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RACHEL - PATHO I FINAL > UNIT 8 - ALTERATIONS IN RESPIRATORY FUNCTION > Flashcards

UNIT 8 - ALTERATIONS IN RESPIRATORY FUNCTION Flashcards

1
Q

ETIOLOGY OF WHICH RESTRICTIVE RESPIRATORY DISORDER?

o BEGINS WITH INHALATION OF PATHOGENS. PATHOGENS THEN ESTABLISH THEMSELVES INSIDE THE LUNGS
o ASPIRATION – VOMITING AND INHALING GASTRIC CONTENTS. BURNS THE BRONCHI AND RESPIRATORY PASSAGES
o ENDOGENOUS – INFECTION THAT OCCURS SOMEWHERE ELSE IN THE BODY. TRAVELS TO THE LUNGS AND ESTABLISHES INFECTION THERE

A

PNEUMONIA

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2
Q

ETIOLOGIC ORGANISMS OF WHICH RESTRICTIVE RESPIRATORY DISORDER?

 STREPTOCOCCUS PNEUMONIAE
 LEGIONELLA PNEUMOPHILA

A

PNEUMONIA

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3
Q

CLASSIFICATION OF WHICH RESTRICTIVE RESPIRATORY DISORDER?

o	NOSOCOMIAL VS COMMUNITY ACQUIRED
o	ETIOLOGIC ORGANISM
     	STREPTOCOCCUS PNEUMONIAE
     	LEGIONELLA PNEUMOPHILA
o	ANATOMIC DISTRIBUTION
A

PNEUMONIA

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4
Q

PATHOGENESIS OF PNEUMONIA:

INVADING ORGANISM SETS OF _____________ REACTION. ALVEOLI FILL WITH EXUDATE RESULTING IN ____________.

A

INFLAMMATORY

CONSOLIDATION

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5
Q

CLINICAL MANIFESTATIONS OF PNEUMONIA CAN VARY WITH AGE, CAUSE, & __________

A

SEVERITY

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6
Q

CLINICAL MANIFESTATIONS OF WHICH RESTRICTIVE RESPIRATORY DISORDER?

o FEVER, CHILLS
o COUGH (MAY OR MAY NOT BE PRODUCTIVE)
o DYSPNEA, CRACKLES OVER AFFECTED LOBE

A

PNEUMONIA

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7
Q

EVALUATION OF PNEUMONIA

__________ DONE TO CHECK FOR CONSOLIDATION
_________ CULTURE

A

XRAYS

SPUTUM

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8
Q 
TREATMENT OF PNEUMONIA IS \_\_\_\_\_\_\_\_\_\_\_:
	OXYGEN PRN
	ANTI-INFECTIVES
	FLUIDS
	ANTIPYRETICS
	EXPECTORANTS
	VENTILATORY SUPPORT
A

SUPPORTIVE

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9
Q

DEFINITION - COLLAPSE OF LUNG TISSUE

A

ATELECTASIS

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10
Q

TYPES OF __________
o OBSTRUCTION
o COMPRESSION BY EXTERNAL MASS

A

ATELECTASIS

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11
Q

PATHOGENESIS OF ATELECTASIS

o AIRLESS ALVEOLI ________ DUE TO ELASTICITY – BECAUSE THEY ARE NOT RECEIVING AIR
o INTERFERES WITH BLOOD FLOW THROUGH LUNGS (DECREASED ____ _________ & ____________)

A

SHRIVEL

GAS EXCHANGE & OXYGENATION

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12
Q

DURING ATELECTASIS, CLIENT BECOMES _____________ VERY QUICKLY

A

HYPOXEMIC

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13
Q

RISK FACTORS FOR ATELECTASIS
o ____________ – SECRETIONS POOL IN LUNGS AND CLOG SMALL BRONCHIOLES. ALVEOLI THAT ARE PASSED THE AREA OF OBSTRUCTION DO NOT RECEIVE AIR AND SHRIVEL. INHIBITS BLOOD VESSELS. IF OXYGEN ISN’T RESTORED THE TISSUE BECOMES NECROTIC AND DIES.
o SURGERY

A

IMMOBILITY

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14
Q

CLINICAL MANIFESTATIONS OF WHICH RESTRICTIVE RESPIRATORY DISORDER?

o	DYSPNEA
o	COUGH
o	FEVER
o	LEUKOCYTOSIS
o	TACHYPNEA
o	FOCAL DECREASED BREATH SOUNDS
o	INCREASED CRACKLES AT LUNG BASES
o	HYPOXEMIA
o	DECREASED DEPTH OF RESPIRATORY EXCURSIONS
A

ATELECTASIS

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15
Q

TREATMENT OF ATELECTASIS

\_\_\_\_\_\_\_\_\_\_\_\_\_\_ IS KEY!!
DEEP BREATHING AND COUGHING
REPOSITIONING
AMBULATION IF NOT CONTRAINDICATED
INCENTIVE SPIROMETRY
A

PREVENTION

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16
Q

CHEST WALL STRUCTURAL ABNORMALITIES

DEFINITION - HUNCHED BACK. ELDERLY WITH OSTEOPOROSIS. INHIBITS CHEST EXPANSION.

