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CPR 2 Exam 2 > Pence Dyspnea Palpitations and Fatigue > Flashcards

Pence Dyspnea Palpitations and Fatigue Flashcards

1
Q

How will an EKG look in a person with a PE?

A
  • Sinus tach
  • Inverted T waves (V1-4) due to RV strain
  • Incomplete or complete RBBB
  • S1, Q3, T3
    • deep S in 1
    • Q wave in 3
    • Inverted T wave in 3
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2
Q

Gold standard imaging for PE?

A
  • CT chest with contrast
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3
Q

What symptoms make up an unstable PE?

A
  • Hypotension
  • RV strain
  • Elevated cardiac enzymes
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4
Q

Treatment for unstable PE

A
  • Resuscitation
    • ventilation or hemmodynamic support
  • Thrombolytic therapy
  • If systemic thrombolysis fails:
    • repeat thrombolysis
    • attempt catheter thrombolysis
    • proceed to surgery for thrombectomy
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5
Q

How do you treat Stable PE?

A
  • Heparin
  • Low molecular weight heparin
    • enoxaparin or lovenox
  • Vitamin K antagonist
    • Warfarin or Coumadin
  • DOACs
    • rivaroxaban apixaban dabigatran endoxaban
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6
Q

What is the reversal agent for LMWH?

A

Protamine Sulfate

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7
Q

What is the reversal agent for DOACs?

A
  • Xa inhibitors
    • Andexanet alpha
    • Dabigatran idarucizumab
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8
Q

What is reversal agent for Warfrin?

A
  • Vitamin K
  • Prothrombin complex concentrate
  • fresh frozen plasma
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9
Q

What is the minimum length of treatment of a PE for all patients?

A

Three months

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10
Q

Who gets indefinite anticoagulation after a PE?

A

Those with underlying disease with high risk of VTE recurrence such as malignancies or genetic mutations

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11
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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12
Q

What is apnea?

A

Reduction in breathing for ten seconds with a noted drop in SpO2 by >3%

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13
Q

What are the two issues of OSA?

A
  • Obstruction:
    • soft tissue or anatomical abnormalities that lead to a patient having a more difficult time keeping airway open during sleep
  • Ventilatory drive:
    • The body’s sensitivity to CO2
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14
Q

What is OSA associated with?

A
  • Htn
  • A.fib/ flutter
  • CAD
  • Type II diabetes
  • At higher risk for occupational hazards
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15
Q

Risk factors for OSA?

A
  • Obesity #1 cause/predictor
  • Large tongue
  • Craniofacial abnormalities
  • Enlarged tonsils
  • Enlarged lymph nodes
  • Males
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16
Q

Symptoms of OSA?

A
  • Excessive daytime sleepiness
  • Partner witnesses gasping episodes
  • STOPBANG
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17
Q

What is STOPBANG?

A
  • Snoring
  • Tired
  • Observed episode
  • Pressure
  • BMI
  • Age >50
  • Neck size
  • Gender
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18
Q

How do you diagnose OSA? Describe the process.

A
  • Polysomnogram (PSG)
  • Gold standard
  • Occurs at home or sleep lab
  • Records sleep activity for 6-7 hrs
  • Monitors EEG, ECG, ocular movement, airflow and O2 saturation
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19
Q

How do you treat OSA?

A
  • Continuous Positive Airway Pressure (CPAP)
    • provides pressure to overcome obstruction
    • 30-50% non compliance
    • Now is a nasal mask but also have oral nasal mask
20
Q

Who does idippathic pulmonary fibrosis occur in?

A

M=F age >60 yo

21
Q

Symptoms of Idiiopathic pulmonary fibrosis?

A
  • Progressive dyspnea
  • Dry cough
  • Fatigue
  • Inability to perform daily activities
  • Prominent inspiratory crackles “Velcro Lung”
22
Q

what will a CT show in a patient with IPF?

A
  • Significant fibrosis bilaterally “honeycombing” with traction bronchiectasis
23
Q

What will PFT and DLCO show in a patient with IPF?

