalities, diplopia, oropharyngeal weakness, vertigo, tinnitus, nausea, dysmetria, ataxia, dysarthria Carotid Artery Contralateral motor and sensory loss, amaurosis fugax, homonymous hemianopsia, Horner's syndrome, facial, asymmetry, aphasia, headache over ipsilateral eye Anterior Cerebral Artery Confusion, personality change, incontinence, contralateral motor or sensory loss greater in leg, rigidity, abulia, perseveration, cognitive impairment, distractibility, apraxia Middle Cerebral Artery Contralateral motor or sensory loss greater in arm, contralateral motor loss in lower face, contralateral visual field loss, language loss, dyslexia, acalculia, agraphia, spatial-perceptual loss, dressing and constructional apraxia Posterior Cerebral Artery Contralateral motor or sensory loss, ipsilateral visual field loss, cortical or bilateral blindness, dysarthria, dysphagia, diplopia, quadriparesis Vertebrobasilar Circulation Cranial nerve deficits, ataxia, blindness or hemianopia, confusion, diplopia, nystagmus, conjugate gaze paralysis, bilateral limb weakness, bilateral paresthesia, slurred speech, facial weakness, tinnitus, vertigo, nausea, transient global amnesia, dysarthria, dysphagia, dysmetria, drop attacks, syncope

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AGACNP Test #2 Questions and
Answers
COPD - answera common preventable and treatable disease characterized by
persistent airflow limitation, usually progressive and associated with an enhanced
chronic inflammatory response in the airways and the lung to noxious particles or
gases.

Small Airways Disease - answerAirway inflammation
Airway fibrosis, luminal plugs
Increased airway resistance

Parenchymal Destruction - answerLoss of alveolar attachments
Decrease of elastic recoil

Airflow limitation - answerSmall airways disease and parenchymal destruction

Modified British Medical Research Council (mMRC) Questionnaire - answer0. Not
troubled with breathlessness except with strenuous exercise.
1. Troubled by shortness of breath when hurrying or walking up a slight hill.
2. Walks slower than people of the same age due to breathlessness or has to stop for
breath when walking at own pace on the level.
3. Stops for breath after walking ~100 m or after a few minutes on the level.
4. Too breathless to leave the house or breathless when dressing or undressing.

GOLD 1: Mild - answerFEV1 > 80% predicted

GOLD 2: Moderate - answer50% < FEV1 < 80% predicted

GOLD 3: Severe - answer30% < FEV1 < 50% predicted

GOLD 4: Very Severe - answerFEV1 < 30% predicted

PFT classification of COPD - answerIn patients with FEV1/FVC < 0.70:

Albuterol - answerShort-acting beta2-agonists

Salmeterol, andacaterol - answerLong-acting beta2-agonists

Ipratropium - answerShort-acting anticholinergics

Tiotropium, aclidinium - answerLong-acting anticholinergics

, theophylline - answerMethylxanthines

beclomethasone - answerInhaled corticosteroids

Milquetoast - answerPhosphodiesterase-4 inhibitors

The most common causes of COPD exacerbations - answerviral upper respiratory tract
infections and infection of the tracheobronchial tree.

The goal of COPD treatment - answerto minimize the impact of the current exacerbation
and to prevent the development of subsequent exacerbations.

indicates respiratory failure in COPD - answerABGs: PaO2 < 60 mm Hg with or without
PaCO2 > 50 mm Hg when breathing room air

Asthma - answerChronic inflammatory disorder of the airways leading to airflow
limitation.Changes that occur within the airway 2nd to inflammation:
Bronchoconstriction; Airway hyperresponsiveness; and Airway edema. Partially
reversible

Asthma treatment step 1 - answerasthma education, environmental control, and as
needed rapid acting beta2-agonists

Asthma treatment step 2 - answerasthma education, environmental control, and as
needed rapid acting beta2-agonists and low dose inhaled corticosteroids or leukotreine
modifer

Asthma treatment step 3 - answerasthma education, environmental control, and as
needed rapid acting beta2-agonists and low dose inhaled corticosteroids plus long
acting beta2-agonist or low dose inhaled corticosteroids plus leukotreine modifer or low
dose inhaled corticosteroids plus sustained released theophylline or medium/high dose
inhaled corticosteriods

Asthma treatment step 4 - answerasthma education, environmental control, as needed
rapid acting beta2-agonists and add two of the following: low dose inhaled
corticosteroids plus long acting beta2-agonist or low dose inhaled corticosteroids plus
leukotreine modifer or low dose inhaled corticosteroids plus sustained released
theophylline or medium/high dose inhaled corticosteriods.

Asthma treatment step 5 - answerasthma education, environmental control, as needed
rapid acting beta2-agonists and add two of the following: low dose inhaled
corticosteroids plus long acting beta2-agonist or low dose inhaled corticosteroids plus
leukotreine modifer or low dose inhaled corticosteroids plus sustained released
theophylline or medium/high dose inhaled corticosteriods. and add low dose oral
glucocorticosteriod or anti IgE treament

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