A

KYPHOSIS

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17
Q

CHEST WALL STRUCTURAL ABNORMALITIES

DEFINITION - (CHEST EXCAVATION) STERNUM IS DISPLACED BACKWARDS.

A

PECTUS EXCAVATUM

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18
Q

CHEST WALL STRUCTURAL ABNORMALITIES

DEFINITION - STERNUM IS PROTRUDING FORWARD. BIRD CHEST.

A

PECTUS CARINATUM

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19
Q

CHEST WALL STRUCTURAL ABNORMALITIES

DEFINITION - SPINE IS ‘S’ SHAPED. INTERFERES WITH MOVEMENT OF RIBS AND INHIBITS MOVEMENT OF CHEST WALL.

A

SCOLIOSIS

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20
Q

CHEST WALL STRUCTURAL ABNORMALITIES SUCH AS KYPHOSIS, PECTUS EXCAVATUM & CARINATUM, & SCOLIOSIS CAN ALL LEAD TO RECURRENT _________ INFECTIONS

A

CHEST

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21
Q

WHICH CHEST WALL INJURY?

o VARIES IN SEVERITY FROM AN ISOLATED RIB FRACTURE TO SEVERE CRUSH INJURY TO CHEST
o RULE OUT UNDERLYING INJURY
o IMPORTANT TO OBTAIN AN ACUTE HISTORY OF THE MECHANISM OF INJURY.
o PAINFUL – INTERFERES WITH LUNG EXPANSIONS. LEADING TO PNEUMONIA OR ATELECTASIS

A

RIB FRACTURES

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22
Q

TREATMENT OF RIB FRACTURE DEPENDS ON __________ OF INJURY

A

SEVERITY

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23
Q

TREATMENT OF RIB FRACTURE
 INCENTIVE SPIROMETRY, DEEP BREATHING AND COUGHING; SUPPORT RIBS WITH PILLOWS DURING COUGHING
 NSAIDS
 ________ SMOKING, OR USE OF BINDERS OR RIB BELTS

A

AVOID

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24
Q

WHICH CHEST WALL INJURY?

o USUALLY 2 FRACTURES PER RIB IN CONSECUTIVE RIBS OR FRACTURE OF STERNUM PLUS CONSECUTIVE RIBS.
o RESULTS IN PARADOXICAL BREATHING (REVERSE OF NORMAL BREATHING INHALATION - CHEST GOES IN, EXHALATION, CHEST GOES OUT)

A

FLAIL CHEST

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25
Q

TREATMENT OF WHICH CHEST WALL INJURY?

PAIN CONTROL AND MANAGEMENT OF UNDERLYING PULMONARY AND/OR CARDIAC INJURY
CHEST TUBES, MECHANICAL VENTILATION

A

FLAIL CHEST

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26
Q

FLAIL CHEST CAN CAUSE ______________

A

PNEUMOTHORAX

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27
Q

DEFINITION - AN ACCUMULATION OF AIR IN THE PLEURAL SPACE

CAUSES ATELECTASIS (GREATER AMOUNT OF AIR = MORE SEVERE ATELECTASIS)

A

PNEUMOTHORAX

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28
Q

PNEUMOTHORAX CAN RESULT FROM ____________ DISEASE (SUCH AS COPD) OR FROM CHEST __________ (RIB FRACTURES)

A

UNDERLYING

TRAUMA

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29
Q 
TYPES OF \_\_\_\_\_\_\_\_\_\_\_\_\_
o	SPONTANEOUS
     	PRIMARY
     	SECONDARY 
o	OPEN 
o	TENSION
A

PNEUMOTHORAX

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30
Q

WHICH TYPE OF PNEUMOTHORAX?

o SPONTANEOUS RUPTURE OF BLEBS (AIR BLISTER) ON VISCERAL PLEURA. MAY OCCUR DURING REST, EXERCISE, OR SLEEP.
o USUALLY OCCURS IN MEN BETWEEN 20 – 40 YRS

A

SPONTANEOUS: PRIMARY

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31
Q

WHICH TYPE OF PNEUMOTHORAX?

o RESULTING FROM TRAUMA OR SPONTANEOUS RUPTURE OF BLEB ON VISCERAL PLEURA SECONDARY TO PRE-EXISTING PULMONARY DISEASE

A

SPONTANEOUS: SECONDARY

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32
Q

WHICH TYPE OF PNEUMOTHORAX?

