Week #10 Flashcards

Question

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

Answer 1

* 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

Answer 2

* 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**

Answer 3

* 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

Answer 4

* 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

Answer 5

* 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%

Answer 6

* Type A H1N1 (swine flu) * Type A H3N2 (hong kong flu) * Type B virus

Answer 7

* 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

Answer 8

* 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

Answer 9

* 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

Answer 10

* 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

Answer 11

* 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

Answer 12

* If severe: * Peripheral oedema * ascites * pleural effusions

Answer 13

* 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

Answer 14

* 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)

Answer 15

* 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

Answer 16

* 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

Answer 17

* pH=7.4 * PaCO₂=40 * HCO₃=25

Answer 18

* With every 10mmHg increase in PaCO₂ the HCO₃concentration 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

Answer 19

* 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

Answer 20

* **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**

Answer 21

* small increase in CO₂leads to a rapid increase in ventilation * whereas large decreases in O₂ are needed before there is an increase in ventilation

Answer 22

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

Answer 23

* 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 CO₂loss to prevent pH from falling too much

Answer 24

* 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

Answer 25

* Obstructive sleep apnoea * central sleep apnoea * obesity hypoventilation syndrome

Answer 26

* 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.

Answer 27

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

Answer 28

* 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

Answer 29

* 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

Answer 30

* 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

Answer 31

* 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

Answer 32

* Streptococcus pneumonia, heamophilus influenza, klebsiella pneumonia pseudomonas aurigenosa, legionella * Mycoplasma pneumonia

Answer 33

* Community acquired pneumonia * Hospital acquired pneumonia * immune deficiency realted pneumona * pneumonia due to aspiration of gastric conentents or URT secretions

Answer 34

* Acute bronchopneumonia, Acute lobarpneumonia * Acute Bronchopneumonia is far more common

Answer 35

* 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

Answer 36

* 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

Answer 37

* Lobarpneumonia

Answer 38

* Respiratory acinus refers to respiratory bronchiol, alveolar duct, alveolar sac and the individual alveoli

Answer 39

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**

Answer 40

* 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

Answer 41

* 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**”

Answer 42

* 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

Answer 43

* 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

Answer 44

* 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

Answer 45

* Increased drive or increased load

Answer 46

* 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

Answer 47

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

Answer 48

* 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

Answer 49

* **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

Answer 50

* 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)

Answer 51

* Whithin the deep veins of the leg * In the soleus muuscle venous plexus

Answer 52

* 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.

Answer 53

* Venous thrombi have layered or laminated structure * Pink is platelets and fibrin and red layers with erythrocytes * This is characteristic of thrombi

Answer 54

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

Answer 55

* occlusive * propagate

Answer 56

* **_Virchow's triad_** 1. **Changes in the vessel wall** (trauma including catheterisation,bacterial infection of the vessel wall) 2. **Changes in the constituents of the blood** – hypercoagulable states 3. **Changes in blood flow** – stasis and turbulence: prolonged immobilisation, dehydration, hypotension, congestive cardiac failure, polycythaemia

Answer 57

* **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

Answer 58

* 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

Answer 59

* Lysis and resolution * Organization-scar tissue replacement * Recanalisation * Embolism

Answer 60

* 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

Answer 61

* 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)

Answer 62

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

Answer 63

* 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

Answer 64

* Acid fast bacteria * Mycobacterium Tuberculosis

Answer 65

* 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

Answer 66

* caseous necrosis

Answer 67

* 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.

Answer 68

* 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 *

Answer 69

* 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

Week #10 Flashcards

(94 cards)