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disease exam 3

respiratory diseases

what is guillain barre syndrome? Relatively rare disorder of the peripheral nervous system in which flaccid paralysis of the skeletal muscles and loss of reflexes develop in previously healthy pt.
Major patho and structural changes of GB syndrome? Mucus accumulation,Airway obstruction,Alveolar consolidation, Atelctasis
Etiology of GB syndrome? not known. Onset frequently occurs 1-4 weeks after a febrile episode like a upper respiratory or GI illness.
signs of GB include? paresthesias, paralysis, CSF findings, abnormal EMG results (EMG measures the nature and speed of electrical conduction along a nerve). CSF will have abnormally high protein level w/ normal cell count
Functional spontaneous recovery for GB syndrome is expected how often? in about 85% to 95% of the cases, although approx 40% of might have minor residual symptoms
common noncardiopulmonary symptoms of GB? Progressive ascending paralysis of the skeletal muscles - usually develop during a single day though can happen over a few days and generally peaks in fewer than 10 days
What are Early symptoms of GB: fever, malaise, nausea, prostration w/ distal paresthesia
what are chest assessment findings common for GB? diminished breath sounds, crackles and rhonchi
what treatment can be used for GB? Plasmapheresis(5 exchanges of 3 L each over 8-10 days is usually adequate.), Infusion of immunoglobulin, Corticosteroids
characteristics of GB? Tingling sensation and numbness (distal paresthesia),Loss of deep tendon reflexes,Sensory nerve impairment, Peripheral facial weakness, Dec gag reflex, Dec ability to swallow
what is myasthenia gravis? Chronic disorder of the neuromuscular junction that interferes w/ the chemical transmission of ACH btw the axonal terminal and the receptor sites of voluntary muscles.,Disorder affects the myoneural junction (motor), sensory function not lost
major P&S changes for MG? Mucus accumulation,Airway obstruction, Alveolar consolidation, Atelecatasis
what is the etilogy of MG? cause appears to be related to circulating antibodies of the autoimmune system (anti-ACH receptor antibodies).
MG is Most common in? young women and older men.disease usually has peak onset in females between 15 and 35 years, compared w/ 40 to 70 years in males.
what are Clinical manifestations associated w/ myasthenia gravis? often provoked by emotional upset, physical stress, exposure to extreme temp changes, febrile illness, pregnancy
diagnosis of MG is based on? clinical history, neuro exam, electromyography, blood analysis, edrophonium test, CT scan, MRI
signs and symptoms of MG include: facial muscle weakness, double vision, difficulty in breathing, talking, chewing or swallowing, muscle weakness in arms and legs, fatigue brought on by repetitive motions, also speech impairment
what is Edrophonium test? MG is usually confirmed w/ the injection of edrophonium (tensilon).
what are Common noncardiopulmonary manifestations of MG? Weakness of striated muscles(ptosis,diplopia,speech impairment,dysphagia), gradual onset,
what are first symptoms of MG? Ptosis followed by diplopia caused by weakness of the external ocular muscles
what should be Frequently measured for MG? pt's vital capacity, blood pressure, oxygen saturation, and ABG
When should Mech vent should be initiated for MG? when the pt's clinical data demonstrate impending or acute ventilatory failure.
what are the actions of Cholinesterase inhibitors used for MG? It inc the concentration of ACH to compete w/ the circulating anti ACH antibodies, which interfere w/ the ability of ACH to stimulate the muscle receptors
how are immunosuppressants used for MG? -corticosteroids e.g. prednisone and similar agents such as cyclophosphamide (cytoxan, neosar) and azothioprine (imuran) are used to suppress the immune system
what is Thymectomy used for in MG? the thymus gland frequently appears to be the source of anti-ACH receptor antibodies- in some pts, muscle strength improves soon after surgery, whereas in others improvement takes months or years.
how is Plasmapheresis used for in MG? blood plasma exchange procedure is used to filter the blood of ACH receptor antibodies
MG is specifically characterized by? fatigue and weakness, w/ improvement following rest.
