resp Flashcards

(119 cards)

1
Q

what are the most common features of PE?

A

tachypnoea
pleuritic chest pain
tachycardia
fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

if your suspicion of PE is low (approx <15%) what tool do you use to rule out PE?

A

PERC - PE rule out criteria

all the criteria need to NOT be present for PERC to be negative and this gives a <2% probability of PE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

CRIteria in PERC

A

AGE >50
Heart rate> 100
oxygen sats < 94
unilateral leg swelling

previous DVT or PE
recent trauma or surgery in past 4 weeks
oestrogen use - HRT contraceptives

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

when do you do a 2 level PE wells score

A

when you suspect PE and its > 15% suspicion lol or when PERC is positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

criteria in 2 level wells score

A

3 POINTS -clinical signs and symptoms of DVT (swelling+ pain minimum)
3 POINTS– PE is most likely diagnosis compared to differentials
1.5 points -tachycardia
1 point - haemoptysis

1.5 points -immobilisation ? 3 days or surg in 4 weeks prev
1.5 points- previous DVT/ PE
1 point- malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

when is a two level PE wells score positive and negative

A

MORE THAN 4 points - likely PE

4 OR LESS - PE unlikely (4 included here)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is first line investigation of PE if wells score >4

A

CTPA and if late start interim anticoagulation if delayed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what to do if CTPA is negative after a positive wells score

A

consider a proximal leg vein ultrasound scan if DVT is suspected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what investigation is first line if PE is unlikely so 4 points or less

A

D dimer test
and if positive immediate CTPA with interim anticoag if late ect and if scan negative consider alternative diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

when is a V/Q scan done instead of CTPA in PE?

A

If renal impairment since V/Q doesnt use contrast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

some ecg findings of pe

A

the classic ECG changes seen in PE are a large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III - ‘S1Q3T3’. However, this change is seen in no more than 20% of patients
right bundle branch block and right axis deviation are also associated with PE
sinus tachycardia may also be seen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

can you see PE in chest x ray? is it done when pe is suspected

A
  • a chest x-ray is recommended for all patients to exclude other pathology
  • however, it is typically normal in PE
  • possible findings include a wedge-shaped opacification
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What needs to be done 6 weeks after a patient has been treated for community acquired pneumonia?

A

Repeat chest x ray

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the curb65 score

A

Score for pneumonia risk stratification
Confusion (abbreviated mental test score <= 8/10)
Urea>7
Resp rate >20
Blood pressure. Syst <90 diast < 60
Age > 65

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is used in gp similar to CURB 65

A

CRB65

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the points in CURB65 score that classify someone as mild moderate and high risk pneumonia

A

0-1 is mild risk
2-3 moderate
>3 high risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Management of low risk community acquired pneumonia

A

Oral amoxicillin and no admission if allergic give a macrolide or tetracycline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Management of moderate or severe CAP

A

dual therapy with amoxicillin and macrolide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

presentation of pleural effusion

A

reduced chest expansion, reduced breath sounds on auscultation, dullness on percussion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

gld stabndard investigation of pleural effusion

A

CXR PA (Posterioanterior)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

other important investigation in pleural effusion

A

pleural aspiration- US guided - using 21G needle and 50ml syringe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is the pleural fluid aspirated in pleural effusion tested for in lab?

A

pH, protein, LDH (lactate dehydrogenase), microbiology, cytology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

when is a pleural effusion considered exudative and when is it considered transudative? when is lights criteria used

A

generally exudative when protein: >30g/L and transudative when < 30g/L -but lights criteria used if 25-35 so only > 35 and <25 is definitive without criteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are lights criteria

