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MCC Part 1 > Pulmonary Medicine > Flashcards

Pulmonary Medicine Flashcards

1
Q

Define dyspnea

A
  • subjective experience of shortness of breath

- common from pulmonary and cardiac disease

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2
Q

Define tachypnea

A
  • increased rate of breathing

>20 breaths/min

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3
Q

Define hyperpnea

A
  • deep and rapid breathing
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4
Q

Define hyperventilation

A
  • increased alveolar ventilation, leading to an alveolar CO2 level below normal
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5
Q

Where is respiratory control centre?

A

Medulla

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6
Q

What inputs into respiratory control centre?

A
  • cortical (voluntary) control
  • mechanical/stretch receptors in chest wall and diaphragm
  • PCO2/pH chemoreceptors in medulla
  • PCO2, PO2, pH receptors in carotid body and aortic arch
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7
Q

What mechanism leads to sensation of dyspnea?

A
  • mechanical receptors in chest wall that feed back to respiratory motor neurons
  • lung stretch receptors
  • irritant receptors in bronchial mucosa activated by stimulation of bronchial mucosa and increased muscle tone and flow
  • central and peripheral chemoreceptors (even in absence of activation of respiratory muscles)
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8
Q

What is Homan sign?

A
  • pain with foot dorsiflexion -> DVT
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9
Q

What does brain natriuretic peptide differentiate?

A

heart failure vs. lung disease
- BNP released by myocytes being stretched
- cleaved into pro-BNP then to biologically active form and inactive amino terminal fragment NT-pro-BNP
-> used to guide CHF therapy
BNP <100 pg/mL or NT-pro-BNP <400 pg/mL: CHF unlikely
BNP >400 pg/mL or NT-pro-BNP >2000 pg/mL: CHF likely

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10
Q

What do you exclude by checking Hct in patient with dyspnea?

A

Anemia

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11
Q

Normal ABG values (sea-level)?

A
  • pH 7.4 (7.36 - 7.44)
  • PCO2: 40 (37 - 42)
  • HCO3: 24 (22 - 26)
  • PO2: 80-100 mmHg
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12
Q

Direction of change with respiratory pH change re: pH and PCO2?

A

Opposite directions

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13
Q

Appropriate compensation for acute resp acidosis

A

HCO3 increase by 10

PCO2 increase by 1

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14
Q

Appropriate compensation for chronic resp acidosis

A

HCO3 increase by 10

PCO2 increase by 3

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15
Q

Appropriate compensation for acute resp alkalosis

A

HCO3 decrease by 10

PCO2 decrease by 2

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16
Q

Appropriate compensation for chronic resp alkalosis

A

HCO3 decrease by 10

PCO2 decrease by 4

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17
Q

What is next step with metabolic acidosis?

A

Anion gap

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18
Q

Calculate anion gap? Normal range?

A

Na - Cl + HCO3

= 14 +/- 2

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19
Q

What is delta gap?

A
  • change in anion gap minus change in HOC3

>+6 = another metabolic process (e.g. metabolic alkalosis)

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20
Q

What does + C-ANCA in patient with dyspnea suggest?

A
  • granulomatosis with polyangitis (Wegener’s)
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21
Q

What investigation is suggestive of FB?

A
  • insp and exp X-ray views to look for gas trapping
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22
Q

Resp acidosis or alkalosis causes?

  • CNS depression
  • Neuromuscular disorders
  • Upper and lower airway abnormalities
  • Lung parenchyma abnormalities
  • Thoracic cage abnormalities
A

Resp acidosis

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23
Q

Resp acidosis or alkalosis causes?

  • hypoxia: pneumonia, pulmonary deem, restrictive lung disease
  • primary hyperventilation: CNS disorder, drugs (salicylate), sepsis, hepatic failure
A

Resp alkalosis

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24
Q

Treatment AECOPD?

