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Respiratory Qs Revision > Qs > Flashcards

Qs Flashcards

1
Q

What’re the 3 centres of brain stem involved in respiration

A

Medulla- DRG (activates diaphragm- inspiration) and VRG (mostly expiration- Abdo muscles).
Lower pins- has apneustic center which enhances inspiration, and upper pons which has pneumotaxic center that inhibits inspiration

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2
Q

What’re the 5 sensors/chemoreceptors and their role

A
  1. Central chemoreceptors- activate VRG and DRG (CSF CO2 main stimuli).
  2. Peripheral chemoreceptors- carotid bodies are main (also aortic arch) respond to low PaO2 and well as high PaCO2- quicker but less market response than central receptors. Carotid messages carried via carotid sinus nerve to brain stem resp centres
  3. Lung stretch receptors- lung distension causes negative feedback via vague nerve to medulla via hering-Breuer reflex-> phrenic nerve thus not activated-> diaphragm thus doesn’t contact
  4. Irritant receptors
  5. Arterial baroreceptors- high BP stimulates carotid/aortic sinus baroreceptors -> reflex hypoventilation
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3
Q

What equals FRC, TLC and VC

A

FRC = ERV + RV

TLC= FRC+ VT+IRV

VC= IRV+VT+ERV

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4
Q

What’re the major determinants of lung compliance

A

Main is lung volume (most compliant at usual interpleural pressures and low at extremes), surfactant, diseases, posture and recent pattern of breathing

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5
Q

What’s equal pressure point

A

Where intrapleural pressure is same as airway pressure - here, flow determined by difference between alveolar and intrapleural pressure. EPP reaches far quicker in asthmatics

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6
Q

What determines flow at dynamic airway compression pressure

A

Alveolar pressure- pleural pressure (I.e. not mouth pressure)

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7
Q

What’s the closing volume? What increases it

A

CV is point of dynamic airway compression. Increases with age, smoking, lung disease, supine posture

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8
Q

Major site of resistance in airways

A

Medium sized bronchioles

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9
Q

At what lung volume is the pulmonary vascular resistance lowest

A

At FRC- it’s increased at both high and low lung volumes.

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10
Q

What’re type A and B V/Q mismatch and when do they occur?

A

Type A is in emphysema- large amount of ventilation occurs - seen in physiological dead space, E.g. emphysema.
Type B mismatch- large areas of blood flow to areas of low flow. Physiological shunt (e.g. chronic bronchitis)

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11
Q

Where is V/Q highest

A

At top of lung, although both ventilation and perfusion are higher at bottom

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12
Q

Lung function test- extrinsic vs intrinsic ILD

A

Extrinsic causes like chest wall abnormalities or neuromuscular diseases DLCO/KCO normal and ratio of RV/TLC is high

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13
Q

Reduced FEV1/FVC, lung volumes also reduced . Ddx?

A

Mixed

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14
Q

Obstructive picture but DLCO normal . Ddx?

A

Chronic bronchitis or asthma

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15
Q

Lung volumes normal, DLCO low, KCO high, Va low. Ddx?

A

Pneumonectomy

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16
Q

Restrictive but normal DLCO. Ddx?

A

Extrinsic RLD: pulmonary (e.g. AS) or nonpulmonary (obesity, APO, diaphragm palsy, scoliosis, myasthenia, muscular dystrophy)

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17
Q

Isolated low DLCO (and low KCO)

A

Pulmonary vascular disease - PE, AVM, pulmonary HTN

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18
Q

Isolated high DLCO

A

Pulmonary haemorrhage

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19
Q

Restrictive with MIP <80%

A

Myasthenia

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20
Q

Causes for when giving oxygen doesn’t fix saturation

A

Methaglobulinemia or shunts

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21
Q

Pattern + causes of fixed upper airway obstruction

A

MIF AND MEF low but both same.

Laryngeal edena, prolonged intubation, tracheal stenosis, retrosternal goiter

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22
Q

Pattern + causes of extrathoracic airway obstruction

A

MIF reduced.

