Clinical Med Part 3 (Pence) Flashcards

1
Q

What is pulmonary hypertension?

A
  • Mean pulmonary artery pressure >20 mmHg
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2
Q

What is the importance of pulmonary hypertension?

A
  • Associated with increased mortality if left untreated

- Onset is insidious and can be overlooked due to vague symptoms or co-morbid conditions

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3
Q

What are some symptoms of pulmonary hypertension?

A
  • Dyspnea on exertion
  • Fatigue
  • Chest pain
  • Presyncope
  • Signs of right sided heart failure
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4
Q

How is pulmonary hypertension diagnosed?

A
  • ECG (showing right ventricular hypertrophy)
  • Labs (increased BNP)
  • TTE
  • Cardiac catheterization
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5
Q

What is the Swanz-Ganz catheter?

A
  • A catheter that is threaded through the venous system and and eventually into the pulmonary artery
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6
Q

What is the treatment for pulmonary hypertension?

A
  • Treat underlying cause

- Symptoms based treatment (graded exercise, supplemental oxygen, diuretics)

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7
Q

What are some medications that are used to treat pulmonary hypertension?

A
  • Prostacyclin agonist (promote vasodilation)
  • Phosphodiesterase inhibitor (reduce breakdown of NO)
  • Endothelium antagonist (inhibit endothelium-1)
  • CCBs (inhibits calcium channels in vascular smooth muscle)
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8
Q

What is a pulmonary embolism?

A
  • Venous thromboembolism located in pulmonary vasculature

- Usually arises from a DVT

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9
Q

What is the importance of a pulmonary embolism?

A
  • Common diagnosis
  • Wide range of risk factors
  • Affects large portion of the population, increased incidence with age
  • High mortality if left untreated
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10
Q

What is Virchow’s triad?

A
  • Hypercoagulability
  • Venous stasis
  • Endothelial injury
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11
Q

What do protein C and S do?

A
  • Block sites at VIII and V to inhibit clotting cascade
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12
Q

What does antithrombin III do?

A
  • Block sites at II and X
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13
Q

What happens in a protein C and S deficiency?

A
  • Ineffective regulation of factor VIIIa and Va
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14
Q

What happens in an antithrombin III deficiency?

A
  • Ineffective regulation of Xa and IIa
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15
Q

What happens in a Factor V leiden mutation?

A
  • Mutation of factor V prevents binding of protein C
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16
Q

What are some symptoms of a pulmonary embolism?

A
  • Chest pain
  • Palpitations
  • Dyspnea
  • Syncope
  • +/- LE edema
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17
Q

How is a pulmonary embolism diagnosed?

A
  • Requires an index of suspicion
  • Wells criteria
  • Elevated D-dimer (good for ruling out PE if D-dimer is normal)
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18
Q

What does an EKG look like in a PE?

A
  • Sinus Tach
  • RV strain
  • Incomplete or complete RBBB
  • S1Q3T3
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19
Q

What does the imaging look like in a PE?

A
  • CT chest with contrast: primary test for diagnosis of PE

- V/Q scan: second line nuclear study (use technegas)

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20
Q

What is the treatment for unstable PE?

A
  • Resuscitation
  • Thrombolytic therapy
  • Attempt catheter directed thrombolysis
  • Proceed to surgery for thromboectomy
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21
Q

What is the treatment for stable PE?

A
  • Heparin (binds antithrombin and inhibits factors IIa and Xa)
  • Low molecular weight heparin
  • Vitamin K antagonist
  • Direct oral anticoagulants
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22
Q

What is the reversal agent for LMWH?

A
  • Protamine sulfate
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23
Q

What is the reversal agent for warfarin?

A
  • Vitamin K, PCC, FFP
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24
Q

What is the reversal agent for DOACs?

A
  • Xa inhibitors inhibitors: andexanet alfa

- Dabigatran: idarucizumab

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25
Q

What is the duration of treatment for PE?

A
  • Minimum of 3 months for all patients

- Extended treatment for those who have traveled, had surgery, or on hormone therapy

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26
Q

When would you give indefinite anticoagulation?

A
  • Those with underlying disease with high risk like malignancy and genetic mutations
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27
Q

What is obstructive sleep apnea?

