Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CBL Year 2 > Breathlessness > Flashcards

Breathlessness Flashcards

1
Q

What is hypoxaemia? also known as hypoxic hypoxia

A

abnormally low arterial partial pressure of oxygen

it is associated with clinical sign of central cyanosis

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

what is hypoxia

A

defined as low tissue partial pressure of oxygen either due to a reduction of the supply of oxygen or the inability to use it

results in organ/tissue dysfunction and even cell death

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

What is the difference between PAO2 and PaO2?

how do you measure them?

A

A: alveolar oxygen pressure
a: arterial oxygen pressure
A: calculated using alveolar gas equation
a: measured by performing an arterial blood gas analysis

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

PAO2 - PaO2 difference in normal individuals

A

healthy young adults about 2kPa

elderly about 5kPa

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

5 causes of hypoxaemia explained

mechanism, notes, PaO2, Aa difference, does O2 help?

A

1) Mechanism: high altitude (climbing Everest)
Notes: fall in barometric pressure leads to an increase inspired O2 tension (PIO2) and PAO2
PaO2: decreases
Aa difference: normal
does O2 help?:yes

2) mechanism : hypoventilation (e.g. opioid overdose)
notes: decreased alveolar ventilation “pump failure” leads to a decrease in PAO2 and an increase in PACO2
PaO2: decreased
Aa difference: normal
does O2 help? yes

3) mechanism: diffusion defect (e.g. fibrosis)
notes: leads to a decrease in PaO2
PaO2: decreases
Aa difference: increased
does O2 help: yes

4) mechanism: V/Q mismatch (e.g. PE)
notes: leads to a decrease in PaO2, PACO2 is low or normal
PaO2: decreases
Aa difference: increased
does O2 help: yes

5)mechanism: right to left cardiac shunt (e.g.congenital cyanotic heart disease
notes: hunted blood bypasses the alveoli and cannot be oxygenated resulting in a very low PaO2
PaO2: decreases
Aa difference: increased
Does O2 help? limited effect, only upon non-shunted blood

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

when should you suspect hypoxia

A 
anxiety
euphoria
confusion/poor judgement/ irritability
lack of coordination
tachypnoea, use of accessory muscles
tunnel-vision
loss of consciousness, coma
seizures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

alveolar ventilation equation

A

VA= R(VT-VD) where R is respiratory rate, VT is tidal volume, and VD is dead space volume.

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

clinical features of type II respiratory failure

A

vary according to underlying cause
headache (cerebral vasodilation)
flapping tremor of the wrist
Bounding pulse

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

Describe a negative feedback loop for acidaemia, hypercapnia and hypoxia

A

those are the stimuli
the receptors are central and peripheral chemoreceptors
the control centre is located in the brainstem, medulla oblongata
the effectors are muscles of the respiratory system that pump to either increase or decrease alveolar ventilation

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

Describe the MRC Dyspnoea scale

A

grade 1 - not troubled by breathlessness except on strenuous exercise
grade 2 - short of breath on hurrying or walking up a slight hill
grade 3 - walks slower than others on level ground, or has to stop for breath when walking at own pace
grade 4 - stops for breath after 100m or after a few mins on level ground
grade 5 - too breathless to leave house, or breathless when dressing/undressing

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

what is stridor

A

high-pitched, wheezing sound caused by disrupted airflow. Stridor may also be called musical breathing or extrathoracic airway obstruction.

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

different types of stridor

A

inspiratory stridor: only hear it when breathing in - indicates an issue with the tissue above the vocal chords

expiratory stridor: only hear it when breathing out - indicates a blockage in the windpipe

biphasic stridor: causes abnormal sound when they breathe in and out - caused by narrowing of cartilage near the vocal chords

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what causes stridor in adults

A 
object blocking airway
swelling in throat or upper airway
bronchitis 
tonsilitis
tracheal stenosis
tumors
etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what causes a wheeze

A

happens when the airways are tightened, blocked, or inflamed, making a person’s breathing sound like whistling or squeaking. Common causes include a cold, asthma, allergies, or more serious conditions, such as chronic obstructive pulmonary disease (COPD).

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

basic description of a pneumothorax

A

is a collapsed lung. A pneumothorax occurs when air leaks into the space between your lung and chest wall. This air pushes on the outside of your lung and makes it collapse. A pneumothorax can be a complete lung collapse or a collapse of only a portion of the lung.

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

causes of a pneumothorax

A

chest injury - blunt or penetrating trauma
lung disease - diseased lungs are more likely to collapse
ruptured air blisters (called blebs) when they burst they allow air to seep into space between lungs and lining causing a pneumothorax (associated with tall underweight people)
mechanical ventilation - when a ventilation device causes an imbalance of air pressure within the chest (very serious)

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

difference between pneumothorax and tension pneumothorax

A

both is air between the parietal and visceral pleura

difference is in a tension pneumo there is a mediastinal shift

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

briefly describe cardiac tamponade

A

happens when extra fluid builds up around the space of the heart - fluid puts pressure on the heart and prevents it from pumping properly

(A fibrous sac called the pericardium surrounds the heart. This sac is made up of 2 thin layers. Normally, a small amount of fluid if found between the 2 layers. The fluid prevents friction between the layers when they move as the heart beats. In some cases, extra fluid can build up abnormally between these 2 layers. If too much fluid builds up, the extra fluid can make it hard for the heart to expand normally. Because of the extra pressure, less blood enters the heart from the body. This can reduce the amount of oxygen-rich blood going out to the body.

