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ASforP > Respiratory conditions and drugs > Flashcards

Respiratory conditions and drugs Flashcards

1
Q

What is croup?

A

Inflammation of the larynx, trachea and bronchi

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2
Q

What is the cause of croup?

A

Usually a viral infection (most commonly parainfluenza ≈75% of all cases) invading the laryngeal mucosa leading to inflammation, hyperaemia and oedema
Can occasionally be bacterial (mycoplasma pneumoniae)

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3
Q

What are the main symptoms of croup?

A

Dyspnoea
Seal bark cough
Stridor
Fever

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4
Q

How can croup cause death?

A

Narrowing of subglottic airways cause dyspnoea (rapid and deep) hypoxia and hypercapnia progressing to respiratory failure and eventually cardiac arrest

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5
Q

What are the signs of peadiatric respiratory distress?

A

Intercostal recession
Tracheal tug
Paradoxical respiration (see-saw breathing)
Dyspnoea
Cyanosis
Hypotonia

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6
Q

What type of virus is parainfluenza?

A

RNA-circus, negative sense, helical, linear, non-segmented virus

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7
Q

What can non vaccinated children presenting with croup symptoms be more susceptible to?

A

Diphtheria infection

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8
Q

Approximately what percent of pre-school children contract croup?

A

6%

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9
Q

At what time of year do croup hospital admissions peak?

A

Late autumn, September to December

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10
Q

At what ages is croup most common?

A

6 months to 3 years, peak incidence is between 18 and 24 months. It is uncommon after the age of 6

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11
Q

Which scoring systems can help with estimating the severity of croup symptoms?

A

Westley croup score
Modified Taussig croup score

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12
Q

How is asthma defined?

A

It is a descriptive term and hard to define. Guthrie (2019) summarises it as “Chronic inflammation of the airway characterised by intermittent airway obstruction and hyperactivity”

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13
Q

What is the pathophysiological process of asthma?

A

Genetic factors give patients hyper-responsiveness then:

Environmental factors (smoking, pollution)
+
Triggers (allergens, irritants)
=
Clinical asthma (oedema, hyper-secretion of mucus)
+
Airway remodelling

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14
Q

What can trigger airway hyperresponsiveness?

A

Upper respiratory tract infections (URTs)
Chest infections
Allergens (Pollen, animal hair, dust, mold etc.)
Air pollution, cigarette smoke, chemicals
Drugs (Aspirin, NSAID’s, Beta-blockers)
Cold air
Exercise

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15
Q

What is COPD?

A

Umbrella term for Emphysema and chronic bronchitis
-Destruction on lung parenchyma and abnormal inflammatory response to noxious particles

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16
Q

How do pre-dispositions and environmental factors cause COPD?

A

Pre-dispositions in the genome negatively affect the lungs’ ability to prevent damage to its tissue. Environmental insults such as pollution and smoking cause free radicals to be produced in the lungs and an inactivation of lung anti-proteases.

Both of these leads to chronic inflammation and damage of airways and parenchyma

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17
Q

What is the Haldane effect?

A

An increase in pO2 causes Hb to lose its affinity for CO2

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18
Q

What are risk factors for spontaneous pneumothorax?

A

Smokers
Males
Tall and slender build
Respiratory diseases (Asthma, COPD, Lung Ca, ILD etc.)
Infection (rarely)

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19
Q

What different classes of pneumonia are there and how are they defined?

A

Many classes all defined by the wider source of infection. Hospital acquired, community acquired etc.

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20
Q

What are the four stages of pneumonia?

A

Early congestion
Red hepatization
Gray hepatization
Resolution

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21
Q

What causes pneumonia?

A

Infection, usually bacterial but can be viral

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22
Q

What is pneumonia?

A

A respiratory illness that causes the alveoli to fill with blood cells, pus, and other liquid.

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23
Q

What are the classic symptoms of pneumonia?

