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2B week 2 - obstructive disease > clinical relevance / extra pbl 2 > Flashcards

clinical relevance / extra pbl 2 Flashcards

1
Q

what spirometry values are abnormal in emphysema and why

A

IRV i increased due to loss of elasticity meaning that air can’t be expelled properly; total lung capacity (TLC) is also increased due to gas trapping

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2
Q

brief overview of TH2 pathway response to allergens

A
  1. dendritic cells pick up allergen -> become APC
  2. APC present to CD4 cells 3. TH2 response initiated -> cytokine release (IL4,5,13)
  3. IL5 attracts eosinophils to the area
  4. IL4 + 13 work in partnership to cause IgE release from B cells
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3
Q

5 investigations useful in asthma diagnosis

A
  1. PEF variability
  2. spirometry with reversibiltiy
  3. FeNO
  4. blood eosinophils
  5. allergy tests
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4
Q

what do steroids aim to treat in asthmatic patients

A

airway inflammation

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5
Q

give 5 clinical features of acute severe asthma

A
  1. PEF 33-50% best
  2. respiratory rate >25/min
  3. HR >110 bmp
  4. inability to complete sentences in one breath
  5. wheeze (progressive, worsening)
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6
Q

7 signs of life-threatening asthma

A
  1. altered conciousness
  2. exhaution
  3. arrythmia
  4. hypotension
  5. cyanosis
  6. silent chest
  7. poor respiratory effort
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7
Q

how is acute asthma treated

A

ABCDE
treat with bronchodilators (SABA), oxygen, corticosteroids (oral pred if poss)

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8
Q

what could cause COPD in a young patient

A

cannabis use

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9
Q

what are 3 key elements to look for in an asthma review

A

inhaler technique; are they taking all the inhalers; triggers (pets, dust etc.)

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10
Q

what is a rescue pack (asthma/COPD)

A

antibiotics and oral steroids for patients with pre-existing condition for use as part of an acute exacerbation plan

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11
Q

3 clinical findings in emphysema

A

reduces cricosternal distance; quiet breathsounds; obstructive pattern (FEV1/FVC)

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12
Q

what is the MRC dyspnoea scale

A
  1. not troubled by breathlessness except on stenuous exercise
  2. short of breath when hurrying
  3. walks slower than contemporaries on level ground due to SOB/ has to stop
  4. stops for breath after 100m/few mins on level ground
  5. too breathless to leave the house/undressing
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13
Q

3 investigations to help confirm a diagnosis of COPD

A
  1. post bronchodilator spirometry (to check its not asthma)
  2. a1 antitrypsin levels
  3. elevatd Hb in FBC (polycythemia)
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14
Q

what is hypoxic drive

A

a form of respiratory drive in which the body uses oxygen chemoreceptors instead of carbon dioxide receptors to regulate the respiratory cycle

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15
Q

what is the O2 target range in a COPD patient

A

86-92%

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16
Q

what are some examples of cardiac causes of acute breathlessness (9)

A

HF; AS; congenital heart disorders; MI; HCM; pericarditis; myocarditis; arrythmias; MS

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17
Q

what are some resp causes of acute breathlessness (10)

A

COPD exacerbation; acute asthma; pneumonia; croup; pneumothroax/haemothorax; ARDS; acute bronchitis; PE; pleural effusion; pulmonary oedema

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18
Q

signs that acute SOB has a resp cause (4)

A

cough, wheeze, stridor, hemoptysis

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19
Q

signs acute SOB has a cardiac cause (4)

A

nausea; chest pain; sweating; palpitations

20
Q

what 3 things are key to ask when taking a SOB history

A
  1. Speed of onset of breathlessness (dinural variation, episodic)
  2. progression and variablity (cant do hobbies now etc.)
  3. exacerbating and relieving factors
21
Q

what type of hypersensitivity reaction is atopy

A

type 1 - exaggerated IgE mediated immune response

22
Q

what immune cell is usually hyper-responsive in atopic people

A

T cells

23
Q

describe second exposure to triggering substances in asthmatics (immunologically)

A
  1. Asthmatics have a naturally high level of IgE antibodies which are bound to receptors on mast cells;
  2. On second exposure, the allergen binds to the IgE and activates these mast cells to degranulate;
    3.This binding causes the release of histamine, heparin, prostaglandins and leukotrienes which causes the contraction of the smooth muscle in the airways and inflammation - occurs through both late and early phase;
  3. early phase histamine release causes : a) Smooth muscle contraction which causes a subsequent difficulty breathing,
    b) Blood vessel dilation causing increased permeability of the blood vessel wall which causes fluid to leak out into the interstitial spaces;
  4. late phase: eosinophils, basophils, Th2 cells and leukotrienes are recruited to the site of the reaction as a result of interleukins –> leukotrienes (LTB4 and LTc4) cause smooth muscle contraction and damage to the epithelium and attract neutrophils, mast cells and eosinophils to their location even after the allergen is gone
24
Q

what is the atopic triad

A
  1. Allergic rhinitis Inflammation of the mucosal membrane lining the nose;
  2. Asthma Inflammation of the lung airways which is usually reversible;
  3. Atopic dematitis Inflammation, redness and swelling of the skin
25
Q

how is the majority of O2 carried in the body

A

the majority of it is bound to respiratory pigments - haemoglobin and myoglobin (mostly all in haemoglobin, the very little bound to myoglobin is stored in the muscles for use during a sudden increase in O2 demand).