If the fluid builds up around the heart too quickly, it can lead to short-term (acute) cardiac tamponade. It’s life-threatening if not treated right away. Another type of cardiac tamponade (subacute) can happen when the fluid builds up more slowly. This is also life-threatening.)

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

describe carbon monoxide poisoning

A

Carbon monoxide poisoning occurs when carbon monoxide builds up in your bloodstream. When too much carbon monoxide is in the air, your body replaces the oxygen in your red blood cells with carbon monoxide. This can lead to serious tissue damage, or even death.

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

deadly forms of cyanide

A

sodium cyanide
potassium cyanide
hydrogen cyanide
cyanogen chloride

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

different ways to classify HF

A 
acute vs chronic
left vs right
systolic vs diastolic
forward vs backward
low output vs high output
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

HF definition

A

an inability of the heart to maintain an adequate perfusion of the tissues (cardiac output) at a normal filling pressure (CVP/JVP)
it is not a diagnosis
it is a syndrome of signs and symptoms that may be caused by a variety of pathological conditions

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

difference between chronic HF and hypovolaemic shock

blood volume, JVP, Pulse rate, BP, CO, TPR, timing, immediate danger to life?

A 
Blood volume: HF ↑, hypo ↓
JVP: HF↑, Hypo↓
Pulse rate: HF⇔, hypo ↑
BP: HF↑or⇔, hypo↓
CO: HF↓, hypo↓
TPR: HF↑, hypo↑↑
timing: HF chronic, Hypo acute
Immediate danger to life: HF no, hypo yes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

pathophysiology of chronic left sided heart failure

A

systolic dysfunction: impaired emptying due to reduced contractility or/and increased after load

diastolic dysfunction: impaired ventricular relaxation or obstruction due to filling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

describe systolic dysfunction in HF

A

diminished capacity of the ventricle to eject blood because of reduced contractility and/or excessive afterload

then end-systolic volume is increased due to the reduction in stroke volume and ejection fraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what conditions lead to impaired contractility (HF)

A

MI or ischaemia
dilated cardiomyopathy
Chronic volume overload (e.g. mitral or aortic regurgitation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Talk through aortic stenosis

A

narrowing of the aortic valve outlet
may result in slow rising pulse and ejection systolic murmur head on auscultation in the aortic area (second right intercostal space) and radiating to the carotids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is meant by an ejection systolic murmur

A

Systolic means when the heart muscle contracts
ejection means because of blood flow through a narrowed or damaged valve
whereas a regurgitant murmur is because of back flow of blood into one of the chamber of the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Aortic stenosis on auscultation

type of murmur, where is it heard loudest, quality?, what can you make a patient do to hear it better?

A

ejection systolic murmur
heard loudest over aortic area (2nd right intercostal space)
has a crescendo-decrescendo quality
loudest on expirations and when a patient is leaning forward

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

mitral regurgitation on auscultation(type of murmur, loudest over?, radiation to?)

A

pan systolic murmur
loudest over mitral area (fifth left intercostal space mid-clavicular line)
radiation of murmur to axilla

pan systolic means: A murmur extending through the entire systolic interval, from the first to the second sound.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

pulmonary stenosis on auscultation

A

ejection systolic murmur
heard loudest over pulmonary area
loudest during inspiration
radiates to left shoulder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

describe diastolic dysfunction (filling) in HF

A

increased stiffness (reduced compliance) of the ventricle impairs filling during diastole (e.g. fibrosis or hypertrophy of ventricular wall or constriction by pericardium)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

define cor pulmonale

A

right sided heart failure due to hypoxic lung disease (e.g. COPD)

Cor pulmonale is a condition that happens when a respiratory disorder results in high blood pressure in the pulmonary arteries (pulmonary hypertension). The name of the condition is in Latin and means “pulmonary heart.”

It’s also known as right-sided heart failure because it occurs within the right ventricle of your heart. Cor pulmonale causes the right ventricle to enlarge and pump blood less effectively than it should. The ventricle is then pushed to its limit and ultimately fails.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

signs of Cor pulmonale

A

nicknamed blue bloater

central cyanosis
raised JVP
pitting oedema
hepatomegaly
parasternal heave (RVH)
tricuspid regurgitation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

compensatory mechanisms in chronic heart failure

A
  • increased renal salt and water retention leading to increased filling pressure (↑JVP) and stroke volume by Frank-Starling mechanism
  • baroreceptor reflex increases sympathetic tone increasing HR and contractility and producing increased peripheral vasoconstriction
  • LVH and remodelling

_all this results in fatigue, and poor exercise tolerance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what is the release of renin stimulated by (think HF) in the renin-angiotensin-aldosterone system

A

1) reduced renal artery pressure secondary to the fall in CO

2) increased renal sympathetic tone (due to baroreceptor reflex)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

detrimental effects of increased filling pressures in the heart (think HF)

A
  • dilated heart is less efficient at contracting (law of Laplace)
  • widening of AV valve orifices leads to regurgitation of blood through valves
  • increased filling pressure of left ventricle leads to pulmonary oedema and breathlessness
  • increased filling pressure of right ventricle leads to peripheral pitting oedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

increased sympathetic tone in HF friend or foe?