A

ONE of the following needs to be true to be indicative

pleural fluid protein/ serum protein > 0.5 is exudative
pleural LDH/ SERUM LDH > 0.6 is exudative
pleural LDH > 2/3 of upper limit of normal serum LDH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
transudative causes
HF hypoalbuminaemia: nephrotic syndrome, liver disease, malabsorption `
26
exudative causes of pleural effusion
pneumonia malignancy connective tissue disorders such as SLE, RA TB pancreatitis PE
27
when do you insert a chest drain for pleural effusion
ONLY when there is indication of infection in there so empyema - more specifically: 1) turbid or purulent pleural fluid 2) or suspected infection and ph < 7.2
28
what are some potential management approaches to reccurent pleural effusions?
repeated aspiration pleurodesis indwelling pleural catheter drug management eg opioids to alleviate dyspnea
29
what is the presentation of pneumothorax
dyspnea, hyperesonance on percussion, unequal expansion, tachycardia, tachypnoea, reduced breath sounds if tension pneumothorax respiratory distress tracheal deviation away from side of pneumothorax, hypotension, respiratory distress
30
how is pneumothorax management decided
based on whether someone is symptomatic and then for the symptomatic ones whether they have certain "high risk characteristics"
31
what is the management for an asymptomatic pneumothorax
conservative REGARDLESS of size ``
32
what are the high risk characteristics that need to be assessed on a symptomatic pneumothorax
haemodynamic compromise (suggesting a tension pneumothorax) significant hypoxia bilateral pneumothorax underlying lung disease ≥ 50 years of age with significant smoking history haemothorax
33
management of pneumothorax without high risk characteristics
there is a choice of intervention, either conservative care or ambulatory device or needle aspiration
34
when do you insert a chest drain for a pneumothorax?
ONLY when there are high risk characteristics on top of symptomatic presentation (and safe to intervene
35
how is safety of intervention determined for a pneuothorax?
2cm laterally or apically on chest x-ray, or any size on CT scan which can be safely accessed with radiological support
36
how is a primary vs secondary spontaneous pneumothorax monitored
primary spontaneous pneumothorax reviewed every 2-4 days as an outpatient secondary spontaneous pneumothorax-- monitored as an inpatient if stable, follow-up in the outpatients department in 2-4 weeks
37
Persistentent / recurrent pneumothorax management
n video-assisted thoracoscopic surgery (VATS) should be considered to allow for mechanical/chemical pleurodesis +/- bullectomy.
38
discharge advice of a pneumothrax
never scuba dive fly two weeks after succesful drainage if no residual air or one week after check xray avoid smoking
39
what is sarcoidosis
multisystem disorder of unknown origin characterised by non caseating granulomas
40
what groups are at higher risk of sarcoidosis?
young adults and in people of African descent
41
features of sarcoidosis
acute: bilateral hilar lympadenopathy, erythema nodosum, swinging fever, polyarthralgia,
42
insidious features of sarcoidosis
insidious: dyspnoea, non productive cough , malaise weight loss
43
other features of sarcoidosis
uveitis lupus pernio hypercalcaemia - because macrophages inside the granulomas cause an increased conversion of vit d to its active form
44
sarcoidosis general prognosis
Sarcoidosis remits without treatment in approximately two-thirds of people
45
what are some poor prognostic features of sarcoidosis?
insidious onset, symptoms > 6 months absence of erythema nodosum extrapulmonary manifestations: e.g. lupus pernio, splenomegaly CXR: stage III-IV features black African or African-Caribbean ethnicity
46
what is the diagnostic proccess for sarcoidosis
diagnostic largely clinical so no specific diagnostic test - ACE levels have a sensitivity 60% and specificity 70% - not reliable to diagnose but potentially monitor progression - hypercalcemia (10%) - raised ESR - chest xray - a bunch of indicative findings - spirometry may show restrictive pattern - tissue biopsy shows non caceating granulomas
47
what the xray features of sarcoidosis and the grades of the disease based on xray fuindings
