respiratory Flashcards
(240 cards)
1
Q
opiate overdose casues what to blood gas
A
respiratory acidosis
2
Q
PE can casue what to blood gas
A
respiratory alkalosis- have low paO2 as well (unlike hyperventilation have norm,al or rasied PaO2)
3
Q
what causes of respiratory alkalosis
A
PE
anxiety induced hyperventiulation
CNS disorderes= stroke, encephalitis, subarachnoid haemorrhage
altitude
pregnancy
salicylate poisoning (initial stages)
4
Q
what causes respiratory acidosis
A
obesity hypoventilation syndrome
life threatening asthma (decompensated)
COPD - high co2
opiate overdose
benzodiazepines overdose
neuromuscular disease
5
Q
whats the effects of salicylate overdose
A
salicylate overdose leads to a mixed respiratory alkalosis and metabolic acidosis. Early stimulation of the respiratory centre leads to a respiratory alkalosis whilst later the direct acid effects of salicylates (combined with acute renal failure) may lead to an acidosis
6
Q
whats the pathophysiology of salicylate overdose
A
In mild toxicity, salicylates directly irritate the gastric lining. They can also cause ototoxicity through a multifactorial process, involving reduced cochlear blood flow secondary to vasoconstriction and changes to cochlear cells.
In higher doses, the pharmacodynamics of salicylate poisoning leads to a mixed respiratory alkalosis and metabolic acidosis. In moderate/severe toxicity, salicylates stimulate the cerebral medulla, leading to hyperventilation and respiratory alkalosis.
Metabolisation of salicylates then causes uncoupling of oxidative phosphorylation, resulting in anaerobic metabolism. This causes heat production and pyrexia and increased lactic acid production, resulting in metabolic acidosis. The acidic effects of salicylates also contribute to the associated acidosis. Hyperventilation then worsens in response to the acidosis until the body can no longer compensate.
7
Q
whats the signs and symptoms of a chest infection
A
sob
fatigue
fever
cough/productive
crackles on auscultation
8
Q
whats the cuases of chest infection
A
streptococcus pneumoniae = most common
haemophilus influenzae
moraxella catarrhalis = immunocompromised/chronic lung disease
psudomonas aerguinsoa = CF/ bronchiectasis
staphylcoccus aureus = CF
atypical:
legionella pneumophila
chlamydia psittaci
mycoplasma pneumonia
chlamydia pneumonia
Q fever
9
Q
whats the antibiotic of choice for chest infection
A
community = amoxicillin
or
doxycyline
or erythromycin or clarithromycin
10
Q
what usually causes aPE
A
usually due to a dvt embolised
11
Q
what risk factors for pe
A
recent surgery
imbolised
long haul flight
pregnacy
med involving oestrogen
cancer
polycythemia
thrombphilia
sle
12
Q
what can you do for VTE prophylaxis
A
asses all pt admitted
LMWH- enoxaparin
antiembolic compression stokings
13
Q
when are LMWH contradinicated
A
active bleeding
existing anticoagulant - warfarin doac
14
Q
when are compression stockings contrainidcated
A
significant peripheral arterial disease
15
Q
differentals of PE
A
MI
CAS
unstable angina
pneumonia
pneumothroax
acute exaserbation of asthma, copd
acute congestive heart failure
disecting/rupture of aortic anyeursm
acute bronchitits
pericardititS
GORD
any casue of collapse
16
Q
presentation of PE
A
pleuritc chest pain
sob
cough with or without blood
hypoxia
tachycardia
tachypnoea
low grade fever
haemodynamiccaly unstable causing low bp
may have s and s of DVT= unilateral leg swelling and tenderness
17
Q
pleurtic chest pains
sob
cough
what could this be
A
PE
other differnetials:
MI
CAS
unstable angina
pneumonia
pneumothroax
acute exaserbation of asthma, copd
acute congestive heart failure
disecting/rupture of aortic anyeursm
acute bronchitits
pericardititS
GORD
any casue of collapse
18
Q
investigations for PE
A
wells score first
if score says likely pe= CTPA = if allergic to contrast or renal impairment do VQscan
if score says unlineky= d dimer and if positive do ctpa
can do cxr to exlcude other casues of symptoms
19
Q
when would you not do a ctpa and what to use instead
A
ctpa require contrast
if renal impairmeent
contrast allergy
at risk from radiation
do vq scan= see mismatch= have well ventialted but not well perfused around area of pe
20
Q
cause of respiratory alklalosis
A
pe= also have low pO2 - due to increase resp rate blowing off loads co2
hyperventialtion- have normal pO2
21
Q
when will a d dimer be postive
A
pe - DVT
prengancy
cancer
surgery
pneumonia
heart failure
22
Q
management of PE
A
supportive- analgesia, oxygen admit to hos[, monitor
intially give LMWH- enoxaparin/ dalteparin straight away before confriming diagnois if delay in the ctpa
long term anticoagulatn:
once diagnosed then need to either be on warfarin, doac or lmwh
warfarin: want inr 2-3
when switching from lwmh continue lmwh for 5 days or when inr 2-3 for 24 hrs (one takes longest)
or go on a doac that doesnt need monitorting = apixaban, rivaroxaban, dabigatran
or be on LMWH
stay on the anticoagulation for:
3 moths if cause is clear and reversible casue then review
or
more than 3 months if cause is unclear or ig cause isnt reversible or recurrent vte = usually 6 months
or
6 moths if active cancer then review
thrombolysis is massive PE with haemodyamic compromise = fibrinolytic medds = streptokinase, alteplase, tenecteplase
by iv cannula or catheter direct thrombosis
23
Q
When is lmwh first line for long term coagulation for PE
A
pregfancy or cancer
24
Q
whats enoxaparin and dalteparin
A
LMWH
25
whats apixaban , dabigatran, rivaroxaban
DOAC
26
whtas sarcoidosis
graulomatous inflammatory condition
27
presentation of sarcoidosis / organs it affects and how
typically involves chest symtpoms
young adults and 60s
woemn and black more
dry cough, fever and erythema nodosum eg. on shins most common presetation
restrictive pattern of lung fuction
lungs: 90%
pulmonary fibrosis
pulmonary nodules