A

beneficial in mild HF but in more severe disturbances the effects may be detrimental:

  1. venoconstriction raises the filling pressure
  2. vasoconstriction leads to increase in afterload and hence myocardial oxygen consumption
  3. uncoupling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are other signalling molecules increased in the plasma in heart failure

A

ADH - promotes water retention by the kidney
BNP (B type natriuretic peptide)- produced by failing myocardium, plasma level correlates with degree of severity, used as a biomarker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

how does cardiac failure produce oedema? (starling forces)

A

increased venous filling pressure leads to an increase in capillary pressure
salt and water retention leads a reduction in the concentration of proteins in plasma and thus a decrease in the colloid osmotic pressure of plasma
these lead to an increase in the production of tissue (interstitial) fluid by capillaries by ultrafiltration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

if you suspect heart failure what four things should you ask about

A
  1. dyspnoea -difficult or laboured breathing (due to pulmonary venous congestion)
  2. orthopnoea - SOB or difficulty breathing when lying flat
  3. PND - paroxysmal nocturnal dyspnoea -SOB that awakens the patient after 1-2 hours of sleep
  4. Fatigue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

4 signs of acute left ventricular failure (LVF)

A
  1. tachypnoea - fast breathing - due to stimulation of J receptors
  2. cold hands - due to increased sympathetic tone
  3. tachycardia - due to increased sympathetic tone
  4. crackles or wheeze - due to pulmonary oedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

describe the abnormal heart sounds you would hear in patients in LVF (left ventricular failure)

A

combination of added heart sounds and tachycardia produces a “gallop rhythm”

S3 (early diastole) - abnormal filling of dilated ventricles

S4 (late diastole ) - atrial contraction against stiff ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

describe the therapeutic strategies in LVF (Left ventricular failure)

A
  • Remove underlying cause if possible
  • Give supplemental oxygen and consider CPAP or NIPPV
  • Use loop diuretics to improve mechanical efficiency by reducing cardiac dilatation and filling pressures
  • Reduce cardiac work by reducing after load (e.g. nitrate vasodilators)
  • . LVAD only available in specialist cardiac units
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

5 causes of high output cardiac failure (what they are, describe them, how it produces high output cardiac failure)

A

1) Severe anaemia - blood contains too few oxygen carrying RBCs - requires heart to pump more blood each minute to deliver enough oxygen to the tissues
2) hyperthyroidism - thyroid gland produces too much thyroid hormone - increases body’s overall metabolism thus increasing demand for blood flow
3) arteriovenous fistula - abnormal connection between an artery and a vein - short circuits the circulation and forces the heart to pump more blood overall to deliver the usual amount of blood to the vital organs
4) Beriberi - deficiency of thiamine (vitamin B1) - leads to increased metabolic demand and increased need for blood flow
5) Paget’s disease - abnormal breakdown and regrowth of bones which develop an excessive amount of blood vessels - increased number of blood vessels require an increased cardiac output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

which comes first right or left sided heart failure

A

left sided heart failure as right sided heart failure usually occurs as a result of LHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

(4) possible pathologies in the lungs (airways and parenchyma) that cause SOB

A

asthma
pneumonia / chest infection
pneumothorax
heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

6 investigations to do with SOB as presenting complaint (thinking lungs) (thinking bloods)

A 
FBC - full blood count
BNP - B natriuretic peptide 
U&E - urea and electrolytes
D-dimer
ABG - arterial blood gas
CRP - C reactive protein

(BNP high in hypoxia because heart has to work hard to pump under oxygenated blood around)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

why do a BNP test when someone is presenting with SOB

A

used in the diagnosis of heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Why do U&Es when someone is presenting with SOB

A

acute kidney injury could cause raised urea and creatinine which could lead to pulmonary oedema

low potassium levels if on salbutamol inhaler (not for diagnosis but important to monitor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

why do a D-dimer when someone is presenting SOB

A

to diagnose PE/DVT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

why do CRP when someone is presenting SOB

A

for respiratory acidosis/alkalosis

A moderately elevated CRP value (10-60 mg/l) is a common finding in viral upper respiratory tract infection, with a peak during days 2-4 of illness.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is CRP raised in?