A

Persistent productive cough (Wheezy in adults, grunty in paeds)
Shortness of breath
Pyrexia
Chest pain
Aching body
Lethargy
Loss of appetite
Crackles on auscultation
Lack of oxygen can cause delerium in older patients

24
Q

What is Virchow’s triad?

A

Triad of factors which contribute to thrombus formation

Stasis (Poor blood flow)
Vessel wall injury (Endothelial damage)
Hypercoagulability (Pre-existing disease/condition)

25
Q

What can effect hypercoagulabilty?

A

Cancer
High oestrogen states
Inflammatory bowel disease
Nephrotic syndrome
Sepsis
Blood transfusion
Thrombophilia

26
Q

What are the high and low risk factors for PE?

A
27
Q

What symptoms occur from a PE?

A

Pleuritic chest pain
Dyspnoea/tachypnoea
Hypoxia
Hypotension
Tachycardia
Haemoptesis

28
Q

What is IRDS?

A

Infant Respiratory Distress Syndrome also known as Neonatal Respiratory Distress Syndrome

29
Q

Who is most at risk of IRDS?

A

Usually affects pre-term babies (surfactant is first produced between 28 and 36 weeks gestation), can also effect full term babies, and babies born to diabetic mothers and via c-section. It is a common cause of neonate death.

30
Q

How can gestational diabetes cause IRDS?

A

Foetal insulin production inhibits the production of phospholipids which is the main component of human surfactant

31
Q

How can C-section cause IRDS?

A

During spontaneous labour there is a decrease in secretion of foetal lung liquid and an increase in its absorption and the release of surfactant is stimulated.

This may be mediated by a raised level of catecholamines in the foetus in response to rupture of membranes and labour.

In C-section the normal changes in surfactant production and absorption can be absent

32
Q

When does IRDS usually present?

A

Immediately after birth or in the few hours following

33
Q

What can cause IRDS?

A

Insufficient surfactant production or surfactant inactivation due to immature lungs or other factors makes gas exchange more difficult

34
Q

What is the function of surfactant?

A

Surfactant counteracts the collapsing forces of the surface tension of the thin layer of water that lines each alevoli.

The surface tension prevents the alveoli from expanding. Without enough surfactant the alveoli collapse with each expiration.

35
Q

Where is surfactant produced?

A

Alveloar type II cells

36
Q

What is the composition of surfactant?

A

80% phospholipids, 10% protein, 10% neutral lipids

37
Q

What leads to diffuse atelectasis in neonates?

A

Insufficient surfactant causes alveloar collapse

38
Q

How does diffuse atelectasis lead to further respiratory distress in neonates?

A

Reduced lung capacity
\/
Decreased pulmonary blood flow
\/
Reflex pulmonary vasoconstriction
\/
Severe hypoxia

39
Q

How does lack of surfactant in neonates perpetuate?

A

An inflammatory response causes an increase in capillary permeability which causes excess fluid and protein (fibrin) to enter the alveoli forming a hyaline membrane and further impairing lung expansion. Oxygen diffusion is further decreased leading to increased WoB, subsequent anaerobic respiration and lactic acidosis. Pulmonary vasoconstriction causes a further decrease in cell function and therefore surfactant production.

40
Q

What treatments can be given for IRDS?

A

Glucocorticoids - Can also be given prophylactically such as inductions
Synthetic surfactant given via ET tube or nebulised (less invasive)
Oxygen therapy (Can cause other issues)
CPAP

41
Q

What airway remodelling occurs with clinical asthma?

A

Fibrotic damage from persistent inflammation
Mucus gland hypertrophy
Smooth muscle hypertrophy
Collagen deposit

42
Q

What pathology occurs in genetic airway hyper-responsiveness?

A

Hyperactive mast cells, T-cells etc. attract inflammatory cells

43
Q

What are the main two clinical features of asthma?

A

Oedema and hyper-secretion of mucus

44
Q

What is cystic fibrosis?

A

Cystic fibrosis (CF) is an inherited disorder that causes severe damage to the lungs, digestive system and other organs in the body.