A
  • oral/ IV steroids x5d
  • abx (increased sputum, purulence, volume): amoxicillin, doxycycline, septra, or 2/3rd gen cephalosporin
  • > likely pathogens H. flu, M. catarrhalis, S. pneumonia
  • second line abx: b-lactam, resp fluoroquinolone
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25
Q

Organisms for CAP?

A
  • S. pneumonia, H. flu, atypicals (C. pneumonia, M. pneumonia, L. pneumophilia)
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26
Q

Treatment CAP?

A

uncomplicated outpt- extended spectrum macrolide or doxycycline
complicated outpt: resp fluoroquinolone (levofloxacin), second line amoxil-clav or 2nd get cephalosporin and macrolide

hospitalized based on pneumonia severity index score
hospital-acquired pneumonia >48h often resistant organisms or gram-negative bacteria - need broad-spectrum abx

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27
Q

ARDS (acute lung injuries) 4 criteria

A
  • acute onset (within 1 wk clinical insult)
  • bilateral patchy airspace disease
  • PCWP <18 mmHg or no clinical evidence of increased LVEDP
  • PO2/FiO2 <300 mmHg (<300 mild, 100-200 moderate, <100 severe)
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28
Q

ARDS dx

A
  • bilateral pulmonary infiltrates
  • resp distress
  • hypoxemia
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29
Q

ARDS etiologies

A
  • aspiration/ toxin inhalants
  • sepsis
  • shock
  • trauma
  • DIC
  • pancreatitis
  • embolism
  • drugs
  • head trauma
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30
Q

ASA toxicity

A
  • metabolic acidosis and resp alkalosis
  • mild: n/v, abdominal pain, tinntus
  • more serious: hyperthermia, tachypnea, resp alkalosis, metabolic acidosis, hypoglycaemia, hypokalmeia, seizure, coma, death
  • > decontamination of gut with charcoal
  • > alkalinize urine and dialysis if severe
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31
Q

What has pauci-immune necrotizing and crescentic glomerulonephritis and pulmonary capillaritis?

A

Granulomatosis and polyangiitis (Wegners) and microscopic polyangiitis
-> high dose steroids and pulsed cyclophosphamide to induce remission then slow taper

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32
Q

What is chronic dyspnea?

A

dyspnea >1mo

2/3 cardiopulmonary

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33
Q

Ddx chronic dyspnea

A
  • COPD
  • asthma
  • CHF/ coronary artery/ CIRCU
  • obesity
  • psychogenic
  • interstitial lung disease
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34
Q

COPD in nonsmoker or pt presenting early condition to r/o?

A

alpha-1-antitrypsin deficiency

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35
Q

Spirometry dx of COPD?

A

FEV1/FVC <0.7

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36
Q

What does cardiopulmonary exercise testing differentiate?

A
  • cardiac and pulmonary pathology
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37
Q

FVC severity COPD?

A 
FEV1/FVC >70% = at risk
FEV1 >80% predicted =mild
FEV1 50-80% predicted = moderate
FEV1 30-49% predicted = severe
FEV1 <30% predicted = very severe
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38
Q

Steps to manage COPD

A 
- education, modulate RF, etc
\+ SABD
\+ LABD
\+/- pulmonary rehav
\+ inhaled steroid to LABD
\+ long-term supplemental O2, surgery, end-of-life care
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39
Q

Nodular pattern of ILD on CXR ddx

A
  • fungal disease
  • metastatic/ lymphangitis carcinomatosis
  • silicosis
  • sarcoidosis
  • histiocytosis X
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40
Q

Dx IPF

A
  • progressive dyspnea
  • bibasilar inspiratory crackles
  • restrictive pattern on PFT and impaired gas exchange
  • bilateral peripheral reticular opacities and sub pleural honeycombing with basal predominance on high resolution CT
  • r/o other causes
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41
Q

What is bronchiectasis

A
  • permanent dilation of airways due to repeat cycles of infection and inflammation

etiology

  • postinfectious
  • idiopathic
  • genetic dz
  • aspiration//GERD
  • immune deficiency
  • rheumatoid arthritis
  • ulcerative colitis
  • ABPA (allergic bronchopulmonary aspergillosis)
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42
Q

What is stridor?