A

In inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

requirement levels of BNP for unlikely HF, referral needed and urgent referral needed

A

unlikely - <300pg/mL
referral - >400pg/mL
urgent - >2000pg/mL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

how to test for CO poisoning

A

can do breath test but levels decline quickly after source is removed
has a half life of 300 mins so can be detected in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

investigations to do if you think circulation is the cause of a patients SOB

A 
FBC
Troponin
Carboxyhaemoglobin
methaemoglobin 
LFTs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what does it mean if a patient has raised carboxyhaemoglobin

A

CO poisoning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what does it mean if a patient has raised methaemoglobin

A

could be congenital or drugs (dapsone, local anaesthetics and antimalarial drugs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what chest wall (or MSK) pathologies would cause SOB

A

osteoporosis - vertebral fractures

Do a bone profile (would show raised ALP if osteoporosis is present)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

name some upper respiratory tract infections

A 
sore throat
pharyngitis
cold
tonsilitis
epiglottitis 
laryngitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what is the upper respiratory tract composed of

A

nasal cavity
pharynx
larynx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

what is the lower respiratory tract composed of

A

trachea
primary bronchi
lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

names some lower respiratory tract infections

A

bronchitis
bronchiolitis
exacerbations of pre-existing lung conditions (asthma/COPD)
Pnuemonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

symptoms of an upper respiratory tract infection

A 
pain
fever 
headache
hoarse voice
stridor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

complications of an upper respiratory tract infection

A

Quinsy (peri-tonsillar abscess)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

signs of an upper respiratory tract infection

A

raised temperature
erythema
exudate

(exudate - fluid that leaks out of blood vessels into nearby tissues)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

symptoms of a lower respiratory tract infection

A 
cough
wheeze
sputum
production
pleuritic chest pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

complications of a lower respiratory tract infection

A

empyema - a collection of pus in the cavity between the lung and the membrane that surrounds it (pleural space).

pulmonary cavity -an abnormal, thick-walled, air-filled space within the lung.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

signs of a lower respiratory tract infection

A 
raised RR
intercostal muscle movement
wheeze
dull percussion
bronchial breathing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

3 important pathogens of an upper respiratory tract infection (URTI)

A

Group A streptococcus
Corynaebacterium diphtheriae
various viral infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

what can group A streptococcus cause? (URTI)

A

fever
pharyngitis
tonsillar enlargement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

complications of group A streptococcus

A

Scarlett fever - need to notify WHO
abscess
rheumatic heart disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

what is rhinovirus

A

the most common culprit behind the common cold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

difference between a lower respiratory tract infection and pneumonia

A

pneumonia shows consolidation on a CXR whereas LRTI doesn’t

any pathogen can cause both pneumonia and LRTI

(Consolidation indicates filling of the alveoli and bronchioles in the lung with pus (pneumonia), fluid (pulmonary oedema), blood or neoplastic cells.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

4 classifications of pneumonia

A

community acquired - no recent hospital contact
hospital acquired - after 48 hrs in hospital
ventilator associated - after 48 hrs on a ventilator
aspiration - not time related

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

hospital acquired pneumonia risk factors

A

post-surgical patients
chronic lung disease
immunocompromised
recent antibiotic exposure (increases infection with resistant organisms)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

things to know about streptococcus pneumoniae (pnuemococcus)

A
  • responsible for 50-66% community acquired pneumonia
  • gram positive coccus, surrounded by polysaccharide capsule
  • over 90 serotypes
  • can cause multiple infections: LRTI/pnuemonia, empyema, meningitis, infective endocarditis, abscesses, otitis media and external
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

things to know about legionella pnuemophilia

type of pneumonia, incubation time, spread by, causes what??

A

atypical pnuemonia
incubation 2-10 days
spread by breathed aerosolised water or soil contaminated with legionella
causes hyponatreamia and liver dysfunction

79
Q

things to know about pneumocystis pneumonia

(associated with, high risk of?, Diagnosis by?

A
  • associated with immunosuppression
  • high risk of pneumothorax
  • Diagnosis by PCR or sputum ( beta glucan usually positive)
80
Q

What TB caused by?

A

by the bacterium - Myobacterium tuberculosis

81
Q

TB symptoms

A
  • a cough for 3 weeks
  • weight loss
  • loss appetite
  • fever
  • fatigue
  • night sweats
82
Q

examination findings and observations of a patient with TB

A

pale
cachexic (loss of body weight and muscle mass)
lymphadenopathy
chest - dull to percuss, bronchial breathing, clear
cardiac - muffled heart sounds
joints - painful and swollen
abdomen - tender, organomegally
CNS - reduced consciousness, focal neurology
high temperature

83
Q

difference between laminar and turbulent flow

A

laminar - smooth and silent

turbulent - chaotic and noisy

84
Q

what is bacteraemia

A

presence of bacteria in the blood

85
Q

what to think when bacteraemia on lab results (conditions)

A

pnuemonia/pyelonephritis/cholecystitis
line associated
contaminated
other (think endocarditis)