The cause of MG is believed to concern antibodies. It is believed that the antibodies disrupt the chemical transmission of ACH at the neuromuscular junction by? 1. blocking the ACH from the receptor sites of the muscular cell, 2. accelerating the breakdown of ACH, 3. destroying the receptor sites
what is seen after the administration of tensilon in a person with MG muscular weakness? a dramatic transitory improvement in muscle function (lasting about 10 min)
what are the most popular cholinesterase inhibitors? most popular agents are edrophonium chloride , neostigmine , pyridostigmine
how does tensilon work? it blocks cholinesterase from breaking down ACH after it has been released from the terminal axon. Action inc the myoneural concentration of ACH, which in turn offsets the influx of antibodies at the neuromuscular junction.
edrophonium chloride (tensilon),
neostigmine (prostigmin)
pyridostigmine (regonol, mestinon)
patho and structural changes associated w/ ARDS are: Interstitial and intra-alveolar edema and hemorrhage, Alveolar consolidation, Intra-alveolar hyaline membrane, Pulmonary surfactant deficiency or abnormality, Atelectasis
what is the Gross appearance of patients with ARDS? lungs look heavy and red, beefy or liver like
ARDS is rest/obstr? Restrictive lung disorder
what was ARDS Historically referred to as? "shock lung syndrome" when disease first identified in WWII
in ARDS the intra-alveolar walls become lined w/ a thick, rippled hyaline membrane identical to the hyaline membrane seen in newborns w/ infant respiratory distress syndrome-
the hyaline membrane seen in ARDS contains contains fibrin and cell debris
etiologies of ARDS #1 Aspiration,Cardiopulmonary bypass,CHF, Disseminated-intravascular coagulation,Drug overdose,Fat or air emboli, Fluid overload, Infections,Inhalation of toxins and irritants,Immunologic reaction,Massive blood transfusion,
what is Disseminated-intravascular coagulation? seen in pts w/ shock, it is a condition of paradoxical simultaneous clotting and bleeding that produces microthrombi in the lungs
what is Septic shock is caused by Infection in blood,Blood vessels dilate,Blood pressure drops
what are clinical manifestations of ARDS? atelectasis, alveolar consolidation and inc a-c membrane thickness
what will a chest assessment of ARDS sound like? dull percussion note, bronchial B.S., crackles
a mild to moderate ABG of ARDS looks like inc pH, dec all else
a severe/acute ventilatory ABG of aRDS looks like dec pH, inc Paco2, inc Hco3, dec Pao2
the chest xray for ARDS shows? increased opacity (whiteness)
what will the mech vent settings be for ARDS? low tidal volume and high RR with PEEP. 4-8 ml/kg and 35 bpm
what is the goal of low tidal volume ventiltilation is to dec high transpulmonary pressure, reduce overdistention of the lungs, dec barotrauma
etiologies of ARDS #2 Nonthoracic trauma,Oxygen toxicity,Pulmonary ishcemia,Radiation induced lung injury,Shock, Thoracic trauma, Uremia
Interstitial lung diseases comprise a large group of pulmonary disorders that are all associated w/ pulmonary inflammatory changes
CILD rest/obst? it Is both restrictive and obstructive disorder or both at the same time
Major patho and structural changes of CILD? Fibrotic thickening of the respiratory bronchioles and alveoli, Granulomas, Destruction of the alveoli and adjacent pulmonary capillaries, Honeycombing and cavity formation, Airway obstruction caused by inflammation and bronchial obstruction
another name for Extrinsic allergic alveolitis is hypersensitivity pneumonitis
Extrinsic allergic alveolitis aka hypersensitivity pneumonitis is the immunologically mediated inflammation of the lungs caused by the inhalation of a variety of antigens like pollen, animal dander, organic dusts, and spores of certain molds. Based on a hypersensitivity reaction
what is an example of Extrinsic allergic alveolitis? Farmers lung- extrinsic allergic alveolitis caused by inhalation of moldy clay
Idiopathic pulmonary fibrosis is a progressive inflammatory disease w/ varying degrees of fibrosis and in severe cases, honeycombing. The precise etiology is unknown.