• CAUSED BY OPENING IN CHEST WALL SECONDARY TO TRAUMA SUCH AS STAB WOUNDS, BULLET WOUNDS. (CHEST INJURY)
• AIR IS DRAWN THROUGH THE WOUND INTO THE PLEURAL SPACE DURING INSPIRATION AND FORCED BACK OUT DURING EXPIRATION. WOUND IN THE CHEST WALL APPEARS TO BE “SUCKING AIR” AND IS VISIBLY BUBBLING; THEREFORE REFERRED TO AS “SUCKING WOUND”
o LEADS TO ATELECTASIS

A

OPEN

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33
Q

PRESSURE IN PLEURAL SPACE EQUALS ___________ PRESSURE

A

ATMOSPHERIC

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34
Q

WHICH TYPE OF PNEUMOTHORAX?

  • SITE OF PLEURAL RUPTURE ACTS AS A ONE-WAY VALVE PREVENTING AIR FROM ESCAPE DURING EXPIRATION
  • AIR ENTERS THE PLEURAL SPACE DURING INSPIRATION; ON EXPIRATION, OPENING IS SEALED AND AIR BECOMES TRAPPED, INCREASING THE PRESSURE WITHIN THE THORACIC CAVITY
  • MEDIASTINUM BECOMES DISPLACED CONTRALATERALLY, COMPRESSING THE HEART AND GREAT VESSELS, INHIBITING VENOUS RETURN
A

TENSION

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35
Q

A ____________ PNEUMOTHORAX IS THE MOST SEVERE.

A

TENSION

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36
Q

CLINICAL MANIFESTATIONS VARY WITH THE ___________ OF THE PNEUMOTHORAX

A

EXTENT

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37
Q

CLINICAL MANIFESTATIONS OF PNEUMOTHORAX

o _____________: CHEST PAIN, DYSPNEA, TACHYCARDIA, DECREASED BREATH SOUNDS ON AFFECTED SIDE

A

INITIALLY

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38
Q

CLINICAL MANIFESTATIONS OF PNEUMOTHORAX

o AS PNEUMOTHORAX ____________: ABSENT BREATH SOUNDS ON AFFECTED SIDE, HYPOXEMIA, LABOURED BREATHING, JUGULAR VENOUS DISTENSION, HYPOTENSION, CONTRALATERAL TRACHEAL SHIFT.

A

PROGRESSES

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39
Q

DIAGNOSIS OF PNEUMOTHORAX IS DONE VIA __________ ________

A

CHEST XRAY

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40
Q

TREATMENT OF PNEUMOTHORAX DEPENDS ON ______ & ________.

o ASPIRATION, O2 THERAPY
o CHEST TUBE INSERTION TO GET RID OF AIR THAT IS COLLECTING IN PLEURAL SPACE.

A

TYPE & SIZE

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41
Q

PLEURAL EFFUSION IS SAME PRINCIPLE AS PNEUMOTHORAX BUT INSTEAD OF AIR IT IS ________ IN THE PLEURAL SPACE

A

FLUID

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42
Q

FLUID IS HEAVY AND SITS AT THE ______________ OF PLEURAL SPACE

A

BOTTOM

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43
Q 
TYPES OF \_\_\_\_\_\_\_\_\_\_ \_\_\_\_\_\_\_\_\_\_:
o	HEMOTHORAX 
o	TRANSUDATE
o	EXUDATE
o	EMPYEMA 
o	CHYLOUS PLEURAL EFFUSION
A

PLEURAL EFFUSIONS

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44
Q

WHICH TYPE OF PLEURAL EFFUSION?

BLOOD IN PLEURAL SPACE USUALLY ASSOCIATED WITH TRAUMA

A

HEMOTHORAX

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45
Q

WHICH TYPE OF PLEURAL EFFUSION?

WATERY DRAINAGE IN PLEURAL SPACE, LOW PROTEIN COUNT (SEEN IN PNEUMONIA)

A

TRANSUDATE

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46
Q

WHICH TYPE OF PLEURAL EFFUSION?

