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Clinical Medicine 2 > Lecture 5 (Meds Pulm)- Exam 2 > Flashcards

Lecture 5 (Meds Pulm)- Exam 2 Flashcards

1
Q

What is the definition of Foregin body aspiration?

A

Definition: Introduction of solid matter into the airway at the level of the glottal opening, larynx, trachea, or bronchi. Potentially life-threatening event because it can block respiration.

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1
Q

Foreign-Body Aspiration
* Common cause of what?
* How many deaths?
* 5th mcc of what?
* Male or females?
* What are teh most common items?

A
  • Common cause of mortality and morbidity in children, especially in those <2 yrs
  • ~1 death per 100,000 children 0 to 4 years old
  • 5th most common cause of unintentional-injury mortality in the US
  • Slightly higher predominance with male children (58%)
  • Most common items – jewelry, coins, food (nuts, seeds, hot dogs), toys, hardware, pins, pen caps, balloons
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2
Q

Foreign-Body Aspiration- clinical presentation
* What does it depend on?
* Most present when?
* What is the mc symptoms?
* What are other symptoms?
* What is the delayed presenation?

A
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3
Q

Foreign-Body Aspiration
* What is the most common foreign bodies (anatomical locations)? What are the sxs?

A

Bronchial foreign bodies are most common: coughing, wheezing & may present with decreased breath sounds (many are missed on initial presentation)
- Right main bronchus (~50%)
-Left main bronchus (~40%)
-Bilateral (~5%)

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4
Q

What foreign bodies is not common? What are the sxs?

A

Laryngotracheal foreign bodies not common: stridor, wheeze, dyspnea, sometimes hoarseness, life threatening (not difficult to diagnose)
* ~5%

up high; block whole airway

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5
Q

Foreign-Body Aspiration -Diagnosis
* What does the history + focused PE show?
* What imaging can be done?
* BUT if you have clinical suspicion is high, what can you do?

A
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6
Q

What does this show?

A
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7
Q

Foreign body aspiration-txt
* What do you need to protect?
* Remove what?
* What has a 95% success rate, good control of airway and visualization, minimal complications?
* What is only done by those with high levels of experience?

A
  • Protect the airway (keep them calm)
  • Remove object quickly but do NOT sweep mouth
  • Rigid bronchoscopy(ER)= ~ 95% success rate, good control of the airway & visualization, minimal complications
  • Flexible bronchoscopy only done by those w/ high levels of experience(OR)
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8
Q

FB aspiration: txt
* If patient cannot be ventilated after the everything, what needs to happen?
* What do you give if infectio from FB?

A
  • If patient cannot be ventilated after the above – cricothyroidotomy may be life-saving
  • Antibiotics and Steroids- only used if infection from FB-> Been there for days
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9
Q

Foreign-Body Aspiration
* What are the complications of FB retention?
* What must be obtained during bronchoscopy?

A
  • Complications:Atelectasis, Bronchiectasis, Post-obstructive pneumonia
  • Cultures obtained during bronchoscopy guide the initial antibiotic choice in treating infected areas
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10
Q

What are the complications of FB extractions?

A

Pneumothorax, Hemorrhage, Respiratory arrest (they occur rarely)

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11
Q

Foreign-Body Aspiration: Anticipatory Guidance
* Not preventable or preventable
* What is available and considered a point of standard of care in pediatric medicine?
* AAP advises what?

A
  • Preventable
  • Age specific educational guidance is available and considered a point of standard of care in pediatric medicine
  • AAP advises educating parents starting at 6 month well visit and every visit after (or as soon as they roll)
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12
Q

Respiratory Distress Syndrome (Hyaline Membrane Disease):
* What is it?

A

Definition: A condition in newborn babies in which the lungs are deficient in surfactant, preventing their proper expansion and causing the formation of hyaline material in the lung spaces

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13
Q

Respiratory Distress Syndrome(Hyaline Membrane Disease)
* When does incidence increase? (Know the ages)

A

Incidence increases with decreasing gestational age
* 100% ≤26 wks GA
* 57% 27-32 wks GA
* 10-1% 33-36 wks GA
* <0.3% 37-40 wks GA

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14
Q

Respiratory Distress Syndrome(Hyaline Membrane Disease)
* What increases with gestational age?
* Some rare cases are what?
* What are the risk factors?
* Leading cause of what?