mediastinal lymohadenopathy
systemic:
fever
weight loss
fatigue
skin: 15%
erythema nodosum
lupus pernio
granulomas can develop in scar tissue
heart:
heart block
bundle branch block
myocardial muscle involvement
cns:
nodules
pituitary involvemnt: diabetes insipidus
encephalopathy
pns:
bells palsy
mononeuritits multiplex
kidneys:
kidney stones= due to ince ca
nephrocalcinosis
interstitial nephritis
liver:20%
liver nodules
liver cirrhopsis
cholestasis
eyes: 20%
uveitis
conjunctivivtis
optic neuritits
bones:
arthritis
arthlagia
myopathy
28
erythema nodosum
polyarthralgia
bilateral mediastinal lymohadenopathy
what is this
lofgrens syndrome = triad of symtpoms
specific presentation of sarcoidosis
29
differentials for sarcoidosis
tb
lymphoma
hypersensitivity pneumonitits
HIV
toxoplasmosis
histoplasmosis
30
investigations for sarcoidosis
bloods:rasied serum ACE= screening test
raised ca
rasied serum soluble interleukin 2 receptor
rasied crp
raised immunglobulins
imagina:
cxr= hilar lymphadenopathy
high reoslution ct of thorax= hilar lymphadenopahty and pulmonary nodules
mri= may show cns involvmennt
pet scan = may show active inflammation in affected areas
hsitology= gold standard of diagnosis = bronchoscopy with ultra sound guided biopsy of mediastinal lymph nodes
= shows non caseating granulomas with epithelioid cells
others to see other organs ivlved=
u and e
lft
opthalmology
ecg, echo
acr - see if proteinuria - nephritits
us of abdo
31
screening test for sarcoidosis
serum ACE - rasied in sarcoidosis
32
definititve diagnosis of sarcoidosis
histology-
bronchoscopy with us guided biopsy of mediastinal lymph nodesshows non-caseating granulomas with epitheloid cells
33
treatment for mild/ no symotoks sarcoidoss
nothing
spontaneously resolve 6 months
34
treatment for symptoms of sarcoidosis
frist line: steroids 6-24 months with bisphosphonates to protect agaisnt osteoporosis
2nd line= methotraxate/ axathioprine
lung trasnplant if sevre
35
risk factors for sleep apnoea
obesity
smoking
males
middle age
alcohol
36
features of sleep apnoea
key feature is day time sleepiness
apnoea episides during sleep= reported by partner = not breathing for max mins during sleep
snoring
morning headache
waking up unrefreshed
concentration problems
reduced o sats during sleep
severe cases cuase hypertension and heart failure and increase risk of mi and stroke
37
management for obstructive sleep apnoea
initaly make sure know what occupation is = if requires fully alrt then need urgent referal ad amend work day duties till assesment
frist = refer to ent or sleep specialist
correct reversible factors= stop smoking, no alcohol, loose weight
second= cpap
sevre cases surgery to reconstruct soft palate and jaw= most common one is uvulopalatopharyngoplasty
38
whtas sleep apnoea
due to collapse of pahryngeal airway during sleep
39
pulmonary hypertension casues strain on which side of heart
right side of heart
40
causes of pulmonary hypertension
1- primary pulmonary hy/ connective tissue disease- sle
2- left heart fdailure due to MI / systemic hypertension
3- chronic lung disease- copd
4- pulmonary vascualr disease= PE
5- miscallaneous stuff- sarcoidosis, glycogen storage disorders, haematoglogical disorders
41
presentation of pulmoanry ht
sob
peripheral oedema
syncope
tachycardia
rasied jvp
hepatomegaly
42
investigations for pulmonary ht
ecg
chest x ray
NT- proBNP
echo
43
right ventricular hypertrophy
may occur when and what ecg changes show this
pulmoarny hypertension
large R wave in V1-V3= right chest leads
large S waves in V4-V6= left chest leads
right axis deviation
right bundle branch block
44
chest xray show in pulmoanry ht
dilated pulmonary arteries
right ventricular hypertrophy
45
whats the management for primary pulmoary ht
iv prostanoids = epoprostenol
endothelin receptor antagonist = macitentan
phosphodiesterase 5 inhibitor= sildenafil
46
treamtent for secondary pulmoanry ht
treat underlying cause eg pe, sle
supportive treatment for complcations too
47
what complciations are there of pulmoanry ht
heart failur
arythmias
resp failure
48
whats a pleural effusion
collection of fluid in the pleural cavity
49
whats exudative and whats transudative
exudative= high in protein- more then 3gtransudative= low in protien- less than 3
50
causes of pleural effusion thats exudative
related to inflammation
pneumonia
lung cancer
TB
rheumatoid arthritits
51
causes of pleural effusion thats transudative
related to fluid shift
congestive heart failure
hypoalbuminaemia
hypothryoidism
meigs syndrome = right sided pleural effusion and ovarian maligancy
52
whats right sided pleural effusion with ovarian malignacy
meigs sundrome
53
presentation of pleural effusion
sob
dullness to percussion over effusion
reduced breath sounnds over effusion
tracheal deviaiotion if bad
54
investigfation for pleural effusion
chest xray
sample fluids= aspiration / chest drain
55
what does pleural effusion look like on cxr
blunting of costophrenic angle
meniscus sign
deviation of trachea and mediastinum in massvie effusion
fluid in lung fissure
56
what look for in pleural effusio naspirationsample
protein count
cell count
pH
glucose
lactate dehydrogenase = LDH
microbio testing
57
treatment for pleural effusio n
if small then conservativr = trwt underlying cause if larger the aspiration, cehst drain
aspiration temporay relieves pressure but they can recur
chest drain= prevent reccurence
58
whats empyema
infected pleural effusion
59
penummonia is improving but pt has ew or ongoing fever
what is this
empyema
60
aspiration of fluid in pleural cavity if pt has empyema shpws what
pus
acidic ph
low glcuose
high LDH
61
treamtent of empyema
chest drain to remove pus
antibitocs
62
whats pneumothorax
air in pleural space = seperates lung from chest wall
63
causes of pneumothroax
iatrogenci - lung biopsy, mechanical ventilation , central line insertion