86
Q

Infective endocarditis definition

A

bacterial (or fungal) infection of a heart valve or area of endocardium

87
Q

how can you get native valve endocarditis

A

cardiac abnormalities
poor dental hygiene
UTI
bowel cancer

88
Q

What is nosocomial infective endocarditis

A

usually >60yrs old

often underlying cardiac disease

89
Q

Some clinical signs of infective endocarditis

A
  • Splinter haemorrhages
  • janeway lesions (non-tender, small erythematous or haemorrhagic macular or nodular lesions on the palms or soles only a few millimeters in diameter )
  • Oslers nodes (tender, raised, fingers and toes, small-raised vasculitis)
90
Q

Major clinical criteria to diagnose infective endocarditis

A

positive blood culture

evidence of endocardial involvement - positive echocardiogram (vegetations, abscess, new valvular regurgitation)

91
Q

Minor clinical criteria to diagnose infective endocarditis

A

predisposition - heart condition

fever ->38

vascular phenomenon - major arterial emboli, septic pulmonary infarcts, intracranial haemorrhage, janeway lesions

immunological phenomena - glomerulonephritis, Osler’s nodes, Roth spots, rheumatoid factors

microbiological evidence - positive blood culture,

echocardiogram - consistent with IE

92
Q

what tests would you do for infective endocarditis? what would you expect these tests to produce?

A
  • multiple sets of blood culture
  • FBC : normocytic, normochromic anaemia, increased WCC (neutrophilia)
  • CRP/ESR: raised
  • Urine: proteinuria and microscopic haematuria
  • echocardiography, Transthoracic vs trans oesophageal
93
Q

when is surgery indicated in infective endocarditis

A 
if there is:
extensive damage to valve
infection of prosthetic valve
worsening renal failure
persistent infection but failure to culture organism
embolisation
large vegetations
94
Q

how much pleural fluid is formed in 24hrs

A

approx 15 ml

95
Q

When will pleural fluid increase

A

when there is:
increased interstitial fluid in the lung (pul oedema)
increased intravascular pressure (because of pul hypertension)
increased pleural fluid protein
increased cytokinase, increased capillary permeability

96
Q

what is pleural fluid produced and absorbed by

A

produced by pleura

absorbed by lymphatic system

97
Q

why does fluid build up in the pleural space when its not supposed to

A

cancer cells can block the lymphatic ducts
lymph nodes around lymphatic ducts can become enlarged and block the ducts
tumour cells secrete more fluid than usual
cytokines increase capillary permeability

98
Q

epidemiology of pleural effusions

A

over 50 causes
commonest is heart failure
strong association with pneumonia
malignancy

99
Q

what is cytology

A

to look for malignant cells

100
Q

management of pleural infection

A

IV antibiotics
drainage of pleural space - usually by placing a chest tube and underwater seal
intra-pleural drugs (fibrinolytic and DNase) useful in loculated cases
some require thoracic surgery (VATS)

101
Q 
(SOB CASE)
20yr man
sudden onset of left sided chest pain
SOB
occurred whilst getting out the car
on examination:
RR 18
SaO2 98%
hyper resonant percussion on left side
no breath sounds left 
diagnosis?
A

Pneumothorax

102
Q

Basic description of VATS surgery for recurrent pneumothorax

A

strip lining of lung and stick lung to the chest wall to stop it collapsing

103
Q

what colour is most potent asbestos

A 
blue asbestos
called crocidolite (amphibole)
104
Q

what colour is least potent asbestos

A

white asbestos

chrysotile (serpentine - curved)

105
Q

brief description of pleural plaques

A

condition is caused from exposure to asbestos
can be calcified or non calcified
occur in greatest areas of friction ( mid zones and diaphragm)
takes 12 years to appear on. CXR and 20 years to calcify
does not undergo malignant change
does not cause disability

106
Q

what does BAPE stand for

A

benign asbestos related pleural effusion

107
Q

what are some asbestos related conditions

A 
pleural plaques
benign asbestos related effusion
diffuse pleural thickening
asbestosis
asbestos related lung cancer
mesothelioma
108
Q

what is mesothelioma (simplistic explanation)

A

cancer of the lining of the lung

does not need much exposure to asbestos to cause this

109
Q

what is asbestosis

A

fibrotic lung disease (thickening or scarring of the tissue)
have to have been exposed to asbestos for many years
can hear fine respiratory crackles on auscultation

110
Q

what is a trapped lung

A

the inability of the lung to expand and fill the thoracic cavity because of a fibrinous restrictive pleural layer that prevents normal visceral and parietal pleural apposition. It is caused by remote inflammation of the pleura and typically presents as chronic stable pleural effusion.

111
Q

how to differentiate between a transudate and exudate pleural effusion

A

if the patient’s serum total protein is normal and the pleural fluid protein is less than 25g/L the fluid is a transudate. If the pleural fluid protein is greater than 35g/L the fluid is an exudate

112
Q

what is the difference between transudate and exudate

A

“Transudate” is fluid buildup caused by systemic conditions that alter the pressure in blood vessels, causing fluid to leave the vascular system. “Exudate” is fluid buildup caused by tissue leakage due to inflammation or local cellular damage.

