Qs Flashcards
(138 cards)
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
2
Q
What’re the 5 sensors/chemoreceptors and their role
A
- Central chemoreceptors- activate VRG and DRG (CSF CO2 main stimuli).
- 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
- 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
- Irritant receptors
- Arterial baroreceptors- high BP stimulates carotid/aortic sinus baroreceptors -> reflex hypoventilation
3
Q
What equals FRC, TLC and VC
A
FRC = ERV + RV
TLC= FRC+ VT+IRV
VC= IRV+VT+ERV
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
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
6
Q
What determines flow at dynamic airway compression pressure
A
Alveolar pressure- pleural pressure (I.e. not mouth pressure)
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
8
Q
Major site of resistance in airways
A
Medium sized bronchioles
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.
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)
11
Q
Where is V/Q highest
A
At top of lung, although both ventilation and perfusion are higher at bottom
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
13
Q
Reduced FEV1/FVC, lung volumes also reduced . Ddx?
A
Mixed
14
Q
Obstructive picture but DLCO normal . Ddx?
A
Chronic bronchitis or asthma
15
Q
Lung volumes normal, DLCO low, KCO high, Va low. Ddx?
A
Pneumonectomy
16
Q
Restrictive but normal DLCO. Ddx?
A
Extrinsic RLD: pulmonary (e.g. AS) or nonpulmonary (obesity, APO, diaphragm palsy, scoliosis, myasthenia, muscular dystrophy)
17
Q
Isolated low DLCO (and low KCO)
A
Pulmonary vascular disease - PE, AVM, pulmonary HTN
18
Q
Isolated high DLCO
A
Pulmonary haemorrhage
19
Q
Restrictive with MIP <80%
A
Myasthenia
20
Q
Causes for when giving oxygen doesn’t fix saturation
A
Methaglobulinemia or shunts
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
22
Q
Pattern + causes of extrathoracic airway obstruction
A
MIF reduced.
Causes: laryngomalacia, vocal cord abnoamalities
23
Q
Pattern + causes of variable intrathoracic airway obstruction
A
MEF reduced.
Causes: tracheomalacia, tracheal tumor
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
25
Causes of left shift
Met hb, high affinity Hb, HbF, CoHb
26
What happens to PaCO2, SaO2 and CaCO2 (oxygen content) in A) Anemia, B) CO poison and C) V/Q mismatch
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
27
What happens to TLC, RV, ERV in
A) aging
B) severe obesity
C) Emphysema
D) Neuomuscular disease
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
28
Main cause of hypoxia
| Main cause of hyper apnea
Hypoxia due to V/Q mismatch, hypercapnea due to hypoventilation
29
For each 10mmHg increase in CO2, how much does HCO3- increase by in acute vs chronic resp acidosis
In acute - by 1-1.5
In chronic by 3-4
30
Equation for A-a gradient in RA
Expected- actual
Expected= 150-(PaCO2/0.8). The 0.8 becomes 1 if exercising
31
What is normal range for A-a gradient
Age/4 +4
32
Equation for A-a gradient in supplemental oxygen
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
33
Causes of high A-a gradient
Main is V/Q mismatch (eg. PE, COPD, pneumothorax), diffusion abnormality (ARDS, ILD) and shunts (TOF, PAVM)
34
Why does hypoxia worsen when IV B2 agonist given in asthmatics
It’s also peripheral vasodilator (dilates smooth muscle in pulmonary arteries)
35
What’s the best measure of aerobic activity / CVS fitness
Max O2 consumption - declines with age. In healthy aging main reason this reduces is due to low HR (I.e. 220-age)
36
What acclimitasions (name 3) in high altitude
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
37
What happens to oxygen curve shift in altitude
Depends..
At moderate altitude- right shift
Very high altitudes- left shift
38
What’s acute mountain illness
| What’s its management for mild and moderate-severe
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
39
What’s HAPE and management
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
40
Describe HAPE and mx
Hallmark is encephalitic features (ataxic gait, reduced mental function). Mx: immediate descent, dex, oxygen
Prophylaxis: Acetazolamide
41
How does BENDS occur ?
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
42
Describe pathophysiology, findings, causes and management of methamoglobulinemia
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+
43
What’re the strongest RFs to VTE with OR of >10
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
44
General approach to PE without haemodynamoc compromise
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.