other names for IPF are acute interstitial fibrosis of the lung, cryptogenic fibrosing alveolitis, hamman-rich syndrome, honeycomb lung, interstitial fibrosis, interstitial pneumonitis
Desquamative interstitial pneumonia (DIP) type of IPF? hyperplasia, desquamation of alveolar type II cells, alveolar spaces are packed w/ macrophages, even distribution of interstitial mononuclear infiltrate. Better prognosis than UIP
Usual interstitial pneumonia (UIP)type of IPF? interstitial and alveolar wall thickening caused by chronic inflammatory cells and fibrosis
what is seen in severe cases of UIP? alveolar walls become fibrotic, honeycombing, inflammatory infiltrate is reduced
who is IPF seen in? Seen most in males between 40 and 70
how is Diagnosis of IPF confirmed? by open lung biopsy
what is Rheumatoid arthritis? primarily an inflammatory joint disease.
How is rheumatoid arthritis a CILD (how does it affect the lungs?) May involve the lungs in the form of pleurisy (w/ or w/o effusion), interstitial pneumonitis, necrobiotic nodules (w/ or w/o cavities), caplan's syndrome, pulmonary hypertension secondary to pulmonary vasculitis, pneumoconiosis
what is the most commonly pulmonary complication associated w/ rheumatoid arthritis? Pleurisy w/ or w/o effusion
Pleurisy is progressive inflammation of the parietal pleura
what is Systemic lupus erythematosus? multisystem disorder that mainly involves the joints and skin. Also may cause problems in the kidneys, lungs, nervous system and heart.
how many cases of lupus involve the lungs? 50-70% of cases involves the lungs
what are the Pulmonary manifestations of lupus characterized by pleurisy w/ or w/o effusion, atelectasis, diffuse infiltrates and pneumonitis, diffuse intersitial lung disease, uremic pulmonary edema, diaphragmatic dysfunction, infections
what is the most common pulmonary complication of lupus? Pleurisy w/ or w/o effusion
Caplan's syndrome aka rheumatoid pneumoconiosis progressive pulmonary fibrosis of the lung commonly seen in coal miners
what is Goodpasture's syndrome? disease of unknown etiology that involves two organ systems- the lungs and the kidneys.
how does goodpasture's syndrome affect the lungs? recurrent episodes of pulmonary hemorrhage and in some cases, pulmonary fibrosis- presumably as a consequence of the bleeding episodes
how does goodpasture's syndrome affect the kidneys? glomerulonephritis characterized by the infiltration of antibodies within the glomerular basement membrane
good pasture syndrome is usually seen in? young adults
what is the Average survival period after diagnosis of good pasture's syndrome? 15 weeks. About 50% of pts die form massive pulmonary hemorrhage, and about 50% die from chronic renal failure
Bronchiolitis obliterans w/ organizing pneumonia- called BOOP is characterized by connective tissue plugs in the small airways and mononuclear cell infiltration of the surrounding parenchyma
etiology of BOOP> Considered idiopathic, but is associated w/ connective tissue disease, toxic gas inhalation, and infection.
Xray of BOOP commonly shows? patchy infiltrates of alveolar rather than intersitial involvement
what are the chest assessment findings for CILD? inc tactile and vocal fremitus, dull percussion, bronchial B.S., crackles
what are the chest xray findings? bilateral infiltrates, granulomas, cavity formation, honey combing, air bronchograms, pleural effusion
All expiratory maneuver findings (eg FVC, FEV, FEF)? decreased
what are the lung volume and capacity findings (eg Vt, RV, FRC)? all decreased except RV/TLC
what are used for treatments for CILD? corticosteroids and plasmapheresis
what disorders are associated with interstitial inflammation accompanied by granuloma formation? extrinsic allergic alveolitis, sarcoidosis, churg-strauss syndrome
what happens in Severe cases of GB? paralysis of diaphragm and ventilatory failure- medical emergency
microscopically what is seen in GB?] nerves show demyelination, inflammation and edema
serum samples taken from GB patients show high antibody titers
if GB is diagnosed early, what is prognosis? excellent
the diagnosis of GB is based on patient's clinical history
GB is more common in: people older than 45 yo, males
Non REM sleep- usually begins immediately after an individual dozes off. Consists of four separate stages, each progressive into deeper sleep
in non REM sleep During stages 1 and 2 vent rate and tidal volume continually inc and dec and brief periods of apnea seen. Cheyne stokes breathing seen in older males
in non REM sleep During stages 3 and 4 ventilation becomes slow and regular. Minute volume is commonly 1 to 2 lpm less. PaCO2 levels are higher (4-8 mm hg), PaO2 levels are lower (3-10 mmhg) and the pH is lower (.03-.05 units)
non REM sleep Lasts 60-90 minutes.
