UNIT 8 - ALTERATIONS IN RESPIRATORY FUNCTION Flashcards
(114 cards)
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
2
Q
ETIOLOGIC ORGANISMS OF WHICH RESTRICTIVE RESPIRATORY DISORDER?
STREPTOCOCCUS PNEUMONIAE
LEGIONELLA PNEUMOPHILA
A
PNEUMONIA
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
4
Q
PATHOGENESIS OF PNEUMONIA:
INVADING ORGANISM SETS OF _____________ REACTION. ALVEOLI FILL WITH EXUDATE RESULTING IN ____________.
A
INFLAMMATORY
CONSOLIDATION
5
Q
CLINICAL MANIFESTATIONS OF PNEUMONIA CAN VARY WITH AGE, CAUSE, & __________
A
SEVERITY
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
7
Q
EVALUATION OF PNEUMONIA
__________ DONE TO CHECK FOR CONSOLIDATION
_________ CULTURE
A
XRAYS
SPUTUM
8
Q
TREATMENT OF PNEUMONIA IS \_\_\_\_\_\_\_\_\_\_\_: OXYGEN PRN ANTI-INFECTIVES FLUIDS ANTIPYRETICS EXPECTORANTS VENTILATORY SUPPORT
A
SUPPORTIVE
9
Q
DEFINITION - COLLAPSE OF LUNG TISSUE
A
ATELECTASIS
10
Q
TYPES OF __________
o OBSTRUCTION
o COMPRESSION BY EXTERNAL MASS
A
ATELECTASIS
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
12
Q
DURING ATELECTASIS, CLIENT BECOMES _____________ VERY QUICKLY
A
HYPOXEMIC
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
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
15
Q
TREATMENT OF ATELECTASIS
\_\_\_\_\_\_\_\_\_\_\_\_\_\_ IS KEY!! DEEP BREATHING AND COUGHING REPOSITIONING AMBULATION IF NOT CONTRAINDICATED INCENTIVE SPIROMETRY
A
PREVENTION
16
Q
CHEST WALL STRUCTURAL ABNORMALITIES
DEFINITION - HUNCHED BACK. ELDERLY WITH OSTEOPOROSIS. INHIBITS CHEST EXPANSION.
A
KYPHOSIS
17
Q
CHEST WALL STRUCTURAL ABNORMALITIES
DEFINITION - (CHEST EXCAVATION) STERNUM IS DISPLACED BACKWARDS.
A
PECTUS EXCAVATUM
18
Q
CHEST WALL STRUCTURAL ABNORMALITIES
DEFINITION - STERNUM IS PROTRUDING FORWARD. BIRD CHEST.
A
PECTUS CARINATUM
19
Q
CHEST WALL STRUCTURAL ABNORMALITIES
DEFINITION - SPINE IS ‘S’ SHAPED. INTERFERES WITH MOVEMENT OF RIBS AND INHIBITS MOVEMENT OF CHEST WALL.
A
SCOLIOSIS
20
Q
CHEST WALL STRUCTURAL ABNORMALITIES SUCH AS KYPHOSIS, PECTUS EXCAVATUM & CARINATUM, & SCOLIOSIS CAN ALL LEAD TO RECURRENT _________ INFECTIONS
A
CHEST
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
22
Q
TREATMENT OF RIB FRACTURE DEPENDS ON __________ OF INJURY
A
SEVERITY
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
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
25
TREATMENT OF WHICH CHEST WALL INJURY?
| PAIN CONTROL AND MANAGEMENT OF UNDERLYING PULMONARY AND/OR CARDIAC INJURY
CHEST TUBES, MECHANICAL VENTILATION
FLAIL CHEST
26
FLAIL CHEST CAN CAUSE ______________
PNEUMOTHORAX
27
DEFINITION - AN ACCUMULATION OF AIR IN THE PLEURAL SPACE
CAUSES ATELECTASIS (GREATER AMOUNT OF AIR = MORE SEVERE ATELECTASIS)
PNEUMOTHORAX
28
PNEUMOTHORAX CAN RESULT FROM ____________ DISEASE (SUCH AS COPD) OR FROM CHEST __________ (RIB FRACTURES)
UNDERLYING
| TRAUMA
29
```
TYPES OF _____________
o SPONTANEOUS
PRIMARY
SECONDARY
o OPEN
o TENSION
```
PNEUMOTHORAX
30
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
SPONTANEOUS: PRIMARY
31
WHICH TYPE OF PNEUMOTHORAX?
o RESULTING FROM TRAUMA OR SPONTANEOUS RUPTURE OF BLEB ON VISCERAL PLEURA SECONDARY TO PRE-EXISTING PULMONARY DISEASE
SPONTANEOUS: SECONDARY
32
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
OPEN
33
PRESSURE IN PLEURAL SPACE EQUALS ___________ PRESSURE
ATMOSPHERIC
34
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
TENSION
35
A ____________ PNEUMOTHORAX IS THE MOST SEVERE.
