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64 Cards in this Set

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SNORING
PARTIAL UPPER AIRWAY OBSTRUCTION, USUALY CAUSED BY TONGUE
STRIDOR
HARSH INSPIRATORY SQUEAL, PARTIAL UPPER AIRWAY OBSTRUCTION
WHEEZING
LOWER AIRWAY, WHISTLING SOUND CAUSED BY NARROWING OF SMALL AIRWAY, HEARD PRIMARILY ON EXPIRATION
RONCHI
RATTLING SOUND IN LARGER AIRWAYS, MUCUS OR FLUID BUILD UP
RALES
CRACKLES, MOIST CRACKLING SOUND, FLUID OR MUCUS IN ALVEOLI, ATELECTASIS-WHEN ALVEOLI ARE REINFLATED
FRICTION RUB
DRY, GRATING, LEATHERYSOUND HEARD ON OSCULATION, DUE TO INFLAMED PLUREA, CAUSES CHEST PAIN ON INSPIRATION
PULSUS PARADOXUS
DECREASE IN SYSTOLIC PRESSURE (10mmHg) OR LOSS OF PERIPHERAL PULSE DURRING INSPIRATION
WHAT ARE SOME CAUSES OF PULSUS PARADOXUS
COPD, ASTHMA, TENSION, TAMPONADE
EUPNEA
STEADY EVEN BREATHS, 12-20 MIN.
TACHYPNEA
RAPID, RATE OVER 20
BRADYPNEA
COMONLY DUE TO NEURO DISTURBANCES, RATE LESS THAN 12
CHEYNE-STOKES
PROGRESSIVE INCREASE IN TITAL VOLUME, FOLLOWED BY DECLINING VOLUME, SEPERATED WITH PERIODS OF APNEA
WHAT DOES SIGHING LEAD TO
HYPERINFLATION OF LUNGS, REINFLATION OF ALVEOLI, DECREASES ATELECTASIS
KUSSMAUL
ABNORMALY DEEP VERRY RAPID SIGHING RESPIRATION, CAUSED BY KETOACIDOSIS OR OTHER METABOLIC ACIDOSIS
BIOTS
IRREGULAR GASPING RESPIRATIONS VARYING IN DEPTH AND INTERUPTED BY APNEA, SEEN IN PATIENTS WITH INCREASING INTERCRANIAL PRESSURE
WHAT IS NORMAL O2 SAT.
95-100 NORMAL, 91-94 MILD HYPOXEMIA, 86-90 MODERATE HYPOXEMIA, <85 SEVERE HYPOXEMIA
HOW IS PEAK FLOW MEASURED
WRIGHT METER ON EXPIRATION, NORMAL-MALE-555-650, FEMALE-400-500,
WHAT ARE CAUSES OF UPPER AIRWAY OBSTRUCTION
TONGUE, TEETH, FOOD, EDEMA, TRAUMA, CROUP, EPIGLOTTITIS
WHAT SHOULD BE ASSESSED ON RESPIRATORY PATIENT
LOC, SPEAK-BREATH-COUGH, ANAPHYLAXIS OR BURNS, ANGEONEUROTIC EDEMA CAUSING LUMP IN THROAT FEELING
WHAT SHOULD BE DONE IF THERE IS OBSTRUCTION
IF PATIENT IS MOVING AIR LEAVE IT ALONE, SWEEP SUCTION REMOVE, HEIMLICH, OR MAGILL FORCEPS&LARYNGOSCOPE
ADULT RESPIRATORY DISTRESS SYNDROME
NON-CARDIOGENIC PULMONARY EDEMA, CAUSED BY INJURY OR ILNESS, PROTINE RICH FLUID LEAKS INTO ALVEOLI, LEADS TO RESPIRATORY FAILURE, ARRHYTHMIAS, BARO TRAUMA, CHF, RENAL FAILUREMANAGED BY PEEP OR CPAP
POSITIVE END EXPIRATORY PRESSURE
INTUBATED PATIENT EXHALES AGAINST METAL, HELPS ALVEOLI STAY INFLATED DURRING EXPIRATION
CONTINUOUS POSITIVE AIRWAY PRESSURE
DELIVERED THROUGH MASK CANULA OR CANNULA ATTACHED TO MACHINE THAT DELIVERS 4-25 CM OF CO2 CONTINUOUSE PRESSURE
HOW IS ARDS MANAGED
IV, BETA ANTAGONISTS, CORTICOSTEROIDS, DIURETICS, ANTIBIOTICS, ANTI-INFLAMITORY MEDS
HOW IS EMPHYSEMA CAUSED