A
  • Surfactant production and quality increase with GA
  • Some rare cases are hereditary
  • Risk factors: Prematurity, Male, Caucasian, Infants of diabetic mothers, Second-born of premature twins, Neonatal infection
  • Leading cause of death in preterm infants
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15
Q

Respiratory Distress Syndrome(Hyaline Membrane Disease)
* What is the pathophysiology?

A
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16
Q

Respiratory Distress Syndrome
(Hyaline Membrane Disease): Clinical presentation
* Presents when?
* What happens with breathing?
* Skin?
* Decreased what?

A
  • Presents within the first minutes to hours after birth
  • Rapid, labored breathing
  • Expiratory grunting
  • Suprasternal and substernal retractions
  • Nasal flaring
  • Cyanosis, lethargy and irregular respirations are signs of worsening pulmonary function
  • Decreased breath sounds, crackles, pale & may have diminished pulses, decreased urine output and peripheral edema
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17
Q

Respiratory Distress Syndrome
(Hyaline Membrane Disease): dx
* How can you tell clinical?
* What can you do before the baby is born?
* What do abgs show?
* What does the CXR show?

A
  • Clinical- preterm infant (worse w/risk factors) with the onset of progressive respiratory failure
  • Prenatally via tests on amniotic fluid (done if gestational age not known and delivery imminent)
  • ABGs revealing hypoxemia and hypercapnia- improves with O2 (pulm issue but if PO2 is not better with O2 then cardiac)
  • CXR= low lung volume, classic diffuse reticulogranular ground glass appearance with air bronchograms
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18
Q

baby born at 20 weeks old- what does this CXR show?

A
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19
Q

Respiratory Distress Syndrome
(Hyaline Membrane Disease)
* What is the txt?

A
  • Treatment includes intratracheal surfactant therapy, supplemental O2 & mechanical ventilation as needed
  • Survival rate >90% with treatment
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20
Q

Respiratory Distress Syndrome
(Hyaline Membrane Disease)
* What is the prevention?

A

Antenatal corticosteroid therapy administered to all pregnant women at 23 - 34 weeks gestation who are at increased risk of preterm delivery within the next 7 days → improved neonatal lung function by enhancing lung maturation and release of surfactant

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21
Q

What is the definition of cystic fibrosis (CF)

A

A hereditary disorder affecting the exocrine glands which causes the production of abnormally thick mucus, leading to the blockage of the pancreatic ducts, intestines, and bronchi and often resulting in respiratory infection.

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22
Q

Cystic Fibrosis
* The most common what? What is the mutation?
* What is the incidence?
* What is the medican predicted survival for CF in US?
* How many ppl are carriers?

A
  • The most common life-shortening autosomal recessive disease among Caucasians (mutation on chromosome 7, CFTR gene)
  • In US occurs ~ 1:3200 Caucasians, 1:10,000 Hispanics, 1:10,500 Native Americans, 1:15,000 African Americans, and 1:30,000 Asian Americans
  • Median predicted survival for CF in US = >40 years old (males>females)
  • ~ 1 in 31 Americans is a symptomless carrier of a defective CFgene
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23
Q

CF
* What gene is mutated?

A

more than 1,700 differentmutationsin the CFTR gene-> can have spin. mutation

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24
Q

What is the pathophysiology of CF?

A

Affects nearly all exocrine glands = abnormal transport of chloride and sodium across secretory epithelia →thickened, viscous secretions in the bronchi, biliary tract, pancreas, intestines, and reproductive system

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25
Q

CF: clinical presentation-pulmonary
* Begins when?
* Chronic what?
* Persistent what?
* Ultimately what happens?
* Chronic hypoxemia results in what?

A
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26
Q

What causes righ ventricular hypertropy in CF?

A

Chronic hypoxemia results in muscular hypertrophy of the pulmonary arteries, pulmonary hypertension and right ventricular hypertrophy

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27
Q

Clinical Presentation of CF: Bacterial Infections
* The lungs of most patients with CF are what?
* What are the most common organism in infants and children?
* What is the most common organism in ALL ages?
* What happens with MRSA?
* What is now present and that now causes rapid pulmonary deterioration?

A
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28
Q

Clinical Presentation of CF: GI
* What happens with pancreas?
* What happens in small intestine?
* What happens in billary?