45
Components of Wells score
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
46
PERC components
Age under 50, HR under 100, sats over 95%, no haemoptysis, no estrogen or prior VTE, no leg swelling and no surgery
47
Which test has highest NPV in excluding PE
V/Q
If CTPA is neg but high pretest probability, anticoagulate or investigate further
48
Which test has highest pick up rates of PE
CTPA
49
Diagnosis of PE in haemodynamoxally compromised patient
Bedside echo first - If RV dysfunction do CTPA if available or treat if high pretest probability
50
Diagnosis of PE in pregnancy
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
51
General management of PE
For high risk PE, use UFH. Otherwise NOAC is non inferior to warfarin and less fatal ICH (but more nonsevere bleeds)
52
Role of filters in PE
50% reduction in PE but 70% increase in DVT
53
Describe platypnea-orthodexoxia syndrome
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
54
What’s the MAIN parameter that PEEP increases
FRC
55
Main lung function changes with pregnancy
FRC lower, minute ventilation and alveolar ventilation increased, TLC slightly reduced, Pa02 same but PaCO2 reduced, RR same
56
Worst prognostic feature in mesothelioma
Sarcomaroidal histology (best is papillary mesothelioma)
57
Management of mesothelioma
Platinum based chemo and pemetrexed- if progresses then gemcitabine
58
Management of COPD infective exacerbation
Pred 37.5 for 5 days, Augmentin or doxycycline to cover haemophilus, strep and moraxella
59
Long term management of COPD
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
In COPD what interventions shown to improve survival
Smoking
Oxygen if under 55 or under 60 if also PH
61
Main cause of death in COPD
COPD exacerbations- commonest being H influenza
62
Which single action provides best long term benefit in asthma
Long term follow up
63
Most sensitive and most specific tests for asmtha
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
Most common cause of occupational asthma
Isocyanates (in spray paint)
65
How to diagnose occupational asthma
Serial peak flow measurements at work and home
66
Management of mild asthma
Regular ICS/SABA or PRN LABA/ICS (SABA alone discouraged now)
67
Lines of management of severe asthma, inc add on therapies
```
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
Diagnostic criteria for CF diagnosis
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
When else does CFTR dysfunction occur
ABPA, chronic rhinosinutis, obstructive azoospermia
70
Commonest features of CF
Commonest is sinusitis, then make inferlity due to absent vas deferens
71
Managing acute infective exacerbation of CF
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
Long term management of CF
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
Main cause of death in CF
Resp failure
Then DIOS (distal intestinal obstruction syndrome)
74
Presentation of AERDS
Chronic rhinosinusitis, polyps, anosmia, eosinophilic. Can be caused by paracetamol too as inhibits COX
75
Management of AERD
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
Causes of bronchiectasis
40% idiopathic
Post infectious, CVID/selective IgA deficiency, COPD, PCD, asthma
77
Long term management steps in bronchiectasis
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
What did using erythromycin for prevention do in bronchiectasis
Reduced H influenza but increased pseudomonas
79
Management of mild-moderate exacerbation of bronchiectasis
AugDF or doxycycline empirically
If culture shows pseudomonas, cipro
For all else continue AugDF
80
Management of severe bronchiectasis exacerbation
Empirically with piptaz OR ceftazadime +/- tobramycin
Then if H influenza or pseudomonas cultured-cont taz. If strep- benpen . If H influenza- ampicillin.
81
What’s the commonest colonised pathogen in bronchiectasis, I like CF
Haemophilus influenza
82
If routine MCS shows pseudomonas, course of action
Fluroquinolones (cipro) for 2 weeks then beta lactams and then inhaled antibiotics for total 3 months
83
CT findings in ABPA
Upper lobe ground glass opacity, cylindrical bronchiectasis, atelactasis
84
Diagnostic criteria for ABPA
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
Management of ABPA exacerbation
Pred and wean over 3 moths
86
Long term management of ABPA
Giving long term abx doesn’t prevent infection and can increase invasive aspergillus
If steroid dependent- itraconazole used (omalizumab May be useful too)
87
RHC findings of Group 1 PAH
| and examples of this group
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
Role of endothelin in Group 1 PAH
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
5 group of agents and examples of them used for Idiopthic IPF
Which have survival benefits
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
ILD can be radiologically divided into UIP or NSIP. List examples AND radiological patterns of both
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
What radiological category does hypersensitivity pneumonitis fot into
In acute cases- NSIP, in chronic UIP!