stage 0 = normal stage 1 = bilateral hilar lymphadenopathy (BHL) stage 2 = BHL + interstitial infiltrates stage 3 = diffuse interstitial infiltrates only stage 4 = diffuse fibrosis
48
when indicated what is the pharmacological manaegement of sarcoidosis
steroids
49
what is the indication for steroids in sarcoidosis
SYMPTOMATIC patients with stage 2 or 3 disease hypercalcemia eye heart or neuro involvement
50
epistaxis types
anterior visible source of bleeding --usually due to insult to the network of capillaries that form Kiesselbach's plexus. Posterior haemorrhages, --more profuse -- from deeper structures. --- older patients ---higher risk of aspiration and airway compromise.
51
management ladder of epistaxis
first aid technique if not have a look and if you can localise source cauterise if cant locate do anterior packing if it doesnt work refer to ent for posterior packing
52
what is the first aid techniwue for epistaxis
lean torso forward and open mouth, avoids aspiration of blood and collection in the nasopharynx and allows spitting of any blood coming to mouth + breath through mouth also pinch cartilagenous part of nose this needs to be done for at least 20 mins!!!
53
if the first aid measures are successful in epistaxis what to do and what to be cautious about when doing this
consider using a topical antiseptic such as Naseptin (chlorhexidine and neomycin) to reduce crusting and the risk of vestibulitis cautions to this include patients that have peanut, soy or neomycin allergies Mupirocin is a viable alternative
54
when may admission be considered after epistaxis episode of a patient
a comorbidity (e.g. coronary artery disease, or severe hypertension) is present, an underlying cause is suspected they are aged under 2 years (as underlying causes such as haemophilia or leukaemia are more likely in this age group)
55
what should be avoided following an epistaxis episode?
patients should be informed that blowing or picking the nose, heavy lifting, exercise, lying flat, drinking alcohol or hot drinks should be avoided
56
Epistaxis that has failed all emergency management
may require sphenopalatine ligation in theatre
57
what is the pathophysiology behind T1Resp failure
T1RF occurs due to a problem with oxygenation, which may occur due to several pathophysiological mechanisms: 1) V/Q mismatch: - The commonest cause of T1RF - An imbalance in ventilation versus perfusion of the lungs leading to inefficient oxygenation - A low V/Q occurs when alveoli are not sufficiently ventilated e.g. in airways disease - A high V/Q occurs when there is limited blood flow in the lungs e.g in pulmonary embolism 2) Diffusion limitation: - Impaired gas exchange across the alveolar membrane - due to inflammation or fibrosis of the membrane e.g. in idiopathic pulmonary fibrosis - due to a decrease in the available surface area for diffusion e.g. emphysema -Carbon dioxide is more soluble than oxygen hence why hypoxaemia is commonly seen without hypercapnia 3) Shunting: - Refers to blood that passes through the lungs without undergoing gas exchange - May be a physiological response to V/Q mismatch as if there are alveoli with very poor ventilation the blood that goes to them will not be ventilated - Anatomical shunting may be seen e.g. in pulmonary arteriovenous malformations Can also cause hypercapnia and T2RF if severe
58
pathophysiology of type 2 resp failure
T2RF occurs due to a problem with ventilation, which may occur in severe shunting or diffusion limitation or more commonly with the following mechanisms: 1) Increase in dead space: - Dead space is ventilated but not perfused and so there is no gas exchange - alveolar dead space increases if capillaries are destroyed e.g. in EMPHYSEMA OR INTERSTITIAL LUNG DISEASE 2) Reduced minute ventilation - Minute ventilation is the total amount of air entering the lungs per minute - If it decreases, there is a decrease in alveolar ventilation - It is equal to respiratory rate x tidal volume - Conditions that reduce respiratory rate include respiratory depressants such as ALCOHOL OR OPIATE MEDICATIONS - Conditions that reduce tidal volume include NEUROLOGIVAL DISORDERS such as motor neuron disease or chest wall deformities
59
Sympotoms of resp failure