A
  • high-pitched sound caused by oscillation of narrowed airway, signifying significant obstruction of large airways -> always prompts urgent airway evaluation
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43
Q

What does wheezing indicate?

A
  • obstructing airway = pathology

- requires sufficient airflow

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44
Q

PFT pattern with obstructive

A
  • FVC normal or reduced
  • FEV1/FVC reduced <70%
  • TLC increased or normal (increased = hyperinflation)
  • RV increased or normal (increased = gas trapping)
  • DLCO normal or reduced in mod-severe emphysema
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45
Q

PFT pattern with restrictive lung

A
  • FVC reduced
  • FEV1/FVC normal
  • TLC reduced <80%
  • RV reduced
  • DLCO reduced
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46
Q

PFT pattern with restrictive chest wall

A
  • FVC reduced
  • FEV1/ FVC normal
  • TLC reduced <80%
  • RV reduced
  • DLCO normal
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47
Q

PFT pattern with pulmonary vascular dz

A
  • FVC normal
  • FEV1/FVC normal
  • TLC reduced <80%
  • RV reduced
  • DLCO normal
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48
Q

Do flow volume curves indicate obstruction?

A
  • yes they give clues to the presence and location of obstruction (upper vs. lower airways) or presence of restriction
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49
Q

3 anatomic areas for obstruction

A
  • extra thoracic upper airways (nose to extrathroacic trachea)
  • intrathoracic upper airways (intrathroacic trachea)
  • lower airways (intrathoracic airways below carina)
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50
Q

Monophasic vs. polyphonic wheeze signifies what?

A
  • monophonic: large airway obstruction

- polyphonic: small airway obstruction

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51
Q

What type of stridor is extrathroacic obstruction?

A

Inspiratory stridor

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52
Q

What type of stridor is intrathroacic obstruction?

A

Expiratory stridor

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53
Q

Initial wheeze investigations

A
  • CBC (re: WBC)
  • ABG (re: hyperpnea, hypoxemia)
  • CXR (re: consolidation, pleural effusion, pneumothorax, heart failure)
  • EKG (re: ACS)
54
Q

Management acute wheeze/ asthma

A
  • O2
  • short acting b-agonist
  • prednisone
  • ipratropium
  • magnesium (very severe re: bronchodilates)
  • epinephrine/ anesthetic gases in ICU
55
Q

Define cyanosis

A
  • physical sign of bluish coloration of skin due to >50 g/L deO2 hemoglobin in blood vessels near skin surface
  • O2 saturation of arterial blood falls <85%
56
Q

What is abnormal deficiency in the concentration of O2 in arterial blood which can be reversed with supplemental O2?

A

Hypoxemia

57
Q

What is the term when the total body is deprived of O2?

A

Hypoxia

58
Q

Central vs peripheral cyanosis

A

Central

  • circulatory or ventilatory problem -> poorer blood oxygenation in lungs or greater O2 extraction due to slowing down of blood circulation in skin bv
  • hypoventilation: normal A-a gradient, elevated PCO2
  • high A-a gradient: shunt, V/Q mismatch

Peripheral

  • blood reaching extremities not O2 rich = skin appears blue
  • can be due to central causes or other etiologies
59
Q

If A-a gradient increased but supplemental O2 doesn’t correct hypoxemia what does that indicate?

A

R-L shunt

60
Q

What is the A-a gradient?

A

Alveolar-Arterial gradient = PAO2 - PaO2

  • normal <10mmHg (5-20 normal range)
  • increased = diffusion defect, V/Q defect or right to left shunt
61
Q

Common causes of cough?

A
  • PND
  • asthma
  • GERD
  • drugs (ACEi)
62
Q

Where are cough receptors (mechanical and chemical)?

A
  • resp epithelium
  • pericardium
  • esophagus
  • diaphragm
  • stomach

-> stimulate via afferent nerves the medullary cough centre that activates exp muscles through efferent nerves

63
Q

Do patients die of asphyxiation or exsanguination with massive hemoptysis?