Most of non REM sleep time is spent in stage 2. person may move into REM sleep at any time though it occurs most often before stage 1 and 2
during REM sleep-vent rate is rapid and shallow, dreaming occurs
during REM sleep the Muscle paralysis that occurs can affect ventilation is two ways Bc the muscle tone of the intercostal muscles is low, the neg intrapleural pressure generated by the diaphragm often causes a paradoxical motion of the rib cage;Loss of muscle tone in the upper airway leads to obstructions
REM sleep Lasts between 5-40 mins, approx every 60-90 min
REM sleep's frequency durign sleep time? Lengthen and become more frequent toward the end of the night's sleep,Consitutes about 20-25% of the total sleep time, Studies show that it is more difficult to awaken a subject during REM sleep
Apnea cessation of breathing for a period of 10 seconds or longer
Sleep apnea is diagnosed in pts who have more than 5 episodes of apnea per hour that may occur in either or both non REM or REM sleep, over a 6 hour period.
generally, the episodes of apnea per hour are more frequent and severe during REM sleep and in the supine body position
Obstructive sleep apnea is caused Caused by an anatomic obstruction of the upper airway in the presence of continued ventilatory effort.most commonly encountered
OSA is Characterized by presence of heightened inspiratory efforts during apneic periods, Apneic episodes followed by increasingly desperate efforts to inhale
during OSA "fricative" breathing is snorting sound may be heard at end of apneic periods
in OSA's Severe cases pt may awaken and sit upright and gasp for air
OSA Pts usually demonstrate perfectly normal and regular breathing patterns during wakeful period
OSA is Seen more commonly in males, esp middle aged men. Approx 1-4% of adult male population appear to be affected.
Pickwickian syndrome and OSA excessive daytime sleepiness- associated with Joe the fat boy from Charles Dickens's The PostHumous papers of the Pickwick club
Some clinical disorders associated with OSA: Obesity,,Anatomic narrowing of upper airway,Deviated nasal septum, or allergic rhinitis, causing mouth breathing, Hypothyroidism,Down syndrome
Clinical manifestations of OSA Chronic loud snoring,Hypertension,Morning headaches,Systemic hypertension,CHF, Nausea,Dry mouth on awakening
Polysomnographic monitoring demonstrates the following in OSA Apnea-related O2 desaturation-4% or greater drop in SpO2;More than 5 obstructive apneas of more than 10 sec per hour of sleep, and one or more of the following: Frequent arousals, Profound bradycardia and/or asystole,Shortened sleep latency
Central sleep apnea occurs when respiratory centers of the medulla fail to send signals to the respiratory muscles
CSA is Characterized by cessation of airflow at the nose and mouth along w/ cessation of inspiratory efforts (absence of diagphragmatic excursions)
CSA is Diagnosed when the frequency of the apnea episodes is excessive (more than 30 in a 6 hour period)
General noncardiopulmonary clinical manifestations of central sleep apnea can be summarized as follows Tendency for the pt to be of normal weight, Mild snoring,Insomnia,Daytime fatigue
Diagnosis of CSA begins w/ a careful history from the pt, esp noting the presence of snoring, sleep disturbance, persistent daytime sleepiness,Blood is evaluated for polycythemia, reduced thyroid function, bicarbonate retention,ABGs
Chest xray, ECG, and echocardiogram helpful in CSA in evaluating the presence of pulmonary hypertension, the state of right and left ventricular compensation, and the presence of any other cardiopulmonary disease
Diagnosis and type of sleep apnea is confirmed w/ polysomnographic sleep studies
Polysomnographic studies include: An EEG and electro-oculogram (EOG) to identify sleep stages,Use of monitoring device for airflow in and out of pt's lungs,An ECG ,Impendance pneumography, intercostal electromyography, esophageal manometry,Ear oximetry or transcutaneous oxygen monitoring
Pts diagnosed as having OSA may undergo a CT scan or head xray to determine site and severity of pharyngeal narrowing
Steps typically involved in diagnosing sleep apnea can be summarized as History, Exam of the neck and upper airway structures, heart and lungs,Spirometry (FV loops in the erect and supine positions) to assess for extrathoracic airway obstruction , ABG, Hemoglobin and carboxyhemoblogin levels, Nocturnal recording oximetry
in sleep apenea, the ABG looks Ph normal, paco2 inc, hco3 inc significantly, dec pao2
Negative pressure ventilation is used for which type of sleep apnea for pts with central sleep apnea
what is def of Drowning? suffocation and death as a result of submersion in liquid.