113
Q

symptoms of pleural infection

A

SOB (dyspnoea)
chest pain
dry, non-productive cough
orthopnoea (inability to breathe unless sat upright or standing erect)

114
Q

what is FEV1

A

forced expiratory volume 1 second
-volume of air expired in first second of maximum force of expiration

(how much air you exhale in 1 second)

115
Q

what is FVC

A

forced vital capacity
-volume of air from maximally forced expiration
( total amount of air you can exhale forcefully in one breath)

116
Q

what is the spirometry ratio?

A

FEV1/FVC

117
Q

what do restrictive lung diseases affect

A

your ability to inhale (things like pulmonary fibrosis)

118
Q

What do obstructive lung diseases affect

A

affect your ability to exhale (COPD and asthma)

119
Q

describe the FEV1/FVC ratio in line with obstructive patterns

A

when the ratio is decreased

diagnosis is reached when ratio is less than 70% for adults and less than 85% for children

120
Q

describe the FEV1/FVC ratio in line with restrictive patterns

A

if FVC is decreased but the ratio FEV1/FVC is normal

reduced TLC

121
Q

what is Tidal volume (TV)

A

amount of air inhaled/exhaled during each normal respiration

122
Q

what is expiratory reserve volume (ERV)

A

the amount of gas that can be expelled at the end of a normal, quiet expiration

123
Q

what is inspiratory reserve volume (IRV)

A

the amount of air that can be breathed in from the end of a normal inspiration

124
Q

what is residual volume (RV)

A

amount of air still left in the lung after maximal expiration

125
Q

how would you measure residual volume (RV)

A

A gas dilution test. A person breathes from a container containing a documented amount of a gas (either 100% oxygen or a certain amount of helium in air). The test measures how the concentration of the gases in the container changes.

126
Q

what is total lung capacity (TLC)

A

vital capacity and residual volume

127
Q

what causes the decreased FEV1/FVC ratio in an obstructive lung condition

A

due to a larger decrease in FEV1 than FVC

128
Q

symptoms of asthma

A 
SOB
cough
wheeze
chest tightness
variable airflow obstruction
129
Q

what is asthma mainly driven by

A

atopy(asthma, eczema, hay fever)

so mainly allergy driven

130
Q

asthma presentation (not symptoms)

A

younger at onset of symptoms
minimal smoking history
personal or family history of asthma or atopy

131
Q

how to diagnose asthma

A

not one test
test for obstruction and atopy
obstruction: spirometry, serial peak expiratory flow rate, reversibility testing, challenge testing
atopy: fractions exhaled nitric oxide, blood/sputum eosinophils, blood IgE, skin prick testing

132
Q

Definition of COPD

A

persistent respiratory symptoms and airflow limitations due to combination airway and/or alveolar abnormalities caused by noxious particles/gases influenced by host factors

133
Q

pathway to diagnose COPD

symptoms, risk factors, how to confirm diagnosis, further investigations

A

symptoms:

  • age >35 years
  • SOB
  • chronic cough
  • sputum
  • frequent winter bronchitis/wheeze

risk factors:

  • smoking
  • occupation
  • exposure to fumes

spirometry:
-to confirm diagnosis of copd

further investigations:

  • CXR to exclude other pathologies
  • FBC to identify anaemia or polycythaemia
  • BMI calculated to identify patients need diet advice
134
Q

some indicators for a diagnosis of COPD

A

SOB that is: progressive over time, characteristically worse with exercise , persistent

chronic cough: may be intermittent and unproductive, recurrent wheeze

chronic sputum production

recurrent lower respiratory tract infections

history of risk factors: tobacco smoke, fumes, occupational dusts/fumes etc.

family history of COPD

135
Q

suggestive features of bronchiectasis

A

large volume of purulent sputum
commonly associated with a bacterial infection
CXR/ CT shows bronchial dilation and bronchial wall thickening

purulent sputum:off-white, yellow or green, and opaque. It indicates the presence of large numbers of white blood cells, especially neutrophilic granulocytes.

136
Q

difference between COPD and asthma with: smoking status, symptoms under 35yo, chronic productive cough, SOB, night time waking with SOB, significant diurnal or day to day variability of symptoms

A

smoking status: nearly all for COPD, possibly for asthma

Symptoms under 35yo: rare - COPD, often-asthma

chronic productive cough: common-COPD, uncommon-asthma

SOB: persistent and progressive - COPD, variable - asthma

night time waking SOB: uncommon-COPD, common-asthma

day to day variability: uncommon-COPD, common-asthma

137
Q

non CF bronchiectasis main cause

A

idiopathic

138
Q

investigations other than CXR/CT for bronchiectasis

A

bloods: CF gene mutation, HIV, ABPA, immunoglobulins, pneumococcal antibodies, autoimmune screens
sputum: MC&S, AFB

139
Q

what is interstitial lung disease

A

an umbrella term used for a large group of diseases that cause scarring (fibrosis) of the lungs. The scarring causes stiffness in the lungs which makes it difficult to breathe and get oxygen to the bloodstream. Lung damage from ILDs is often irreversible and gets worse over time.