A
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29
Q

CF is the third leading cause for what transplant?

A

liver transplantation in late childhood dt Biliary cirrhosis→ hepatobiliary disease

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30
Q

What are all the other clinical presentation findings for CF?

A
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31
Q

CF dx:
* What can you do for screening?
* What combo do you need?

A
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32
Q

What are the three ways that show Evidence of cystic fibrosis transmembrane conductance regulator (CFTR) dysfxn?

A
  • Elevated sweat chloride ≥60 mmol/L
  • Presence of two disease-causing variants inCFTR, one from each parental allele
  • Abnormal nasal potential difference
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33
Q

What is the primary test for dx of CF? What are the result levels?
* When can you preform the text/
* How is it stimulated? (what meds)

A
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34
Q

CF management:
* What do you need to monitor patients with?
* Whhat are the findings to the monitoring?
* What may also be useful to monitor extent of disease?

A
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35
Q

Explain this when the genetic testing come back positve for CFTR mutation on chromsome 7

A
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36
Q

Cystic Fibrosis- Managment
Pulmonary Function tests:
* Best indication of what?
* What age groups do you need to modify this?
* What are the expected results?

A
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37
Q

Cystic Fibrosis management
* What can be given?
* What are the airway clearance therapies?
* What is the preventation?
* Bronchodialators?
* What are the anti-inflam therapies?
* How do you prevent actute exacerbations?

A
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38
Q

Cystic Fibrosis- managment:
* What do you give for constipation?
* What do you do for the pancreatic?
* What do yoy need to monitor?
* What vitamins are needed?
* What are the blood tests needed?

A
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39
Q

Cystic Fibrosis- Management
* Requires what?
* Experience who?
* What do families and patients often need what?
* What needs ot be discussed?

A
  • Requires multi-disciplinary support
  • Experienced physician, dietician, physical therapist, respiratory therapist, pharmacist and social worker
  • Families & patients often need support groups and counseling
  • Advance care directives & lung transplant evaluations need discussion
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40
Q

Cystic Fibrosis- Prognosis
* Determined by what?
* What is inevitable?
* What has extended life expectancy?
* What is the life expectancy?
* What is recommended for planning pregnancy?

A
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41
Q

What is croup (Laryngotracheobronchitis)

A

Definition: inflammation of the larynx and trachea in children, associated with infection and causing breathing difficulties.

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42
Q

What is the viral form of croup? (What ages, caused by what, sx)

A

classic croup; occurs commonly in children 6 months - 3 yrs old
* caused by respiratory viruses
* viral symptoms (eg, nasal congestion, fever) are usually present

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43
Q

What is the spasmodic form of croup? (What ages, what is common, sx)

A

Spasmodic croup—occurs in children 6 months - 3 yrs old
* always occurs at night, fever is typically absent
* recurrent nature, “frequently recurrent croup”
* familial predisposition may be more common in children with a family history of allergies

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44
Q

Croup-viral:
* Most common in who? Uncommon in who?
* What is the male to femal ratio?
* What is the most common pathogen? Most common when? What are also pathogens?
* Most frequent time of occurance?

A
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45
Q

Mc pathogen for viral croup?

A

parainfluenza

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46
Q

What is the pathophysiology of croup-viral?

A

infection → inflammation of larynx, trachea, bronchi, bronchioles and lung parenchyma resulting in swelling and exudate, anatomic hallmark is narrowing of the subglottic airway

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47
Q

Croup-Viral: clinical presentation:
* What type of cough?
* Aggravated by what?
* Typcially begins as what?
* No fever or fever?
* What type of voice?
* Breathing may be what? What can result?
* Inspiratory what?

A
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47
Q
A
48
Q

what disease do you see a barking cough, that typically begins as a URI?

A

CROUP

49
Q

Croup-viral: Dx
* What does history and exam show?
* What are the DDXs?
* What do you do if dx is unclear?

A
50
Q

What x-rays do you order for croup? What do they show? ⭐️

A

AP and lateral neck x-ray = sub-epiglottic narrowing – “steeple sign”

51
Q

Croup- Viral: txt
* What is the txt? (What do you do with increasing severity?

A
52
Q

Croup- Viral
* What is the prognosis?
* What do you need to educate on?