26
Q

2 ways O2 can be carried in the body

A

bound to haemoglobin; dissolved in the blood plasma

27
Q

what 3 factors determine the rate of O2-haemoglobin dissociation

A

[H+], temperature, 2,3-Diphosphoglycerate (2,3-DPG)

28
Q

what is the Bohr effect

A

a shift to the right of the O2-haemoglobin dissociation curve due to a lower affinity for O2 in more acidic/CO2 rich conditions

29
Q

why is the O2-Haemoglobin curve sigmoidal?

A

It gets easier for the next oxygen to bind to haemoglobin with every O2 that binds prior to - when one O2 molecule bind
there is a structural change in the whole haemoglobin molecule which allows for increased access to the Haemgroup in the other subunits of the protein

30
Q

3 ways CO2 is transported in the body

A
  1. dissolved into the blood plasma/RBCs as bicarbonate (the majority);
  2. in solution in the blood plasma or cytoplasm of RBCs;
  3. bound to protein subunits of haemoglobin/ to other plasma proteins
31
Q

what is chloride shift

A

an exchange of ions that takes place in our red blood cells in order to ensure that no build up of electric change takes place during gas exchange - bicarb out and Cl- in

32
Q

why is chloride shift reversed in the lungs compared to the rest of the blood

A

to allow HCO3- to enter and be converted by carbonic anhydrase to CO2 and then diffuses into the alveolar air

33
Q

CO2 -> HCO3- reaction

A

CO2+H2O ⇌ H2CO3 ⇌ H+ +HCO3-
initial step involves the use of carbonic anhydrase

34
Q

what is the Haldane effect

A

oxygenation of blood in the lungs displaces carbon dioxide from hemoglobin, increasing the removal of carbon dioxide

35
Q

what are the 4 types of respiratory acid-base disorders (and what is unbalanced in them)

A
  1. respiratory acidosis (the blood pCO 2 rises and pH falls)
  2. respiratory alkalosis (pCO 2 falls and pH rises, occurs during hyperventilation)
  3. metabolic acidosis (excessive production of H+ or excessive excretion of CO3-)
  4. metabolic alkalosis (excessive intake of bicarbonate or excessive loss of acidic fluid e.g. during vomiting)
36
Q

how does the paraympathetic system control the RT

A

Ach release causes bronchoconstriction - useful when there is a need to reduce the flow of
air to the lungs, such as during an asthma attack

37
Q

what is the main NT involved with RT sympathetic control

A

adrenaline - relaxation of smooth muscle

38
Q

symp/parasymp control of mucous and blood vessels i the RT

A

sympathetic: decreases muscous secretion and BV constriction;
parasympathetic: promotes mucus secretion and BV dilation

39
Q

what is the pulmonary plexus

A

Network of autonomic nerves and ganglia located at pulmonary hila of each lung

40
Q

role of the pulmonary plexus

A

Regulates bronchial smooth muscle tone, mucus secretion, vascular permeability,
and blood flow

41
Q

pulmonary plexus nerve supply

A

sympathetic - indirectly from the cervical sympathetic ganglia via the cardiac plexus; directly from the sympathetic cardiac nerves from the paravertebral ganglia of
T2 to T6 segments of the spinal cord
parasympathetic - vagal trunks (cranial nerve X) via several cardiac nerves

42
Q

how to calculate alveolar ventilation

A

VCO2/FCO2

v - volume of CO2 produced
f - fraction of alveolar ventilaiton that is CO2

43
Q

biochem make up of surfactant

A

Phospholipids make up around 75% - form a lattice structure called tubular myelin that forms film that spreads over
entire surface of alveoli;
main ion is Ca2+;

44
Q

5 funcitons of surfactant

A
  1. Reduces surface tension in alveoli and prevents collapsing tendency of lungs;
  2. stabilise the alveoli to withstand collapsing
  3. play an important role in inflation of lungs after birth
  4. Defense against infection and inflammation
  5. Stops transudation of fluid from blood into alveoli
45
Q

what is cor pulmonale

A

right heart failure - most commonly due to COPD, occurs due to loss of vascular bed and chronic hypoxic pulmonary vasoconstriction (HPV) due to alveolar wall destruction

46
Q

common signs of cor pulmonale (6)

A

Fainting spells during activity;
Chest discomfort/pain; Swelling of the feet or ankles; Symptoms of lung disorders, such as wheezing or coughing or phlegm production; Bluish lips and fingers (cyanosis)

2B week 2 - obstructive disease (4 decks)

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