140
Q

when to consider interstitial lung disease

A

progressive SOB
Dry cough
restrictive lung disease - reduced gas transfer
Hx of CTD, occupations/hobbies/pets
medications
CXR can be normal CT central to diagnosis

141
Q

when to consider idiopathic pulmonary fibrosis

A 
progressive SOB
dry cough
insidious onset (proceeding in a gradual, subtle way, but with very harmful effects.)
clubbing
dry inspiratory basal crackles
142
Q

what is sarcoid

A

An inflammatory disease marked by the formation of granulomas (small nodules of immune cells) in the lungs, lymph nodes, and other organs. Sarcoid may be acute and go away by itself, or it may be chronic and progressive.

143
Q 
sarcoid complications
(cardiac, endocrine, skin, neurosarcoid, eyes)
A

cardiac - heart block, arrhythmia, failure
endocrine - hypercalcaemia
skin - lupus pernio, erythema nodosum
neurosarcoid - cranial nerve palsies, psychiatric
eyes - uvetis

144
Q

function of the interstitium

A

a reservoir and transportation system for nutrients and solutes distributing among organs, cells, and capillaries, for signaling molecules communicating between cells, and for antigens and cytokines participating in immune regulation.

145
Q

what is Hypersensitivity Pneumonitis

A

an immune system disorder in which your lungs become inflamed as an allergic reaction to inhaled microorganisms, plant and animal proteins or chemicals.

146
Q

What does CPAP stand for? what is it?

A

continuous positive airway pressure

positive airway pressure ventilation in which a constant level of pressure greater than atmospheric pressure is continuously applied to the upper respiratory tract of a person.

147
Q

what does PEEP stand for

A

positive end expiratory pressure

148
Q

what does NIV stand for

A

non invasive ventilation

149
Q

What does BiPAP stand for

A

bilevel positive airway pressure

150
Q

two simplistic causes of respiratory failure

A

lung failure: gas exchange failure manifested by hypoxaemia

pump failure: ventilatory failure manifested by hypercapnia

151
Q

basic description of type one respiratory failure

A

failure of 1 process

problem with gas exchange (problem with lung itself)

152
Q

pathophysiology of type 1 respiratory failure

A

problems with diffusion or ventilation perfusion mismatch

diffusion: surface area, concentration gradient, thickness of membrane and solubility

ventilation perfusion mismatch: blood is supplied to alveoli that arent ventilated (also known as a shunt)

153
Q

3 processes that cause type 1 respiratory failure

A
  1. anything that affects diffusion of oxygen
  2. any thing that affects perfusion of ventilated alveoli
  3. anything that affects ventilated of perfused alveoli
154
Q

what are things that affect the diffusion of oxygen

A
  • fluid filling alveolar spaces
  • loss of lung tissue leading to reduced surface area
  • thickening of alveolar membrane
155
Q

examples of fluid filling alveolar spaces

A

oedema
pus (pneumonia)
inflammation
blood (pulmonary haemorrhage)

156
Q

examples of loss of lung tissue leading to reduced surface area

A
  • emphysema
  • surgery
  • trauma
  • fibrosis
  • pneumothorax
157
Q

examples of thinking of alveolar membrane

conditions

A
  • interstitial lung disease

- oedema

158
Q

what would affect perfusion of ventilated alveoli

A

blockage of a pulmonary artery

159
Q

what causes a blockage of a pulmonary artery

A

pulmonary embolism

160
Q

what would effect ventilation of a perfused alveoli

A
  • reduced ventilation or collapse of an alveoli
  • extra pulmonary: due to heart/vessels having an abnormal connection leading to communication between the right and left heart
161
Q

examples of reduced ventilation or collapse of an alveoli (things that cause it)

A

atelectasis
pleural effusion
small & large airway obstruction
fluid filling alveolar spaces

162
Q

management of type 1 respiratory failure

A

oxygen therapy
usually aim SaO2>94%
increase the amount of oxygen
increase the pressure you give oxygen

163
Q

Briefly describe CPAP

who is it given to

A

continuous positive airway pressure

  • tight fitting mask attached to a machine which delivers pressurised air plus oxygen
  • 1 pressure level that provides positive end expiratory pressure (PEEP)
  • stops the small airways and alveoli from collapsing during expiration so increases surface area for gas exchange and reduces shunting
  • given to people suffering with type 1 respiratory failure
164
Q

what is type 2 respiratory failure

A

failure of 2 processes
reduced ventilation leads to high PaCO2 and secondary low PaO2

this is where you have low O2 with high CO2

165
Q

physiology of type 2 respiratory failure

A
  • CO2 excretion is proportional to alveolar ventilation
  • decreased alveolar ventilation leads to accumulation of CO2(reduced respiratory effort, failure to overcome increased resistance
166
Q

mechanism leading to type two respiratory failure from the brain/CNS

A

decreased respiratory drive -> decreased respiratory rate -> alveolar hyperventilation

167
Q

examples of brain/CNS causes of type two respiratory failure

A

opiate toxicity
anaesthetics
CNS disease (trauma, encephalitis, stroke)
Ondines curse

