Respiratory Conditions Flashcards

1
Q

Define sarcoidosis

A
  • Condition where chronic inflammation granulomas form.
  • Granulomas are inflammatory nodules full of macrophages.
  • Granulomas form over various organs, including liver, heart, lungs, eyes and kidneys
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2
Q

Eye symptoms of sarcoidosis

A

CON U

Conjunctivitis
Optic neuritis
Uveitis

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3
Q

Liver symptoms of sarcoidosis

A

Liver nodules
Cirrhosis
Cholestasis

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4
Q

Sarcoidosis systemic symptoms

A

Fever
Fatigue
Weight loss

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5
Q

Heart symptoms of sarcoidosis

A

British heart Market

Bundle branch block
Heart block
Myocardial muscle involvement

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6
Q

Kidney symptoms of sarcoidosis

A

Kidney stones (due to hypercalcaemia)
Nephrocalcinosis
Interstitial nephritis

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7
Q

CNS symptoms of sarcoidosis

A

Nodules
Pituitary involvement (diabetes insipidus)
Encephalopathy

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8
Q

PNS symptoms of sarcoidosis

A

Facial nerve palsy
Mononeuritis multiplex

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9
Q

Bones symptoms of sarcoidosis

A

Arthralgia
Arthritis
Myopathy

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10
Q

Lofgren’s Syndrome

A

This is the triad which is typically assoicated with sarcoidosis.
-Erythema nodosum
-Bilateral hilar lymphadenopathy
-Polyarthralgia (joint pain in multiple joints)

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11
Q

what blood tests are used to investigate sarcoidosis?

A

Raised angiotensin-converting enzyme (ACE) (often used as a screening test)
Raised calcium (hypercalcaemia)

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12
Q

imaging for sarcoidosis

A

Chest x-ray may show hilar lymphadenopathy
High-resolution CT scanning may show hilar lymphadenopathy and pulmonary nodules
MRI can show central nervous system involvement
PET scan can show active inflammation in affected areas

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13
Q

Tests for sarcoidosis

A

U&Es for kidney involvement
Urine albumin-creatinine ratio to look for proteinuria
LFTs for liver involvement
Ophthalmology assessment for eye involvement
ECG and echocardiogram for heart involvement
Ultrasound for liver and kidney involvement

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14
Q

what is the managment of sarcoidosis?

A

1st line
-steroids
- bisphosphonates

2nd line
- Methotrexate

severe managment
- lung transplant
—————————————————————-

  • Interestingly, Sarcoidosis can resolve itself (50% of patients) within two years.
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15
Q

Sarcoidosis progression

A
  • pulmonary fibrosis and pulmonary hypertension.
  • 10% rate of mortality
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16
Q

-20-40 year old
-black female
-presenting with a dry cough
-shortness of breath.
-Has painful red lesions on shins

A
  • typical presentation of sarcoidosis
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17
Q

Syndromes associated with sarcoidosis

A

Lofgren’s syndrome is an acute form of the disease characterised by bilateral hilar lymphadenopathy (BHL), erythema nodosum, fever and polyarthralgia. It usually carries an excellent prognosis

In Mikulicz syndrome* there is enlargement of the parotid and lacrimal glands due to sarcoidosis, tuberculosis or lymphoma

Heerfordt’s syndrome (uveoparotid fever) there is parotid enlargement, fever and uveitis secondary to sarcoidosis

*this term is now considered outdated and unhelpful by many as there is a confusing overlap with Sjogren’s syndrome

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18
Q

what is the electrolyte abnormality associated with sarcoidosis?