def of Near drowning? victim survives liquid submersion, at least temporarily
def of Dry drowning? glottis spasms and prevent water from passing into the lungs. Lungs are usually normal
def of Wet drowning? glottis relaxes and allows water to flood the TBT and alveoli. When fluid is initially inhaled, the bronchi constrict in response to parasympathetic reflexes- then the patho processes responsible for noncardiogenic pulmonary edema begin
If a victim was submerged in unclean water, pathogens and solid material may be aspirated.can lead to pneumonia and ARDS
Major pathologic changes of the lungs in near drowning are the same in fresh water and sea water -both result in reduction in pulmonary surfactant, alveolar injury, atelectasis and pulmonary edema
how many people drown each year? Between 6000 and 8000 people drown each year in the US.
Children under the age of 5 account for 40% of deaths. Additional 20% of deaths occur in ages between 5 and 20
the major P&S changes of near drowning are: laryngospasm and bronchial constriction, intersitial edema including engorgement of the perivascular and peribronchial spaces, alveolar walls and interstitial spaces, dec pulmonary surfactant, inc surface tension, atelectasis, frothy white secretions
clinical manifestations of near drowning? atelectasis, alveolar consolidation, inc a-c membrane, bronchospasm
in near drowning apnea is related to the length of time the victim is submerged
what are the chest assessment findings of near drowning? crackles and rhonchi
what does the ABG look like in the early and advanced stages of near drowning? low pH, high Pa2, low HCO3 (lactic acidosis is common), low Pao2
First objective by first responder is to remove the person from the water and if the pt has no spontaneous ventilation and pulse, to call for help and immediately initiate CPR,Should be wrapped in warm, dry coverings
If pt has been submerged for less than 60 mins in cold water, fixed and dilated pupils means does not necessarily mean poor prognosis
Virtually every near drowning victim suffers from hypoxemia, hypercapnia, acidosis
The degree of hypoxemia is directly related to the amt of a-c damage-chest xray should be obtained
Intubation and mech vent should be performed immediately for anyone w/ no spontaneous breathings or pts who are unable to maintain a PaO2 of 60 mmhg w/ a FIO2 of .5 or lower.
For wet drowning, how should ventilation be handled? mech vent w/ PEEP or CPAP should be administered
radiographic deterioration may occur in near drowning pts within first 48-72 hours
what is Thermal injury injury caused by inhalation of hot gases. Usually confined to upper airway-nasal cavity, oral cavity, nasopharynx, oropharynx, larynx
Airways distal to the larynx and the alveoli are usually spared serious thermal injury bc of The remarkable ability of the upper airways to cool hot gases, Reflex laryngospasm, Glottic closure
what is classic predictor of thermal injury? Presence of facial burns
Thermal injury to the distal airways results in mucosal edema, vascular congestion, epithelial sloughing, obliterative bronchiolitis, atelectasis, pulmonary edema
Direct thermal injuries usually do not occur below the level of the larynx, except in the rare instance of steam inhalation.
in Early stage (0-24 hours postinhalation)of smoke inhalation injury TBT becomes more inflamed initially. Process causes an overabundance of bronchial secretions to move into the airways, resulting in bronchospasm. Also, smoke slows down the mucociliary escalator which inc mucus retention
Smoke inhalation may also cause noncardiogenic high permeability pulmo edema- "leak alveoli"
Intermediate stage (2-5 days postinhalation) Necrotic debris, excessive mucus production, and mucus retention lead to mucus plugging and atelectasis. Mucus accumulation also leads to bacterial colonization, bronchitis, pneumonia.