TENSION
36
CLINICAL MANIFESTATIONS VARY WITH THE ___________ OF THE PNEUMOTHORAX
EXTENT
37
CLINICAL MANIFESTATIONS OF PNEUMOTHORAX
o _____________: CHEST PAIN, DYSPNEA, TACHYCARDIA, DECREASED BREATH SOUNDS ON AFFECTED SIDE
INITIALLY
38
CLINICAL MANIFESTATIONS OF PNEUMOTHORAX
o AS PNEUMOTHORAX ____________: ABSENT BREATH SOUNDS ON AFFECTED SIDE, HYPOXEMIA, LABOURED BREATHING, JUGULAR VENOUS DISTENSION, HYPOTENSION, CONTRALATERAL TRACHEAL SHIFT.
PROGRESSES
39
DIAGNOSIS OF PNEUMOTHORAX IS DONE VIA __________ ________
CHEST XRAY
40
TREATMENT OF PNEUMOTHORAX DEPENDS ON ______ & ________.
o ASPIRATION, O2 THERAPY
o CHEST TUBE INSERTION TO GET RID OF AIR THAT IS COLLECTING IN PLEURAL SPACE.
TYPE & SIZE
41
PLEURAL EFFUSION IS SAME PRINCIPLE AS PNEUMOTHORAX BUT INSTEAD OF AIR IT IS ________ IN THE PLEURAL SPACE
FLUID
42
FLUID IS HEAVY AND SITS AT THE ______________ OF PLEURAL SPACE
BOTTOM
43
```
TYPES OF __________ __________:
o HEMOTHORAX
o TRANSUDATE
o EXUDATE
o EMPYEMA
o CHYLOUS PLEURAL EFFUSION
```
PLEURAL EFFUSIONS
44
WHICH TYPE OF PLEURAL EFFUSION?
BLOOD IN PLEURAL SPACE USUALLY ASSOCIATED WITH TRAUMA
HEMOTHORAX
45
WHICH TYPE OF PLEURAL EFFUSION?
WATERY DRAINAGE IN PLEURAL SPACE, LOW PROTEIN COUNT (SEEN IN PNEUMONIA)
TRANSUDATE
46
WHICH TYPE OF PLEURAL EFFUSION?
WATERY BUT HAS HIGH PROTEIN COUNT (SEEN IN TUMORS – LUNG CANCER)
EXUDATE
47
WHICH TYPE OF PLEURAL EFFUSION?
PUS IN PLEURAL SPACE (SEEN IN LUNG ABSCESSES)
EMPYEMA
48
WHICH TYPE OF PLEURAL EFFUSION?
