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Patho II > Respiratory System Diseases > Flashcards

Respiratory System Diseases Flashcards

1
Q

Bronchiectasis: description

A

Obstructive lung disease (no cure)

  • Abnormal permanent dilation of large bronchi, resulting in weakness
  • Weakened bronchial wall can outpouch- leading to more retained materials and weakening and destruction of the bronchial walls
  • Increase in lung infections
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2
Q

Bronchiectasis: causes

A

1) Localized: from an airway obstruction ie tumors or foreign bodies
2) Generalized:
- congenital abnormalities
- lung infection (TB, fungal, abscesses)
- cystic fibrosis
- exposure to toxic gases

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3
Q

Bronchiectasis: development and progression of bronchial obstruction and infection

A

1) bronchial obstruction (mucus plug, tumor, etc)
2) Alveoli lose surface tension leading to atelectasis
- less O2 to body, can lead to full lung collapse
3) smooth muscle relaxation and dilation of the airways
- airway remains patent unless there’s an obstruction
4) Infection and Inflammation r/t debris accumulation and bacterial growth
5) impaired ciliary fxn d/t bacterial growth
6) chronic inflammation and development of new infections

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4
Q

Bronchiectasis: manifestations

A
  • Recurrent infection
  • Fever
  • Coughing
  • Producing copious amounts of foul-smelling, purulent sputum
  • Hemoptysis (coughing up blood)
  • Weight loss
  • Anemia (can be a cause or manifestation)
  • Marked dyspnea and cyanosis (again, d/t infections)
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5
Q

Cystic Fibrosis: Description

A

Genetic disorder which affects exocrine glands (systemic)
production of large amounts of thick mucus - secretions from exocrine glands inspissate (thicken) in ducts and act like a sponge => pull in fluid => pulling fluid and electrolytes out of other systems (ie lungs)

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6
Q

Cystic Fibrosis: genetics

A

autosomal recessive on chromosome #7

  • 1/29 carry the gene
  • > 200 types of defects (variability and severity of expression varies greatly)
  • Not sex-linked
  • most fatal genetic disease in Caucasian newborns, Dx usually b/t 1 month and 2 years old
  • – median survival = age 38
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7
Q

Cystic Fibrosis: pulmonary effects

A
  • secretions pull fluid out of alveoli, decreasing surface tension and leading to absorption atelectasis
  • blocks alveolar ventilation
  • chronic inflammation
  • edema of capillary-alveolar interface (even when it’s not blocked) d/t fluid in interstitium
  • bronchial scarring & fibrosis destroys airways
  • reduced lung compliance d/t alveolar rigidity
  • barrel chest
  • increased risk of pneumonia and chronic bronchitis
  • – s. aureus = yellow sputum/ pseudomonas = green
  • linked to bronchiectasis - can impact e/o
  • incr. incidence of nasal polyps
  • digital clubbing
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8
Q

Cystic Fibrosis: GI effects (pancreas)

A

Pancreatic duct clogs with mucus
- digestive enzymes can’t reach SI
- enzymes begin to digest the pancrease - destroying parenchymal tissue
- Destroys both exocrine and endocrine fxn
===> decr. insulin / DM

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9
Q

Cystic Fibrosis: GI effects (liver and spleen)

A

Small bile duct obstruction means bile can’t get through

  • backs up into liver and destroys it
  • biliary cirrhosis
  • liver failure

Portal vein moves blood from spleen/GI into liver

  • incr. Portal vein pressure = Portal hypertension
  • blockage leads to collateral vessel creation which bypass the liver; unfiltered blood in the body
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10
Q

Cystic Fibrosis: GI effects (intestine)

A

Blocks digestion and absorption

  • malabsorption of fats, CHO, proteins
  • In infants: failure to thrive d/t poor nutritional status
  • poor nutritional status all ages
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11
Q