Dyspnoea Headache Light-headedness Confusion Drowsiness Agitation Symptoms related to underlying cause e.g. productive cough and fever in pneumonia
60
signs of resp failure
Tachypnoea (although respiratory rate may be low in some cases of T2RF e.g. opiate overdose) Cyanosis Accessory muscle usage Nasal flaring Signs of central nervous system dysfunction e.g. reduced GCS, irritability Signs related to underlying cause e.g. wheeze in a COPD exacerbation
61
signs related to hypercapnea
Flushed skin Bounding peripheral pulses Asterixis Tachycardia or arrhythmia Drowsiness
62
definition of resp arrest
Respiratory arrest is the complete cessation of respiratory effort. It typically is the result of progressive respiratory distress and can result in cardiac arrest.
63
Epidemiology of resp arrest
Respiratory disease resulting in distress is a relatively common reason for paediatric hospital admission in the UK. Fortunately, progression to respiratory arrest is rare. Infants, particularly those under 3 months of age, are particularly prone to apnoea.
64
causes of reso arrest
Respiratory distress and ultimately arrest can be the result of: Infections: Croup, Epiglottitis, Bronchiolitis, Pneumonia Inflammation and bronchoconstriction: Asthma, viral-induced wheeze Foreign body aspiration Neuromuscular: respiratory muscle paralysis Cardiovascular conditions: myocarditis, dilated cardiomyopathy, pericarditis
65
management of resp arrest
A-E maintain airway with head tilt chin loift or jaw thrust oxygen >94 iv access iv resus bolus balanced isotonic fluids If the respiratory distress and arrest result in cardiac arrest, CPR should be commenced following the ALS algorithm.
66
complications of cardiac arrest
Hypoxic brain damage Cardiac arrest Death
67
prognosis of resp arrest
There are generally poor outcomes associated with cardiorespiratory arrest in children and infants. Early detection and involvement of PICU are associated with the best outcomes.
68
what antibiotic prophylaxis is given to bronchiectasis patients who are carriers of pseudomonas aeruginosa
nebulised colomycin
69
Most common organisms isolated from patients with bronchiectasis:
Haemophilus influenzae (most common) Pseudomonas aeruginosa Klebsiella spp. Streptococcus pneumoniae
70
Bronchiectasis: management
physical training (e.g. inspiratory muscle training) - has a good evidence base for patients with non-cystic fibrosis bronchiectasis postural drainage antibiotics for exacerbations + long-term rotating antibiotics in severe cases bronchodilators in selected cases immunisations surgery in selected cases (e.g. Localised disease)
71
Bronchiectasis: symptoms and signs
persistent productive cough. Large volumes of sputum may be expectorated dyspnoea haemoptysis Signs abnormal chest auscultation coarse crackles wheeze clubbing may be present
72
diagnostic investigation of bronchiectasis
high resolution chest CT
73
most common chemical causing occupational asthma
isocyanates - the most common cause example occupations include spray painting and foam moulding using adhesives platinum salts soldering flux resin glutaraldehyde flour epoxy resins proteolytic enzymes
74
investigation for occupational asthma
Serial measurements of peak expiratory flow are recommended at work and away from work.
75
management of occupational occupation asthma
Referral should be made to a respiratory specialist for patients with suspected occupational asthma.
76
what is gout
Gout is a form of arthritis that occurs when monosodium urate crystals deposit in joints. This causes both acute inflammation (gout flares) and in the longer-term, a chronic gouty arthritis with tophi (hard deposits of monosodium urate crystals in soft tissues).
77
describe tophaceous gout
long term manifestation of gout Patients will usually have a history of longstanding recurrent acute gout Tophi are firm white nodules of sodium monosulphate crystals under the skin They commonly occur on extensor surfaces of joints such as knees or elbows, the Achilles tendons, backs of hands and feet and on the helices of the ears Usually they are painless however they can become infected, inflamed or ulcerated They may discharge white material onto Chronic gouty arthritis may present with tender and stiff joints with reduced range of motion