LYMPHATIC FLUID LEAKING INTO PLEURAL SPACE
CHYLOUS PLEURAL EFFUSION
49
COLLECTION OF FLUID IN PLEURAL SPACE EXERTS PRESSURE ON THE ________ CAUSING ___________ ATELECTASIS AND MAY DISPLACE MEDIASTINAL STRUCTURES
LUNGS
| COMPRESSION
50
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
DRAINAGE
| increases
51
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
EXTENT
FLUID
EXUDATE
52
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
ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)
53
PATHOGENESIS OF ARDS:
ACUTE PHASE
__________ DAMAGES STRUCTURAL FRAMEWORK OF LUNG
INCREASE IN ___________ FACTORS
CYTOKINES
| COAGULATION
54
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)
FIBROBLAST
THICKNESS
DECREASES
55
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
ARDS
56
DIAGNOSIS OF ARDS
o HISTORY OF _____________ EVENT
o VQ MISMATCH, ABG’S, CXR
PRECIPITATING
57
TREATMENT OF ARDS
o VENTILATORY SUPPORT (MECHANICAL VENTILATION)
o TREATMENT OF ___________ CONDITION
UNDERLYING
58
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
CYSTIC FIBROSIS (CYSTIC = DUCT)
59
```
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
```
MUCUS
60
GASTROINTESTINAL EFFECTS OF CYSTIC FIBROSIS
(MUCUS PREVENTS LIVER AND PANCREAS FROM SECRETING __________)
o FAILURE TO THRIVE, MALABSORPTION
o DIABETES, PANCREATITIS, HEPATIC FAILURE
ENZYMES
61
TREATMENT FOR CYSTIC FIBROSIS
NO CURE
MANAGED BY SUPPLEMENTING ______________ ENZYMES SUCH AS COTEZYME
DIGESTIVE
62
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
AGES
63
DEFINITION - LUNG DISEASE CAUSED BY CHRONIC EXPOSURE TO INDUSTRIAL PRODUCTS
PNEUMOCONIOSIS
64
FINE PARTICLE SILICA(DUST) INHALATION
SILICOSIS
65
DEFINITION – IN BUILDINGS IN 50S AS FIRE RETARDANT
ASBESTOSIS
66
DEFINITION – COAL MINER’S LUNG, ACCUMULATION OF SOOT, FINE PARTICLE DUST
ANTHRACOSIS
67
DEFINITION – PESTICIDES, FINE HAY PARTICLES
FARMER’S LUNG
68
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
LYSOZYMES
| ALVEOLI
69
WHICH INFECTIOUS DISORDER?
* CAUSATIVE ORGANISM: BORDETELLA PERTUSSIS **
* DROPLET INFECTION – HIGHLY CONTAGIOUS
PERTUSSIS – WHOOPING COUGH
70
PATHOGENESIS OF PERTUSSIS
ATTACHED TO _____ IN RESPIRATORY TRACT PRODUCES A TOXIN WHICH INITIATES AN _______________ RESPONSE
CILIA
| INFLAMMATORY
71
PERTUSSIS CAN BE DANGEROUS IN INFANTS & BABIES BECAUSE OF __________ SPASMS. CAN CAUSE VOMITING, INCREASING RISK OF _______________.
COUGHING
| ASPIRATION
72
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
COLD
73
CLINICAL MANIFESTATIONS OF PERTUSSIS
• BRUISING AROUND _______
• BROKEN ________ _________ IN EYE FROM COUGHING
EYES
| BLOOD VESSELS
74
EVALUATION & TREATMENT OF PERTUSSIS
• ____________ SWAB (BP SWAB)
• CXR
• ANTIBIOTICS
NASOPHARYNGEAL
75
USED IN PREVENTION OF PERTUSSIS?
IMMUNIZATION (85% PREVENTION)
76
COMPLICATIONS OF PERTUSSIS
o RISK OF _____________ IN INFANTS ( 1 – 3 INFANTS DEATHS PER YEAR IN CANADA)
o PETECHIAE, BRUISING, FRACTURED _____, PNEUMONIA
ASPIRATION
| RIBS
77
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
TUBERCULOSIS
78
```
POPULATIONS AT RISK FOR TUBERCULOSIS (________ POPULATIONS LIVING IN _______ AREAS)
o ELDERLY
o HIV
o HOMELESS
o REFUGEE CAMPS
o TRAVELERS
```
LARGE
| SMALL
79
ACTIVE TUBERCULOSIS
o ALVEOLAR MACROPHAGES ATTEMPT TO INGEST INHALED ______________.
o CHARACTERIZED BY CASEATION ___________ AND __________
(PERSON DOES NOT HAVE HEALTHY IMMUNE SYSTEM)
MYCOBACTERIUM
NECROSIS
CAVITATION
80
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.
MYCOBACTERIUM
GRANULOMA
MACROPHAGES
81
PERSONS WITH DORMANT TUBERCULOSIS MAY HAVE A __________ TUBERCULIN SKIN TEST.
THEY HAVE TUBERCLES ON _______. BUT NO OTHER EVIDENCE FOR DISEASE IS VISIBLE.
POSITIVE
| LUNGS
82
REACTIVATION OF TUBERCULOSIS CAN OCCUR WHEN SOMEONE _____________ INFECTED WITH DORMANT TB'S IMMUNE SYSTEM BEGINS TO ______ REACTIVATING TB. _________ CAN NO LONGER CONTROL INFECTION.
PREVIOUSLY
FAIL
MACROPHAGES
83
PRIMARY INFECTION OF TUBERCULOSIS MAY BE ________________.
ASYMPTOMATIC
84
```
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
```
ACTIVE
85
```
EVALUATION OF TUBERCULOSIS:
o MANTOUX TEST:
MEASURED BY ______________ (HARDNESS) OF 10MM(DOES NOT CONFIRM ACTIVE DISEASE) – FEELS LIKE A CYST
CXR
SPUTUM CULTURES
```
INDURATION
86
TREATMENT OF TB
| o _____________ AGENTS
ANTITUBERCULAR
87
SEVERE ACUTE RESPIRATORY SYNDROME (SARS) IS A SEVERE FORM OF PNEUMONIA CAUSED BY SARS ASSOCIATED _________________ (SARS-COV).
CORONAVIRUS
88
SARS QUICKLY LEADS TO RESPIRATORY ___________
FAILURE
89
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
SARS
90
PERSONS WITH SARS ARE CONTAGIOUS WHEN :
THEY ARE ________________.
CDC RECOMMENDS ISOLATION FOR ____ DAYS POST SYMPTOMS
SYMPTOMATIC
| TEN
91
SARS IS HIGHLY CONTAGIOUS & IS TRANSMITTED VIA _____
AIR
ITS AIRBORNE. THIS WAS AWKWARD TO WORD.
92
THERE IS CURRENTLY NO RAPID SCREENING _____ FOR SARS
TEST
93
BLOOD TESTS THAT CAN BE PERFORMED FOR SARS?
_______ (ENZYME-LINKED IMMUNOABSORBENT ASSAY)
RT-PCR (REVERSE TRANSCRIPTION-POLYMERASE CHAIN REACTION)
VIRAL SWABS OF RESPIRATORY _____________
ELISA
| SECRETION
94
```
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 _____
```
38°C
RISK
SARS
95
TREATMENT FOR SARS:
________ PRECAUTIONS &
_________ SUPPORT
ISOLATION
| VENTILATORY
96
INFLUENZA IS A ______________ ILLNESS
RESPIRATORY
97
OUT OF INFLUENZA A, B & C. INFLUENZA __ IS THE MOST SERIOUS.
A
98
ORTHOMYOMYXOVIRIDAE – FAMILY THAT ____________ COMES FROM. THIS COMES FROM BIRDS.
INFLUENZA
99
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
```
INFLUENZA
100
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
INFLUENZA.
101
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 ______
LUNGS
EMBOLUS
DVT
102
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
```
SLUGGISH
PROMOTES
INCREASED
103
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).
DEEP VEINS
PULMONARY
OCCLUDE
DEATH
104
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
SEVERITY
105
DIAGNOSIS OF PULMONARY EMBOLISM:
o CXR; PFT
o _________ (TEST FOR PULMONARY EMBOLISM) ***
o VQ SCAN
o ANGIOGRAM
D-DIMER
106
TREATMENT OF PULMONARY EMBOLISM:
o RISK FACTOR ANALYSIS AND ELIMINATION OF _____________ FACTORS
o ANTICOAGULATION
o SUPPLEMENTAL ____________ AND/OR ___________ SUPPORT
PREDISPOSING
OXYGEN
VENTILATORY
107
LUNG CANCER ______ CELL OR _______ CELL
SMALL CELL OR NONSMALL CELL
108
SMALL CELL LUNG CANCER
o __________ GROWING (SPEED)
o _____________ TO TREATMENT
o GROWS IN CENTRAL ________ REGION
RAPID
UNRESPONSIVE
BRONCHI
109
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
OUTSIDE
DOUBLES
POOREST
110
NONSMALL CELL LUNG CANCER
SQUAMOUS CELL
GROWS _________ (LOCATION)
_______ FOUND
GROWS _________ (SPEED)
CENTRALLY
EASILY
SLOWLY
111
NONSMALL CELL LUNG CANCER
ADENOCARCINOMA
_______ GROWING CANCER (SPEED)
GROWS ___________ (LOCATION)
GROWS MORE ________ THAN SQUAMOUS CELL
SLOW
PERIPHERALLY
QUICKLY
112
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
```
```
CLUSTERS
PERIPHERALLY
SLOW
EASY
SUCCESS
```
113
PERSISTENT NAGGING________ IS USUALLY FIRST SIGN OF LUNG CANCER
COUGH
114
```
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
```
OBSTRUCTION
| INFLAMMATION