A

Restrictive pattern and decreased DLCO

24
Q

How do you treat Idiopathic Pulmonary Fibrosis? Survival rate?

A
  • Supportive care
  • Steroids
  • Immunomodulators
  • Anti fibrotic therapy
  • 50% 3-5 yrs after diagnosis
25
Q

What is sarcoidosis?

A
  • non caseating granuloma
  • Can affect most organ systems lungs are most common
  • Heterogenous prognosis
26
Q

Clinical presentation of Sarcoidosis?

A
  • cough dyspnea of insidous onset
  • Cutaneous involvement
    • lupus pernio
    • erythema nodosum
    • maculopapular rash
  • Anterior uveitis
  • Lofgren’s syndrome
  • Heerfordt’s syndrome
  • Asx in 20-3-%
27
Q

What is Lofgren’s syndrome?

A
  • Seen in sarcoidosis
  • Erythema nodosum
  • Hilar lymphadenopathy
  • fever
  • arthritis
28
Q

What is Heerfordt’s syndrome?

A
  • Seen in sarcoidosis
  • anterior uveitis
  • Parotitis
  • Cranial nerve VII palsy
  • Fever
29
Q

What do you see on sarcoidosis radiology?

A
  • hilar lymphadenopathy
  • minimal dz findings to diffuse fibrosis
30
Q

Sarcoidosis PFTs?

A
  • normal, restrictive, or obstructive pattern
  • +/- reduced DLCO
31
Q

Treatment of sarcoidosis?

A
  • Supportive care
  • Immunosuppression
    • steroids are first line
    • methotrexate, asathipprine, cyclophosphamide
    • Biologics
32
Q

What are the staages of sarcoidosis?

A
  1. Hilar LAD
  2. Hilar LAD + infiltrates
  3. Infiltrates only
  4. Fibrosis

not a progression of disease

33
Q

What dose Granulomatosis with Polyangiitis cause?

A
  • systemic small vessel vasculitis affecting sinuses kidneys and lungs
  • results in destruction of lung parenchyma, diffuse alveolar hemorrhage, ulceration in the tracheobronchial tree and glomerulonephritis
34
Q

Clinical presentation of GPA? Labs?

A
  • Dyspnea
  • Cough
  • Hemoptysis
  • Fever
  • Saddle nose
  • Chronic sinusitis/rhinitis
  • Recurrent otitis media
  • +C-ANCA
35
Q

Treatment of GPA?

A
  • steroids and cyclophosphamide
36
Q

Radiology of GPA?

A
  • lung nodules
  • patchy ground glass opacities
  • hilar LAD
37
Q

What is goodpasture syndrome?

A
  • AI condition against the glomerular and alveolar basement membrane
  • results in destruction of lung parenchyma diffuse alveolar hemorrhage and glomerulonephritis
38
Q

Clinical presentation of goodpastures syndrome and labs?

A
  • Weight loss
  • fever
  • proteinuria
  • hematuria
  • dyspnea
  • hemoptysis
  • cough
  • hypoxemia
    • anti-GBM
39
Q

Treatment of Goodpasture’s?

A

Plasmapheresis + steroids + cyclophosphamide

40
Q

What is hypersensitivity pneumonitis

A
  • extrinsic allergic alveolitis caused by repeated exposure to Ag of environmental or occupational nature in a sensitized individual
41
Q

History of hypersensitivity pneumonitis?

A
  • cough dyspnea low fever
  • Recent or chronic exposure to allergen
    • gets better when outside of the environment
42
Q

Histoloogy of Hsn pneumonitis?

A
  • Plasma cells
  • +/- non caseating granulomas
43
Q

PFT’s of hsn pneumonitis?

A
  • Restrictive pattern
  • +/- DLCO
44
Q

Pneumoconiosis?

A
  • Inflammation from inhaling inorganic dust
    • results in fibrosis
45
Q

Silicosis risks?

A
  • miners
  • stone cutters
  • sand blasting
  • quarry workers

CPR 2 Exam 2 (17 decks)

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