Cystic Fibrosis: Cardiac effects

A

Chronic lung disease leads to Right sided HF => Cor pulmonale

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12
Q

Cystic Fibrosis: Reproductive effects

A

Males: obstructed vas deferens leading to aspermia
Females: thick mucus secretion in cervix blocks entrance - sterility

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13
Q

Cystic Fibrosis: Sweat glands effects

A

(Normal sweat is isotonic [mostly H2O] because Cl- gets reclaimed and Na+ follows)

Impaired reabsorption of ions in sweat ducts

  • 4-5x the concentration of salt in sweat compared to normal
  • leads to heat prostration (exhaustion), cellular dehydration, hyponatremia, hypochloremia
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14
Q

Cystic Fibrosis: Dental effects

A

Salivary ducts close leading to caries and gingivitis

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15
Q

Cystic Fibrosis: Respiratory manifestations

A
  • wheezing
  • chronic cough
  • dyspnea
  • tachypnea
  • barrel chest
  • cyanosis
  • may need daily chest physiotherapy to loosen mucus, lots of coughing, saline…
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16
Q

Cystic Fibrosis: Developmental manifestations

A
  • delayed weight gane
  • slowed bone growth
  • delayed sexual development
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17
Q

Cystic Fibrosis: GI manifestations

A
  • *Fat is needed for energy and myelination of nerves – especially for babies!!!**
  • inspissated meconium in fetal gut
  • meconium ileus (emergent, can’t pass meconium)
  • GERD
  • recurrent abdominal pain
  • distention
  • no bile = steatorrhea
  • vit deficiencies (A,D,E,K)
  • rectal prolapse from straining
  • inspissated mucofecal masses
  • chronic constipation w hemorrhoids
  • voracious appetite d/t malabsorption
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18
Q

Cystic Fibrosis: diagnosis

A 
Sweat test 
- 1month-20 years old
- > 60 mEq/L Cl- in sweat
Genetic Screening
- recombinant DNA
- Amniocentisis
CXR
- hyperinflation
- widespread consolidation
- fibrotic changes
- bronchiectasis
- Blebs
- RUL (right upper lobe??) involvement (why?) 
Stool
- trypsin and chymotrypsin absent
- fecal fat 15-30g (norm = 4g)
19
Q

Pulmonary Hypertension: description and etiology

A

(normal lung BP = 25/10)

Increased pressure in pulmonary circulation (>30syst & >12 diast)

Can be primary (idiopathic), genetic (autosomal DOMINANT), or secondary (d/t:

  • alveolar hypoventilation
  • COPD
  • Chronic bronchitis, emphysema
  • CF
  • other causes)

*she also said something about low pH leads to vasoconstriction which leads to PulmHTN…

20
Q

Pulmonary Hypertension: Signs and Symptoms

A
  • murmurs & S3/S4
  • dyspnea
  • JVD
  • chest pain
  • palpitations
  • dizziness
  • syncope
  • cough
  • lower extremity dependent edema
21
Q

Pulmonary Hypertension: Diagnosis

A
  • EKG: R ventricular hypertrophy and R axis deviation
  • PFT & ABG: arterial hypoxemia, reduced diff. capacity
  • V/Q scan: to rule out pulmonary embolism
  • CXR: enlarged central pulmonary arteries
  • Echo doppler: R ventr enlargement and overload
  • ***Cardiac cath: R cath to measure pressure
  • angiography as indicated by V/Q
22
Q

Cor Pulmonale: description

A

R ventricular dysfunction caused by pulmonary circulation chaos

  • Acute: pulmonary embolism or other trigger causes pulmonary HTN => Acute dilation of RV
  • **the right ventricle can EXPLODE so deal with this!!!!
  • Chronic: vascular or pulmonary parenchymal disease leads to hypertrophy and dilation of the RV
23
Q

Cor Pulmonale: Manifestations

A

Lung manifestations:
cough with or without sputum, dyspnea w/ exertion, rhonchi and wheezing
RHF manifestations:
S3 and tricuspid regurgitation, atypical chest pain,
JVD, hepatomegaly, ascites (backwards)
Cyanosis