Causes: laryngomalacia, vocal cord abnoamalities

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23
Q

Pattern + causes of variable intrathoracic airway obstruction

A

MEF reduced.

Causes: tracheomalacia, tracheal tumor

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24
Q

Causes of right shift oxygen Hb curve and what it represents

A

Right shift in high offload to tissues

Seen in high CO2, acidosis, 2,3 DPG, high temperature

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25
Q

Causes of left shift

A

Met hb, high affinity Hb, HbF, CoHb

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26
Q

What happens to PaCO2, SaO2 and CaCO2 (oxygen content) in A) Anemia, B) CO poison and C) V/Q mismatch

A

A) only the Ca02 content low
Anemia is the main reason for reduced oxygen delivery despite normal arterial oxygen Sats

B) again only CaCo2 low, unless you request oxyHb specifically in Sa02 when it would then be low

C) all low

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27
Q

What happens to TLC, RV, ERV in

A) aging
B) severe obesity

C) Emphysema
D) Neuomuscular disease

A

A) RV higher, ERV lower (thus FRC only slightly higher) and IC same

B) RV higher, ERV much lower (FRC lower), IC also lower

C)RV much higher, ERV slightly lower and IC higher

D) RV much higher, ERV much lower and IC much lower

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28
Q

Main cause of hypoxia

Main cause of hyper apnea

A

Hypoxia due to V/Q mismatch, hypercapnea due to hypoventilation

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29
Q

For each 10mmHg increase in CO2, how much does HCO3- increase by in acute vs chronic resp acidosis

A

In acute - by 1-1.5

In chronic by 3-4

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30
Q

Equation for A-a gradient in RA

A

Expected- actual

Expected= 150-(PaCO2/0.8). The 0.8 becomes 1 if exercising

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31
Q

What is normal range for A-a gradient

A

Age/4 +4

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32
Q

Equation for A-a gradient in supplemental oxygen

A

Expected is Pa02/FiO2

Note FiO2= oxygen there’re on divided by 100 (e.g, at 100% O2, FiO2 is 1!

Normal via this method is >400

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33
Q

Causes of high A-a gradient

A

Main is V/Q mismatch (eg. PE, COPD, pneumothorax), diffusion abnormality (ARDS, ILD) and shunts (TOF, PAVM)

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34
Q

Why does hypoxia worsen when IV B2 agonist given in asthmatics

A

It’s also peripheral vasodilator (dilates smooth muscle in pulmonary arteries)

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35
Q

What’s the best measure of aerobic activity / CVS fitness

A

Max O2 consumption - declines with age. In healthy aging main reason this reduces is due to low HR (I.e. 220-age)

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36
Q

What acclimitasions (name 3) in high altitude

A

Most important is hyperventilation- initially limited by alkalosis but then renal kicks in and can continue. Acetazalamide taken prophylaxis can increase HCP3 loss by kidney and thus can hyperventilate more

Also polycythemia and oxygen curve shift

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37
Q

What happens to oxygen curve shift in altitude

A

Depends..
At moderate altitude- right shift
Very high altitudes- left shift

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38
Q

What’s acute mountain illness

What’s its management for mild and moderate-severe

A

Mostly above 2500m about 8-12 hrs post

Headache, fatigue, dizzy, nausea, hypoxia, alkalosis, fluid retention and reduced urine.
Mx if mild- nil

If moderate-severe oxygen, acetazamide, dex and consider descent Do NOT ascend further

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39
Q

What’s HAPE and management

A

Often above 8000 and progresses from AMS. Due to breakdown of pulmonary blood-gas barrier due to maladaptive process to hypoxia. Largely genetically determined
High pulmonary artery pressure and uneven vasoconstriction are key

Symptoms: non productive cough, SOBOE progressing to SOB at rest (this is key). X-ray looks far worse than patient.
Mx: oxygen is KEY, acetazopamide. Not all need descent

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40
Q

Describe HAPE and mx

A

Hallmark is encephalitic features (ataxic gait, reduced mental function). Mx: immediate descent, dex, oxygen
Prophylaxis: Acetazolamide

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41
Q

How does BENDS occur ?