A
  • Disruption in breathing pattern while sleeping that results in excessive daytime somnolence despite adequate sleep periods and not explained by other causes
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28
Q

What is apnea?

A
  • Reduction in breathing for at least 10 seconds with a noted drop in SpO2 by >3%
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29
Q

What are the two issues that are related to breathing disorders?

A
  • Obstruction (soft tissue or anatomical abnormalities)

- Ventilatory drive (body sensitivity to CO2)

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30
Q

Why is obstructive sleep apnea important?

A
  • OSA is associated with:
  • HTN
  • A fib/flutter
  • CAD
  • Insulin resistance (T2DM)
  • Occupational hazard
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31
Q

What are some OSA risk factors?

A
  • Obesity
  • Large tongue
  • Craniofacial abnormalities
  • Enlarged tonsils
  • Enlarged lymph nodes
  • Male sex
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32
Q

How could micrognathia affect OSA?

A
  • Reduces that amount of airway that is available
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33
Q

What are some symptoms of OSA?

A
  • Excessive daytime somnolence
  • Partner witness apnea episodes or voices concern of gasping episodes
  • STOPBANG questionairre
34
Q

How is OSA diagnosed?

A
  • Polysomnogram (gold standard)

- Occurs in a sleep lab or at home

35
Q

What are some treatment options for OSA?

A
  • CPAP

- Oral appliances (work by thrusting the mandible forward and result in opening airway)

36
Q

What is interstitial lung disease?

A
  • Heterogeneous group of pulmonary disorders with a variety of different causes that present with the same characteristics.
37
Q

What are some characteristics in interstitial lung disease?

A
  • Restrictive pattern on PFT
  • Decreased DLCO
  • Dyspnea on exertion
  • Absence of primary infection or malignancy
38
Q

What are the symptoms of interstitial pulmonary fibrosis?

A
  • Progressive dyspnea
  • Dry cough
  • Fatigue
  • Inability to perform activities of daily living
39
Q

What is a key characteristic of interstitial pulmonary fibrosis?

A
  • Prominent inspiratory crackles sounding like velcro
40
Q

What does CT show of interstitial pulmonary fibrosis?

A
  • Significant fibrosis bilaterally “honeycombing” with traction bronchiectasis
41
Q

What do PFTs show of interstitial pulmonary fibrosis?

A
  • Progressive restrictive pattern

- Decreased DLCO

42
Q

What is the treatment for idiopathic pulmonary fibrosis?

A
  • Supportive care (O2, physical rehab)
  • Steroids
  • Immunomodulators
  • Anti-fibrotic therapy
43
Q

What is sarcoidosis?

A
  • Disease of multisystem involvement of unknown cause, characterized by the presence of non-caseating granulomas
44
Q

Who is more likely to have sarcoidosis?

A
  • African americans have a 3:1 chance compared to caucasians
  • Females are more likely than male
  • Older people
45
Q

What is the clinical presentation of someone with sarcoidosis?

A
  • Asymptomatic
  • Cough, dyspnea
  • Cutaneous involvement
  • Ocular symptoms
  • Lofgren’s syndrome
  • Heerfordt’s syndrome
46
Q

What does radiology find in sarcoidosis?

A
  • Most common finding is hilar lymphadenopathy

- Can range from minimal disease finding to diffuse fibrosis

47
Q

What do the PFTs look like in sarcoidosis?

A
  • Normal, restrictive, or obstructive pattern

- +/- reduced DLCO

48
Q

What is the treatment of sarcoidosis?

A
  • Supportive care (O2, rehab, nutritional counseling, social services)
  • Immunosuppression (steroid, methotrexate)
49
Q

What is the cause of granulomatosis with polyangiitis?

A
  • Systemic small vessel vasculitis most often affecting the sinuses, kidneys, and lungs
50
Q

What is the clinical presentation for granulomatosis with polyangiitis?

A
  • Dyspnea
  • Cough
  • Hemoptysis
  • Fevers
  • Saddle nose
  • Chronic sinusitis/rhinitis
  • Recurrent otitis media
51
Q

What do the labs and imaging show in granulomatosis with polyangiitis?