A

hyperkalemia
- macrophages in the granulmoa cause increased conversion of vitamin D to its active form (1,25-dihydroxycholecalciferol)

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19
Q

Heerfordt’s syndrome (uveoparotid fever)

A

parotid enlargement, fever and uveitis secondary to sarcoidosis

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20
Q

what are the stages of sarcoidosis?

clue: 4 stages

A

A chest x-ray may show the following changes:
stage 0 = normal
stage 1 = bilateral hilar lymphadenopathy (BHL)
stage 2 = BHL + interstitial infiltrates
stage 3 = diffuse interstitial infiltrates only
stage 4 = diffuse fibrosis

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21
Q

Step one management of asthma (newly diagnosed)

A

Short acting beta agonist (Saba)
Salbutamol

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22
Q

Step 2 asthma control (not controlled on previous step or newly diagnosed asthma with more than 3 week or nigh time waking in week)

A
  • SABA
  • ICS
23
Q

Step 3 of asthma management

A
  • SABA
  • low dose ICS
  • leukotriene receptor agonist (LTRA)
    Continue LTRA based on patient’s response
24
Q

Step 4 asthma management

A

-SABA
- ICS
- LABA
- can continue LTRA if tolerated

25
Q

Step 5 asthma management

A

SABA +/- LTRA
med dose of ICS

Switch ICS/ LABA for MART that includes low dose ICS

26
Q

Step 6 asthma management

A

SABA +/- LTRA + medium dose ICS MART

Alternatively consider fixed dose of moderate dose ICS + separate LABA

27
Q

Acute exacerbation of asthma

A

acute exacerbation of asthma (or an asthma attack) is the progressive worsening of symptoms including dyspnoea, wheeze, cough, and chest tightness over an acute or subacute time period.

  • reduced pulmonary function, demonstrated by a reduced peak expiratory flow rate (PEFR
28
Q

Moderate acute asthma exacerbation:

A
  • Increasing symptoms.
    -PEFR >50-75% of the patient’s best or predicted score.
    -No features of acute severe asthma.
29
Q

Acute severe asthma exacerbation:

A

-PEFR 33-50% of the patient’s best or predicted score.
-Respiratory rate (RR) ≥ 25 breaths per minute.
-Heart rate (HR) ≥ 110 beats per minute.
-Inability to complete sentences in one breath.

30
Q

Life-threatening asthma exacerbation:

A

-PEFR <33% of the patient’s best or predicted score.
-SpO₂ <92%.
-In life-threatening asthma exacerbations, PaCO₂ will be normal. If the PaCO₂ rises, then this is now classed as a near-fatal asthma exacerbation.
-PaO₂ <8kPa.
-Absence of audible breath sounds over the chest (silent chest).
-Cyanosis (usually of the lips).
-Reduced respiratory effort.
-New-onset arrhythmia.
Exhaustion.
-Reduced Glasgow coma score (GCS).
-Hypotension.

31
Q

Near-fatal asthma exacerbation:

A

Raised PaCO₂ (>6kPa) and/or need for mechanical ventilation.

32
Q

what can cause an asthma exaccebation

A

-provoked by viruses (the most common being rhinovirus)
-bacteria
-allergens such as mold and pet dander
-or tobacco smoke.

33
Q

How to assess fr asthma

A

-PEFR or forced expiratory volume in one second (FEV1).
-PEFR is expressed as a percentage of the patient’s best or predicted score prior to coming into hospital. The predicted score is based on the patient’s age and height, but should only be used if the patient does not have an accurate best score from the last two years.

34
Q

proper inhaler technique

A
  1. Remove cap and shake
  2. Breathe out gently
  3. Put mouthpiece in mouth and as you begin to breathe in, which should be slow and deep, press canister down and continue to inhale steadily and deeply
  4. Hold breath for 10 seconds, or as long as is comfortable
  5. For a second dose wait for approximately 30 seconds before repeating steps 1-4.
35
Q

mesothelioma diagnosis

A

histology, following a thoracoscopy

36
Q

what is Mesothelioma

A

Cancer of the mesothelial layer of the pleural cavity that is strongly associated with asbestos exposure

In small cases, the abdomen can also be affected

37
Q

features of mesothelioma

A

Dyspnoea, weight loss, chest wall pain
Clubbing
30% present as painless pleural effusion
Only 20% have pre-existing asbestosis
History of asbestos exposure in 85-90%, latent period of 30-40 years