WATERY BUT HAS HIGH PROTEIN COUNT (SEEN IN TUMORS – LUNG CANCER)

A

EXUDATE

47
Q

WHICH TYPE OF PLEURAL EFFUSION?

PUS IN PLEURAL SPACE (SEEN IN LUNG ABSCESSES)

A

EMPYEMA

48
Q

WHICH TYPE OF PLEURAL EFFUSION?

LYMPHATIC FLUID LEAKING INTO PLEURAL SPACE

A

CHYLOUS PLEURAL EFFUSION

49
Q

COLLECTION OF FLUID IN PLEURAL SPACE EXERTS PRESSURE ON THE ________ CAUSING ___________ ATELECTASIS AND MAY DISPLACE MEDIASTINAL STRUCTURES

A

LUNGS

COMPRESSION

50
Q

CLINICAL MANIFESTATIONS ARE ASSOCIATED WITH THE EXTENT OF ATELECTASIS (AMOUNT OF________________) SYMPTOMS WORSEN AS DRAINAGE __________.

o DYSPNEA, TACHYPNEA, TACHYCARDIA, DECREASED BREATH SOUNDS ON AFFECTED SIDE
o FEVER ASSOCIATED WITH INFECTION (EMPYEMA)
o HYPOXEMIA, LABOURED BREATHING, HYPOTENSION, CONTRALATERAL TRACHEAL SHIFT

A

DRAINAGE

increases

51
Q

TREATMENT: IN ACCORDANCE TO _____________ OF EFFUSION

o THORACENTESIS – INSERT LONG THIN NEEDLE AND ASPIRATE ______. OR PUT CHEST TUBES IN TO DRAIN OVER SEVERAL DAYS
o LAB ANALYSIS OF ___________ TO DETERMINE CAUSE OF EFFUSION
o SUPPORTIVE: OXYGEN PRN, IV FLUIDS, ANTIBIOTICS TO TREAT INFECTION

A

EXTENT
FLUID
EXUDATE

52
Q

WHICH RESTRICTIVE RESPIRATORY DISORDER?

FORM OF RESPIRATORY FAILURE.
CAUSES
o DIRECT – PNEUMONIA, SMOKE INHALATION, CHEMICAL INHALATION, INHALATION OF TOXIC FUMES, NEAR DROWNING
o INDIRECT – CAUSED BY OTHER DISEASES SUCH AS PANCREATITIS, DRUG OVERDOSE

A

ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)

53
Q

PATHOGENESIS OF ARDS:

ACUTE PHASE
 __________ DAMAGES STRUCTURAL FRAMEWORK OF LUNG
 INCREASE IN ___________ FACTORS

A

CYTOKINES

COAGULATION

54
Q

PATHOGENESIS OF ARDS:

FIBROPROLIFERATIVE PHASE
 ___________ CELLS DEPOSIT PROTEIN ALONG WALLS OF ALVEOLI OCCUR WITH THE INCREASED INFLAMMATION. THIS INCREASES THE ____________ OF THE ALVEOLI AND _____________ GAS EXCHANGE.
 PROMINENT FIBROSIS (THICKENING)

A

FIBROBLAST
THICKNESS
DECREASES

55
Q

CLINICAL MANIFESTATIONS OF WHICH RESTRICTIVE RESPIRATORY DISORDER?

o DYSPNEA, TACHYPNEA, TACHYCARDIA, INCREASED RESPIRATORY EFFORT.
o HYPOXEMIA UNRESPONSIVE TO INCREASING FRACTIONS OF INSPIRED OXYGEN (FI02), POOR LUNG COMPLIANCE
o CAN RESULT IN RESPIRATORY FAILURE AND IF NOT REVERSED – DEATH
o RESTLESSNESS, EXHAUSTION, DECREASED MENTAL STATUS

A

ARDS

56
Q

DIAGNOSIS OF ARDS
o HISTORY OF _____________ EVENT
o VQ MISMATCH, ABG’S, CXR

A

PRECIPITATING

57
Q

TREATMENT OF ARDS
o VENTILATORY SUPPORT (MECHANICAL VENTILATION)
o TREATMENT OF ___________ CONDITION

A

UNDERLYING

58
Q

WHICH RESTRICTIVE RESPIRATORY DISORDER?