A

Asphyxiation

64
Q

Define massive hemoptysis

A
  • expectoration >100-600 mL blood over 24h period

+ features hemodynamic instability, altered gas exchange, or resp difficulties

65
Q

What is most common site of hemoptysis?

A
  • bronchial arteries due to higher pressures (vs. pulmonary arteries)
66
Q

What do bronchial arteries supply?

A
  • airways
  • hilarious LN
  • visceral pleura
  • some of mediastinum
67
Q

Can blood from respiratory source present as coffee ground emesis?

A

Yes if swallowed

68
Q

Anatomic classification of lower resp tract (LRT) disorders

A
  • large airways (obstructive lung dz)
  • small airways
  • interstitium
  • vascular
  • extra pulmonary
69
Q 
Diagnosis of:
- nocturnal wheeze, cough or dyspnea
- chest tightness
- waxing and waning sx
- nocturnal sx
- seasonal variation
- sx exacerbated by cold, exercise, dust
\+/- nasal polyps
CXR often normal
A

Asthma

70
Q 
Diagnosis of:
- dyspnea (hallmark), esp on exertion
- chronic cough, sputum production
- hx smoking
- frequent resp infection 
o/e - prolonged expiration on forced exhalation (>6sec), reduced breath sounds, increased AP diameter, paradoxical breathing if severe
- pulmonary HTN if severe
CXR - increased AP diameter, hyperinflation, bullae
A

COPD

71
Q 
Diagnosis of:
- chronic resp infection
- chronic cough
- purulent sputum production 
- fever
- weakness
- wt loss
- hemoptysis
- dyspnea (less frequently)
\+/- nasal polyps or sinusitis
crackles on auscultation
CXR - normal; dilated bronchi, tram tracks
A

Bronchiectasis

72
Q 
Diagnosis of:
- orthopnea
- nocturnal wheeze, cough, dyspnea
- leg swelling
- dyspnea on exertion
- fatigue 
o/e - bibasilar crackles, elevated JVP, valvular disease, leg swelling
CXR - vascular redistribution to apical area, fluid in fissures, fluffy opacities, pleural effusions, Kerly B lines, peribronchial cuffing
A

CHF

73
Q

Diagnosis of:
- progressive dyspnea on exertion then at rest
- hypoxia (later stages)
- dry cough
- occupation/ drug exposure
- autoimmune history
o/e - clubbing, fine crackles, rheumatologist dz, pulmonary HTN
CXR variable - may have nodules or reticulations

A

Interstitial lung

74
Q 
Diagnosis of:
- history stroke/ seizure
- neuromuscular dz
- EtOH or drug abuse affecting LOC
- use of sedating medications
- elderly
- GERD
o/e - crackles, wheeze, fever
CXR - range to pneumonia or ARDS
A

Aspiration

75
Q

Diagnosis of:
- sudden dyspnea on exertion or rest
- leg swelling
- risk factors DVT
o/e - fever, tachypnea, tachycardia
- hypotension, elevated JVP, pulses if large
CXR - often normal- may have Hampton hump (infarction); Westermark sign (oligemia)

A

PE

76
Q

Asthma paroxysmal or persistent symptoms?

A
  • dyspnea
  • wheeze
  • chest tightness
  • cough
  • sputum production
77
Q

What is associated with allergies, atopic dermatitis, seasonal allergic rhinitis, conjunctivitis

A

Asthma

78
Q

How do you diagnose asthma?

A

Reversible airway obstruction (FEV1 gold standard)

  • clinical history + spirometry
  • peak expiratory flow variability
  • metacholine challenge
  • exercise challenge
79
Q

Positive response to bronchodilators in diagnosis of asthma?