38
Q

Managment of mesothelioma

A

Symptomatic
Industrial compensation
Chemotherapy, Surgery if operable
Prognosis poor, median survival 12 months

39
Q

investigation and diagnosis of mesothelioma

A

suspicion is normally raised by a chest x-ray showing either a pleural effusion or pleural thickening
the next step is normally a pleural CT
if a pleural effusion is present fluid should be sent for MC&S, biochemistry and cytology (but cytology is only helpful in 20-30% of cases)
local anaesthetic thoracoscopy is increasingly used to investigate cytology negative exudative effusions as it has a high diagnostic yield (around 95%)
if an area of pleural nodularity is seen on CT then an image-guided pleural biopsy may be used

40
Q

acute exacerbation of COPD in whom a respiratory acidosis (PaCO2>6kPa, pH <7.35 ≥7.26) persists despite immediate maximum standard medical treatment
Important

A

Non-invasive ventilation is needed

41
Q

Fine end-inspiratory crepitations

A

idiopathic pulmonary fibrosis

42
Q

symptoms and onset of acute bronchitis

A

cough: may or may not be productive
sore throat
rhinorrhoea
wheeze

usually normal chest expansion but some patients also have
Low-grade fever
Wheeze

43
Q

How to differentiate between acute bronchitis and pneumonia

A

History: Sputum, wheeze, breathlessness may be absent in acute bronchitis whereas at least one tends to be present in pneumonia.

Examination: No other focal chest signs (dullness to percussion, crepitations, bronchial breathing) in acute bronchitis other than wheeze. Moreover, systemic features (malaise, myalgia, and fever) may be absent in acute bronchitis, whereas they tend to be present in pneumonia.

44
Q

diagnostics of bronchitis

A

acute bronchitis is typically a clinical diagnosis
however, if CRP testing is available this may be used to guide whether antibiotic therapy is indicated

45
Q

Managment of bronchitis

A

analgesia
good fluid intake
consider antibiotic therapy if patients:
are systemically very unwell
have pre-existing co-morbidities
have a CRP of 20-100mg/L (offer delayed prescription) or a CRP >100mg/L (offer antibiotics immediately)
NICE Clinical Knowledge Summaries/BNF currently recommend doxycycline first-line
doxycycline cannot be used in children or pregnant women
alternatives include amoxicillin

46
Q

Pulmonary arterial hypertension

A

Pulmonary arterial hypertension (PAH) is a rare, progressive disorder characterized by high blood pressure in the arteries of the lungs, leading to right heart failure and ultimately death if untreated.

47
Q

etiology of PAH

A

PAH can be idiopathic, heritable, or associated with other conditions such as connective tissue diseases, congenital heart disease, HIV infection, or drug/toxin exposure.

48
Q

PAH symptoms

A

Symptoms include shortness of breath, fatigue, chest pain, fainting, swelling in the ankles or abdomen, bluish lips or skin (cyanosis), and palpitations.

49
Q

PAH diagnostics

A

Diagnostic tests include echocardiography, right heart catheterization, chest X-ray, pulmonary function tests, blood tests (BNP, NT-proBNP), and imaging studies (CT, MRI).

50
Q

PAH treatments

A

Treatment may include medications such as calcium channel blockers, prostacyclin analogs, endothelin receptor antagonists, and phosphodiesterase-5 inhibitors, as well as lung transplant in severe cases.

51
Q

Prognosis of PAH

A

Prognosis varies depending on the underlying cause, severity of symptoms, and response to treatment, but PAH is generally a progressive and life-threatening condition if left untreated.

52
Q

Managment of PAH if
negative response to acute vasodilator testing

A

prostacyclin analogues: treprostinil, iloprost
endothelin receptor antagonists
non-selective: bosentan
selective antagonist of endothelin receptor A: ambrisentan
phosphodiesterase inhibitors: sildenafil

53
Q

positive response to acute vasodilator testing

A

oral calcium channel blockers