INHERITED DISEASE WITH A GENETIC ABNORMALITY.
CHARACTERIZED BY EXCESSIVE SECRETION OF THICK MUCUS AND CONCENTRATED SWEAT, OFTEN CAUSING OBSTRUCTION OF GI AND RESPIRATORY TRACTS

A

CYSTIC FIBROSIS (CYSTIC = DUCT)

59
Q 
RESPIRATORY EFFECTS OF CYSTIC FIBROSIS
(\_\_\_\_\_\_\_\_\_\_\_  BLOCKS DUCTS IN RESPIRATORY TRACT)
o	COUGH, WHEEZE, RECURRENT PNEUMONIA
o	BARREL CHEST, CLUBBING BC OF HYPOXEMIA
o	BRONCHOSPASM
o	MUCUS IN LUNG
o	CAUSES HYPOXEMIA
A

MUCUS

60
Q

GASTROINTESTINAL EFFECTS OF CYSTIC FIBROSIS
(MUCUS PREVENTS LIVER AND PANCREAS FROM SECRETING __________)
o FAILURE TO THRIVE, MALABSORPTION
o DIABETES, PANCREATITIS, HEPATIC FAILURE

A

ENZYMES

61
Q

TREATMENT FOR CYSTIC FIBROSIS
NO CURE
MANAGED BY SUPPLEMENTING ______________ ENZYMES SUCH AS COTEZYME

A

DIGESTIVE

62
Q

AS THE CLIENT WITH CYSTIC FRIBROSIS ____ THEY CAN DEVELOP:
o PANCREATITIS
o LIVER FAILURE
o DIABETES
o RESPIRATORY PROBLEMS BC LUNGS BEGIN TO FAIL, BECOME HYPOXEMIC
 CAN GO INTO RESPIRATORY FAILURE
 NEED LUNG TRANSPLANT EVENTUALLY

A

AGES

63
Q

DEFINITION - LUNG DISEASE CAUSED BY CHRONIC EXPOSURE TO INDUSTRIAL PRODUCTS

A

PNEUMOCONIOSIS

64
Q

FINE PARTICLE SILICA(DUST) INHALATION

A

SILICOSIS

65
Q

DEFINITION – IN BUILDINGS IN 50S AS FIRE RETARDANT

A

ASBESTOSIS

66
Q

DEFINITION – COAL MINER’S LUNG, ACCUMULATION OF SOOT, FINE PARTICLE DUST

A

ANTHRACOSIS

67
Q

DEFINITION – PESTICIDES, FINE HAY PARTICLES

A

FARMER’S LUNG

68
Q

PNEUMOCONIOSIS PATHOGENESIS

• MACROPHAGES (WBCS) SECRETE _____________ WHICH DESTROY ALVEOLAR WALLS
• MACROPHAGES SEE PARTICLES AS FOREIGN INVADERS AND TRY TO DESTROY THEM, IN THE PROCESS THE ___________ ARE SCARRED
o LEADS TO STIFF FIBROTIC LUNGS

A

LYSOZYMES

ALVEOLI

69
Q

WHICH INFECTIOUS DISORDER?

  • CAUSATIVE ORGANISM: BORDETELLA PERTUSSIS **
  • DROPLET INFECTION – HIGHLY CONTAGIOUS
A

PERTUSSIS – WHOOPING COUGH

70
Q

PATHOGENESIS OF PERTUSSIS

ATTACHED TO _____ IN RESPIRATORY TRACT PRODUCES A TOXIN WHICH INITIATES AN _______________ RESPONSE

A

CILIA

INFLAMMATORY

71
Q

PERTUSSIS CAN BE DANGEROUS IN INFANTS & BABIES BECAUSE OF __________ SPASMS. CAN CAUSE VOMITING, INCREASING RISK OF _______________.

A

COUGHING

ASPIRATION

72
Q

PATHOGENESIS OF PERTUSSIS

 INCUBATION PERIOD 5 – 21 DAYS
 PRODROME: 1 – 2 WKS
RHINORRHEA (RUNNY NOSE), FEVER, MALAISE (RESEMBLES BAD _________)
 PAROXYSM : 1 – 6 WKS; PAROXYSMAL COUGHING SPASM (ASSOCIATED WITH VOMITING)
 CONVALESCENCE: WKS – MONTHS

A

COLD

73
Q

CLINICAL MANIFESTATIONS OF PERTUSSIS
• BRUISING AROUND _______
• BROKEN ________ _________ IN EYE FROM COUGHING

A

EYES

BLOOD VESSELS

74
Q

EVALUATION & TREATMENT OF PERTUSSIS
• ____________ SWAB (BP SWAB)
• CXR
• ANTIBIOTICS

A

NASOPHARYNGEAL

75
Q

USED IN PREVENTION OF PERTUSSIS?