78
diagnostic investigation for gout and some others
Joint aspiration is the gold standard diagnostic investigation Needle-shaped monosodium urate crystals with negative birefringence are seen in gout Synovial fluid should also be sent for gram stain and culture to rule out septic arthritis Tophi can be biopsied to look for these crystals Blood tests: Serum uric acid should be measured in all patients with suspected gout consider screening for risk factors
79
first linemanagement. of gout
NSAIDs or colchicine are first-line the maximum dose of NSAID should be prescribed until 1-2 days after the symptoms have settled gastroprotection (e.g. a proton pump inhibitor) may also be indicated offer urate-lowering therapy to all patients after their first attack of gout
80
main side effect of cholchicine
diarrhoea
81
when is urate lowering therapy definitely indicated
>= 2 attacks in 12 months tophi renal disease uric acid renal stones prophylaxis if on cytotoxics or diuretics
82
what is taken with allopurinol
colchicine cover should be considered when starting allopurinol. NSAIDs can be used if colchicine cannot be tolerated
83
which medication makes gout worse
thiazides
84
medication that is goot for gout and hypertension
losartan
85
which vitamin may help in decreasing serum uric acid levels
vit c
86
what type of hypersensitivity reaction are most allergens
type 1 hypersensitivity reactions (IgE mediated) non IgE mediated hypersensitivity reactions also exist and tend to occur more slowly - these are cell-mediated
87
serum specific IgE how long does it take to be resulted
may take several weeks
88
what allergens do you test in a skin prick test?
Some patients may be "sensitised" to specific allergens i.e. they have positive test results but no symptoms of allergy when exposed to that allergen Because of this, testing should be targeted based on the clinical history as otherwise false positive results are common
89
what is done in cases of confirmed food allergy long term
follow-up testing may be done to see if patients have developed tolerance to that allergen important since one of the complications is malnutrition in children being limited from having limited diets
90
definition of malnutrition
a Body Mass Index (BMI) of less than 18.5; or unintentional weight loss greater than 10% within the last 3-6 months; or a BMI of less than 20 and unintentional weight loss greater than 5% within the last 3-6 months
91
how common is malnutrition in >65y
Around 10% of patients aged over 65 years are malnourished, the vast majority of those living independently, i.e. not in hospital or care/nursing homes.
92
screening tool for malnutrition
MUST (Malnutrition Universal Screen Tool).
93
management of malnutrition
not totally straight forward and identical always but dietician support if the patient is at high-risk a 'food-first' approach with clear instructions (e.g. 'add full-fat cream to mashed potato'), rather than just prescribing oral nutritional supplements (ONS) such as Ensure if ONS are used they should be taken between meals, rather than instead of meals
94
definition of obesity
A BMI of 30 or higher is considered indicative of obesity.
95
what is metabolic syndrome
Metabolic syndrome, on the other hand, is a constellation of metabolic abnormalities, including central obesity, insulin resistance, high blood pressure, and dyslipidemia. While obesity is a component of metabolic syndrome, individuals with metabolic syndrome may not meet the BMI criteria for obesity.
96
risk factors of obesity
genetics environmenta; socioeconomic psychilogical medical conditions eg PCOS and Hypothyroidism
97
investigations in obesity
BMI Measurement: Calculate the BMI using an individual's weight and height. Waist Circumference: Measure the waist circumference to assess central obesity. Blood Pressure: Monitor blood pressure levels regularly. Fasting Blood Glucose: Screen for impaired glucose tolerance or diabetes. Lipid Profile: Assess lipid levels, including cholesterol and triglycerides. Liver Function Tests: Evaluate liver health as obesity can lead to non-alcoholic fatty liver disease (NAFLD).
98
medical therapy in obesity examples and when to consider