Cystic fibrosis affects the cells that produce mucus, sweat and digestive juices. These secreted fluids are normally thin and slippery. But in people with CF, a defective gene causes the secretions to become sticky and thick. Instead of acting as lubricants, the secretions plug up tubes, ducts and passageways, especially in the lungs and pancreas. This causes lung infections and problems with digesting food.

45
Q

How do beta-2 agonists cause bronchodilation?

A

They bind to beta-2 receptors (G protein coupled receptors) in the lungs. This causes the GDP on the alppha sub-unit to be hydrolysed and exchanged for GTP. The now activated alpha sub-unit activates adenylate cyclase. cAMP is then generated from ATP forming PKA. This causes an inactivation of the myosin light chain kinaese and a decrease in calium and therefore bronchodilation

46
Q

How do anticholinergenics like ipratropium bromide work?

A

Anticholinergic bronchodilators (or muscarinic receptor antagonists) block the parasympathetic nerve reflexes that cause the airways to constrict, so allow the air passages to remain open. Muscarinic receptor antagonists bind to muscarinic receptors and inhibit acetylcholine mediated bronchospasm.

Anticholinergenics dry the body out by reducing secretions (Can’t see, pee, spit or shit), these are standard effects of all acetylcholine blockers.

47
Q

What should LABAs be used in conjuction with, why?

A

LABAs should only be used when combined with inhaled corticosteroids

Long-acting β agonists (LABAs) might increase the risk of asthma mortality when used by patients with unstable asthma without concomitant inhaled corticosteroids or scheduled medical review.

48
Q

Why do you not pierce capsule inhalers more than once?

A

You may shatter the capsule and breathe in the fragments

49
Q

What is the difference in technique for using a Dry Powder Inhaler (DPI) and pressurised Metered Dose Inhalers (pMDI), breath-actuated metered dose inhalers and soft mist inhalers?

A

DPI - quick sharp deep breath in
pMDI/breath-actuated/soft mist - long slow breath in

Hold breath for 10 seconds or as long as possible with all inhalers

50
Q

Hoe do steroids help with asthma and COPD?

A

They reduce inflammation of the airway and reduce secretions

51
Q

How do mucolytics work?

A

They break down mucus and/or help draw more water into your airway. These actions thin out the mucus making it easier to clear

52
Q

What is Montelukast?

A

Montelukast is one of a group of medicines called leukotriene receptor antagonists, it blocks the effects of these inflammatory chemicals relieving symptoms. Montelukast is an add-on treatment, which means you take it alongside your preventer inhaler.

53
Q

What are the serious side-effects of montelukast?

A

Neuropsychiatric reactions

Including speech impairment, obsessive-compulsive symptoms, mood changes, depression and hallucinations

54
Q

When should asthma/COPD patients take their rescue packs?

A

When flare ups are unresponsive to their reliever inhaler and with the following symptoms:

Steroid:
Increased breathlessness/wheeze
New/increased cough
New/increased chest tightness

Antibiotic:
Fever
Change in sputum
-amount, consistency, colour

55
Q

How do beta-2 agonists affect potassium and glucose levels?

A

Beta-2 agonists have been shown to decrease serum potassium levels via an inward shift of potassium into the cells due to an effect on the membrane-bound Na/K-ATPase, which can potentially result in hypokalemia.

Beta-2 agonists also promote glycogenolysis, which can lead to inadvertent elevations in serum glucose.

56
Q

What is theophylline and how does it work?

A

Theophylline is the most commonly prescribed xanthine.

It inhibits phosphodiesterase and blocks adenosine receptors causing bronchodilation.

57
Q

What are Phosphodiesterases (PDEs)?

A

Phosphodiesterases (PDEs) are enzymes involved in the homeostasis of both cAMP and cGMP.
Their main function is to catalyze the hydrolysis of cAMP, cGMP, or both (termination phase).

ASforP (22 decks)

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