A

On rapid ascent after diving . During diving nitrogen (which is poorly soluable and in high concentrations) forces into our body tissues (mainly fat) and if ascent quickly it comes out as bubbles-> pain, blindness, deafness
Treat by recompressing

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42
Q

Describe pathophysiology, findings, causes and management of methamoglobulinemia

A

MetHb is when Hb bound to ferric iron (Fe3+) which cannot bind oxygen. Body tries to compensate by left shift.
Presents as asymptomstic cyanosis and hypoxia, anemia and saturation gap . Key is regardless of extent of MetHb, SpO2 plateau at 85%
Causes- cytochrome b5 reductase deficiency, puruvate linase deficiency, nitrogen ingestion, meds like dapsone, sulphonamides and local anaesthetics

Mx: if MetHb >20%, methylene blue can restore Fe2+

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43
Q

What’re the strongest RFs to VTE with OR of >10

A

Fracture of lower limb, hospitalisation for heat failure or AF within 3 months, MI within 3 months, THR/TKR within 3 months, prior VTE, major trauma and spinal cord injury

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44
Q

General approach to PE without haemodynamoc compromise

A

Do Wells score. If low test probability (score under 2)- use PERC- is PERC net exclude and PERC pos to D dimer. If d dimer positive- CTPA

IF Wells shows intermediate (2-6) do D dimer.

If Wells is high risk do CTPA.

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45
Q

Components of Wells score

A

3 points each for clinical signs of DVT, and alternative diagnosis less likely
1.5 points for prior PE/DVT, HR over 100, surg within 4 weeks

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46
Q

PERC components

A

Age under 50, HR under 100, sats over 95%, no haemoptysis, no estrogen or prior VTE, no leg swelling and no surgery

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47
Q

Which test has highest NPV in excluding PE

A

V/Q

If CTPA is neg but high pretest probability, anticoagulate or investigate further

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48
Q

Which test has highest pick up rates of PE

A

CTPA

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49
Q

Diagnosis of PE in haemodynamoxally compromised patient

A

Bedside echo first - If RV dysfunction do CTPA if available or treat if high pretest probability

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50
Q

Diagnosis of PE in pregnancy

A

If leg symptoms do USS

If no leg symptoms, do CXR and if normal do V/Q- if neg great, if positve treat with LMWH, if inconclusive do CTPA

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51
Q

General management of PE

A

For high risk PE, use UFH. Otherwise NOAC is non inferior to warfarin and less fatal ICH (but more nonsevere bleeds)

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52
Q

Role of filters in PE

A

50% reduction in PE but 70% increase in DVT

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53
Q

Describe platypnea-orthodexoxia syndrome

A

SOB on standing up, arterial desaturation in upright position, and improvement in supine position. Causes can be broadly categorized into 4 groups: intracardiac shunting, pulmonary shunting, ventilation-perfusion mismatch, or a combination of these.

Diagnosed on TTE

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54
Q

What’s the MAIN parameter that PEEP increases

A

FRC

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55
Q

Main lung function changes with pregnancy

A

FRC lower, minute ventilation and alveolar ventilation increased, TLC slightly reduced, Pa02 same but PaCO2 reduced, RR same

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56
Q

Worst prognostic feature in mesothelioma

A

Sarcomaroidal histology (best is papillary mesothelioma)

57
Q

Management of mesothelioma

A

Platinum based chemo and pemetrexed- if progresses then gemcitabine

58
Q

Management of COPD infective exacerbation

A

Pred 37.5 for 5 days, Augmentin or doxycycline to cover haemophilus, strep and moraxella

59
Q

Long term management of COPD

A

1st line LANA. If persistent- LAMA and LABA. If FEV1 under 50 (esp with eosinophils over 300)- LABA/ICA
If still symptoms - triple therapy