A
  • Typically lasts 3-4 days
  • Educate parents regarding signs and symptoms of respiratory distress, to keep the patient as comfortable as possible through hydration, antipyretics.
53
Q

What is Epiglottitis?

A

Definition: inflammation of the epiglottis and adjacent supraglottic structures, potentially life-threatening condition

54
Q

Epiglottitis
* What are the causes?
* Occurs in who? Why have rates decreased?

A

Rapidly progressing infection of the epiglottis: bacterial, viral, & fungal pathogens, non-infectious causes

Occurs in Children and Adults- rates have declined due to vaccines
* -Children: 0.6 to 0.8 cases per 100,000
* -Adults: 0.6 to 1.9 cases per 100,000
* -median age of children has increased from 3 years to ~ 6 to 12 years
* -more common in males (58% of cases)

55
Q

What is the pathogen that causes the most cases of epiglottis?

A

Most cases: Bacterial= Haemophilus influenzaetype b (Hib)
* H. influenzae(types A, F, and nontypeable), Streptococci, Staphylococcus aureus, group AStreptococcus, Neisseria meningitides, Pasteurella multocida

56
Q

Epiglottitis:
* What are the risk factors? (children and adults)

A

Risk Factors
* Children: incomplete or lack of immunization for Hib and immune deficiency
* Adults: hypertension, diabetes mellitus, substance abuse, and immune deficiency, BMI >25, presence of an epiglottic cyst

57
Q

What is the pathophysiology of epiglottitis?

A

Colonized bacteria from the nasopharynx spread locally to cause a supraglottic cellulitis resulting in edema and accumulation of inflammatory cells of the epiglottis → threatened airway obstruction

58
Q

Epiglottitis-presentation
* How will children present?
* How is this a pediatric emergency?
* How will adults presents?

A
  • Children: “Tripod” position, abrupt onset, fever, anxiety, sore throat, stridor, drooling, dysphagia, hoarse voice, respiratory distress
  • Pediatric emergency – potential for rapid progression to complete airway obstruction
  • Adult: sore throat out of proportion to exam, presentation is slower with symptoms developing over 24 hr
59
Q

Epiglottitis-DX
* How do you dx this?

A
  • Clinical suspicion
  • Visualization: erythematous, edematous epiglottis w/ or w/o laryngoscopy
  • Most will go to OR for direct visualization and airway support
59
Q

What will the imaging show with epiglottitis?

A

Imaging: soft tissue lateral neck Xray-> Thumbprint Sign

60
Q

Epiglottitis-txt
* What do you need to manage immediately?
* Admit where?
* What do you do once airway secured?
* What is the empiric combo therapy?

A
61
Q

What is the definition of pertussis-whooping cough

A

Definition: a highly contagious acute respiratory illness caused by the Bordetella pertussis bacteria. Whooping cough is characterized by fits of coughing followed by a noisy, “whooping” sound while inhaling.

62
Q

Pertussis – “Whooping Cough”
* What is the cause?
* Increase incidence when?
* How is it transmitted?
* In the US, it cycles how?

A
  • Etiology – gram-negative coccobacillus – Bordetella pertussis
  • Increased incidence summer and fall
  • Transmission via respiratory droplets
  • In US it cycles q3-5yrs – the incidence of pertussis has been rising since the 1990s (increased rates of infection in adolescents and adults)
63
Q

Pertussis
* Highly what? Explain
* Who has the highest risk of mrobidity and mortality?
* Who may serve as a reservoir and present risk to infants?
* What is the incubation period?

A
64
Q

What is the preventation of pertussis?

A

Since 1997, acellular pertussis vaccine (DTaP) has been recommended for all five childhood doses. Prior to 1997, whole-cell pertussis vaccine (DTwP) was administered.

65
Q

What are the ages and types of vaccines for whooping cough?

A
66
Q

Pertussis-Presentation
* What type of symptoms?
* Paroxysms of what?
* Increased production of what?
* What can happen?
* Infants may progress to what?
* How long is the cough?

A
67
Q

What is ths catarrhal pertussis stage?

A

Catarrhal – URI symptoms, nighttime cough may occur, lasts 1-2 wks

68
Q

What is the paroxysmal pertussis stage?