Consider medications such as orlistat (a lipase inhibitor) or GLP-1 receptor agonists (e.g. liraglutide) for individuals who do not achieve weight loss goals through lifestyle changes alone.
99
when to give GLP-1 analogues
adjunct to diet and exercise for weight management in individuals with a BMI ≥35, or ≥30 with weight-related comorbidities such as type 2 diabetes or hypertension
100
liraglutide therapy action if 12 weeks no loss of at least 5% O initial body weight
stop it
101
bariatric surgery when offered
Recommended for individuals with severe obesity (BMI ≥ 40) or those with a BMI ≥ 35 with significant obesity-related comorbidities.
102
types of bariatric surgery
gastric bypass, sleeve gastrectomy, adjustable gastric banding, and biliopancreatic diversion.
103
what conditions is OSA a risk factor for
strongly linked with cardiovascular disease and the metabolic syndrome, and is a significant risk factor for coronary artery disease, type 2 diabetes and stroke. daytime sleepiness- driving concerns
104
initial screening tools for obstructive sleep apnoea
STOP-Bang asks about snoring, sleepiness, apnoeas, hypertension, obesity, neck circumference, age and sex and gives a low, medium or high risk of OSA. The Epworth sleepiness scale focuses on daytime sleepiness - gives a result of either normal or mild, moderate or severe excessive
105
definitive diagnostic investigation of OSA
polysomnography (also called a sleep study) which would usually be arranged by a specialist clinic.
106
WHEN SHOUld patients be referred urgently for polysomnography?
Excessive sleepiness is impacting on their safety to work (e.g. professional driver) They have a related comorbid condition such as treatment resistant hypertension or COPD They have upcoming major surgery They are pregnant
107
when should patients be non urgently referred for polysomnography?
pt who have moderate or severe OSA or mild OSA which is impacting quality of life should be referred routinely to a sleep clinic for consideration of polysomnography.
108
what does polysomnography measure
how many episodes of apnoeas or hypopnoeas lasting 10 seconds or more patients have per hour of sleep (referred to as the apnoea-hypopnoea index or AHI). Five or more is diagnostic of OSA and severity is classified as below: Mild OSA: AHI 5-14 per hour Moderate OSA: AHI 15-30 per hour Severe OSA: AHI over 30 per hour The number of episodes of oxygen desaturation per hour is also measured, with more episodes of desaturation predictive of poorer cardiovascular outcomes.
109
what is conservative management of OSA
Patient education, especially concerning driving Advise to sleep on their side rather than supine where possible Weight loss advice and support Reduction in alcohol intake Smoking cessation
110
first line MEDICAL MANAGEMENT of OSA
CPAP therapy
111
second line medical management of OSA if CPAP not tolerated
intra- oral mandibular advancement device is another option
112
driving advice for mild/ suspected OSA
If OSA is suspected or mild, advise patients not to drive until symptoms are controlled. If this is not achieved within 3 months, they should inform the DVLA.
113
driving advice for moderate or severe OSA
patients should inform the DVLA immediately and not drive; this will be reviewed by the DVLA and they may be allowed to drive once symptoms are controlled.
114
COMPLICATIONS OF OSA related to daytime sleepiness
Road traffic collisions - patients with OSA have a 2.5x increased risk compared to those without the condition Accidents at home or at work Deterioration in mental health, including irritability and depression
115
Cardiovascular and metabolic complications of OSA
Stroke Coronary artery disease Hypertension that may be treatment resistant Congestive heart failure Type 2 diabetes
116
features of klebsiella pneumonia
(typically following aspiration) and urinary tract infections. Features of Klebsiella pneumonia: more common in alcoholic and diabetics 'red-currant jelly' sputum often affects upper lobes
117
deterioration/ complication associated with NIV
pneumothorax
118
describe features of erythema nodosum
PAINFUL Red rash on shins
119
two common organ systems affected by sarcoidosis
lungs and nlymphatic system (so parotid lyphadenopathy)