spontaneous
lung pathology- infection, astha, copd
64
presentation of pneumothroax
sudden sob
pleuritc pain - can radiate
cyanosiis
ipislateral reduced breath sounds
ipsilateral hyperresonance on percussion and hyperinflation
65
typical person to present with pneumothorax
tall young thin male presenting with breathlessness and pleuritic chest pain possibly while playing sport
66
investigations for pneumothorax
cxr
bloods
consider ct chest if too small to see on cxr
67
what does no lung markings show on cxr
pneumothroax
also measure the size of lung edge to iside chest wall at level of hilum
68
management of penumothorax
no sob
and less than 2cm of air on cxr = no treatment and will resolve, folow up in 2-4 weeks
if sob and or more than 2cm air = aspiration and reasess
if aspiration fails 2 times chest drain
if unstable / bilateral / secondary oneumothroax then chest drain
69
where chest drain go
triangle of safety
5th intercostal spacce mid axillarly line and anterior axillary line
needle above rib to avoid neurovascular bundle at bottom of ribcxr to cehck in postion after inserttion
70
whats tnesions pneumothroax and cause
trauma to chest wall creating a one way valve
air comes in each breath but non can go out so increase pressure each breath psushes mediastium across= kinks big vessels and causes cardiorespiratior arrest
71
signs of tension pneumothroax
tracheal deviation away from pneumothroax= air pushing it away
decreased air entry in affected side
increase respnance on percussion on affected side
tachycarida
hypotension
72
management of tension oneumothorax
insert a large bore cannula in secind intercostal space in midclavicular line
then once pressure relieved insert chest drain
73
whats sarcoidosis
74
whats pneumonia
infection of lung tissue
casues inflammation of lung tissue and produciton of sputum that fills airways and alveoli
75
presentation of pneumonia
sob
cough - producitve
haemoptysis
fever
pleuritic chest pain- inspiratory pain
delerium
sepsis
bronchial breath sounds - harsh breath sounds in and out due to consolidation
focal course crackles
dullness to percussion- consolidation/lung tissue collapse
76
signs of sepsis secondary to pneumoni a
fver
confusion
tachycardia
tachypnoea
hhypoxia
hypotension
77
how to asses severity of pneumonia
CURB 65
dont use urea in cap
confusion
urea over 7
resp rate 30 or over
bp systolic under 90 or diastolic 60 or less
65 or over
if 2 or more then consider hosp admission
78
casues of pneumonia - common ones
streptoccus pneumonia - most common cap in healthy
haemophilus influenxa- also v common casue cap in healthy
moraxella aeurginsoa = immunocompromised/ chronic lung condition
pseudomonas aeurginosa = CF/brocnhiectasis = common hap casue
staphylcoccus aureus = cf and durg users - needles
79
casues of penumonia atypical
atypical- not treated by pencillins wont work
legions of pscitatti mcq
legionella pneumophila = infected water/ac - think if been on holiday
casues hyponatraemia due to casuing SIADH
mycoplasma pneumoniae = rash- eythmeatous multiform- pink ring with pale centre - children can get neuro symtpoms
chlamydophila pneumoniae= mild to moderate pneumonia - school age - chronic pneumonia and wheeze
coxiella burnetti- Q fever = exposrue to animals and their bodily fluids
chlamydia psittaci = contact with infected birds
80
farmer got sob and productive cough and fever casue ?
Q fever= coxiella burneti
causes pneumonia
exposure to animals and their bodily fluids
81
man has fever and productive cough and pleuritic chest pain
owns a bird
chlymaydia psittaci
= contact with infected birds
82
fungal casue of pneumonia that seen in immunoscompromised pts. esp those with new hiv/ low cd4 count
PCP= pneumocystis jiroveci
83
investigfations for pneumonia
if crb 65 is 0-1 no need
if in hosp do
cxr= see consolidaiton
fbc- raised wbc
u and e - urea
crp- rasied
if moderate to severe also do:
sputum culture
blood culuture
legionella and pneumococccal urinary antigens
if immunocomprosied may not have raised inflammatory markers as they may not ahve any inflammatory response
84
treatment of pneumonia if atypical casue
macrolides(clarithromycin)
or fluroquines (levofloxacin)
or tetracyclines (doxycycline)
85
treatment for pcp
co-triomoxazole
86
patient siwth low cd4 are prescribed what to protect agaisnt pcp
oral co-triomoxazole as prophylaxis
87
treament for pneumonia if mild cap
5 day course- amoxicillin/ macrolide = oral
88
treatment dor mod-severe cap
7-days course- amoxicillin and macrolide
89
complications of pneumonia
sepsis
empyema
pleural effusion
lung absess
death
90
whats fev1
forced expiration volume in one second
measures how easily air can flow luot of lungs
91
FEV1 is low means
obstructive
air struggling to flow out
92
whats fvc
forced vital capaicty
total maount of air can be exhaled after full inspiration
measures to total volume of air a person can take into the lungs
93
FVC low means
restrictive - restriction of filling the lungs up
94
FEV1:FVC ratio less than 75%
obstructive
fvc normal but cant blow air out quick cus obstructing but can get air into the lungs and out but its just slow but still has the full capcaity of lungs
95
whats obstrucitve picture in fev1:fvc ratio
less than 75%
96
how to see if ashtma or copd on lung function test
test for reversibility - asthma is copd isnt
give bronchodilator - salbutamol- then do spirometry again
if fev1:fvc improve then asthma
97
if FEV1:FVC ratio is normal / rasied measn
restrictive
they are either both equally reduced so normal or can even be raised becasue the FEV1 can be raied becasue tight lungs so push air out
fvc be reduced becasue cant ge tthe air into the lungs
98
restrictive pattern in spirometry
FEV1:FVC ratio normal or rasied
both are euqally reduced
ott fev1 can be normal / raised
fvc reduced
99
causes of restrictive pattern