A

coughing spells increase in severity, may exceed 5 coughs per expiration →“whoop” (a rushed inspiration)
* Copious mucous expectorant, post-tussive vomiting, infants may become cyanotic, coughing spells increase in frequency during the first 1-2 weeks, remain the same intensity for 2-3 weeks, and decrease gradually, stage may last 2-8 weeks

69
Q

What is the convalescent pertussis stage?

A

cough subsides over several weeks to months, average~ 4 weeks post infection (“100 day cough”), the cough may persist for many more weeks and is likely to return if patient has a URI in the following months.

70
Q

Pertussis-dx
* clinical dx?
* Dx can be confimed if what?
* How is it dx (lab)?
* What do you need to notify lab?
* What is the preferred test?

A
71
Q

Pertussis txt:
* Who needs to be hospitalized?
* What is the isolation in hospital?
* What is supportive care?
* Can it be treated as outpatient? explain?

A
  • Hospitalization: children < 4 months, respiratory distress, pneumonia, inability to feed, cyanosis or apnea, seizures
  • Isolation in hospital: standard precautions & droplet precautions until 5 days of antibiotics completed or 21 days after the onset of symptoms in untreated patients
  • Supportive care: fluids, nutrition, may require supplemental O2 or intubation (Cough suppressants and expectorants are not recommended)
  • May be treated as outpatient if older and not in respiratory distress – but may requires 21 days of isolation
72
Q

Pertussis medication:
* What antibiotics?
* Most effective when?
* Minimal effect when?
* Antibiotic therapy should always be initiated for what?

A

Medications
* Macrolide antibiotics (erythromycin, azithromycin-> this can be the only one used for under one month, clarithromycin);
* Trimethoprim-sulfamethoxazole (TMP-SMX) is an alternative for children older than two months
* Most effective in the catarrhal stage
* Minimal effect in later stages BUT – is utilized to prevent possible spread

Antibiotic therapy should always be initiated for secondary bacterial complications such as pneumonia, otitis.

73
Q

Pertussis
* What is the preventaion?
* What is the prophylaxis? Given when?

A
74
Q

Respiratory Syncytial Virus (RSV)
* What is this?

A

a paramyxovirus that causes disease of the respiratory tract. It is a major cause of bronchiolitis and pneumonia in young children and may be a contributing factor in sudden infant death syndrome.

75
Q

Respiratory Syncytial Virus (RSV)
* Seasonal outbreak where?
* US: when does it occur?
* Almost all children are infected by what age?
* MCC of what?

A
  • Seasonal outbreaks throughout the world
  • US: annual outbreaks Winter through Spring (Oct-May)
  • Almost all children are infected by age 2
  • Most common cause of lower respiratory tract infection in children <1 yr

  • Global hospitalization rates in children <5 years was 4.4 per 1,000
  • ~ 57,000 hospitalizations per year in US in children < 5 years
76
Q

Respiratory Syncytial Virus (RSV)
* What is the mortality rate globally?

A
  • 2.3 % of deaths among neonates 0 - 27 days of age (because mom’s antibodies)
  • 6.7 % of deaths among infants 28 - 364 days of age
  • 1.6 % of deaths among children 1- 4 years of age
77
Q

What are the risk factors of RSV?

A
  • Infants younger than six months of age who are born during the first half of the RSV season
  • Infants and children with underlying lung disease, such as chronic lung disease (bronchopulmonary dysplasia, cystic fibrosis, asthma)
  • Prematurity (<35 weeks gestation)
  • Congenital heart disease
  • Infants exposed to secondhand smoke
  • Trisomy 21
  • Immunocompromised patients
78
Q

Respiratory Syncytial Virus (RSV)
* What type of virus? Which one?
* What are the two subtypes?
* What is the transmission?

A
  • RNA virus -member of the Pneumoviridae family
  • Two subtypes: A and B, both present in most outbreaks
  • Transmission = primarily by inoculation of nasopharyngeal or ocular mucous membranes after contact with virus-containing secretions or fomites, direct contact is the most common route but aerosol droplets also a cause
79
Q

RSV
* Can survive for how long?
* What is critical to prevent health care associated spread?
* Infants most often follows infection of who?
* What is the incubation period?

A
  • RSV can survive for several hours on hands and fomites
  • Hand washing and contact precautions are critical to prevent health care-associated spread
  • Infants most often follows infection of older siblings or daycare
  • Incubation period=4-6 days
80
Q

What is the pathophysiology of RSV?