A

IMMUNIZATION (85% PREVENTION)

76
Q

COMPLICATIONS OF PERTUSSIS

o RISK OF _____________ IN INFANTS ( 1 – 3 INFANTS DEATHS PER YEAR IN CANADA)
o PETECHIAE, BRUISING, FRACTURED _____, PNEUMONIA

A

ASPIRATION

RIBS

77
Q

WHICH INFECTIOUS RESPIRATORY DISORDER?

o CAUSED BY BACTERIUM MYCOBACTERIUM TUBERCULOSIS
o BACILLI – ARE SUPER TOUGH
o MODE OF TRANSMISSION – CAUSED BY INHALATION OF BACTERIUM
o AEROSOLIZED DROPLET

A

TUBERCULOSIS

78
Q 
POPULATIONS AT RISK FOR TUBERCULOSIS (\_\_\_\_\_\_\_\_ POPULATIONS LIVING IN \_\_\_\_\_\_\_ AREAS)
o	ELDERLY
o	HIV
o	HOMELESS
o	REFUGEE CAMPS
o	TRAVELERS
A

LARGE

SMALL

79
Q

ACTIVE TUBERCULOSIS

o ALVEOLAR MACROPHAGES ATTEMPT TO INGEST INHALED ______________.
o CHARACTERIZED BY CASEATION ___________ AND __________
(PERSON DOES NOT HAVE HEALTHY IMMUNE SYSTEM)

A

MYCOBACTERIUM
NECROSIS
CAVITATION

80
Q

DORMANT TUBERCULOSIS

o ALVEOLAR MACROPHAGES ATTEMPT TO INGEST INHALED ______________.
o CHARACTERIZED BY PRESENCE OF ____________ (TUBERCLES) (HEALTHY IMMUNE SYSTEM LIMITS DAMAGE CAUSED BY INFECTION) ______________ SEAL INFECTION AND PREVENT IT FROM BECOMING FULL BLOWN DISEASE. LIMITS EXTENT OF INFECTION.

A

MYCOBACTERIUM
GRANULOMA
MACROPHAGES

81
Q

PERSONS WITH DORMANT TUBERCULOSIS MAY HAVE A __________ TUBERCULIN SKIN TEST.
THEY HAVE TUBERCLES ON _______. BUT NO OTHER EVIDENCE FOR DISEASE IS VISIBLE.

A

POSITIVE

LUNGS

82
Q

REACTIVATION OF TUBERCULOSIS CAN OCCUR WHEN SOMEONE _____________ INFECTED WITH DORMANT TB’S IMMUNE SYSTEM BEGINS TO ______ REACTIVATING TB. _________ CAN NO LONGER CONTROL INFECTION.

A

PREVIOUSLY
FAIL
MACROPHAGES

83
Q

PRIMARY INFECTION OF TUBERCULOSIS MAY BE ________________.

A

ASYMPTOMATIC

84
Q 
CLINICAL MANIFESTATIONS OF \_\_\_\_\_\_\_\_\_ TUBERCULOSIS:
o	FEVER
o	FATIGUE
o	MALAISE
o	WEIGHT LOSS
o	NIGHT SWEATS
o	COUGH (MAY BE PRODUCTIVE, MAY COUGH UP BLOOD)
o	SPUTUM PRODUCTION
o	HEMOPTYSIS
A

ACTIVE

85
Q 
EVALUATION OF TUBERCULOSIS: 
o	MANTOUX TEST:
	MEASURED BY \_\_\_\_\_\_\_\_\_\_\_\_\_\_ (HARDNESS) OF 10MM(DOES NOT CONFIRM ACTIVE DISEASE) – FEELS LIKE A CYST 
	CXR
	SPUTUM CULTURES
A

INDURATION

86
Q

TREATMENT OF TB

o _____________ AGENTS

A

ANTITUBERCULAR

87
Q

SEVERE ACUTE RESPIRATORY SYNDROME (SARS) IS A SEVERE FORM OF PNEUMONIA CAUSED BY SARS ASSOCIATED _________________ (SARS-COV).