anythig that restricts chest wall and lung expansion to draw air in
interstitial lung disease- pulmonary fibrosis
sarcoidosis
scoliosis
obesity
MND
100
whats peak flow and how to use and when to use
= fastest point (peak) of a persons expiratory flow of air
use to see obstrutive lung disease and esp how asthma controlled - obstructive air can fill all lungs but does so slowliy in and out
it demonstrates how much obstruction there is to the outflow in pts lungs
stand tall
from good tight seal
deep breath in
blow fast and hard as can
x3 and take best number
compare what shuld be of sex age ehight etc
and gives perceetnage of predicted
101
whats asthma
reverisble airway obstruciton
102
pathology of ashtma
chronic inflammatory condtion that causes episodic exaserbations of bronchoconstction
inflammation casues excess mucus secretion = cough and further blockage
constriction casued by hypersensitivity and can be triggered by enviromental factors
103
trigers of ashtma
infection
night and early morning
allergens
cold air
damp/dusty air
animals
exercise
strong emotions
after nsaids, beta blockers
occupational
104
what meds exaserbate asthma
nsaids
beta blockers
105
presentation of asthma
episodic
diurnal variability - worse at night
cough with wheeze and sob
hx of atopy- eczema, hayfever, food allergy
fam hist
bilateral widespread polyphonic wheeze
106
diangosis nice of asthma
do investigations before treatment
1st line= FeNO - above 40 postive
spiroemtry with bronchodilator reversibilty - improve fev1 by 12 % or more and increase volume by 200ml or more
if uncertain after that:
peak flow - PEFR - 2-4 weeks if 20% variable
direct bronchial challenge test with histamine/ mathacholine
107
managment of asthma according to nice
1= saba = salbutamol/ terbutaline
2= add ICS = beclometasone/ butesonice/ flucticasone/ mometasone
3= add oral leukotriente receptor antagonist = monteleukast
4= add LABA inhaler - only contrinue if good repsonse - review 4-8 weeks = salmeterol
5= consider changing to MART
6= increase ICS dose to medium
7= consider increase ics to high dose/ oral theophylline / inhlaed LAMA
8= refer to specialst
108
what mart options are there and what is mart
fast acting LABA and ICS
use 1/2 in morn and eve and then when needed
fostair= formoterol + beclasmetasone
symbicort = formoterol + budenoside
seretide= salmeterol + fluticasone
109
whats saba and action and options
salbutamol
terbutaline
short acting beta 2 agonsit
relacion of smooth muscle
110
what ics are there and side effects
beclometasone
butsenonide
fluticasone
mometasone
maitence/prevernter - take regualry
se= thrush, hoarse voice, osteoporosis- ensure ca intake and exercise
111
se of saba/laba
tremor- excess use measn not controlled
tachycardia, headaches, hypokaleamia = causes blood potassium to move into cells
112
what laba options are ther
salmeterol
formoterol
113
lama
name and mechanism
tiotropium
blocks ach r
ach - pns activates to casue contraction so blcok this casues bronchodilation
114
leukotriene receptor antagonist
name and mechasnim
monteleukast
leukotrienes are produced by immune system
cause inflammation, bronchoconstriction, mucus secretion
anatagonist so block leukotrienes so block allthis
115
theophylline
action
relax bronchial smooth muscle and reduce inflammation
has a narrow therpaeutic index so needs monitoring blood levels as can then be toxic
monitor after 5 days starting and then after 3 days for each dose change
116
which asthma drug do you need to monitor blood for
theophylline
117
what is a low, med. high ics dose
400micrograms or less = low
400-800 micrograms= med
over 800 high dose
118
theophylline toxicty/ posioning symtoms
vomiting
agitation
restlessness
dialted pupils
sinus tachycardia
hyperglycemia
serious:
haemetemesis
convulsion-seizures
supraventriocular and ventricular aryhtmias
severe hypokalameia
119
presentation of acute asthma
progressively worseing sob
use of accesory msucles
symmetrical wheeze on asucultation
tachypnoea
chest sound tight and reduced air entry
120
what moderate acute asthma attack
pefr 50-75% predicted
121
whats severe acute asthma attack
PEFR 33-75%
or
resp rate more than 25
or
hr over 110
or
unable to complete snetnece
122
whats life threatening acute asthma attack
PEFR less than 33%
or
sats less than 92%
or
tired
or
no wheeze- silent cehst
or
cyanotic
or
haemodynamically unstbale.- low bp
or
confusion
123
abg of person initally acute asthma attack
repsiratory alkalsos- breathing wuick so blow off co2
124
abg of lifethreatening acute asthma attack
normal pco2
/ hypoxia
concerning as patient is then tiring ans not breathing as much
125
abg of near fatal acute ashtma attack
repsiratory acidosis due to high co2 - vvv bad
126
patient has respiratory acidosis in acute asthma attack
how bad is this
near fata
127
pt has normal pco2/ hypoxia in acute astham attack
how bad is this
life threathening
means not brehting much as pt is tiring
128
treatment for acute ashtma attack
if moderate :
nebulsised SABA - salbutamol 5mg and repeat every 30 mins
if no imporvemnt add nebulised ipratroium bromide
give steroids- iv hydrocortisone or oral prednisolone - contiunue for 5 dys
abx if bacterial infection casue
if severe aslo give :
oxygen so sats maintained 94-98%
aminophylline iv - senior dp
consider iv salbutamol
life threatening:
add
iv magensium sulphate - senior
hdu/icu
intubation- need consider early as intubating when severe bronchoconscrition is hard
129
monitor acute asthma attack
o2 sats - below 92% life threatning - aim for 94-98%
resp rate
resp effort
peak flow
chest asucultation
monitor serum potassium as salbutamol can casue hypokalameia as casue k to go into cells
onitor hr as salbutamol will also casue tachycardia
130
pt has pneumonia but no acute exaserbation of copd (no wheeze, no dysponea)
pt has copd
should give steroids??