A

replicate in the nasopharynx →infects the small bronchiolar epithelium→ extends to the type 1 and 2 alveolar pneumocytes →lower respiratory tract infection 1-3 days later with includes mucus buildup, airway obstruction, air trapping, and increased airway resistance

81
Q

Respiratory Syncytial Virus (RSV)
* How does it present?
* Commonly assocaited with what?

A
82
Q

Respiratory Syncytial Virus (RSV): DX
* How do you dx clinically?
* What tests that can be done?
* What is the imaging?

A
83
Q

What does the CXR look like with RSV?

A
84
Q

Respiratory Syncytial Virus (RSV)
* What is the txt?
* What is not recommended?
* What is reserved for patients with evidence of pneumonia on CXR or with co-morbid bacterial infections?
* What is not typically used with first infection but sometimes repeat infections?

A
  • Supportive care= hydration, relief of nasal congestion/obstruction & monitoring for disease progression
  • Antiviral treatment not recommended
  • Antibiotics reserved for patients with evidence of pneumonia on CXR or with co-morbid bacterial infections
  • Bronchodilators- not typically used with first infection but sometimes repeat infections
85
Q

What is the txt for sereve resp distress with RSV?

A

Severe Resp Distress= Hospitalization, O2 to keep sats >90-92%, high-flow nasal cannula, CPAP and intubation in some cases

86
Q

Respiratory Syncytial Virus (RSV): patient education
* SXS?
* Spread?
* Nose?
* Avoidance of what?
* When do seek what?

A
87
Q

What is the definition of childhood asthma?

A

A respiratory condition marked by spasms in the bronchi of the lungs, causing difficulty in breathing, usually results from an allergic reaction or other forms of hypersensitivity

88
Q

Childhood asthma:
* How many kids affected?
* Gender ratio?
* Race?
* Asthma is the most common what?
* Leading cause of what?

A
  • 1 in 12 children = About 6 million children in US ages 0-17 yrs have asthma
  • Male > Female (under 20 yrs old)
  • African American ~14%, Puerto Rican ~13.6%, Multiple Race Non-Hispanic ~13%
  • Asthma is the most common chronic disease among children worldwide
  • A leading cause of hospitalization and school absenteeism

  • According to WHO – over 339 million people are affected globally
  • In 2019- Hospital Inpatient Stays 8%, ER Visits 74%, Office Visits 6%
  • Costs ~ $82 Billion per year
89
Q

What is the pathophysiology of childhood asthma? ⭐️

A
90
Q

Childhood Asthma
* What are the histological findings? How is this done?

A

Mucous plugging, eosinophilic inflammation, epithelial desquamation and hyperplasia, goblet cell metaplasia, subbasement membrane thickening, subepithelial fibrosis, smooth muscle hypertrophy/hyperplasia & submucosal gland hypertrophy

  • (only done with endobronchial/transbronchial biopsies & autopsy)
91
Q

Risk Factors: Pre- & Perinatal for childhood asthma? (think hx, maternal age, deficiencies, toxins, perinatal factors)

A
92
Q

Risk Factors of asthma: Childhood
* Who is more affected (gender with age ranges)
* Atopy has increase what?
* Exposure to what?
* What type of infections?
* Air?
* Skinny or obesity?
* Early what?

A
93
Q

Childhood Asthma
* What are common triggers?

A
94
Q

What are common medications that can trigger asthma?

A

NSAIDS, beta blockers, sometimes ACE inhibitors, Aspirin, (not used <18 yrs old unless directed)

95
Q

Childhood Asthma: clinical presentation
* what is going on with respiratory? (3)
* What is happening to the chest?
* Often followed by what?
* May be what?
* What happens at night?

A
96
Q

Childhood Asthma: clinical dx
* What do you need to look with personal hx, family hx and pmhx?

A
  • History- pattern of respiratory symptoms that occur following exposure to triggers & resolve with avoidance or asthma medication
  • Family Hx – list family members with asthma and severity
  • PMHx- Asthma is often diagnosed before the age of 7 years in ~ 75% of patients
97
Q

What do you need to make sure to document with childhood asthma?