60
Q

In COPD what interventions shown to improve survival

A

Smoking

Oxygen if under 55 or under 60 if also PH

61
Q

Main cause of death in COPD

A

COPD exacerbations- commonest being H influenza

62
Q

Which single action provides best long term benefit in asthma

A

Long term follow up

63
Q

Most sensitive and most specific tests for asmtha

A

Sensitive is direct bronchoprovocation with methacholine or histamine (should show fall in FEV1 by > 20%)

Most specific is indirect bronchoprovocarion with mannitol or hypertonic saline or exercise/eucapneic voluntary hyper apnea (positive if >10% fall in FEV1)

64
Q

Most common cause of occupational asthma

A

Isocyanates (in spray paint)

65
Q

How to diagnose occupational asthma

A

Serial peak flow measurements at work and home

66
Q

Management of mild asthma

A

Regular ICS/SABA or PRN LABA/ICS (SABA alone discouraged now)

67
Q

Lines of management of severe asthma, inc add on therapies

A 
High dose ICS/LABA
Iv magnesium (relaxes smooth muscle- calcium antagonst)
IF allergic (high IgE, ABPA) omalizumab, (IgE antagonist), oral steroids

If esonophilic asthma (over 150), oral steroids , mepolizumab, benralizumab (IL5 antagonist)

If nonesonophilic asthma, LABA/LAMA, theyophiline (PDE3 and PDE4 inhibitor)

If

68
Q

Diagnostic criteria for CF diagnosis

A

If symptoms/FHx, positive neonatal screen- do sweat chloride. If >60= CF, if <30= no CF

If between 30-60= CFTR genetic analysis. If it shows 2 mutations- CF

69
Q

When else does CFTR dysfunction occur

A

ABPA, chronic rhinosinutis, obstructive azoospermia

70
Q

Commonest features of CF

A

Commonest is sinusitis, then make inferlity due to absent vas deferens

71
Q

Managing acute infective exacerbation of CF

A

Firstly do routine sputum MCS 3 monthly- 70% are colonised with pseudomonas if over 25 rs (under that staph is commonest). After initial pseudomonas identification- aggressive therapy

For acute sickness- give piptaz and tobramycin OR AugDF

72
Q

Long term management of CF

A

Azithromycin 500mg 3 times per week has antibacterial/antipseudomonas effect AND anti inflammatory effect (don’t use in NTM due to risk of resistance developing)

Ivacaftor is a CFTR potentiator- increases chloride secretion and reduces excessive sodium and water absorption-> prevents airway dehydration . Improves lung function and reduces exacerbations BUT no effect alone in del508 mutants (this causes folding problem) . Thus given with lumacaftor (in del508 homozygotes) and tezacaftor (also useful in del508 heterozygotes)

Dornase alpha (DNAse) improves FEV1 and reduces exacerbations. Inhaled hypertonic saline reduces exacerbations. PEP therapy

73
Q

Main cause of death in CF

A

Resp failure

Then DIOS (distal intestinal obstruction syndrome)

74
Q

Presentation of AERDS

A

Chronic rhinosinusitis, polyps, anosmia, eosinophilic. Can be caused by paracetamol too as inhibits COX

75
Q

Management of AERD

A

Monteleukast (leukotrione antagonist), mepolizumab, dapilumab (IL4, IL13 antagonist)
Also aspirin desensitisation and intravascular steroids and sinus surgery

Note eosinophilic asthma is associated with AERD and treated similar

76
Q

Causes of bronchiectasis

A

40% idiopathic

Post infectious, CVID/selective IgA deficiency, COPD, PCD, asthma

77
Q

Long term management steps in bronchiectasis

A

3 monthly sputum MCS and aggressively treat pseudomonas if cultured

Step 1= PT, pulmonary rehab

Step 2= if despite above 3 or more exacerbations= mucoactive trewtment and PT reassessment

Step 3= If despite above 3 or more = long term macrolide (If pseudo cultured can give anti pseudo instead)

Step 4= of despite above 3 or more = long term macrolide AND inhaled ABX (colistin/tobramyin/aztreonam)

78
Q

What did using erythromycin for prevention do in bronchiectasis

A

Reduced H influenza but increased pseudomonas

79
Q

Management of mild-moderate exacerbation of bronchiectasis

A

AugDF or doxycycline empirically
If culture shows pseudomonas, cipro
For all else continue AugDF

80
Q

Management of severe bronchiectasis exacerbation

A

Empirically with piptaz OR ceftazadime +/- tobramycin

Then if H influenza or pseudomonas cultured-cont taz. If strep- benpen . If H influenza- ampicillin.