Egg shelf classification shows silicosis (black lung)
92
Causes of UL fibrosis
CHARTS
| Coal miners pneumoconiosis, hypersensitivity pneumonitis, ankylosing spondylitis, Radiation, TB, Silicosis/Sarcoidosis
93
Causes of LL fibrosis
ACID
| Asbestosis, CT diseases (except AS), IPF, drugs (bleomycin, amiodarone, MTX)
94
Treatment of IPF and their SE
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
IPF exacerbation management
Steroids
96
NSIP management
Steroids wean over 6 months , steroid sparing agents, lung transplant
97
Stages of sarcoidosis
Stage 1= bilateral Hilary lymphadenopathy, stage 2= BHL + infiltrates
Stage 3= infiltrates
Stage 4= fibrosis
98
Diagnosis of sarcoidosis
Tissue diagnosis needed l, unless Lofgren
Endobrobchial USS guided trans bronchial needle aspiration has highest yield
99
Management of sarcoidosis
Most don’t need treatment
| If symptomatic pulmonary disease, cardiac or neurological disease or symptomatic hypercalcelia= steroids
100
What’re the sarcoidosis syndromes/types
Lofgrens = acute, bilateral Hilary lymphadenopathy, erythema nodosum, fever, polyarthralgia. Carries except prognosis
Hearfordt = parotid enlargement, fever, uveitis
Mikulicz = enlarged parotid, lacrimal glands
101
What’s most diagnostic of obesity hypoventilation
PaCO2 >45 when awake
102
Describe management alogorithm for primary pneumothorax
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
Management alogorithm for secondary pneumothorax
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
MAnatement of iotrogenic
If no COPD etc, observe alone, majority resolve on their own and recurrence very rare
105
Risk of over drainage of pneumothorax
Re-expansion pulmonary edema (RPE)
106
Describe Fleischner society rules for lung mass
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
Triad of symptoms in fat embolism
| When does it present
Mostly due to long bone and pelvic fractures 1-3 days post the fractures- hypoxemia, petechial rash, neurological abnormalities , ARDS picture.
108
Outside of NIV, which device provides the highest Fi02
Non rebreather mask (95%)
109
List the 4 commonest causes of polycythemia and state what happens to RBC mass, plasma volume and EPO with them
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
What’re the prognostic indicators in parapnuemonic infections
Serum urea, age, pleural fluid appearance and serum albumin
111
Lights criteria needed to meet to say exudate
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
What’s the most sensitive marker for transudate
Pleural:serum albumin <0.6
113
Management of pleural infections
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
Describe LAM (lymphangioleiomyomatosis)
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
Describe pulmonary alveolar proteinosis
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
What’re the 3 options for prevention of PJP post lung transplant
Bactrim (also gives prophylaxis to toxo), dapsone (causes MetHb), pethidine nebs
117
NIV vs CPAP
What settings to start NIV
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
How to calculate expected HCO3
24+ (PaCO2-40)/10
119
Diagnosis of central, pleural, peripheral and peribronchoal lesions
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
Which lung cancer most likely to cause cavitation lesion
Squamous cell
121
Describe pulmonary langerhans cell histiocytosis (PLCH)
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
How to investigate for contact allergy
Patch test
123
Most sensitive test for atopic dermatitis
Serum IgE
124
Approach to unconvincing antibiotic allergy patient
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
Does desensitisation work in opidoid, red man syndrome, contrast allergies
No because all these are anaphylactaoid (where last cell degranulation occurs without IgE cross linking) thus no specific IgE
126
Type of hypersensitivity caused by latex
Commonest is type 4 contact dermatitis
| IgE mediated can also occur
127
Difference between the two types of angioedemas
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
What’re the three types of HAE and how to manage them
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
CSF finding in narcolepsy
Low hypocretin
130
Narcolepsy diagnostic criteria
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
Management of narcolepsy (and cataplexy)
Narcolepsy= modafinil or amphetamines
| Venlafaxine and SSRI and sodium icy are prevent cataplexy
132
Management of central sleep apnoea
Adaptive seroventilation BUT CANNOT use of CCF as increases mortality
133
What is REM sleep behaviour disorder and 1st line treatment
It’s parasomnia with dream enactment after losing REM sleep Antonia
Mostly in LBD, Parkinson’s
Management- high dose melatonin
134
Common cause of periodic limb movement disorder
Iron deficiency as iron is cofactors for dopamine
135
Definition of OSA
AHI over 15 or over 5 and symptoms
136
Cause of tiredness and CVS risk in OSA
Tired due to repeated arousals
| CVS risk due to desaturation
137
Benefits of CPAP in OSA
Improves BP, sleepiness, depression and erectile dysfunction (May reduce stroke)
Most importantly reduces MVAs
138
RFs for OSA
Obesity, macroglossia (amyloidosis, hypothyroidism, acromegaly), Marfan, large tonsils