yes
give steroids to copd pts with pneumonia even if no sign of acute exaserbation
131
gynaecomastia is associated with what lung cacner - paraneoplastic syndrome
adenocarcinoma
132
paraneoplastic syndromes asscoaited with small cell lung cancer
SIADH-> hyponatraemia
ectopic ACTH= cushings syndrome
lambert - eaton myasthenic syndrome - diff walking and muscle tenderness. weakness worsens as use increases
133
FVC and FEV1 in restrictive pattern
both equally reduce so that the ratio is then normal or can be raised becasue the FEV1 can be okish becasue the restricted lngs can push the air out as they restricted anyway
134
obstructive spirometry and casues
FEV1 - significantly reduced - air slow to move out
FVC - reduced or normal
FEV1% (FEV1/FVC) - reduced - less than 0.75 (0.7)
Asthma
COPD
Bronchiectasis
Bronchiolitis obliterans
135
restrictive pattern and casues in spirometry
FEV1 - reduced
FVC - significantly reduced
FEV1% (FEV1/FVC) - normal or increased
Pulmonary fibrosis
Asbestosis
Sarcoidosis
Acute respiratory distress syndrome
Infant respiratory distress syndrome
Kyphoscoliosis e.g. ankylosing spondylitis
Neuromuscular disorders
Severe obesity
136
casue of copd
smoking
air pollution
alpha 1 anti trypsin deficiency
work place dust and fumes
137
pathology of copd
empysema = alveolar walls damaged and so air trapped in them = pink puffers = hyper inflated and barrel cehst as air trapped in them . increased resp rate and purse lips
chronic bronchitits= chronic inflammaation - thick sticky mucus blocks airways and inflammation and swelling makes worse = blue bloaters
138
presentation of copd
wheeze
cough- often productive
recurretn resp infections
barell chest
chronic sob
139
cxr findings and oxamination for copd
barrel chest
bullae may be there in empysema
hyperresonance percussion
140
differentials for copd
lung cancer
fibrosisi
heart failure
asthma- see reversibility
unusual to have haemoptysis, finger and chest pain in copd
no finger clubbing
141
hyper resonance percussion occurs in what
asthmna
severe empysema
pneumothorax
142
how to diangose copd
clinical and spirometry
obstructive picture - FEV1/FVC ratio less than 0.7 (70%)
no dramatic reversibility with b2 agonist
143
whats the severity stages of copd
all have fev1/fvc ratio less than 0.7
stage 1: FEV1 more then 80% predicted
stage 2: FEV1 50-79% predicted
stage 3 : FEV1 30-49% predicted
stage 4: FEV1 less than 30%
144
other investigatins for copd can be done
cxr to rule out other patholgoies
gbc = see if polycythameia (if chronic hypoxic then increase hb) and anemia
bmi
sputum culutre- asses for chronic infection
ecg and echo- asses heart function
ct thorax- lung cancer , fibrosis, bronchiectasis
serum alpha 1 antitrypsin - of deficiency empysema is worse and early onset
TLCO is low in copd (asthma its raised)
145
managemnt of copd
stop smoking
pneumococcal and flu vaccone
stage 1: SABA/SAMA(ipratropium bromide)
stae 2 if no response to steroids or asthma like features) = LABA + LAMA (anoro ellipta, ultrobreehaler, dualar genuair)
stage 2 if athmatic features/response to steroids= LABA + ICS
stage 3= LABA + LAMA + ICS= trimbo/ trelelg elipta
severe:
oral theorphylline
nebulsisers
home oxygen therpay if hypoxic at rest (no smoking though) , polycythamia, cyanosis, heart failure secondary to pulmonary ht= cor pulmonale
prophylactic abx= azithromycin
oral mucolytic= carbocisteine
146
exaserbation of copd
= acute worsening of symptoms
cough
wheeze
spututm
sob
fever
inc rr/ hr
147
most common casue of copd infective exaserbations
haemiphilus influenza
148
investigations for copd exaserbatin
cxr - pneumonia etc
fbc - wbc
abg - see what co2 levels are
ecg - arhtmia and heart strain
u and e check electrolytes
sputum culutre
blood culture if septic
149
treamten tof copd exaerbation
at home:
increase doses / take regular of inhaler/ nebulsier (what normally use)
prednisolone 30mg od for 5 days
abx may be needed= amoxicillin/ doxycylicn / clarithromycin
in hosp:
oygen= venturin mask if retianing co2 keep sats 88-92%
if not retaining co2 then can aim for normal sats of 94-98
nebulised bronchodilators- saba/sama = salbutamol/ipatropium
steroids - 200mg hydrocortison (possibly iv), 30-40mg oral prednisolone
abx
physio
severe:
iv aminophylline
niv
intubation
doxapram if no niv/intubation appropriate
150
how many times pt with copd exaserbations with steroids need consider for prophylaxis for ...