81
Q

What’s the commonest colonised pathogen in bronchiectasis, I like CF

A

Haemophilus influenza

82
Q

If routine MCS shows pseudomonas, course of action

A

Fluroquinolones (cipro) for 2 weeks then beta lactams and then inhaled antibiotics for total 3 months

83
Q

CT findings in ABPA

A

Upper lobe ground glass opacity, cylindrical bronchiectasis, atelactasis

84
Q

Diagnostic criteria for ABPA

A

MUST have asthma and/or CF. AND both of positives skin prick or raised IgE levels to aspergillus fumigatus. AND elevated IgE (>1000).
AND at least two of: radiology consistent, total eosinophils >0.5, positive aspergillus or raised IgG to aspergillus

85
Q

Management of ABPA exacerbation

A

Pred and wean over 3 moths

86
Q

Long term management of ABPA

A

Giving long term abx doesn’t prevent infection and can increase invasive aspergillus

If steroid dependent- itraconazole used (omalizumab May be useful too)

87
Q

RHC findings of Group 1 PAH

and examples of this group

A

Inc idiopathic, CT diseases, HIV, schostomatosis

In echo RSVP is above 40 for all or tricuspid regurgitation velocity over 2.9.
Then if mean arterial pressure is over 20 (some say 25) that’s diagnostic of raised pressure. For the cause look at PAWP and if that’s under 15= not from LA= precapillary
Then do vasoreactivity testing with epoprostenol

88
Q

Role of endothelin in Group 1 PAH

A

ET-A and ET-B act on smooth muscle to cause vasoconstriction of smooth muscle, whilst on endothelium they stimulate release of NO causing vasodilation

89
Q

5 group of agents and examples of them used for Idiopthic IPF
Which have survival benefits

A

All get diuretics if RV failure

  1. Endothelin receptor antagonists- bosentan (endothelin A and B antagonist), ambrisentan (only A antagonist) and Macitentan (A and B antagonist- improves mortality!)

Phosphodiesterase type 5 inhibitors: sildenafil-> pulmonary vasodilation

Guanylate cyclase stimulator= riociguat. Dual actions- increases sensitivity to NO, and directly stimulates NO receptor->

Prostacyclin analogues- Improves mortality!

Calcium channel blocker of vasoreactive positive

Most get combo therapy with tadalafil and abrisentan.

90
Q

ILD can be radiologically divided into UIP or NSIP. List examples AND radiological patterns of both

A

UIP- idiopathic pulmonary fibrosis, asbestosis, RA
HRCT- honecombing, traction bronchiectasis, reticular opacities lower lobes, no atypical features.

NSIP- clinical diagnosis include NSIP, all CTD except RA, HIV, drugs (bleomycin, amiodarone, MTX, nitrofurantoin)
HRCT shows ground glass opacities, reticular opacity, traction bronchiectasis, diffuse disease

91
Q

What radiological category does hypersensitivity pneumonitis fot into

A

In acute cases- NSIP, in chronic UIP!

Egg shelf classification shows silicosis (black lung)

92
Q

Causes of UL fibrosis

A

CHARTS

Coal miners pneumoconiosis, hypersensitivity pneumonitis, ankylosing spondylitis, Radiation, TB, Silicosis/Sarcoidosis

93
Q

Causes of LL fibrosis

A

ACID

Asbestosis, CT diseases (except AS), IPF, drugs (bleomycin, amiodarone, MTX)

94
Q

Treatment of IPF and their SE

A

Pirferidone (antifibroblast- main SE photosensitovoty) and Nintedanib (TKI- diarrhoea)

Neither cure but both improve FEV1

Nintedanib has shown effectiveness in severe disease called chronic fibrosing progressive ILD