A
  • +C-ANCA

- Lung nodules, patchy ground glass opacities, hilar LAD

52
Q

What is the treatment for granulomatosis with polyangiits?

A
  • Steroids + cyclophosphamide
53
Q

What is goodpasture’s syndrome?

A
  • Autoimmune condition with antibodies against basement membrane of alveolar and glomerular parenchyma
54
Q

What is the clinical presentation of goodpasture’s syndrome?

A
  • Weight loss
  • Fevers
  • Proteinuria
  • Hematuria
  • Dyspnea
  • Cough
  • Hemoptysis
  • Hypoxemia
55
Q

What do the labs and radiology show in goodpasture’s syndrome?

A
  • +anti-GBM

- Bilateral ground glass opacities indicative of diffuse alveolar hemorrhage

56
Q

What is the treatment of goodpasture’s syndrome?

A
  • Plasmapheresis + steroids + cyclophosphamide
57
Q

What are some ILD associated connective tissue diseases?

A
  • Systemic sclerosis
  • Rheumatoid arthritis
  • Dermatomyositis/polymyositis
58
Q

What is hypersensitivity pneumonitis?

A
  • Extrinsic allergic alveolitis
59
Q

What causes hypersensitivity pneumonitis?

A
  • Caused by repeated exposure to specific antigen of environmental or occupation nature in a sensitized individual
60
Q

What are some common names of hypersensitivity pneumonitis?

A
  • Farmer’s lung
  • Bird fancier’s lung
  • Woodworker’s lung
  • Baker’s lung
61
Q

What is the clinical presentation for hypersensitivity pneumonitis?

A
  • Cough
  • Dyspnea
  • +/- fevers
62
Q

What do PFTs show in hypersensitivity pneumonitis?

A
  • Restrictive pattern

- +/- reduced DLCO

63
Q

What is the treatment for hypersensitivity pneumonitis?

A
  • Remove patient from antigen
64
Q

What is pneumoconiosis?

A
  • ILD caused by the inhalation of inorganic dust that results in tissue inflammatory response causing fibrosis
65
Q

What do PFTs show in pneumoconiosis?

A
  • Restrictive pattern

- +/- reduction in DLCO

66
Q

What is the treatment of pneumoconiosis?

A
  • Removal from occupational exposure
  • Smoking cessation
  • Immunizations
  • Oxygen therapy
67
Q

What causes silicosis?

A
  • Inhalation of silica “crystalline quartz”
68
Q

What occupations typically have silicosis?

A
  • Miners
  • Stonecutters
  • Sand blasting
  • Quarry workers
69
Q

What is asbestosis?

A
  • Fibrosis due to inhalation of asbestos
70
Q

What occupations typically have asbestosis?

A
  • Construction
  • Insulation
  • Demolition
  • Automobile workers
71
Q

What does radiology show in asbestosis?

A
  • Multiple nodular opacities
  • Pleural effusions
  • Pleural fibrosis
  • May see blurring of diaphragm/cardiac sihouette
72
Q

What may be at in increased risk in asbestosis?

A
  • Malignant mesothelioma

- Lung cancer

73
Q

What is coal workers pneumoconiosis?

A
  • FIbrosis caused by inhalation of coal dust
74
Q

What is simple CWP?

A
  • Asymptomatic

- Radiology has small nodules at apex

75
Q

What is complicated CWP?

A
  • Symptomatic (cough, dyspnea, sputum production)
  • PFTs: restrictive pattern
  • Radiology shows large nodules and patchy infiltrates
76
Q

What is berylliosis?

A
  • Fibrosis due to beryllium exposure

- Have increased chance of lung cancer

77
Q

Who is most like to have berylliosis?

A
  • Manufacturing of alloys and electronic devices
78
Q

What does the acute version of berylliosis look like?

A
  • Similar reaction to hypersensitivity pneumonconiosis
79
Q

What does chronic berylliosis look like?

A
  • Insidious onset

- Thought to be from cumulative exposure of beryllium

80
Q

What do PFTs and radiology show in berylliosis?

A
  • Hilar LAD, diffuse infiltrates

- Restrictive pattern

81
Q

What is the treatment of berylliosis?

A
  • Steroids

- Removal from beryllium environment