Organisms commonly cultured from smoke inhalation injury are gram positive staph, gram negative klebsiella, enterobacter, e. coli, pseudomonas.
Noncardiogenic pulmo edema and ARDS may develop at any time during intermediate period
When chest wall burns are present, situation may be further aggravated by the pts' inability to breath deeply and cough as result of pain, use of narcotics, immobility, inc airway resistance, dec lung and chest compliance.
Late stage (5 or more days postinhalation) Infections resulting from burn wounds on the body surface are the major concern during this period- infections often lead to sepsis and multiorgan failure,Pneumonia and pulmo embolism may cause problems
Sepsis induced multiorgan failure is primarily cause of death in what stage? late stage post inhalation
Long term effects of smoke inhalation rest/obst? both
Restrictive lung disorder- develops from alveolar fibrosis and chronic atelectasis
Obstructive lung disorder- caused by inc and chronic bronchial secretions, bronchial stenosis, bronchial polyps, bronchiectasis, bronchiolitis.
Major patho and structural changes of Thermal injury upper airway-nasal cavity, oral cavity, pharynx: blistering, mucosal edema, vascular congestion, epithelial sloughing, thick secretions, acute UAO
major P&S changes of Smoke inhlations injury TBT, alveoli: inflammation of TBT, bronchospasm, excessive bronchial secretions and mucus plugging, dec mucosal ciliary transport, atelectasis, alveolar edema and frothy secretions, ARDS, BOOP, alveolar fibrosis, bronchiectasis
The prognosis of fire victims usually is determined by 1. extent and duration of smoke exposure, 2. chemical composition of the smoke, 3. size and depth of body surface burns, 4. temp of gases inhaled, 5. age, 6. pre-existing health status
When smoke inhalation injury is accompanied by a full thickness or third degree skin burn, the mortality rate almost doubles
First degree (min depth to skin) superficial burn, damage limited to the outer layer of the epidermis. Burn characterized by red skin, tenderness, pain. No blisters. Healing time: 6-10 days. Result of healing: normal skin.
Second degree (superficial to deep thickness of skin) burns in which damage extends through the epidermis and into the dermis but not sufficient enough to interfere w/ regeneration of epidermis. Blisters present. Healing time: 7-21 days.
Third degree (full thickness of skin including tissue beneath skin): burns in which both epidermis and dermis are destroyed, w/ damage extending into underlying tissues. Tissue may be charred or coagulated.
Principal goals in initial care of smoke inhalation and thermal injuries: immediate assessment of pt's airway, respiratory status, CV status, percentage of body burned, depth of burns, IV line should be started immediately to admin fluids and meds, Clothing should be removed or soaked, burn wounds covered,Infection control
Fluid resuscitation w/ ringer's lactate solution is usually initiated according to the parkland formula which is? 4 ml/kg of body weight for each percent of BSA burned over a 24 hour period.
The pts's hemodynamic status will usually remain stable at this fluid replacement rate, w/ an avg urine output target of 30-50 ml/hr
The pts's hemodynamic status will usually remain stable at this fluid replacement rate,and a central venous pressure target of 2-6 mm hg.
fluid resuscitation can lead to overhydration and acute upper airway obstruction and pulmo edema
If secondary infection occurs during second degree burn, damage may be equal to a third degree burn.
Result of healing during second degree burn? normal to hairless and depigmented skin w/ texture that is normal, pitted, flat or shiny
Healing of third degree burns: may occur after 21 days or never occur w/o skin grafting if area is large.
Results of third degree burn hypertrophic scares (keloids) and chronic degranulation.
fluid resuscitation can lead to] overhydration and acute upper airway obstruction and pulmo edema
Created by: blueseas
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