95
Q

IPF exacerbation management

A

Steroids

96
Q

NSIP management

A

Steroids wean over 6 months , steroid sparing agents, lung transplant

97
Q

Stages of sarcoidosis

A

Stage 1= bilateral Hilary lymphadenopathy, stage 2= BHL + infiltrates
Stage 3= infiltrates
Stage 4= fibrosis

98
Q

Diagnosis of sarcoidosis

A

Tissue diagnosis needed l, unless Lofgren

Endobrobchial USS guided trans bronchial needle aspiration has highest yield

99
Q

Management of sarcoidosis

A

Most don’t need treatment

If symptomatic pulmonary disease, cardiac or neurological disease or symptomatic hypercalcelia= steroids

100
Q

What’re the sarcoidosis syndromes/types

A

Lofgrens = acute, bilateral Hilary lymphadenopathy, erythema nodosum, fever, polyarthralgia. Carries except prognosis

Hearfordt = parotid enlargement, fever, uveitis

Mikulicz = enlarged parotid, lacrimal glands

101
Q

What’s most diagnostic of obesity hypoventilation

A

PaCO2 >45 when awake

102
Q

Describe management alogorithm for primary pneumothorax

A

If asymptomatic and under 2cm= oxygen and observe for 24 hours

If asymptomatic but over 2cm, or if symptomatic and under 2cm= needle aspiration and oxygen

If patient unstable or needle aspiration failed=chest drain (if taking too long urgent decompression)

If chest drain/tube failed to reexpand or persistent leaks from tube= VATS pleurodesis

103
Q

Management alogorithm for secondary pneumothorax

A

If over 50 and >2cm or SOB= chest drain/tub

If over 50 but under 2cm= needle aspiration, if remains over 1cm= chest drain

Permanently avoid diving

104
Q

MAnatement of iotrogenic

A

If no COPD etc, observe alone, majority resolve on their own and recurrence very rare

105
Q

Risk of over drainage of pneumothorax

A

Re-expansion pulmonary edema (RPE)

106
Q

Describe Fleischner society rules for lung mass

A

If solitary module under 3cm and low risk patient= no nothing. If patient high risk= repeat CT 12 months

If single nodule 6-8cm or multiple modules under 6mm= repeat CT 12 months

If multiple modules over 6cm= CT 3-6 monthly

107
Q

Triad of symptoms in fat embolism

When does it present

A

Mostly due to long bone and pelvic fractures 1-3 days post the fractures- hypoxemia, petechial rash, neurological abnormalities , ARDS picture.

108
Q

Outside of NIV, which device provides the highest Fi02

A

Non rebreather mask (95%)

109
Q

List the 4 commonest causes of polycythemia and state what happens to RBC mass, plasma volume and EPO with them

A

EPO secreting tumor, chronic hypoxemia, PCV, high affinity Hb all cause high RBC mass and normal plasma volume, and all but PCV also cause high EPI

110
Q

What’re the prognostic indicators in parapnuemonic infections

A

Serum urea, age, pleural fluid appearance and serum albumin

111
Q

Lights criteria needed to meet to say exudate

A

At least one of

Pleural fluid protein to serum protein ratio of >0.5; pleural fluid LDH:serum LDH >0.6
Pleural fluid level >2/3 of upper value of normal LDH

112
Q

What’s the most sensitive marker for transudate

A

Pleural:serum albumin <0.6

113
Q

Management of pleural infections

A

ICC if pH <7.2, presence of organisms in culture

No need to give Abx for atypical sad those bugs don’t cause pleural infections

114
Q

Describe LAM (lymphangioleiomyomatosis)

A

Progressive systemic diseases causing cystic lung diseases, mainly in young women, many related to tuberous sclerosising complex
CT classically shows thin walled cystic changes

115
Q

Describe pulmonary alveolar proteinosis

A

Surfactant builds up in alveoli causing SOB, due to reduced granulocytr-macrophage colony stimulating factor resulting in build up of debris
HRCT shows extensive white patches within kings