3-4 cases per year of exaserbations using steroids to treat then consider prophylaxis for osteoporisis
151
ABG has high co2 and high bicarb and normal ph
retaing co2 but chronic as kidneys able to compensate
152
pt abg got copd
high co2
relaitvely high bicarb
ph acidodic
copd exaserbation
normally high levels bicarb to compensate for retaining co2 but kidneys cant keep up wth the incerase co2 as acute exaeerbation cant get it out
153
retaining co2 acutely abg
resp acidosis
154
whatrs NIV
alternative to full intubation and ventilation
mid point
full face/tight fitting nasal mask to blow air frocefully into lungs
155
whats BiPAP and when used
bilevle postivie airway pressure
cycle high and low pressure correspondong to breathing in and out
higher pressure inspiration
used in t2 resp faulure- typically copd
ipap= pressure during inspiration
epap= pressure during expiration = less but still some to stop airways collapsing
the pressures are based off body. ass
average male starts ipap= 16-20cm H2O
epap= 4-6cm H2O
then can increase ipap by 2-5cm increments until acodisis is resovled
156
criteria for bipap
respiratory acidosis:
pH less than 7.35
paco2 more than 6
despure adequate med treatment
157
contraindications for bipap
pneumothroax untreated
structural/ patholgy abnormalities affecting face, gi tract and airway
do cxr prior to starting if this can be done
158
when to monitor abg in bipap
1 ahr after ever change
and
every 4 hrs until stable
159
whats cpap and when used
continuous possitive pressure
keeps airways expanded all time so air can travel in and out
uses: in airways prone to collapse
obstructive sleep apnoea
congestive cardiac failure
acute pulmonary oedema
160
whats. interstitial lung disease
conditions that affect the lung parenchyma casuing inflammation and fibrosis= replacment of normal elastic tissue and lung function with scar tissues thats stiff and not function effectviely
161
types of interstital lung disease= fibrosis
idiopathic pulmonary fibrosis
secondary pulmonary fibrosis
asbestosis
cryptogenic organsisng pneumonia
hypersenstivitiy pneumonitit s(extrinsic allergic alvelolitis)
drug induced
can get from infection eg. pneumonia ]can be focal or can be diffuse (extrnisic allergic alveolitits/idiopathic pulmoanry fibrosis)
162
diangsos of pulmonary fibrosis
HRCT- ground glass apperance
and with clinical features
if unclear do lung biopsy
163
managment of pulmoanry fibrosis / interstial lung disease
generally poor progniosis and limited rx
damage is irreveersibl
rmeove andtreat the underlying cause
home o2 if hypoxic at rest
stop smoking
physio and rehab
penumoccoal and flu vaccine
advanced care planning
lung transplant
164
presentation of pulmonary fibrosis
persistant sob and dry cough for over 3 months
50 and over
bibasal fine crackles inspiratory
finger clubbing
can have a restricitve pattern on spirometry
165
whats idiopathic pulmonary fibrosis
progressive pulmonary fibrosis with no clear casue
166
treatment idiopathic oulmonary fibrosis
pirfenidone = anti fibrotic and anti inflammatiory
nintendanib= monocolonal ab targetting tyrosine kinase
167
whats drugs can induce pulmoanry fibrosis
amiodarone
methotrexate
nitrofurantoin
cyclophosphamide
168
what casues are there of secodnary pulmonary fibrosis
rheumatoid arthritis
alpah 1 anti trypsin deficieny
skorgrens syndrome
sle
systemic sclerosis
169
what type of hyersenstivity rxn is hypersenstivity pneumonitits (extrinsic allergic alveolitits)
type 3 hypersentitivty rnx to enviroemntal allergen
170
causes of hypersenstivity pneumonitits (extrinsic allergic alveolitits)
farmers lung= rxn to mouldy spores in hay
bird fanciers lung= rxn to bird droppings
mushroom wokrers lung= rxn to specfic mushroom antigen
malt workers lung = rxn to mould on barley
171
investigatios for hypersenstivity pneumonitits (extrinsic allergic alveolitits)
bronchoalveolar lavage=> increased lymphocytes and mast cells
172
treat hypersenstivity pneumonitits (extrinsic allergic alveolitits)
remove allergen
oxygen and steroids where needed
173
whats cryptogenic organising pneumonia
focal area of inlammation of lung tissue- leads to focal areas of pulmoanry foibrosis
174
cayses of cryptogenic organising pneumonia
idiopathic
triggered by infection
inflamm disorder
radiation
meds
envromental toxins
allergens
175
presentation of cryptogenic organising pneumonia
fevr
sob
cough
lethargy
- like pneumonia
176
cryptogenic organising pneumonia cxr
focal consolidation- look like pneumonia
177
definitive investigation for cryptogenic organising pneumonia
lung biopsy is definitive
178
treamtne tof cryptogenic organising pneumonia
systemic corticosteroids
179
what irritants can casue pulmoanry fibrosis/ interstial lung disease
silica
coal dust
asbestotis
180
whats asbesosis
lung fibrosis related to inhallation of asbetso
181
whats asbestots
fibrogenic and oncogenic
takes decades to develop
182
inhalation of asbestos can casue what probelms
adenocarcinoma
mesothelioma
pulmonary fibrosis
pleural thickening and pleural plaques
pts with heslth conditions reated to exposure (exceptnplaques) can get compensation
183
if pt dies with known asbestos exposure hwat needs be done
refer to coroner
184
whats cystic fibrosis
autosomal recessive condition affecting the mucus glands => thick and stcky
185
what gene is afected in CF and whats most comon mutation
CFTR gene on chr 7
delta F508
186
key consequences of CF
thick pancreatic and bilary secretion=>
blockage of ducts
lack digestive enzymes to get to the system as blocked = pancreatic liipase esp
low volume and thick airway secretions=>
decresed airway celarance-> bacterial colonisation and suseptible to airway infections
congenital bilateral absence of vas deferens =? male infertility- have ehalthy sperm but sperm cant ge tout
187
presentation of cf
normally picked up at birth
meconium ileus = not pass meconium in frst 24 hrs as thick and sticky in cf=, abdo distention and vomiting
recurrent LRTI
failure to thrive
pacnreatitis
chronic cough
thick sputum production
parent says child is salty to kiss
steathorrea- loose ad greasy
nasal polyps
finger clubbing
crackles and wheeze on asucultation
abdo distenition
188
dianosis of CF
most picked up with blood spot testing newborn
sweat test- gold standard- chloride levels over 60mmol/l is positive
genetic test for CFTR gene - amniocentesis, chorionic vilus, bloood test
189
common microbial colonisiers for CF
staphlycoccus aureus -> can give long term prophylaxis flucloxacillin
haemophilus influenza
klebsiella pneumonia
e coli
burkhodhena capacia
psuedomonas aeurginosa- hard to treat and worsesn cf prognosis - avoid cf pts seeing eachother as risk colonsiers passing it on - treat colonisation with long term nebulised abx = tobramycin. oral ciprofloxacin
190
maangemnt of cf
physio
high calorie intake- physio, coughing, malunutrition, increase resp effort, infections
creon- for replacement of lipase if needed
prophylactic flucloxacillin (staph aureus)
treat chest infections
bronchodilators- salbutamol
nebulised DNase= break down resp secretions
nebulsied hypertonic saline
vaccination - pneumoncoccal influenza, varicella
other:
liver tranplant and lung trasnplant in end stage failure
feritlitt rx= sperm extraction
genetic counselling
191
number of carriers of cf
1 in 25
192
both parents are healthy, one sibling has cystic fibrosis and a second child does not have the disease, what is the likelihood of the second child being a carrier?