24
Q

Cor Pulmonale: Causes

A 
Can be restrictive or obstructive
Pulmonary Tree
- COPD
- Pulmonary fibrosis (restrictive)
- Pulmonary resection
- Granulomatous disease (sarcoidosis, RA, SLE),
- Bronchiectasis
- CF
- Malignancy

Pulmonary Vessels

  • Primary Pulm HTN
  • Pulm Embolism
  • Pulm vascular disease 2ndary to syst illness
  • IV drug abuse

Thoracic Cage

  • obesity
  • kyphoscoliosis
  • neuromusc disease (ie MS, MG)
  • sleep apnea

Chronic hypoxia at high altitudes

25
Q

Pulmonary HTN and Cor Pulmonale: Treatment

A
  • Treat w/ low flow O2 - arterial O2 to >60mmHg
  • Bronchodilators on a routine schedule
  • Diuretics for fluid removal (monitor electrolytes!)
  • Vasodiltors: require cardiac monitoring
  • Cardiac cath
  • AVOID sedatives/respiratory depressants
26
Q

Pleural effusion: Types and descriptions

A

Pleural effusion = fluid in the pleural space
- always caused by underlying disease

TRANSUDATE = fluid with low protein (high hydrostatic pressure or low osmotic pressure)

  • most common cause is incr. pulmonary venous pressure from HF
  • Alveoli and pleura filled with fluid squished out of the capillaries
  • Low serum albumin d/t loss of osmotic pressure

EXUDATE = fluid high in protein and cellular content

  • inflammatory (pneumnia, TB) or malignant process
  • gross bloody effusion: malignancy or chest trauma
  • cellular content: WBCs or cancer cells
  • Presence of air: bronchopleural fistula d/t TB, pneumonia, malignancy
  • — air at apex, fluid at base
  • fluid = usually pus (empyema)
  • High fibrin content means pleural adhesions, which restricts ventilation
  • Chylothorax - d/t lymphatic obstruction (Lymph fluids in the pleural space)
27
Q

Pleural effusion: Manifestations

A

PE varies based on rapidity of collection and volume (ie HF = slow, stab wound = quick)

  • Pain: initially most common sx
  • pleural friction rub
  • effusion can move between pleural and pericardial space (to test, hold breath during auscultation)
  • Dyspnea: effusion compresses normal lung, esp if developed rapidly/large quantity
  • Tachypnea
  • Cough, hemoptysis
  • Breath sounds: reduced, absent, only bronchial
  • Mediastinal shift: trachea and mediastinum shift away from large, one-sided PE
28
Q

Pleural effusion: diagnosis and treatment

A

*treat underlying factors

  • Thoracentesis: performed at bedside - needle inserted for analysis (may need to be repeated to prevent fibrosis/ provide symptomatic relief)
  • Cone Biopsy: extract pleural tissue to test for TB or malignancy
  • Chest tube (continuous drainage) esp w/ empyema
  • Decortication/ peeling of pleural layers: may be necessary to avoid scarring if fibrous adhesions have occured
  • Pleurodesis: purposeful scarring, adheres lungs; late stage response.
29
Q

Pneumothorax: description

A

Rapid accumulation of intrapleural air and collapse of lung

Caused by any opening into pleural space through the visceral pleura, chest wall, mediastinum

30
Q

Spontaneous Pneumothorax

A

Unexpected; caused by rupture of blebs

  • primary or congenital (mostly tall and thin males)
  • secondary to emphysema w/ the blebs
  • air gains access to pleural cavity through defect in bronchus or alveoli
  • Primary Sx: chest or shoulder pain worse with inspo/cough
  • Dyspnea: from pain/ lung collapse
  • decreased resp excursions/ asymmetry
  • decr breath and voice sounds
31
Q