116
Q

What’re the 3 options for prevention of PJP post lung transplant

A

Bactrim (also gives prophylaxis to toxo), dapsone (causes MetHb), pethidine nebs

117
Q

NIV vs CPAP

What settings to start NIV

A

Both provide EPAP to keep airway open but NIV also gives pressure support (PS+EPAP=IPAP) to increase tidal volume and reduce CO2

EPAP is 10% body weight and start IPAP at 10 (IPAP is EPAP+ pressure support)

118
Q

How to calculate expected HCO3

A

24+ (PaCO2-40)/10

119
Q

Diagnosis of central, pleural, peripheral and peribronchoal lesions

A

Central= flexible bronchoscope, sputum cytology

Peripheral= radial EBUS, transthoracic needle aspiration

Pleural = pleural biopsy or thoracocentesis

Peribronchoal/mediastinal= linear EBUS, bronchoscope with transthoracic needle aspiration.

120
Q

Which lung cancer most likely to cause cavitation lesion

A

Squamous cell

121
Q

Describe pulmonary langerhans cell histiocytosis (PLCH)

A

Smoking related granulpma disease- local infiltrates of langerhan cells seen mixed with eosinophils centered around terminal bronchiole . Associated with lymphoma, leukaemia, lung cancer. Most spontaneously revert once smoking ceased

122
Q

How to investigate for contact allergy

A

Patch test

123
Q

Most sensitive test for atopic dermatitis

A

Serum IgE

124
Q

Approach to unconvincing antibiotic allergy patient

A

Avoid drug but if urgently needed do desensitisation rapidly. If less urgent can test for the allergy with RAST blood and if positive do skin prick test - if negative- graded oral challenge

125
Q

Does desensitisation work in opidoid, red man syndrome, contrast allergies

A

No because all these are anaphylactaoid (where last cell degranulation occurs without IgE cross linking) thus no specific IgE

126
Q

Type of hypersensitivity caused by latex

A

Commonest is type 4 contact dermatitis

IgE mediated can also occur

127
Q

Difference between the two types of angioedemas

A

Those associated with urticaria (always histamine mediated) and those not associated with urticaria (still mostly histamine medicated, but also 20% bradykinin medicated like C1INH deficiency

128
Q

What’re the three types of HAE and how to manage them

A

Type 1 HAE= low C4, low C1INH
Type 2= low C4, normal C1INH but low functional C1INH

Type 3= completely non functional C1INH

C3 normal in all

Acquired C1INH has low C1q (normal in HAE) - seen in lymphomas

Mx= icatibant (bradykinin receptor blocker) or C1INH infusion

Prevention= TXA, danazol,

129
Q

CSF finding in narcolepsy

A

Low hypocretin

130
Q

Narcolepsy diagnostic criteria

A

MSLT is gold . Shows multiple sleep latency time under 10 minutes and 2 episodes of REM during the MSLT within 15 minutes OR evidence of cataplexy

131
Q

Management of narcolepsy (and cataplexy)

A

Narcolepsy= modafinil or amphetamines

Venlafaxine and SSRI and sodium icy are prevent cataplexy

132
Q

Management of central sleep apnoea

A

Adaptive seroventilation BUT CANNOT use of CCF as increases mortality

133
Q

What is REM sleep behaviour disorder and 1st line treatment

A

It’s parasomnia with dream enactment after losing REM sleep Antonia
Mostly in LBD, Parkinson’s
Management- high dose melatonin

134
Q

Common cause of periodic limb movement disorder

A

Iron deficiency as iron is cofactors for dopamine

135
Q

Definition of OSA

A

AHI over 15 or over 5 and symptoms

136
Q

Cause of tiredness and CVS risk in OSA

A

Tired due to repeated arousals

CVS risk due to desaturation

137
Q

Benefits of CPAP in OSA

A

Improves BP, sleepiness, depression and erectile dysfunction (May reduce stroke)

Most importantly reduces MVAs

138
Q

RFs for OSA

A

Obesity, macroglossia (amyloidosis, hypothyroidism, acromegaly), Marfan, large tonsils

Respiratory Qs Revision (1 decks)

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