2 in 3 chances
know they dint have it
and both parents must be carriers so got two xaxA and so dont have xaa cus know they dont have it. left have got xaxA and xaxA and xAxA. so 2 in 3 chance of carrying
193
when to monitor cf patients and monitoring for what
every 6 months
sputum colonsidation for psuedomonas
diabetes
osteporosis
vit d deefciecny
liver failure
194
what can cf patietns develop
90% develop pancreatic insufficnecy
50% cf related diabetes and and require insulin
30% develop liver disease
most males infertile due to absent vas deferens
195
whats bronciectasis
chronic resp disease characterised by permantne t bronchial dialtion due to irreversible damage to broncial wall
196
caues of bronciectasis
previous severe lrti = most common casue
eg. oenumonia, pertussis, pulmonarry tb, mycoplasma, influenza etc
pulmonary disease- copd, asthma= frequent exaserbations
ongenital- CF, primary cilairy dyskinesia , alpha 1 anti tryppsin deficiency - empysema
connetive tissue disease- rhemuatoid arthritis, sle, sarcoidosis
idiopathic- 40%
IBD - more common in UC
197
presnetation of bronchectasis
persitant couch with mucuopurulent sputum - 8 weeks or more
hameotpysis
exertional dynspnoea and gets worse pregresdively so then at rest sob
fatigue
rhinosinututs symptoms - nasal discahrge, obstruction,
histroy of a trigger
weight loss
course crackles esp on lower zones
wheeze
high pitch inspiratory squeaks
large airay rhonci
finger clubbing
198
investigations for bronciectasis
sputum culute - see if colonising pathogen
cxr- may be normal. may see tram lines and ring shadows
spirometry- obstruction
o2 sats
HRCT= broncial dialtion,
test fpr a casue- anti ccp, ana, anca, ige, ciliary dyskinesa, RA etc
crp rasied in acute exaserbation
199
differentiels for brocniectasis - presitant cough with sputum, haemptysis, sob, fatigue, tiger, weight loss, course crackles, wheeze, high putch inspiratory squeak, rhinositits sympotoms
asthma= have diurnal variaiton, history of atopy, bronchodilation reversibility
copd= have decreased breath sounds, no high pitch sqeak, ct may be normal
penumonia- more acute onset, day not months to years
cxr show consolidation
chronic sinusitis= vesicular breath sounds, radiology invetigations normal
200
pathology of bronciectasis
inital insul eg, infection activates immune cells
immune cells reasle cystokines and proteases
inflamamtio casues damage to muscle and elastin casuing dilation
but in bronciectasis this cant be reveresed eg. due to impaired mucociliary clearnace, dysregulated immunuty
dilaition then predisposes to microbial colonisation and then all hapens again so get more and more dialted
201
treatment for bronchestasis
stop smoking
follow up in secindary care if had 3 or more exaserbaions in a year, chronic psudomonas, mrsa, deteroiring,allergic oulpnary aspergillos, asscoatedwith RA, ibd, priamry cilairy dyskinesia, immune deficient
pulmoanry rehab
anual vacines
mucoactie agents- carbocistein/nebulsied saline
long term abx if 3 or more exaserbation in a year= azithromycin 3 /7
bronchodilator- laba
treat underlying condition
long termo2 if sats below 88% on room air
lung resection of localsied
lung trasnplant if under 65 depsite med rx no better
202
complications of broncoectasis
infective exaserbations and chornic colonisation
haemoptysis
pneumothorax
resp failure
cor pulmonale due to pulmonary ht
chest pain
corary heart disease
anxiety and depression
nutirtional deficnect ]fatigue
lung transplant comlications
macrolides (axithromycin) = long QT , tinnutus, hearing loss
203
se of long term use of macrolides - azithromycin which is used in long term abx if 3 or more exaserbation in 1 year of bronciectasis, copd
long QT
tinnitus
hearing loss
204
whats TB
mycobacterium tuberculsos
acid fast baccili that stain red with zihel neelsen staining
205
acid fast baccilli that stain red with ziehl neelsen staining
TB
206
what stating use for TB
zeihl neelsen- stain red
207
disease course of TB
v slow divding and need lots oxygen- hence often in lungs
trasmoission via saliva droplets
spreads through body in blood and lymph
granulomas form containg the baceria
most cases can celar and kill infection
latent tb= immune system encapsulates site of infection to stop progression bt can reactivate
seocndary tb = latent tb reactivated
208
diseminated tb
immune system cant control the disease - severe- mililary TB
209
site of infection of mycobacterium tuberculosis
lungs most common
extrapulmoanry:
bones and joints
cutaneous tb
GI
genitourinary
pleura
CNS
pericardium
210
vaccin for TB
BCG
live atenuated- cehck not got hiv . immunosupressed before giving it
before vaccine do mantoux test and give vaccine if test is negatve
give vaccine:
BCG vaccine is offered to patients that are at higher risk of contact with TB:
Neonates born in areas of the UK with high rates of TB
Neonates with relatives from countries with a high rate of TB
Neonates with a family history of TB
Unvaccinated older children and young adults (< 35) who have close contact with TB
Unvaccinated children or young adults that recently arrived from a country with a high rate of TB
Healthcare workers
211
risk factors tb
known contact with active TB
immirants from area of high rate tb
peoplewith close relative.close contat from countires of hogh rate tb
immunocompreommsied
homeless, drug users, alcoholics
212
presentation TB
fever
chronic gradual worsening of symtoms
most pulmoary tb
lethargey
weight loss
haemoptyisis
cough
lymphadenomapthy
erythema nodosum
spinal pain in spine TB =potts disease
213
investigations TB
mantoux test to see if got tb= used tuberculin into skin, wait 72hrs and if induration 5mm or more postive. then do interferon gamma realease assay to see if active - this test confirms latent tb
ziehle neelsen stain- bright red
cxr
214
see on cxr for primary tb
pathcy consolidation
pleural effusions
hilary lymphadenopathy
215
see on cxr for reactivated tb
patchy / nodular consolidation with cavitations esp inthe upper zones
216
see on cxr in diseminated TB
millet seeds throughput lung fields
217
managment of latent tb
if ehalthy do nothing
if at risk of reactivation (immuncompsormised etc)
:
rifampacin and isonazid = 3 months
or
isonazid 6 months
218
managemnt of acute pulmoaryTB
ripe
rifampacin 6 months
isonazid 6 months
pyrazinamide 2 months
ethambutol 2 months
test for other disease- hiv, hep b and c
contact test tb
notify public health
isolate for 2 weeks once started rx
extrapulmoarny disease= corticosteroids
219
se of rifampacin
hepatoxocity
red/ orange disolcouration of secretion- tears and urine
induced cyp450 enxyme so drugs metabolsied by this less effective- COCP
(red and orange pissin)
220
se of isonazid
peripheral neuropathy
hepatoxicity
(im so numb a szid)
221
isonazid what other med take too
pyrixodine - b6 to prevent peripheral neuropahty
222
pyrazinamide se
hepatoxicity
hyperuricaemia = gout
223
se ethambutol
colour blindess adn reduced visual acuity
(eye thambutol)
224
which tb meds can casue hepatoxocitiy
rip
rifampacin
isonazid
pyrazinamide
225
tb rx
orange urine and red tears
which meds causes
rifamacin
226
tb rx
difficulty recognising coliurs
which med
ethambutol
227
tb rx
painful elbows
whioch med
pyrazinamide
casues hyperuricaemia - gout
228
tb rx
feels numbness in toes and unusual sensation
ned casues
isoniazid
229
arterial blood gas
first look at what
oxygen
PaO2= are they hypoxic - if hypoxic then respiratory failure
then look at FiO2- fraction of inhaled 02
room air= 21%
venturi mask can control FiO2
pther masks can only give approximate FiO2
230
types of resp failure
type 1= normal CO2, low O2
type 2- rasied CO2, low O2
231
once looked at co2 and oxygen look at what
pH
acidoitic, alkaltoic or noral
full compensation? partial compensation?
eg. COPD have full metabolic compensation chronic high CO2 and so kidneys have tome and make bicarb high so balance sout the high co2
232
repsiratory acidosis whats this
high PaCO2
low pH high CO2
acutely retaining co2- unable to blow it off
233
where bicarb come from
produced by kidneys
take time to be produced
if bicarb high then chirnically retaitning CO2 (if the co2 is high this is)
eh. copd
acute resp acidosis the bicarb be low cus isnt fast enough to keep up with rising co2
234
acute exaserbation COPD ABG
acidotic
rasied CO2
raised bicarb
- kidneys cant keep up. norally the bicarb is rasied to compensate for the high co2 but now the co2 risijg too fast in the exaserbation so acidotic despite higher bicarb than normal
235
respiratory alkalsosi
rasied resp rate- blowing off too much CO2
high pH
low PaCO2
236
casues of resp alklasosis
hyperventialtion
PE
237
high pH
low PaCO2
normal/ high O2
hyperventilation
resp alklaisis with normal / high o2
= hyperventialtion
238
high oH
low PaCO2
low PaO2
PE
resp alkalosis with low po2= PE
239
metabolic acidosis causes
low pH
low bicarb
casues:
rasied lactate- anerobic resp= tissue hypoxia - damge
raised ketones= DKA
increased H ions = renal failure (cant excrete them), type 1 renal tubular necorisis, rhambomyolysisi (casues aki cus myoglobuin )
reduced bicarb= renal fialure, diarhoea (stool contains bicarb), type 2 acute tubular necorisis
240
metbaolic alkalsosis casues
hgih pH
high bicarb
casues:
loss H ions = Gi tract (vomiting)
loose H ions from kidneys= too much aldosterone (aldosterone enoucarges excretion h ions and k ions and reabsorbtion na and water)
high aldosterone=
heart failure (trying inc bp cus heart not pumping enough around so inc Bp by inc aldosterone)
conns synrome = priamry hyperaldosteronism
liver cirrhosis
loop diruetic
thiazide diuretics