A

Make sure to document age of onset (if patient has diagnosis of asthma), symptom progression, response to bronchodilators, history of use of corticosteroids, current medications & frequency used, ER visits, hospitalizations (intubations)

98
Q

⭐️

Childhood Asthma: PE findings
* Vitals: Make sure to check what?
* General: What do you need to document?
* HEENT: What may be present?
* Cardiac: What may be present?
* Skin: what may be present?
* Resp: What do you need to document?

A
99
Q

⭐️

Childhood Asthma
* Asthmatic wheezing usually involves what?
* This is different from what?

A
  • Asthmatic wheezing usually involves sounds of multiple different pitches starting and stopping at various points in the respiratory cycle, varying in tone and duration over time, do not clear with cough, bilateral
  • Different from FB aspiration= monophasic wheezing of a local bronchial narrowing with a single pitch, repeatedly begins and ends at the same point in each respiratory cycle
100
Q

⭐️

Childhood Asthma
* What are the exam findings that suggest severe airflow obstructions (PE, position, use of, pulse)?

A
101
Q

Childhood Asthma
* What is a poor predictor of the severity of airflow obstruction?
* Wheezing may be heard in patients with what?
* Widespread airway narrowing may be present in who?

A
  • Presence or absence of wheezing on physical examination is a poor predictor of the severity of airflow obstruction
  • Wheezing may be heard in patients with mild, moderate, or severe airway narrowing
  • Widespread airway narrowing may be present in individuals without wheezing

Wheezing ≠ Severity

102
Q

Childhood Asthma
* What is status asthmaticus?

A

acute asthma exacerbation in which bronchial obstruction is severe → continues to worsen/not improve despite adequate standard therapy → respiratory failure

103
Q

What are the sxs of status asthmaticus?

A
  • Poor respiratory effort, appears exhausted
  • Silent chest due to limited airflow is an ominous sign
  • Paradoxical thoracoabdominal movement
  • Bradycardia
  • Absent pulsus paradoxus
  • Cyanosis
  • Hypotension

  • medical emergency-ICU and possible intubation
104
Q
  • Not all wheezing is asthma- think about:
A
105
Q

Childhood Asthma
* How do you dx non-clinical?

A
106
Q

What is the preferred method of diagnosis of airflow obstruction?
* National Asthma Education and Prevention Program (NAEPP) advises what? What is the exception?

A
  • Spirometry: preferred method of diagnosis of airflow obstruction
  • National Asthma Education and Prevention Program (NAEPP) advises all patients >5 yrs must perform test to confirm diagnosis of asthma
  • <5 years old use history, exam and response to medication
107
Q

What is the spirometry values for obstruction?

A

FEV1< 80% predicted and
FEV1/FVC ratio < 0.85 (85 %)

108
Q

What number do you need to remember if asthma is not controlled on that big ass chart?

A

2s

109
Q

What are other studies that can be done with childhoos asthma?

A
110
Q

When do you need to obtain CXR in childhood asthma? (5)

A
111
Q

What will the CXR show with a patient with childhood asthma? (4)

A
  • Hyperinflation
  • Interstitial prominence
  • Peribronchial thickening
  • Mucoid impaction with atelectasis
112
Q

Childhood Asthma: Txt for acute exacerbation
* What is the goal?
* SABA?
* SAMA?
* Systemic glucocorticords?
* ICS?
* What is supplement

A
113
Q

⭐️

Childhood Asthma: asthma management
* What is the txt (4)

A
114
Q

Childhood Asthma: asthma control and prevention
* What are the 3 types you can use?
* What is no longer recommended?

A
115
Q

Childhood Asthma: goals
* Freedom of what?
* Few to no what?
* Minimal need for what?
* Reduce what?
* Optimize what?
* Maintence of what?
* Satisfaction with what?

A
116
Q

Childhood Asthma
* What does peak flow meters do?
* What age can this be used?

A

measure the maximal rate that a person can exhale during a short maximal expiratory effort after a full inspiration
* Children: based on personal best, usually must be ≥ 5 yrs old

117
Q

asthma

Reasons to Refer to Specialist: Pulmonology, Allergy
* Use of what/
* Recurrent what?
* Hx of what? (2)
* ED visits?
* Hospitalizations?

A
118
Q

What does the GINA show?

A

Clinical Medicine 2 (16 decks)

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