168
Q

mechanism leading to type two respiratory failure from the spinal cord, peripheral nerves, neuromuscular junction

A

decrease in signals to the muscles of respiration -> insufficient inflation of the chest wall to generate pressures needed for ventilation -> alveolar hypoventilation

169
Q

examples of the spinal cord, peripheral nerves, and neuromuscular junction that cause type two respiratory failure

A 
spinal cord lesions
transverse myelitis
Guilian Barre syndrome
poliomyeltis
motor neurone disease
botulism
170
Q

mechanism leading to type two respiratory failure from the muscles

A

decreased motor input from respiratory muscles -> alveolar hypoventilation

171
Q

examples of the muscle cause leading to type two respiratory failure

A

respiratory muscle fatigue from increased work of breathing
inherited muscular dystrophies
inflammatory myopathies
disuse atrophy

172
Q

mechanism leading to type two respiratory failure from the chest wall

A

non compliant chest wall requires increased effort from inspiratory muscles to move -> alveolar hypoventilation

173
Q

examples of the chest wall causes leading to type two respiratory failure

A

obesity
chest wall trauma
kyphoscoliosis

174
Q

mechanism leading to type two respiratory failure from the airways

A

airway obstruction and loss of elastic recoil -> hyperinflation and increased respiratory muscle load and work of breathing -> respiratory muscle fatigues -> alveolar hypoventilation

175
Q

examples of airway causes leading to type two respiratory failure

A 
upper airway obstruction
COPD
asthma exacerbation
bronchiectasis 
cystic fibrosis
176
Q

mechanism leading to type two respiratory failure from the alveolar unit

A

loss of elastic recoil and hypoxia -> respiratory muscle fatigue -> alveolar hypoventilation

177
Q

examples of the alveolar unit causes of type two respiratory failure

A

pulmonary oedema

pneumonia

178
Q

3 categories of type 2 respiratory failure

A

acute
chronic (compensated)
acute on chronic (decompensated)

179
Q

how to tell the difference between acute, chronic and acute on chronic type 2 respiratory failure

A

do a blood gas
acute & chronic - acidic
acute on chronic - alkaline

180
Q

blood gas difference between type 1 and 2 respiratory failure (PaO2, PaCO2, pH, HCO3-)

A

PaO2 - 1) low 2) low
PaCO2 - 1) low or normal 2) raised
pH - 1) normal 2) low
HCO3- - 1) normal 2) low if acute, raised if chronic

181
Q

symptoms of type 2 respiratory failure

A

SOB
anxiety
headache
symptoms due to underlying conditions

182
Q

signs of type 2 respiratory failure

A

increased RR
tachycardia
unable to talk in full sentences
increased work of breathing/accessory muscle use
cyanosis
signs of CO2 retention (asterixis - CO2 retention flat, confusion/reduced GCS, warm peripheries)

183
Q

signs and symptoms of chronic type 2 respiratory failure

A

daytime sleepiness
morning headache
impaired cough (neuromuscular patients)
signs of heart failure

184
Q

First line investigations for respiratory failure

A 
pulse oximetry (oxygen saturations)
arterial blood gas
venous blood gas
CXR
Bloods 
ECG
185
Q

what is pulse oximetry affected by

A 
nail polish
dark skin
anaemia
movement
CO
186
Q

what is venous blood gas used for (respiratory failure)

A

useful for pH, PaCO2, and HCO3-

187
Q

why are bloods helpful with respiratory failure

A

high Hb might suggest polycythaemia due to chronic hypoxia

(polycythaemia:an abnormally increased concentration of haemoglobin in the blood, either through reduction of plasma volume or increase in red cell numbers. It may be a primary disease of unknown cause, or a secondary condition linked to respiratory or circulatory disorder or cancer.)

188
Q

management for type 2 respiratory failure

A

ABCDE approach initially
address any hypoxia (aim to keep sats between 88-92 to avoid over oxygenating)
remove aggravating factors
treat the cause

189
Q

describe NIV and BiPAP

A

have 2 pressure levels

  • high one for breathing in, known as inspiratory positive airway pressure which increases inspiratory volume and improves CO2
  • low one for breathing out, known as expiratory positive airway pressure it splints the airway open in expiration and improves O2
190
Q

when would you NOT use BiPAP

A

for patients with Asthma or pneumonia who go into type 2 respiratory failure

191
Q

management of acute type 2 respiratory failure in a patient with COPD

A

ABCDE approach
titrate the oxygen (88-92%)
optimise with bronchodilators (salbutamol nebulisers), steroid and antibiotics if appropriate
address any other factors that may be contributing
if not improving or severely unwell then start BiPAP

192
Q

what is obesity hypoventilation syndrome

A

combination of following three things when other causes of type two respiratory failure has been excluded

BMI >30
day time hypercapnia
sleep disordered breathing

193
Q

clinical features of obesity hypoventilation syndrome

A 
snoring
apnoeas when sleeping
morning headache
drowsiness
day time sleepiness
decreased mental

CBL Year 2 (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions