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Respiratory Block > Week #10 > Flashcards

Week #10 Flashcards

1
Q

What are some of the common symptoms of influenza?

A
  • fever, chills, cough, headache, muscle aches, fatigue, loss of apetite.
  • Normal chest X-ray
  • Acute infection lasting about 7 days or longer
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2
Q

What is the incubation period and infectious period of influenza infection?

A
  • 1-5 days
  • 5-6 days
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3
Q

How much does influenza cost Australia per year?

how many deaths worlwide are caused by influenza?

A
  • $600 million
  • 250,000-500,000 deaths
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4
Q

What is the linkage that the viral heamaglutinin makes with the _____ on non ciliated respiratory epithelium.

A
  • SA alpha2-6 linkage to galactose
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5
Q

Viruse replicates in the upper and the lower respiratory tracts but mainly in the ______

A
  • large airways
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6
Q

What is the cause of the influenza like symptoms due to cytokines

A
  • Fever is caused by IL-1
  • head and muscular aches casued by IFN
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7
Q

Early on influenza virus will infect the non ciliated epithelium but then goes onto infect the ciliated epithelium of trachea and bronchi, this can lead to secondary infeciton by which pathogens and can cause what?

A
  • H. influenzae, Staph aureus, Strep. pneumoniae.
  • Can cause death from bacterial pneumonia
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8
Q

What is the structure of the influenzae virus and to what virus family does it belong?

A
  • Influenza is an enveloped virus with a genome comprising segments of single stranded RNA of negative sense
  • member of the Orthomyxoviridae family
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9
Q

What are the three types of infleunza and what are there features

A
  • Influenza A and B can infect humans and cause infleunza
  • Type C can infect humans but is a minor human pathogen
  • Type A also has subtypes
  • Type A subtypes and B virus also have viral strains.
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10
Q

How many segements of genome does the influenza virus have and how is each RNP structured?

A
  • 8 segments
  • each segemnt is strucutred like a pan-handle
  • each segment has 3 polymerase subunits for the RNA dependent RNA polymerase
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11
Q

What is the role of the following influenza proteins:

np

M2

NS1

A
  • np is a nuclear protein capsid protecting each of the RNPs
  • M2 is an ion channel
  • NS1 is a protein that counters the effects of IFN
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12
Q

What is the role of HA and NA?

A
  • HA binds to the Galactose and initiated entry into the host cells
  • NA functions to snip of the SA off the galactose so that the virus particle may not re-infect the same cell when it leaves the cell.
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13
Q

Heamaglutin acts as a trimer and NA acts as a tetramer? true or false?

A

True

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14
Q

Type A virus has ___ different HA subtypes

and ___ different NA subtypes

A
  • 16
  • 9
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15
Q

What is the replication cycle of influenza virus?

A
  • Viral hemagglutinin (HA) binds to receptor (sialic acid linked to galactose) on surface of respiratory epithelial cell
  • Virus taken into cell by receptor-mediated endocytosis
  • As the endosome becomes more acid the HA
    changes conformation leading to fusion of viral
    envelope with the endosomal membrane
  • The 8 viral RNPs escape the endosome
    and go to the nucleus
  • Viral RNA replication and mRNA synthesis
  • Viral RNPs form
  • HA, NA expressed on cell surface after glycosylation in ER and golgi
  • Viruses acquire their surface glycoproteins and envelope as they bud out of the cell
  • Viral neuraminidase (NA) cuts sialic acid receptors from the cell surface so that newly budded virus won’t bind back to the dying cell
  • Newly formed virus requires the action of tryptase Clara to become infectious
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16
Q

What is the role of the enzyme tryptase Clara?

and why is it so important for influenza infection?

A
  • When a virus buds out of a cell it is not virulent until it has undergone cleavage by tryptase Clara
  • The HA must be cleaved by tryptase clara and this enzyme is only found in the respiratory tract.
  • this cleavage occurs so to expose hydrophobic residues required for endosome escape
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17
Q

Explain the two main types of immunity generated to influenza virus?

A
  • CD8 cytotoxic T cells
    • kils infected cells
    • is broadly cross reactive due to the fact that it recognises internal viral proteins which are conserved across sub-types and strains-not between A and B though
  • Antibody
    • developing antibody to HA (and NA) speeds clearance of virus
    • acts by inhibiting attachment (or release) of virus. Ab and C’ lysisof cells, promoting phagocytosis etc
    • Pre-existing Ab will protect against infeciton by neutralising input virus
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18
Q

Explain the conceot of antigenic drift and drift

A
  • drift is mutaitons accumulating in viral proteins due to the error prone nature of the RNA dependent RNA polymerase
  • antigenic drift is when these mutaiton occur in the antigenic site of the HA or NA
  • viruses with mutations that diminish binding of the Ab will be selected for
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19
Q

How many antigenic sites are there on a HA trimer?

and what would happen if all were mutated

A
  • 5 sites
  • an epidemic
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20
Q

What are some of the sites of vaccine based therapy to influenza virus?

A
  • The HA to prevent entry
  • or Ab to NA to prevent escape of the virus
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21
Q

What is contained within the influenza vaccine?

What kind of immunity does it induce?

What are some of its problems?

A
  • Influenza A H1N1 and H3N2 subtypes and influenza type B and another Type B strain that is distinct
  • inactivated preperation and so only induces Ab type defences
  • Vaccine has to be updated every year due to antigenic variation due to antigenic drift
  • Less than 70% effective and even worse in the elderly
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22
Q

What are some of the tagets of antiviral (influenza) drugs?

A
  • Ion channel blockers inhibit the function of the M2 ion channel, preventing endosome escape of RNPs
  • NA inhibitors block efficient release
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23
Q

What is the HA conformational change importnat for?

How do antiviral drugs that block the M2 ion channel work?

A
  • H+ ions enter the endosome to acidify it and it causes the HA to undergo a conformational change and this allows fusion of the virus envelope with the endosomal membrane
  • but then we need to acidify the viral particle as well so that the RNPs can escape
  • The M2 ion channel on the sirface of the virus allows H+ ions to enter and this allows escape of the RNPs
  • So anti-viral drugs inhibit viral escape from the endosome
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24
Q

What are the names of the two M2 ion channel blockers?

A

Amantadine

Rimantadine

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25
Q

What do relenza and tamiflu do? and how are they adminiterred?

A
  • Relenza and Tamiflu block the action of the NA
  • Relenza is adminiterred through inhalation
  • Tamiflu is adminiterred orally there seems to be resistance to this drug
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26
Q

What is antigenic shift?

A
  • Sudden appearance of a new HA influenza virus
  • New HA must come from an animal
  • No one has immunity so it results in a pandemic
  • very rare
  • bird viruses use alpha2-3 linkage to SA so must mutate this before they can infect humans as the receptors in the human respiratory tract are mainly alpha2-6 galactose
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27
Q

What is a way a new human subtype viruse can be created?

A
  • Can be achieved through viral reassortment when a human influenza and a avian influenza infects a pig which has both alpha2-3 and alpha2-6 linked SA galactose in its respiratory tract.
  • this can lead to new HA viruses using the human virus receptor that recognises SA alpha Gal
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28
Q

Swine flu H1N1

A
  • H1N1 virus
  • respiratory symptoms as in seasonal influenza; not systemic
  • spread very rapidly despite best efforts
  • overall not as lethal as H5N1
  • greater ability to replicate in lungs than seasonal influenza
  • deaths in younger people
    • possibly somme immunity left over from those born before 1920 due to earlier seasonal H1N1
  • Pregent women, obvese individuals and indigenous patients most susceptibe
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29
Q

Why is H5N1 so bad?
Why is it capable of systemic spread?

A
  • No one will have immunity to it
  • Has a potential for systemic spread because it has a different cleavage site that can be cleaved by an enzyme found in all cells.
  • case fatality rate of 80%
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30
Q

What influenza viruses are currently circulating?

A
  • Type A H1N1 (swine flu)
  • Type A H3N2 (hong kong flu)
  • Type B virus
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31
Q

How does asbestos cause lung disease and what form of lung disease is it?

A
  • Asbestos causes interstitial lung disease due to exposure.
  • progressive, diffuse inflammation and fibrosis of lung parenchyma causing disruption and destruction of the A-C membrane
  • Gas exchange and mechanical defects with PaO2 reduced, increased A-a gradient, decreased lung volumes (restrictive ventilatory defect), decreased compliance and increased work of breathing
  • Patients present with progressive exertional breathlessness and cough
  • Clubbing, crepitations, perhaps cyanosis on examination
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32
Q

What would the cardiac finding likely be of someone with lung disease due to asbestos and pulmonary oedema?

What would be the likely pathophysiological causes of the pulmonary hypertension?

A
  • Sinus tachycardia due to decreased stroke volumes
  • right ventricular heave
  • Loud P2 and 4th heart sound
    • pulmonary semilunar valve sound and 4th heart sound is blood rushing into stiff or hypertrophic ventricle
      • so most likely RV hypertrophy
  • pulmonary systolic ejection murmur
  • triscuspid pansystolic murmer
    • means blood is being lost from ventricle into atrium due to valve incompetence. This is mostly likely due to the increased pulmonary pressure, the RV will dilate and this will cause valve incompetence
  • Increased JVP with v waves
    • elevated as increased RV pressure and increase RA pressure

Pathophysiological Causes of the pulmonary hypertension

  • destructionof pulmonary capillaries
    • the process of inflammation and fibrosis destroys the capillary bead and this leads to increased pressures
  • spasm of pulmonary arterioles
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33
Q

What is the likely diagnosis of a patient with these symptoms:

non smoker, previously very fit

  • 6 months of intermittent SOB
  • “anxiety”
  • No abnormalities on examination
  • normal CXR and ECG
  • Spirometry normal, DCO 80% predicted
  • Brisk walk-no distress, pulse 135, SaO2 98% => 90%
A
  • Oxygen saturation at 90% is bery low even for someone who is exercising
  • Probably not airway disease as there is no wheezing
  • probably not interstitial lung disease as there would be more crepitations
  • Perhaps a pulmoanry embolism which has caused blood clot in thelungs
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34
Q

What can a ventilation perfusion scan be used for, and how does it work?

A
  • Inject a radioactive substance into the blood and see if it will get lodged in any of the arterioles
  • If the dispersal is even then there is no ventilatory mismatch
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35
Q

What is the effect of pulmoanry hypertension on right atrial and systemic venous pressures?

A
  • They will be increased
  • Pressure increases in right ventricle, right atrium and then venous pressure will rise and then this will lead increased pressure in the capillary bed and this can lead to peripheral oedema
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36
Q

What is the effect of increased systemic venous pressure on the systemic capillary bed?

A
  • If severe:
    • Peripheral oedema
    • ascites
    • pleural effusions
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37
Q

What are some of the causes of pulmonary hypertension?

A
  • Mechanisms that increase vascular resistance (main category)
    • vasoconstriction-low alveolar O2 (including hypoventilation)
    • obstruction-embolism, primary pulmonary hypertension(uncommon condition)
    • obliteration-arteritis (less likely), emphysema, pulmonary fibrosis
  • Increased left atrial pressure
    • mitral stenosis, LVF
  • Increased pulmonary blood flow
    • left to right shunts, high flow states, excess central volume
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38
Q

How can pulmonary hypertension lead to heart failure and what kind?

A
39
Q

Acid base disorders

How can one differentiate between a respiratory and a metabolic acidosis?

How do we know if each of the conditions is compensated or not?

A
  • If CO2 is elevated then it is a respiratory acidosis and is probably associated with hypoventilation
  • Metabolic acidosis is where there is a loss of HCO3 or an addition of acid

Compensation

  • Bicarbonate retention for respiratory acidosis will occur over days so that the pH comes up a bit to the lower end of normal (still not quite normal)
  • Compensation for metabolic acidosis will occur in seconds and will involve hyperventilation (low PaCO2)
40
Q

What are some of the causes of a metabolic acidosis?

A
  • loss of HCO3
    • diarrhoea would be the most common cause
  • addition of acid
    • exercise with the addition of lactic acid
    • ischeamic tissue will also cause increased lactic acid
    • ketoacidosis-starvation
41
Q

How can we differentiate between a respiratory alalosis and a metabolic alkalosis?

What is the compensation for each of these?

A
  • Respiratory due to low CO2 (hyperventilation)
    • could be due to anxiety, altitude hypoxia etc
  • Metabolic due to increased HCO3 or loss of acid
    • Loss of acid could be due to vomiting

Compensation

  • Bicarbonate excretion for respiratoyr alkalosis (days)
  • Mild hypoventilation for metabolic alkalosis
    • person is at risk of hypoxia though
42
Q

What are the normal blood gas values for pH, PaCO2 and HCO3?

A
  • pH=7.4
  • PaCO2=40
  • HCO3=25
43
Q

How can we tell if the increase in HCO3 concentration in respiratory acidosis is due to renal compensation or just the equation being pushed to one side?

A
  • With every 10mmHg increase in PaCO2 the HCO3 concentration increases by aproximately 3.5.
  • So full compensation HCO3 should come up a bit higher
  • and pH should come a bit back up to normal
44
Q

What are the two central controllers for breathing and what do they do?

A
  • Brainstem
    • neurons in medulla and pons
    • autonomic rhythmic inspiratory stimuli, and sometimes expiratory stimuli
    • in-put from peripheral sensors
    • can be over-ridden by cortex
    • major output is to the phrenic nerve
  • Cortex
    • voluntary hyperventilation leading to hypocapnoea
    • to a lesser extent, hypoventilation leading to hypercapnoea
45
Q

Explain the role of the central chemoreceptors and the peripheral chemoreceptors

A
  • Central chemoreceptors
    • situated on ventral surface of medulla, surrounded by CSF
    • respond to CSF [H+]
    • CSF [H+] is a reflection of CO2 in cerebral capillaries
    • Increased PaCO2 => increased CSF [H+] => increased ventilation
    • do not respond to PaO2
  • Peripheral chemoreceptors
    • situated in carotid bodies at bifurcation of common carotid arteries in neck, and aortic bodies around arch of aorta
    • rapid response
    • responds to decreased PaO2, decreased pH, increased PaCO2 => increased ventilation
46
Q

How does the ventilatory response to variation in CO2 vs variation in O2 differ?

A
  • small increase in CO2 leads to a rapid increase in ventilation
  • whereas large decreases in O2 are needed before there is an increase in ventilation
47
Q

What is minute ventilation (VE)

A
  • Ve is the respiratory equivalent to Cardiac output
  • amount of air goinf in and out per minute
  • respiratory rate multiplied by stroke volume
48
Q

Describe the VE vs Work relationship

A
  • As work increases minute ventilation increases linearly
  • and then at about 60% maximum work there is an inflection
    • this inflection is called anaerobic threshold
    • below this point the ventilation is increasing to match CO2 production and O2 consumption
    • So at this inflection point there is more anaerobic metabolism and this generates lactic acid
    • So now a metabolic acidosis.
    • With high levels of work PaCO2 actually decreases a bit as the body increases ventilation even more to increase CO2 loss to prevent pH from falling too much
49
Q

What are some of the causes of hypoventilation?

A
  • Reduced respiratory centre activity
    • reduced drive (e.g. low CO2 or high pH)
    • Supression of activity by drugs, trauma, vascular accidents etc
  • Neuromuscular disease
    • nerve paralysis (drugs, polio, Guillian-Barre, trauma etc)
    • muscle weakness (drugs, motor neurone disease, muscular dystophy)
  • Chest wall deformity (gross)
  • Obesity (gross)
  • Sleep disorded breathing
50
Q

What are three causes of sleep disorded breathing?

A
  • Obstructive sleep apnoea
  • central sleep apnoea
  • obesity hypoventilation syndrome
51
Q

What is Obstructive Sleep Apnoea (OSA)?

A
  • Transient obstruction of the throat during sleep preventing breathing, and disturbing sleep
  • Occurs in peeople who snore (but not all snorers have OSA)
  • Obstruction occurs during sleep because of:
    • airway muscles relax (floppy throat-especially in REM)
    • Throat already narrowed
    • Tongue falls backwards (especially if supine)
  • When brain is in REM sleep it may not be receptive to external stimuli and may not realize that the airway is blocked and then when the brain wakes up into light sleep and then airway muslce contracts agains and airways open up more
    • so sleep is being interrupted and we don’t get the restorative sleep-very fragmented sleep.
52
Q

What is the cycle of events for a person with OSA?

A
  1. Sorning in light sleep
  2. Complete obstruction (apnoea) in deep sleep
  3. Reduced blood O2, increased CO2, other stimuli
  4. Brain “wakes” in lighter sleep (arousal)
  5. Muscles contract, airway opens, breathing recommences
  6. Back into deep sleep, obstructs again

Often more that 60 events every hour throughout sleep

Very fragmented sleep => sleep deprivation

Bed partner often makes diagnosis

53
Q

What is tested in an overnight sleep test?

A
  • Measure airflow from the nose
  • Measure oxygen saturation in blood
  • Measure muscle contraction in chest

With OSA there is a lag between low airflow and the recording of low oxygen due to the blood flow time

With central sleep apnoea the brain stops sending signals for the muscles to contract so we can differentiate between central sleep apnoea and OSA by looking at the muscle contractions

54
Q

What is the treatment for OSA?

A
  • nasal CPAP
  • continuous positive airway pressure
  • air is there to keep the airway open
  • Can use a mouth guard to push jaw forward to stop toungue falling back
55
Q
  • If a morbidly obese person (BMI=50) presents with excessive sleepiness during the day, non-smoker, no previous heart or lung disease and the ABG shows:
  • pH 7.37, PaO2=52mmHg, PaCO2=68mmHg, HCO3=34mmol/L
  • With cellulitis in right lower leg and bilateral oedema
  • What do they have?
  • How would we confirm the diagnosis
  • What would the treatment be?
A
  • compensated respiratory acidosis
  • A-a gradient is normal
  • rigth heart failure has caused the bilateral leg oedema due to the constriction of pulmonary vessels due to the hypoxia (V/Q mismatch)
  • Need to do a sleep study to confirm diagnosis but it is likely that it could be a severe OSA patient
  • patient must loose weight, use CPAP or BiPAP at night
56
Q

Why would be careful treating someone of has chronic hypoxia with excessive oxygen?

A
  • Because hypoxic drive is what is pushing ventilation
  • and because the set point has been lowered due to the chronic hypoxia giving excessive oxygen could stop ventilatory drive
57
Q

What are some of the common bacterial causes of typical pneumonia?

What are some of the common bacterial causes of atypical pneumonia?

A
  • Streptococcus pneumonia, heamophilus influenza, klebsiella pneumonia pseudomonas aurigenosa, legionella
  • Mycoplasma pneumonia
58
Q

What are the 4 clinical based classifications of pneumonia?

A
  • Community acquired pneumonia
  • Hospital acquired pneumonia
  • immune deficiency realted pneumona
  • pneumonia due to aspiration of gastric conentents or URT secretions
59
Q

What are the two pathology based calssifications of pneumonia?

Which is more common?

A
  • Acute bronchopneumonia, Acute lobarpneumonia
  • Acute Bronchopneumonia is far more common
60
Q

What are 5 lung defense mechanisms that can be compromised?

A
  • loss of cough reflex
  • impairment of mucociliary function
  • accumulation of secretions
  • interferance with the phagocytic or bacteriocidal action of alveolar macrophages
  • pulmonary congestion or oedema
61
Q

What is the difference between acute lobapneumonia and acute bronchopneumonia

What are the common causes of each

A
  • Difference depends mainly on the distribution of the pneumonia
  • Acute Bronchopneumonia
    • infection starts in terminal bronchiol and then spreads out into alveolar parenchyma-often bilateral and multifocal
    • often low virleunce organism
  • Lobar pneumonia
    • when inflammatory oedema spreads rapidly through the lobe
    • high virulence organism
    • 80% caused by streptococcus pneumonia
62
Q

Would pleurasy (inflammation of pleura) be more likely occur in lobarpneumonia or bronchopneumonia?

A
  • Lobarpneumonia
63
Q

what is the respiratory acinus?

A
  • Respiratory acinus refers to respiratory bronchiol, alveolar duct, alveolar sac and the individual alveoli
64
Q

What are the two stages of lobar pneumonia?

A

earlier stage of lobar pneumonia is red due to blood cells-red hepatization
but then becomes white as the polymorphs take over and the RBC break down-grey hepatization

65
Q

What is a lung Abscess?

What are some of the common causes of lung Abscess?

A
  • A lung abscess is a collection of pus in the lung

Causes

  • Aspiration– mixed infection with anaerobic
    bacteria (bacteroides)
    • gastric contents, URT secretions
  • Obstruction of the bronchial tree
    • bronchiol carcinoma
  • Haematogenous seeding of the lung from an extra-pulmonary infection (e.g. osteomyelitis)
  • Certain types of bacterial pneumonia: Strep pyogenes, Staph aureus. Klebsiella pneumonia
  • Acute bronchopneumonia in debilitated hosts
  • aspiration of a foreign body and trauma
66
Q

What are some of the characteristics of viral pneumonia?

A
  • Viral infections don’t produce consolidations-not neutrophil rich, lymphocytes dominate
  • Can cause bronchiolitis and inflammation of the alveolar septa (lymphocytic)
  • Most are cytopathic i.e. they cause death of
    epithelial cells within the upper and lower
    respiratory tract, predisposing to secondary
    bacterial infections and severe pulmonary oedema.
  • Viral pneumonias at autopsy (e.g. influenza
    pneumonia) are heavy, wet and red or “boggy”
67
Q

What is Bronchiectasis?

A
  • Bronchiectasis is permenant dilatation of the large cartilage containing bronchi.
  • Chronic bacterial infection leads to weakening of bronchiol wall which results in scar tissue deposition which then contracts and causes some dilatation. There is then some pooling of secretions in the lung that cannot be cleared. Stasis is the basis for infection
68
Q

What are some of the complications of bronchiectasis?

A
  • Copious offensive sputum production
  • Poor drainage of secretions leads to recurrent
    bacterial pneumonia and abscesses
  • Rupture of vessels in bronchial walls leads to
    haemoptysis
  • Pulmonary fibrosis leading to right ventricular
    failure (known as cor pulmonale)
  • Cerebral abscesses
    • spread of infection from lung to brain
  • Amyloidosis
    • accumulation of innapropriately folded proteins
69
Q

What are the components of ventilatory work?

A
  • mainly inspiratory work
  • stretching work-elastic work
    • ussually lung is compliant and the elastic work is low
  • airflow work-resistive work
    • Normally low resistance and no obstruction
70
Q

What are the two contributers to Shorteness of breath?

A
  • Increased drive or increased load
71
Q

What doe crepitaitons indicate?

A
  • Crepitations indicate problem with the alveoli capillary
  • Could be a reulst of air bubbling through fluid in pulmonary oedema etc
  • Or lung alveoli pop open at the end of inspiration when lungs are stiff and scarred like in interstitial lung disease
72
Q

What are the spirometry and X-ray findings of a patient with interstitial lung disease?

A
  • diffuse interstitial lung disease lung spirometry will be restrictive and on X-rays the lungs will be more white than usual.
73
Q

What are some of the respiratory causes of breathlesness?

A
  • AIRWAYS DISEASE
    • Upper airways - tumour, foreign body, angioneurotic odema, CROUP
    • Lower airways - asthma, COPD, bronchiolitis
  • ALVEOLAR DISEASE
    • Pneumonia, lung collapse, pulmonary odema, pulmonary fibrosis
  • PULMONARY VASCULAR DISEASE
    • Pulmonary embolism, vasculitis, primary pulmonary hypertension
  • PLEURAL and CHEST WALL DISEASE
    • Pleural effusion, pneumothorax, chest wall deformity
  • RESPIRATORY MUSCLE DISEASE
    • Respiratory muscle weakness, phrenic nerve palsy
74
Q

What are 3 examples of Medically undiagnosed Dyspnoea

(MUD)

A
  • Breathlessness in you athletes
    • Exercise induced bronchoconstriction in 30-40% of athletes
    • responds to asthma treatment
    • Vocal Cord Dysfunction (Laryngeal Dysfunction)
    • Incidence in athletes but described more than in general population
    • Responds to speech therapy, CBT
  • Disease or Deconditioned
    • Difficult to tell
    • Can do a incremental exercise test
    • Someone who is deonditioned will have a steep HR response
    • We may find other stuff like cardiac disease when we do this as well.
    • Or can try a 3 month training program and see if there breathlessness has improved
  • Phycogenic or disease?
    • symptoms releated to anxiety or depression
    • seeing that most tests are negative probably best to stop taking tests and see if we ca sought out underlying anxiety causes first
75
Q

What is thye difference beween a clot and a thrombus?

A
  • A thrombus is a solid mass composed of blood compoennts formed in an artery or vein during life
  • the word “clot” is not a synonym for thrombus: a clot is a solid mass composed of blood components which forms after death (post-mortem)
76
Q

What is a common site for venous thrombi to form?

A
  • Whithin the deep veins of the leg
  • In the soleus muuscle venous plexus
77
Q

In which part of the vein does the thrombus usually form?

A
  • Venous thrombus initiate in the locality of venous valves
  • The thrombi often commences in a pocket just upstream of a venous valve venous thrombus is typically occlusive and is often red due to erythrocytes and it can propagate and get bigger and bigger.
78
Q

Describe the basic histology of a venous thrombus

A
  • Venous thrombi have layered or laminated structure
  • Pink is platelets and fibrin and red layers with erythrocytes
  • This is characteristic of thrombi
79
Q

Compare the colour of venous thrombi and arterial thrombi

A
  • Venous thrombi are red because they are relatively
    rich in erythrocytes
  • in contrast to arterial thrombi, which are more often grey or white
80
Q

Venous thombi are usually _______ and have the ability to _______ (extend in both upstream and downstream directions)

A
  • occlusive
  • propagate
81
Q

What are some of the predisposing factors to venous thrombosis?

A
  • Virchow’s triad
    1. Changes in the vessel wall (trauma including catheterisation,bacterial infection of the vessel wall)
  1. Changes in the constituents of the blood –
    hypercoagulable states
  2. Changes in blood flow – stasis and turbulence:
    prolonged immobilisation, dehydration, hypotension, congestive cardiac failure, polycythaemia
82
Q

What are two examples of genetic causes to hypercoagulabilty of the blood?

A
  • Factor V Leiden point mutation in factor V prevents activated protein C, a natural anticoagulant,
    from binding to a cleavage site. Sufferers have a 5 fold increase risk in thrombosis formation (venous)
    • 50% of patients with DVT have this mutation
  • Prothrombin III deficiency leading to circulating levels of prothrombin
  • 3 uncommon genetic diseases:
    1. Antithrombin III deficiency
    2. Protein C deficiency
    3. Protein S deficiency
83
Q

List some secondary (acquired) causes of hypercoagulability

A
  • Surgery
  • Massive trauma and burns
  • Malignancy – release of thrombogenic substances fromtumours especially mucinous adenocarcinomas
  • Obesity – mechanism unknown
  • Smoking – probably
  • Hyper-oestrogenic states (pregnancy and the Oral Contreceptive Pill)
  • Nephrotic syndrome (both cause and effect of renal vein thrombosis)
  • Anti-phospholipid antibody syndrome
84
Q

What are the most common fates of vebous thrombi?

A
  • Lysis and resolution
  • Organization-scar tissue replacement
  • Recanalisation
  • Embolism
85
Q

What is the difference between a thrombus and an embolis?

A
  • An embolus is a mobile mass of material within the
    vascular system able to lodge within a vessel, occlude its lumen and obstruct blood flow.
  • A thromboembolus is a detached piece of thrombus
86
Q

What is a saddle thromboembolis?

A
  • Pulmonary thromboembolus lodged at the bifurcation of the pulmonary artery
  • Mainly red with pale areas
  • Coiled shape tends to reflect shape of the vein of origin
  • Occlusive
  • Sudden death (cardiac arrest with electromechanical
    dissociation)
87
Q

What is a pulmonary thromboembolis?

A
  • Embolis in the right or left pulmonary artery
  • Clinical effects
    • Sudden death
    • Dyspnoea, chest pain and circulatory failure mimicking myocardial infarction
88
Q

What is a small pulmonary thromboembolis?

A
  • thromboembolis in the small pulmonary arteries
  • can cause pulmonary infarct
    • Sharply demarcated
    • Wedge shape
    • Pleural base
    • Red
    • Occluded artery at the apex
  • Clinical
    • Dyspnoea
    • Haemoptysis
    • Pleuritic chest pain
  • Note that not all pulmonary emboli cause infarction and with the dual blood supply they often don’t
89
Q

Ziel Nielsen stain is fused for the staining of what kind of bacteria?

A
  • Acid fast bacteria
  • Mycobacterium Tuberculosis
90
Q

What is a granuloma?

A
  • lump of macrophages
  • Type IV hypersensitivity reaction
  • Response of the body to an organsm that is difficult to eradicate completely
  • So we wall it off instead
91
Q

What kind of necrosis is tyopical of infection with Mycobacterium tuberculosis?

A
  • caseous necrosis
92
Q

Explain the cause, the appearance (with names) and the outcome of primary TB infection

A
  • Primary occurs in a person with no previous exposure
    • usually mild or sub-clinical
  • Characterised by granulomas and caseous necrosis in the periphery of the lung
    • This area is known as a Ghon Focus
  • Sread of bacteria can spread to the hilar lymph nodes can cause caseaus necrosis in this area as well
  • Ghon focus and caseating hilar lymph node is known as a Ghon complex
  • In most patients, immune response controls the infection and the Ghon complex heals by fibrosis, often with some calcification.
93
Q

Explain the cause the appearance and the outcome (complications) of secondary TB infection

A
  • Occurs in patietns that have been previously infected and the TB infection reactivates for some reason
    • old age
    • corticosteroids etc
  • Secondary TB is a lung disease that effects the apex of the lung
  • the extent of the caseous necrosis is much mroe severe than in primary TB
  • The characteristic feature is cavitation of the caseous necrosis
  • Cavitation occurs when the caseous necrosis erodes into the wall of the bronchus and discharges into the bronchio tree.
  • The body can localise the infection by producing a fibrosing wall around the area of cavitation
  • So can be controlled but hte fibrosis itself can be a problem so the host tesponse is the cause of the lung damage.

Complications

  • progressive spread of the caseous necrosis into the lung
  • blood vessels can become eroded leading to heamoptysis
  • dessimination of infection via the bronchiol tree
  • pleura can become inflammed and fibrotic
  • Infected lung can become scarred
    *
94
Q

What is Miliary TB?

A
  • Numeous tubercles widely scattered through the lung parenchyma
  • Caused by desemination of M. tuberculosis through the blood vessels
  • this can occour in any organ-systemic process
  • Very high mortality
  • Is more common in secondary TB but can also occur in primary TB as well

Respiratory Block (4 decks)

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