A

CORONAVIRUS

88
Q

SARS QUICKLY LEADS TO RESPIRATORY ___________

A

FAILURE

89
Q

PATHOGENESIS OF WHICH INFECTIOUS RESPIRATORY DISORDER?

o INCUBATION PERIOD 2 TO 7 DAYS
o ONSET: FEVER, CHILLS, MYALGIA, HEADACHE
o NONPRODUCTIVE COUGH; PROGRESSES TO PNEUMONIA
o MAY DEVELOP HYPOXEMIA

A

SARS

90
Q

PERSONS WITH SARS ARE CONTAGIOUS WHEN :
 THEY ARE ________________.
 CDC RECOMMENDS ISOLATION FOR ____ DAYS POST SYMPTOMS

A

SYMPTOMATIC

TEN

91
Q

SARS IS HIGHLY CONTAGIOUS & IS TRANSMITTED VIA _____

A

AIR

ITS AIRBORNE. THIS WAS AWKWARD TO WORD.

92
Q

THERE IS CURRENTLY NO RAPID SCREENING _____ FOR SARS

A

TEST

93
Q

BLOOD TESTS THAT CAN BE PERFORMED FOR SARS?

_______ (ENZYME-LINKED IMMUNOABSORBENT ASSAY)
RT-PCR (REVERSE TRANSCRIPTION-POLYMERASE CHAIN REACTION)
VIRAL SWABS OF RESPIRATORY _____________

A

ELISA

SECRETION

94
Q 
SARS MAY BE SUSPECTED IN A PATIENT WITH:
o	FEVER OF \_\_\_\_\_ AND
o	HISTORY OF 
	TRAVEL TO HIGH \_\_\_\_ AREAS OR
	CONTACT WITH SOMEONE WITH A DIAGNOSIS OF \_\_\_\_\_
A

38°C
RISK
SARS

95
Q

TREATMENT FOR SARS:

________ PRECAUTIONS &
_________ SUPPORT

A

ISOLATION

VENTILATORY

96
Q

INFLUENZA IS A ______________ ILLNESS

A

RESPIRATORY

97
Q

OUT OF INFLUENZA A, B & C. INFLUENZA __ IS THE MOST SERIOUS.

A

A

98
Q

ORTHOMYOMYXOVIRIDAE – FAMILY THAT ____________ COMES FROM. THIS COMES FROM BIRDS.

A

INFLUENZA

99
Q

CLINICAL MANIFESTATIONS OF WHICH INFECTIOUS RESPIRATORY DISORDER?

o	FEVER (38 ° - 40° C)
o	MYALGIA (SORE MUSCLES), HEADACHE
o	OCULAR SYMPTOMS (RUNNY EYES)
o	NONPRODUCTIVE COUGH, NASAL DRAINAGE
o	USUALLY SELF-LIMITING – CAN PROGRESS TO PNEUMONIA
A

INFLUENZA

100
Q

COMPLICATIONS OF WHICH INFECTIOUS RESPIRATORY DISORDER?

o CROUP, VIRAL PNEUMONIA, SECONDARY BACTERIAL INFECTIONS
o CARDIAC COMPLICATIONS
o REYE’S SYNDROME (ENCEPHALOPATHY – BRAIN DAMAGE, SECONDARY TO INFECTION)
o GUILLAIN-BARRE SYNDROME

A

INFLUENZA.

101
Q

VASCULAR DISORDERS
PULMONARY EMBOLISM – BLOOD CLOT TO ______
BLOOD CLOTS HAVE DEVELOPED IN LUNGS OR DEVELOP ELSE WHERE IN THE BODY.
AN _______ (PIECE OF BLOOD CLOT) BREAKS OFF AND TRAVELS TO LUNGS.
OFTEN CAUSED BY ______

A

LUNGS
EMBOLUS
DVT

102
Q

VIRCHOW TRIAD (FACTORS CONTRIBUTING TO THROMBOSIS)

o	VENOUS STASIS (\_\_\_\_\_\_\_\_\_ BLOOD FLOW) 
	PROLONGED IMMOBILITY
o	HYPERCOAGULABILITY (\_\_\_\_\_\_\_\_\_\_\_\_\_ BLOOD CLOTTING)
	POLYCYTHEMIA VERA (\_\_\_\_\_\_\_\_\_\_ COAGULABILITY)
	MEDICATIONS (BIRTH CONTROL)
o	INFLAMMATION OF BLOOD VESSEL 
	HYPERGLYCEMIA CAN INFLAME BLOOD VESSEL
	WHEN WE START AN IV (VENIPUNCTURE)
	SMOKING
A

