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Week 2 Flashcards

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1
Q

Where are the peripheral chemoreceptors? What do they do?

A

aortic bodies on the arch of the aorta

carotid bodies on the carotid sinus

Sense tension of O2, CO2 and H+ in blood.

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2
Q

Name some autoimmune causes of interstitial lung disease

A
  • Wegener’s
  • Churg-Strauss
  • Systemic Lupus Erthyematosus
  • Bechet’s
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3
Q

COPD clinical syndrome - symptoms

A

chronic, not episodic associated with smoking daily productive cough progressive breathlessness frequent infective exacerbations CB - wheezing Emphysema - reduced breath sounds

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4
Q

What is the target of muscarinic receptor antagonist drugs? I.e. SAMAs, LAMAs (give examples of both)

A

M3 receptor on smooth muscle

SAMA - ipratropium (non-selective), oxitropium

LAMA - tiotropium, aclinidium

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5
Q

Treatment of stable COPD

A

Dependent on GOLD staging. A - SAMA/SABA B - LAMA C - LABA/LAMA or ICS/LABA D - ICS/LABA/LAMA (C and D are dependent on 2 or more exacerbations per year)

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6
Q

Name that cell!

A

Neutrophil, single multi-lobed nucleus

Increase in

  • stress, both physiological and pathological (acute infection, trauma, infarction, inflammation)
  • steroids, causes ‘de-margination’
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7
Q

How is stimulation of the dorsal neurones terminated?

A

Pneumotaxic centre (PC), located superiorly to the dorsal neurones gets excited by dorsal firing and inhibits inspiration. Without the PC, breathing would be prolonged, with lots of inspiratory gasps and brief expirations

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8
Q

Where are M3 receptors found? What do they do?

A

Smooth muscle

Mediate contraction to ACh. Also present on mucous-producing cells and evoke increased secretion

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9
Q

Which ILD is erythema nodosum associated with?

A

Sarcoidosis

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10
Q

Briefly outline the asthma treatment pyramid?

A

(bottom to top)

  • Reliever - SABA
  • Preventer - ICS
  • Controller (2nd line additive to ICS) - theophylline, LTRA, LABA/LAMA
  • Controller - oral steroid
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11
Q

When are tests most useful with regards to prevalence measure?

A

When prevalence is at 50%

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12
Q

What Clotting factors are involved in Prothrombin Time (PT)?

A

II, V, VII and X

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13
Q

How is COPD severity assessed?

A

GOLD staging, management is dependent on this.

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14
Q

What clotting factors are involved in Activated Partial Thromboplastin Time (aPTT)?

A

II, V, VIII, IX, X, XI and XII

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15
Q

What external influences are there on the respiratory centres responsible for breathing rhythm?

A

Higher brain centres

Stretch receptors in the walls of bronchi and bronchioles, guards against hyperinflation (Hering-Breur reflex)

Juxtapulmonary receptors - stimulated by pulmonary capillary congestion and pulmonary oedema i.e. heart failure

Joint receptors - impulses from moving limbs increases breathing

Baroreceptors

Central and peripheral chemoreceptors - sense the values of gas tensions, example of negative feedback control

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16
Q

Respiratory acidosis

A

Increasing [H+] due to increasing pCO2

[H+] is proportional to pCO2/[HCO3-], so HCO3- will also have to rise to compensate, kidneys excrete extra [H+] (occurs slowly)

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17
Q

What is the best drug combination for treating someone with moderate COPD?

A

Combo of LABA and LAMA, superior to either drug alone at increasing FEV1.

These drugs work in different but complimentary ways to one another to cause smooth muscle relaxation

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18
Q

What do alveolar macrophages release in response to cigarette smoke in patients with COPD? What is then released next?

A
  • neutrophil chemotactic factors
  • cytokines (IL-8)
  • mediators (Leukotriene B4)
  • TNF alpha oxygen radicals.

Proteases (collagenase, elastase) released by neutrophils, causing mucous hypersecretion in chronic bronchitis or alveolar wall destruction in emphysema.