SMOKING #1, POLLUTION, CHEMICALS, CHRONIC ASTHMA, 50% MORTALITY RATE WITH IN 10 YEARS, INCREASED MUCOUS ALLOWS AIR IN BUT NOT OUT , AIR TRAPING OCCURS
HOW IS COPD CAUSED
SMOKING CAUSES INFLAMITORY REACTION, PROMOTES INFLUX OF LEUKOCYTES THAT RELEASE CHEMICAL MEDIATORS THAT DIALATE VESSELS AND MAKE THEM PERMIABLE, AND BREAK DOWN ELASTIN, LEADS TO EMPHYSEMA
POLYCYTHEMIA
ELEVATED HEMATOCRIT, INCREASED RBC TO HELP O2 TRANSPORT, THIS THICKENS BLOOD, INCREASED WORKLOAD OF HEART
COR PULMONALE
RIGHT VENTRICULAR HYPERTROPHY, LEADS TO RIGHT VENTRICULAR HEART FAILURE
THORACIC HYPER-EXPANSION
BARREL CHEST, RESULTS FROM AIR TRAPED FROM LOSS OF ELASTIC RECOIL, EXPIRATION BECOMES AN ACTIVE PROCESS
CHRONIC BRONCHITIS
MUCOUS PRODUCING COUGH, RESULTS FROM EXPOSURE TO IRRITANTS AND EXCESSIVE MUCOUS SECRETIONS
BRONCHIECTASIS
ABNORMAL DILATION OF BRONCHI DUE TO PUS-PRODUCING INFECTIONS OF THE WALL
WHAT MAKES COPD BREATHING EASIER
SITTING WITH ELBOWS RESTING ON THIGHS OR TABLE, BREATHING THROUGH PURSED LIPS
HOW DO YOU TELL IF COPD IS EMPHYSEMA OR BRONCHITIS
USE OF ACCESSORY MUSCLES WITH EMPHYSEMA-EXPIRATION, BRONCHITIS-INSPIRATION/EXPIRATION
PINK PUFFER
EMPHYSEMA
BLUE BLOATER
CHRONIC BRONCHITIS
WHAT ARE SOME FINDINGS OF COPD'ER
WHEEZING, RONCHI, RALES, REDUCED BREATH AND HEART SOUNDS DUE TO REDUCED AIR EXCHANGE, INCREASED THORACIC CAVITY
WHAT ARE LATE SIGNS OF COPD'ER
PERIPHERAL CYANOSIS, CLUBBING OF FINGERS, RIGHT SIDED HEART FAILURE SIGNS, CARDIAC DISRHYTHMIAS
WHAT IS TREATMENT OF COPD
O2, IV-TKO, CARDIAC MONITOR, PULSE OX, ENCOURAGE COUGH IF PRODUCTIVE
COPD MEDICATIONS
B2 ANTAGONIST BRONCHODILATORS(IPRATROPIUM,NEBULIZED ATROPINE,TERBUTALINE,ALBUTEROL,METAPROTERENOL), XANTHINE BRONCHODILATORS(AMINOPHYLLINE), CORTICOSTEROIDS
WHEN DO MOST ASTHMA DEATHS OCCUR
OVER 45, 50% OCCUR BEFORE REACHING ER
EXTRINSIC ASTHMA
CHILDHOOD ONSET, GENETICALLY PREDISPOSED, 50% DEVOLOPE PRIOR TO AGE TEN, USUALY RESOLVES WITH AGE, CAUSED BY RELEASE OF IgE
ATOPY
IF ONE PARENT IS SENSITIZED 40% OF OFFSPRING WILL HAVE ALLERGIES, IF BOTH PARENTS 80% WILL HAVE ALLERGIES
INSTRINSIC ASTHMA
STARTS IN ALDLT WITHOUT STRONG HISTORY, 33& PRIOR TO AGE 30, USUALY PERSISTANT, CAUSED BY SNS-PNS RESPONSE ACh
ASTHMA DEVELOPMENT
HYPOXIA, BRONCHIOL MUSCLES CONTRACT, HYPERSECRETION OF MUCUS,INFLAMATION OF BRONCHIAL WALLS
ASTHMA PHASE 1
BRONCHOCONSTRICTION, EDEMA, DECREASED EXPIRATORY AIR FLOW, MUCUS PLUGGING, INFLAMMATION OF BRONCHIAL WALLS, USUALLY RESOLVES IN 1-2 HOURS OR WITH BETA2 DRUGS
ASTHMA PHASE 2
INCREASE IN EDEMA, BRONCHIAL CONSTRICTION, DECREASSE IN EXPIRATORY FLOW, OCCURS WITHIN6-8 HOURS AFTER PHASE 1 ATTACK, DOES NOT RESPOND TO BETA 2 DRUGS, STEROIDS ARE NEEDED
ASTHMA TREATMENT
IF FATIGUED PREPARE TO VENTILATE, ADMINISTER BRONCHODILATORS, STEROIDS(METHYLPREDNISONE/HYDROCORTISON) MAY TAKE 2-6 HOURS, MAGNESIUM SULFATE (PHASE 2 OR STATUS) TO LOWER ACh RELEASE, THE LONGER TIME BEFORE TREATMENT THE LESS LIKELY BETA2 WILL WORK
STATUS ASTHMATICUS
PHASE 2 PRECIPITATED BY VIRAL INFECTION, CAN NOT BE BROKEN WITH BETA 2,NEEDS ANTICHOLINERGIC, CORTICO STEROIDS, MAGNESIUM, ANTIBIOTICS
OTHER ASTHMA MEDS
ANTICHOLINERGIC AGENTS, CORTICO STEROIDS, MAGNESIUM, ANTIBIOTICS, KATAMINE, HELI-OX-HELIUM,
PNEUMONIA
INFLAMMATION OF RESPIRATORY BRONCHIOLS, ALVEOLI, 5TH MOST COMMON CAUSE OF INFECTIOUS DISEASE DEATHS
LUNG CANCER
NEOPLASM-NEW GROETH OR TUMOR, MOST OCCUR BETWEEN 55-65, #1 CAUSE IS SMOKING, #2 CAUSE IS RADON GAS,
LIST FOUR TYPES OF LUNG CANCER
ADENOCARCENOMA-MOST COMMON, SMALL CELL CARCINOMA, EPIDERMOID CARCINOMA, LARGE CELL CARCINOMA
CAUTION
CHANGE IN BOWELOR BLADDER, A SORE THAT DONT HEAL, UNUSUALY BLEEDING OR WEIGHT LOSS, THICKENING OR LUMP, INDEGESTION, OBVIOUS CHANGE IN WART OR MOLE, NAGGING COUGH OR HOARSENESS
CARBON MONOXIDE
COLORLESS, ODORLESS, TASTLESS GAS, COMBINES WITH HEMOGLOBIN 200-250 TIMES TIGHTER THAN O2
SIGNS/SYMPTOMS OF CO POISON
<10%- NONE, 20%- HEADACHE, NAUSEA, VOMITING, FATIGUE, 30%-ALTERED CNS, DIZZINESS, VISION, 40-60%- COMA, HALF LIFE IS 4 HR IN ROOM AIR, 30-40 MIN IN 100% 02
PULMONARY EMBOLUS
BLOCKAGE OF PULMONARY ARTERY, 90% ARISE FROM LEGS, 11% OF DEATHS WITHIN ONE HOUR, 38% IN 2ND HOUR,
WHAT FACTORS CAUSE PE
VENOSTASIS-TRAVEL,OBESITY, VENOUS INJURY, INCREASED COAGULATION, PREGNANCY, DISEASE, MULTIPLE TRAUMA
TUBERCULOSIS
TRANSMITTED BY SMALL DROPLETS FROM COUGH OR SNEEZE, PROTECTED BY STRONG COATING THAT HELPS IT SURVIVE, SIGNS ARE FEVER, NIGHT SWEATS, MALAISE, WEIGHT LOSS, COUGH WITH GREEN OR YELLOW SPUTUM
AMYOTROPHIC LATERAL SCLEROSIS
LOU GEHRIGS, PROGRESSIVE DEGENERATION OF CNS NERVES, 80% BETWEEN 40-70, 50%DIE IN 3 YRS, SET AIRWAY, VENT, O2, IV TKO
GUILLIAN-BARRE
ILNESS AFTER INFECTION, EXPOSURE TO TOXINS, CERTAIN VACCINES, 50% FOLLOW MILD UPPER RESPIRATORY OR UPPER GI INFECTION, RESOLVES ITSELF IN A FEW WEEKS OR MONTHS, DAMAGED MYLIN COVERING, HOSPITALIZE, GIVE FLUIDS
MYAESTHENIA GRAVIS
PRONOUNCED MUSCLE WEAKNESS, CIRCULATING ANTIBODIES BLOCK ACH RECEPTORS THAT AFFECT POSTSYNAPTIC ACH RECEPTORS, NERVE IMPULSES DONT CAUSE MUSCLE CONTRACTIONS
MANAGEMENT OF MG
AIRWAY SUPPORT, DRUGS-ANTICHOLINEESTERASE, STEROIDS, IMUNOSUPPRESSANTS, PLASMA EXCHANGE, SURGERY- THYMECTOMY TO REMOVE TUMOR
CARPOPEDAL SPASMS
HYPERVENTILATION LEADS TO INCREASED AMOUNT OF BOUND CALCIUM LEADING TO SPASMS IN FINGERS AND TOES
POLIO
VIRUS THAT LIVES IN DIRT, ONCE IN STOMACH IT GOES TO CNS, PTS ARE PLACED ON IRON LUNG