A

> 12% and 200mL increase in FEV1 or FVC = positive response

80
Q

Define properly controlled asthma

A
  • daytime sx <4/wk
  • night sx <1/wk
  • capable of normal physical activity, no work/school absence
  • mild/few exacerbations
  • rescue puffer <4 dose/wk
  • FEV1 >90% patient’s best
  • PEF >90% patient’s best
  • PEF diurnal variation <10-15%
  • sputum eosinophils <2-3%
81
Q

Treatment of asthma

A

education re: trigger avoidance

mild intermittent - short acting b-agonist

mild persistent - low dose inhaled corticosteroids plus short acting b-agonist for sx relief

moderate persistent - medium-dose inh corticosteroids or low-medium dose inh corticosteroid with long acting b-agonist plus short acting b-agonist (sx)

severe persistent - high-dose inh corticosteroid and long acting bronchodilator +/- anti-IgE tx (omalizumab) +/- leukotriene receptor antagonist +/- oral corticosteroid

82
Q

Main cellular mechanisms involved in asthma?

A

Mast cells - early phase allergen; release histamine, tryptase, leukotriene, cytokines -> smooth muscle contraction

Eosinophils - late phase allergen; release major basic protein, eosinophilic cationic protein, leukotrienes -> airway narrowing and hyperactivity, mucous secretion -> airway remodelling

T cells - initiation and sustaining airway inflammation -> Th2 immune deviation (IL4, 13) -> increased IgE production by B lymphocytes

83
Q

Treatment for mast cell mechanism in asthma?

A
  • b2-agonist/ anticholinergic for smooth muscle relaxation

- anti-IgE Ab to prevent activation

84
Q

Treatment for eosinophil mechanism in asthma?

A
  • leukotriene receptor antagonists (mast cells and eosinophil action)
85
Q

Treatment for T cell mechanism in asthma?

A

Corticosteroids to inhibit pro inflammatory cytokines

86
Q

Types of lung cancer?

A

Small cell lung cancer (SCLC)

Non-small cell lung cancer (NSCLC)

  • adenocarcinoma
  • SCC
  • large cell carcinoma
87
Q

What does pancoast tumor involve?

A
  • often in apical tumor

- involves brachial plexus -> shoulder pain

88
Q

What is SVC syndrome?

A
  • common in central tumors

- SVC compression -> dyspnea, venous distention in neck, swelling of face

89
Q

Common lung mets sites?

A
  • brian
  • bone
  • liver
  • adrenal
  • skin
90
Q

Paraneoplastic syndromes with lung cancer?

A
  • cushing (SCLC)
  • hypercalcemia (SCC)
  • SIADH (SCLC)
91
Q

What is a pleural effusion?

A
  • imbalance between formation and removal of pleural fluid

- pulmonary, pleural or extrapulmonary dz

92
Q

Symptoms of pleural effusion?

A
  • dyspnea most common

+/- cough, chest pain, orthopnea

93
Q

Does pleural fluid have low or high protein? pH? Glucose?

A
  • low protein (<2g/dL)

- pH and glucose similar to blood

94
Q

How is pleural fluid formed?

A
  • mainly from parietal pleura

- turnover re: vascular and interstitial exchange

95
Q

Does parietal or visceral pleura have higher hydrostatic pressure? Flow of fluid in which direction?

A
  • parietal = 30 mmHg
  • visceral = 10 mmHg
    fluid: parietal -> visceral pleura
96
Q

What is exudative pleural effusion? Causes?

A
  • inflammation in lung/ pleural or impaired lymphatic drainage, including movement of fluid from extrathoracic spaces
  • local factors
    Causes = DELII MICE
  • drugs (amiodarone, nitrofurantoin, cytotoxic)
  • extrapulmonary
  • lymphatic abnormalities
  • infectious (empyema, parapneumonic, abscess, TB)
  • inflammatory (pancreatitis, PE, sarcoidosis, radiation, radiation, ARDS, asbestos, ureic pleurisy)
  • malignancy (carcinoma, lymphoma, mesothelioma, chylothroax)
  • iatrogenic
  • connective tissue dz
  • endocrine
97
Q

What is transudative pleural effusion? Causes?

A
  • imbalance of hydrostatic and oncotic pressures in chest, including movement of fluid from extra thoracic spaces (peritoneal/ retroperitoneal)
  • systemic factors

Causes

  • CHF
  • cirrhosis
  • nephrotic syndrome
  • peritoneal dialysis
  • hypoalbuminemia
  • constrictive pericarditis
  • atelectasis
  • SVC obstruction
  • urinothorax
  • Meig syndrome
98
Q

Lights criteria for exudates

A
  • pleural fluid protein divided by serum protein >0.5
  • pleural fluid LDH divided by serum LDH >0.6
  • pleural fluid LDH > 2/3 upper limes of normal serum LDH
    any of these 3 criteria = pleural effusion exudative
99
Q

Physical exam signs of pleural effusion

A
  • reduced breath sounds
  • dullness to percussion
  • reduced tactile fremitus
  • egophony
  • pleural friction rub
100
Q

Complications of thoracentesis

A
  • pneumothorax
  • reexpansion pulmonary edema
  • hemothorax/ bleeding
  • infectoin
  • abdominal puncture
101
Q

Common tests to order for pleural fluid analysis?

A

Pleural fluid

  • LDH
  • total protein
  • glucose
  • pH
  • cell count
  • differential
  • cytology (gram stain)

Serum

  • LDH
  • total protein
  • glucose
102
Q

Define pneumothroax

A
  • air in pleural space
103
Q

Sx tension pneumothorax?

A
  • rapid, laboured breathing
  • cyanosis
  • tachycardia
  • hypotension
  • tracheal shift away from side of pneumo
  • absent breath sounds on ipsilateral side
  • JVP distended
  • pulses paradoxus
  • abdominal distention
104
Q

Sx spontaneous pneumothorax? Classification?

A

variable sx re: size

  • dyspnea
  • chest pain

primary - unknown cause
secondary - underlying etiology

105
Q

Causes of secondary pneumothorax?

A
  • airway dz - emphysema, COPD, CF, asthma
  • infectious - pneumocystis jiroveci pneumonia, necrotizing pneumonia
  • interstitial dz - IPF, pulmonary Langerhans cells histiocytosis, sarcoidosis, LAM
  • CT disorder - Marfan, RA, ankylosing spondylosis, Ehlers-Danlos syndrome
  • malignancy - lung CA, metastatic
  • trauma/ iatrogenic
106
Q

What is postthrombotic syndrome?

A
  • chronic pain, swelling, ulceration of skin
  • 1/3 pt with DVT
  • latency up to 10yr
107
Q

Are thrombi resulting in PE often from proximal or distal leg veins?

A

proximal leg veins

- can begin as calf vein thrombi and extend proximally

108
Q

What do you want to rule out in patients with no obvious cause for DVT, recurrent idiopathic thrombosis or patients >60yr?

A

Malignancy

109
Q

Ddx unilaterla/ local edema

A
  • DVT
  • lymphatic obstruction
  • ruptured popliteal cyst
  • cellulitis
  • postphlebitic syndrome
  • trauma
  • thyroid dz
110
Q

Classic triad for DVT?

A
  • calf pain
  • edema
  • pain on dorsiflexion of food - Woman sign
111
Q

Sx PE

A
  • dyspnea
  • pleuritic CP
  • RR> 20
  • cough
  • hemoptysis
112
Q

DVT risk factors?

A
  • pregnancy
  • malignancy
  • hip surgery
  • major knee surgery
  • immobilization
  • OCP
  • nephrotic syndrome
  • sepsis
  • anticardiolipin Ab
  • protein C and S and antithrombin deficiency
  • previous VTE
113
Q

Wells criteria (DVT)

A

Sx

  • active cancer = 1
  • paresis, paralysis, recent plaster cast = 1
  • recently bedridden >3d or major surgery <4wk = 1
  • localized tenderness over deep veins = 1
  • entire leg swollen = 1
  • calf swelling >3cm compared to other leg measured 10cm below tibial tuberosity = 1
  • pitting edema = 1
  • collateral superficial veins = 1
  • alternative dx as likely or greater than DVT = -2
114
Q