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19
Q

What is pneumoconiosis? Give some causes

A

Another ILD, a “mineral dust disease” Causes are fibrogenic and non-fibrogenic. Fibrogenic - asbestosis, silicosis Non-fibrogenic - siderosis (iron), stanosis (tin), baritosis (barium)

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20
Q

What’s the difference between -aemia and -osis? I.e. acidaemia and acidosis

A

Acid/Alkalaemia is referring to an increase or decrease in [H+]

Acid/alkalosis is referring to the process tending to cause an increase or decrease in [H+]

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21
Q

Where are M1 muscarinic receptors found? What do they do?

A

Ganglia

Facilitate fast transmission mediated by ACh acting on nicotinic receptors

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22
Q

How does the body compensate in the case of…

  • excess H+
  • excess CO2
A
  • too much H+, body blows out more CO2
  • too much CO2, body excretes H+ via the kidneys

H+ + HCO3- ⇔ H2CO3 ⇔ CO2 + H2O

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23
Q

Describe developing red cells - where do they develop, what do they contain and what do they require?

A
  • Where? Bone marrow
  • Contain? A nucleus, unlike matured RBCs
  • Require? Vitamin B12 and folate for the nucleus to mature before its removal
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24
Q

What groups of neurones are involved in active expiration?

A

VENTRAL neurones get excited during increased firing of dorsal neurones. Go on to excite internal intercostal and abdominal muscles, leading to forceful expiration.