Closed pneumothorax

A

Leak closes quickly - if small can heal itself

  • closes immediately leaving only a partial collapse
  • interferes least w/ resp (other lung unaffected)
  • Leak in visceral pleura closes quickly
  • Symptoms more when fxn compromised by other disease
  • up to 30% heal w/o chest tube - watch for resolution
32
Q

Tension pneumothorax

A
  • lethal - medical emergency*
  • Valve-like opening in visceral pleura allows inspiration, closes for expiration
  • air accumulated under positive pressure completely collapsing lung and compressing contents of mediastinum (DEVIATION of other lung, aorta, vena cava, heart, trachea to other side)
  • prevents respiration => cyanosis, shock, death
  • Cardiac tamponade: parietal pleura continuous w/ pericardium
33
Q

Open pneumothorax

A

Penetrating injury - opening remains w/ collapse of lung

  • No negative pressure = affected lung does not expand at all
  • Postive pressure in trachea on expiration - expand on expiration
  • Air in trachea is rebreathed by unaffected lung
  • paradoxical/ see-saw breathing: chest rises on expirations and falls on inspiration (affected side)
34
Q

Hydropneumothorax

A

Accompanied by transudate
air moves to the top of lung and fluid at base
- could be caused by a misplaced IV cath in sublcavian v. - punctures pleura and infuses IV into it

35
Q

Hemopneumothorax

A

accompanied by blood

Mostly with chest trauma or surgery where blood vessels are cut

36
Q

Chest tubes

A

Thoracotomy tubes, called “trochar”

  • remove air/ fluid from space and reexpand lung
  • after chest srugery
  • inserted b/w ribs (6th-7th ICS for fluid)
  • Trochar in the pleural space has small openings
  • For air & fluid: need two tubes joined by a connector to a drain
37
Q

Under/water seal

A

(all chest drainage systems have this component)

  • allows bubbling of air through it; air can’t return
  • bubbling = air leak, fistula has not closed
  • tidaling = up and down movement, should occur until lung is fully expanded then no movement
  • rolling boil = leak
38
Q

Care of patient with a chest tube

A

Pleurevac/thoraklex must be below level of chest tube at all times* works with gravity*
- fluid drainage facilitated by semi-Fowler’s position/ turning toward side of tube
- avoid dependent loops of tubing - cause change in pressure
- do not milk tuing - causes increased negative pressure
- Check for respiratory distress (any kinks? all connections good? any leaking at insertion site?)
Don’t change dressing

39
Q

Care of patient with a chest tube: mobility

A

They need to move - otherwise can get pneumonia/ frozen shoulder

  • encourage full ROM on affected side
  • deep breathing and coughing ESSENTIAL to prevent atelectasis
  • Deep inspo expands lung and pushes air and fluid into tube
  • Pt can ambulate… disconnect from wall!!!! Carry tube
40
Q

Care of patient with a chest tube: clamping

A

NEVER clamp unless it’s been opened by damage, then change quickly
- clamping will result in a tension pneumothorax

41
Q

Care of patient with a chest tube: suction

A

amt ordered by physician via pleuravac

  • gentle continuous bubbling is all that’s necessary
  • use wall unit/devide to regulate pressure
  • always check fluid levels, record, sign off
  • usually stops in 3-4 days
  • Check VS and make assessment if bloody drainage occurs
  • Auscultate lungs
42
Q

Chest tube removal

A

(RN assists, done by MD, PA, NP)
CXR first: is lung re-expanded?
Give pain meds first
- suture clipped
- patient takes deep breath and bears down
- regular gause and occlusive tape to prevent air entry
- CXR done after - has pneumothorax reoccured?
- check VS and breath regularly

43
Q

Psychosocial impact of resp disorders

A

Developmental: loss of self esteem, fear of dying, physical changes
Economic: disruption/ loss of employment, cost of care
OCcupational/ Recreational: loss of opportunities, restriction of activities
Social: Change in sexual fxn, social isolation, change in role performance.

Patho II (12 decks)

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