Wells pretest probability (DVT)

A 
0 = low risk = 3% probability
1-2 = moderate risk = 17% probability
>3 = high risk = 75% probability
115
Q

Wells criteria (PE)

A
  • clinical sx DVT = 3
  • PE as likely as alternative dx = 3
  • HR >100 bpm = 1.5
  • immobilization or surgery <4wk = 1.5
  • prior DVT or PE = 1.5
  • hemoptysis = 1
  • malignancy = 1
116
Q

Wells pretest probability (PE)

A

0-2 pt = low risk = 3% probability
2-6 pt = intermediate risk = 20% probability
>6 pt = high risk = 60% probability

117
Q

What anticoagulant works right away to manage DVT/PE?

A

Heparin - inhibits activated coagulation factors

unfractionated

  • inhibits thrombin and factor Xa
  • PTT monitoring
  • difficult to maintain therapeutic range

LMWH

  • inhibits factor Xa
  • no monitoring
  • more reliable dose relation
  • not safe with renal failure
118
Q

Slower anticoagulant for managing DVT/PE?

A

Coumadin

  • inhibits synthesis of vitamin K-dependent coagulation factors
  • follow INR with 2-3 target

-> overlap start with heparin x5d

119
Q

Anticoagulant complications?

A
  • bleeding
  • thrombocytopenia (HIT) with heparin
  • osteoporosis with long term use of LMWH
  • drug interactions with warfarin
  • teratogenicity with warfarin
120
Q

Length of anticoagulant tx?

A
  • time-limited factor: 3mo
  • idiopathic - 6 mo
  • ongoing RF or second event - life
121
Q

Thromboprophylaxis guidelines

A

Low risk - early ambulation

Moderate risk - low dose unfractionated heparin q12

  • LMWH (dalteparin or enoxaparin)
  • pneumatic compression stockings

High risk - low dose unfractionated heparin q8

  • LMWH (dalteparin or enoxaparin)
  • pneumatic stockings + elastic stockings

Very high risk - LMWH (dalteparin or enoxaprin)

  • PO coumadin
  • pneumatic stockings/ elastic stockings + low dose heparin/ LMWH
122
Q

Treatment unilateral cellulitis

A

Mild
- no systemic infection
tx - PO abx
- Penicillin or Ceftriaxone or Cefazolin or Clindamycin

Moderate
- systemic infection
tx - IV abx
- Penicillin or Ceftriaxone or Cefazolin or Clindamycin

Severe

  • decompensated or immunocompromised
  • r/o necrotizing process, send cultures, empiric broad spectrum IV abx
  • Vancomycin + Piperacilin/ Tazobactam
123
Q

What is a genetic condition resulting from hypersensitivity reactions to allergens?

A

Atopy

124
Q

With Ig do mast cells have high affinity for surface receptor?

A

IgE

- coated with IgE antibody

125
Q

How is mast cell activated in allergies? What happens?

A
  • allergin binds IgE on surface of mast cell and cross-linking activates mast cell
  • > release of granules = histamine, proteoglycans (heparin), serine proteases
  • > make and release prostaglandin D2, leukotriene C4 and cytokines
126
Q

What causes:

  • dilation of post capillary venules
  • bronchial and smooth muscle contraction
  • increase in nasal mucus production
  • increase in blood vessel permeability leading to edema
A

Histamine

127
Q

Do you need previous sensitization for IgE allergies?

A

Yes - need to have made IgE Ab

128
Q

Sx allergic rhinitis?

A
  • sneezing
  • itchy eyes
  • rhinorrhea
129
Q

What is angioedema?

A
  • rapid swelling of skin, mucosa and submucosal tissue

- often associated with allergy, can be hereditary

130
Q

Ddx wheeze

A
  • asthma
  • FB
  • aspiration
  • GERD
  • CF
  • bronchitis
  • tumor
  • COPD

MCC Part 1 (22 decks)

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