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25
What's the difference between allergic and non-allergic rhinitis?
Allergic rhinitis involves IgE and is very similar to allergic asthma Non-allergic rhinitis doesn't involve IgE and the causes are numerous
26
What equation underpins all acid-base things? Why is acid-base regulation important?
H+ + HCO3- ⇔ H2CO3 ⇔ CO2 + H2O The body produces 60 millimol of H+ a day via metabolism, and most of this needs to be excreted via urine to tightly maintain a H+ of 35-45 nanomol/L Rearranged equation: [H+] is proportional to pCO2/[HCO3-]
27
Where are M2 receptors found? What do they do?
Post-ganglionic neurone terminals Act as inhibitory autoreceptors, **reducing the release of ACh**
28
Diagnose - [H+] is elevated, HCO3- is decreased What is the compensatory response?
Metabolic acidosis pCO2 is lowered, excess is blown off
29
Treatment of acute asthma attack
Oral Pred nebulised high dose salbutamol +/- nebulised ipatropium +/- aminophylline/magnesium At least 60% O2
30
What are the features of the Non-rebreather mask?
Up to 85% FiO2 Uncontrolled FiO2 Flow limited to outflow of wall (15L) "Go-to" mask in ABCDE situations
31
Steroid treatments in COPD could lead to infective exacerbations because of their immunosuppressive activity. How are they prescribed?
In combination with a LABA, reduces exacerbations in eosinophilic COPD
32
What are the three types of anaemia?
Microcytic - iron deficiency e.g. in chronic blood loss Macrocytic - vit B12/folate deficiency e.g. nuclear defects Normocytic - acute blood loss. Anaemia of chronic disease e.g. due to inflammation or infection
33
Benefits of a spacer device?
reduces oropharyngeal and laryngeal side effects reduces systemic absorption from swallowed fraction reduces particle size and velocity improves lung deposition
34
What is SaO2? And what is SpO2?
SaO2 is the oxygen saturation of arterial blood SpO2 is the percutaneous oxygen saturation (sats detected by a pulse oximeter)
35
What blood measurement could a deficiency in B12 and folate be seen in?
Mean Cell Volume (MCV)
36
Which part of the respiratory tree is the conducting zone (gas transport) and which is the acinar zone (gas exchange)?
conducting - 1-17, large airways, down to the bronchioles acinar - 17-23, terminal bronchioles and alveolar sacs
37
What are the key features of Chronic Bronchitis and Emphysema, the two forms of COPD?
CB * inflammation of bronchi and bronchioles * cough, with **clear mucoid sputum** * infections with purulent sputum (containing pus) * increasing breathlessness Emphysema * **distension** and **damage** to the alveoli * **destruction** of acinal pouching in alveolar sacs
38
Metabolic alkalosis
Decreasing [H+] due to increasing HCO3- [H+] is proportional to pCO2/[HCO3-], CO2 needs to rise to maintain ratio, so **ventilation is decreased** (occurs quickly)
39
What was the Helena study?
Smoking was banned in restaurants, bars, taxis etc. in an isolated town, ppn 66,000 and one hospital for cardiac care. Heart attack rates fell by 58% in 6 months.
40
Name that cell!
Lymphocyte - one very big purple nucleus Have numerous functions. Important in viral infections
41
What is FiO2?
Fraction of inspired oxygen, the fraction of oxygen that a patient is inhaling from an oxygen device
42
What are some types of Hypersensitivity pneumonitis? What type of hypersensitivity is this?
Farmer's Lung Bird Fancier's Lung etc. etc. Type III Hypersensitivity (immune complex accumulation, i.e. antigen-antibody complexes aren't cleared by the innate immune system)
43
Why is tiotropium superior to ipratropium?
Tiotropium has a much longer half-life at M3 receptors, giving it functional selectivity. M1 and M3 blockage is desirable, but M2 block leads to increased release of ACh
44
What are the features of the nasal cannula?
well-tolerated low flow only uncontrolled FiO2, dependent on the patient's own nasal breathing
45
Diagnose - [H+] is decreased, pCO2 is decreased What is the compensatory response?
Respiratory alkalosis HCO3- is lowered
46
Disease in the lungs is obstructive/restrictive. Disease in the airways is obstructive/restrictive.
lungs - restrictive airways - obstructive
47
What are the features of the Variable Performance Mask?
5-15L/min Uncontrolled FiO2 Unable to cope with high flow requirements
48
Give some examples of anti-histamines (H1 receptor antagonists)
Loratidine Fexofenadine Cetirizine
49
Give the %s of each of the white blood cells in a normal individual's blood
neutrophils ~60% lymphocytes ~ 28% monocytes ~8% eosinophils ~3% basophils ~1%
50
What feature of muscarinic antagonists means that they have few adverse effects?
Little systemic absoprtion due to quaternary ammonium group
51
Compared to obstructive diseases, what are compliance and elasticity like in restrictive diseases?
Compliance is down Elasticity is up Harder to get air INTO the lungs
52
Where are the central chemoreceptors? What do they do?
Near the surface of the medulla respond to the H+ of the cerebral spinal fluid
53
Treatment of acute COPD
nebulised high dose salbutamol + ipatropium Oral Pred antibiotic (if infection - amox/doxy) 24-28% O2, non-invasive ventilation
54
What other conditions, without anaemia, might you see macrocytic cells in?
Alcohol excess Liver disease Hypothyroidism
55
What are the features of the Venturi Mask?
Fixed performance Comes in a variety of %s
56
Diagnose - [H+] is elevated, pCO2 is increased. What is the compensatory response?
Respiratory acidosis HCO3- is raised
57
Name that cell!
Eosinophil, red granule appearance Seen in parasitic infections, as well as hypersensitivity/allergic reactions