SLUGGISH
PROMOTES
INCREASED

103
Q

PATHOGENESIS OF PULMONARY EMBOLISM

INITIALLY A BLOOD CLOT (THROMBUS) FORMS WITHIN THE ______ ________. THE CLOT BECOMES AN EMBOLUS, IT BECOMES DISLODGED FROM ITS ORIGINAL SITE AND TRAVELS THROUGH THE SYSTEMIC CIRCULATION AND INTO THE __________ CIRCULATION. THE CLOT EVENTUALLY TRAVELS INTO A BRANCH OF THE PULMONARY CIRCULATION. IT CAN EITHER ____________ A SMALL VESSEL CAUSING TEMPORARY SYMPTOMS UNTIL THE FIBRINOLYTIC SYSTEM DESTROYS IT. IT MAY MANIFEST AS MULTIPLE SMALL EMBOLI, OR IT MAY BE LARGE ENOUGH TO BLOCK THE FLOW OF BLOOD DISTAL TO THE OBSTRUCTION, CREATING _______ OF PULMONARY TISSUE (AN INFARCTION).

A

DEEP VEINS
PULMONARY
OCCLUDE
DEATH

104
Q

CLINICAL MANIFESTATIONS OF PULMONARY EMBOLISM VARY WITH ___________:

o INITIALLY – ANXIETY, RESTLESSNESS
o DYSPNEA, TACHYPNEA, CHEST PAIN, TACHYCARDIA
o AS IT WORSENS – MAY EXPERIENCE HEMOPTYSIS
o HYPOXIA/CYANOSIS
o MASSIVE OCCLUSION FROM POOR BLOOD FLOW TO TISSUE – PROFOUND SHOCK

A

SEVERITY

105
Q

DIAGNOSIS OF PULMONARY EMBOLISM:

o CXR; PFT
o _________ (TEST FOR PULMONARY EMBOLISM) ***
o VQ SCAN
o ANGIOGRAM

A

D-DIMER

106
Q

TREATMENT OF PULMONARY EMBOLISM:

o RISK FACTOR ANALYSIS AND ELIMINATION OF _____________ FACTORS
o ANTICOAGULATION
o SUPPLEMENTAL ____________ AND/OR ___________ SUPPORT

A

PREDISPOSING
OXYGEN
VENTILATORY

107
Q

LUNG CANCER ______ CELL OR _______ CELL

A

SMALL CELL OR NONSMALL CELL

108
Q

SMALL CELL LUNG CANCER

o __________ GROWING (SPEED)
o _____________ TO TREATMENT
o GROWS IN CENTRAL ________ REGION

A

RAPID
UNRESPONSIVE
BRONCHI

109
Q

SMALL CELL LUNG CANCER

o GROWS FROM THE _______ OF LUNG INSIDE
o ___________ IN SIZE IN 33 DAYS
o USUALLY ISN’T FOUND UNTIL IT HAS SPREAD CONSIDERABLE
o HAS ________ OUTCOME

A

OUTSIDE
DOUBLES
POOREST

110
Q

NONSMALL CELL LUNG CANCER

SQUAMOUS CELL
 GROWS _________ (LOCATION)
 _______ FOUND
 GROWS _________ (SPEED)

A

CENTRALLY
EASILY
SLOWLY

111
Q

NONSMALL CELL LUNG CANCER

ADENOCARCINOMA
 _______ GROWING CANCER (SPEED)
 GROWS ___________ (LOCATION)
 GROWS MORE ________ THAN SQUAMOUS CELL

A

SLOW
PERIPHERALLY
QUICKLY

112
Q

NONSMALL CELL LUNG CANCER

LARGE CELL CARCINOMA
	GROWS IN \_\_\_\_\_\_\_\_\_ 
	GROWS \_\_\_\_\_\_\_\_\_\_\_ (LOCATION)
	\_\_\_\_\_\_  GROWING (SPEED)
	FAIRLY \_\_\_\_ TO FIND & INDENTIFY
o	IF FOUND EARLY THERE MAY BE \_\_\_\_\_\_  IN TREATING THEM
A 
CLUSTERS
PERIPHERALLY
SLOW
EASY
SUCCESS
113
Q

PERSISTENT NAGGING________ IS USUALLY FIRST SIGN OF LUNG CANCER

A

COUGH

114
Q 
EFFECTS OF LUNG CANCER
o	\_\_\_\_\_\_\_\_\_ OF AIRFLOW
o	\_\_\_\_\_\_\_\_\_\_\_\_\_\_
o	PLEURAL EFFUSION, HEMOTHORAX, PNEUMOTHORAX
o	PARANEOPLASTIC SYNDROME (SIADH) – TUMORS MANUFACTURES AND SECRETES ADH
	SWELLING
	HYPONATREMIA
o	SYSTEMIC EFFECTS
A

OBSTRUCTION

INFLAMMATION

RACHEL - PATHO I FINAL (2 decks)

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