58
Name that cell!
Basophil... Seen in hypersensitivity reactions
59
Treatment of ILD
Remove trigger Immunosuppression: 1st line - systemic corticosteroids, inhaled isn't effective = ORAL PRED. 2nd line - oral azathioprine (steroid sparing immunosuppressant)
60
How does V/Q vary within the lung?
Apex - good ventilation, poor perfusion = high V/Q Base - poor ventilation, good perfusion = low V/Q
61
What makes up the remaining 55% of total blood?
Plasma - 90% is water - proteins - albumin, immunoglobulins, clotting factors etc. - nutrients and salt
62
Situation - COPD patient with chronically compensated elevated CO2 levels (CO2 retainer) in resp failure and put on high inspired oxygen. What are the 3 mechanisms by which CO2 will increase in this patient's blood?
Haldane effect Ventilation/Perfusion mismatch Removal/reduction of hypoxic drive
63
Name some causes of respiratory acidosis and alkalosis
acidosis - choking, bronchopneumonia, COPD/asthma alkalosis - hysterical overbreathing, mechanical over-ventilation, raised intracranial pressure
64
Upon being presented with antigen by a dendritic cell, what cytokines does Th0 release and what do they go on to do?
IL-4, IL-6, IL-12, TGF beta and IFN gamma * TGF beta and IL-6 - Th17 activation * IL-12 and INF gamma - Th1 activation * TGF beta - Treg cell activation (suppresses Th2) * IL-4 - Th2 activation
65
Clinical syndrome of ILD - symptoms
* Breathless OE * Cough, no wheeze * Finger clubbing * Inspiratory lung crackles * Central cyanosis if hypoxaemic
66
What's the difference between Type I and Type II respiratory failure?
Type I - hypoxaemia **without** an increase in CO2 in the blood (hypercapnia). Typically caused by a V/Q mismatch, but also caused by high altitudes, alveolar hypoventilation and a shunt (mix of oxygenated and deoxygenated blood) Type II - **hypoxaemia with hypercapnia**. Caused by increased airway resistance (COPD/asthma), decrease in area of the lung available for gas exchange, deformities and neuromuscular problems
67
3 components of the asthma triad
airway hyperresponsiveness reversible airway obstruction airway inflammation
68
Name that cell!
Monocyte, one big nucleus Active in chronic infections, malignancies and immune disorders
69
Suspicious of asthma? Ask about...
Triggers! Allergens - animal dander, pollen, dust mites etc. Others - exercise, cold weather, smoke, drugs (NSAIDs, beta blockers)
70
In blood, 'formed elements' account for 45% of total blood, and constitute red cells, white cells and platelets. What are all the types of white cells?
Granulocytes - neutrophils, basophils, eosinophils Agranulocytes - lymphocytes, monocytes
71
In a respiratory acid or alkalosis, the primary change is seen in pCO2/HCO3- In a metabolic acid or alkalosis, the primary change is seen in pCO2/HCO3-
Respiratory - primary change is in pCO2 Metabolic - primary change is in HCO3-
72
Respiratory alkalosis
Decreasing [H+] due to decreasing pCO2 [H+] is proportional to pCO2/[HCO3-], so HCO3- will have to lower to compensate, **kidneys retain [H+]** (slow process)
73
What do red cells not contain, compared to every other cell in the body.
A nucleus, instead they contain haemoglobin
74
What is the major rhythm generator in breathing? How is this rhythm generated?
A network of neurons called the **Pre-Botzinger Complex**, found in the **MEDULLA** is excited by the apneustic centre (AC). This excites DORSAL neurones Firing generates muscle contraction of inspiratory muscles (active inspiration), firing stops = passive expiration
75
How do you calculate specificity?
True negatives/(true negatives + false positives)
76
What are some chronic adaptations to high altitude hypoxia?
increased RBC production increased 2,3-BPG production within RBCs increased number of capillaries increased number of mitochondria
77
What pro-inflammatory cytokines are released by Th2 cells during asthma? (4)
* IL-4 * IL-5 * IL-13 * TGF beta IL-4 and IL-13 act on B cells to activate mast cells IL-4 and TGF beta act on Th9 cells IL-5 acts on eosinophils
78
Metabolic acidosis
increasing [H+] due to decreasing HCO3- [H+] is proportional to pCO2/[HCO3-], CO2 needs to be lost so there is **increased ventilation** (occurs quickly)
79
Name some causes of metabolic acidosis and alkalosis
acidosis - impaired [H+] excretion, increased [H+] production, loss of HCO3- alkalosis - loss of [H+] in vomit, alkali ingestion, potassium deficiency
80
Sarcoidosis clinical syndrome - symptoms and signs
erythema nodosum bilateral hilar lymphadenopathy lung infiltrates appearance of NON-CASEATING GRANULOMAS (type IV hypersensitivity reaction) Lack of energy, weight loss, fever, uveitis
81
Asthma clinical syndrome - symptoms
episodic diurnal variability non-productive cough, wheeze triggers family history
82
Diagnose - [H+] is decreased, HCO3- is increased What is the compensatory response?
Metabolic alkalosis pCO2 is increased, ventilation rate lowers
83
Hallmarks of remodeling in chronic asthma?
thickening of the basement membrane collagen deposition in the submucosa hypertrophy of smooth muscle
84
How do you calculate sensitivity?
True positives/(true positives + false negatives)
85
What is PDE4? Name a drug that acts on PDE4 and describe how it works
Phosphodiesterase 4, prominent PDE expressed on neutrophils, T cells and macrophages. **Rofumilast**, approved for severe cases of COPD, may have inhibitory effects on inflammatory and immune cells through inhibiting the PDE4 receptor.

Respiratory (11 decks)

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