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Respiratory block > Misc. > Flashcards

Misc. Flashcards

1
Q

What is the CFTR channel responsible for?

A

Moving Chloride ions outside of cells in the lungs and other organs.

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2
Q

What are the consequences of a mutation in the CFTR gene?

A

CFTR is unable to move Chloride ions out of cells, resulting in buildup of sticky mucous on the outside of cells.

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3
Q

What are the characteristics of Type 1 hypersensitivity?

A

Allergy
Immediate
Th2 cells promote IgE secretion (via IL-4)
Mast cell degranulation (bind FcER on IgE)
May be local (common) or systemic (rare: anaphylaxis)
e.g. Atopy
Two Phases: immediate = mast cell degranulation; delayed: cytokine and chemokine release

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4
Q

What are the characteristics of Type 2 hypersensitivity?

A

Antibody mediated
IgM and IgG against cell-bound or extracellular matrix antigen.
e.g. Graves Disease.

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5
Q

What are the characteristics of Type 3 hypersensitivity

A

IgM and IgG immune complex deposition

e.g. SLE

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6
Q

What are the characteristics of Type 4 hypersensitivity?

A

Delayed type hypersensitivity
CD4 mediated
e.g. Coeliac disease, TB

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7
Q

What are the characteristics of allergens (ingested vs. inhaled)

A

Inhaled: highly soluble proteins carried by small proteins
Ingested: slowly degraded molecules, very stable.

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8
Q

What occurs in the “sensitisation” phase of Type 1 Hypersensitivity?

A

Th2 cell differentiation

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9
Q

What happens in Coeliac disease and what kind of hypersensitivity is it?

A

Type 4/DTH
T-cells recognise Gliadin Peptides (rich in glutamine and proline)
Transglutaminase enables HLA-DQ2 to bind Gliadin

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10
Q

In what forms is CO2 transported in the blood? in what proportions?

A

10% dissolved
30% attached to proteins
60% bicarbonate

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11
Q

What enzyme is responsible for the formation of Bicarbonate in the blood?

A

Carbonic anhydrase

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12
Q

Out of CO2 and O2, which diffuses more quickly across the A-C membrane?

A

CO2 diffuses 20 times faster than O2.

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13
Q

In general, what is the reason for increased PACO2?

A

Inadequate alveolar ventilation:

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14
Q

What is the relationship between Arterial CO2 concentration and Alveolar ventilation?

A

Pa(CO2) is proportional to the inverse of Alveolar ventilation.

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15
Q

Which nerve supplies the diaphragm?

A

Phrenic

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16
Q

What do the External intercostal muscles do? Which nerve provides their innervation?

A

Increase A-P thorax diameter

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17
Q

Which muscles are involved in active expiration?

A

Abdominal muscles

Internal intercostals

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18
Q

The Work of Breathing is the sum of which two forces?

A

Resistive + Elastic

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19
Q

What is meant by the Resistive forces of breathing?

A

The resistance to air-flow by the walls of the tube through which it is travelling (i.e. increased resistance with decreased diameter)

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20
Q

What is meant by the Elastic forces of breathing?

A

Force required to expand the lungs against the elastic forces generated by the surface tension in alveoli and the lung tissue itself.

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21
Q

What is Compliance?

A

(Change in volume)/(change in pressure) a way of determining the elastic properties of the lung.

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22
Q

What breathing pattern would you observe in a patient with Airflow obstruction?

A

Deep, slow breaths

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23
Q

What breathing pattern would you seen in a patient with stiff lungs/reduced compliance?

A

Rapid, shallow breaths

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24
Q

What do the following stand for? PaO2, PaCO2.

What are their normal values?

A

Arterial PO2 and PCO2.

Their normal values are 100mmHg and 40mmHg respectively.

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25
Q

Where are central chemoreceptors located?

A

Ventral surface of medulla

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26
Q

What do central chemoreceptors respond to?

A

CSF [H+] (i.e. [CO2] of blood)

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27
Q

Where are peripheral chemoreceptors located?

A

Carotid bodies: bifurcation of common carotid arteries in the neck
Aortic bodies: Around the arch of aorta

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28
Q

What do peripheral chemoreceptors respond to?

A

Decreased PaO2
Decreased pH
Increased PaCO2

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29
Q

What limits exercise capacity in a healthy person?

A

Heart-rate

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30
Q

What are two muscles involved in active exhalation?

A

Sternocleidomastoid + scalene

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31
Q

What is Pulsus Paradoxus?

A

An increased difference between the blood pressure at inhalation vs. exhalation.
An abnormally large decrease in systolic BP during inhalation.

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32
Q

What are three possible causes of an increased A-a Gradient?

A

Right to Left Intrapulmonary Shunt (due to fluid filled alveoli)
V/Q Mismatch (due to lung dead space)
Alveolar hypoventilation

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33
Q

What is A-a gradient a measure of?

A

Efficiency of gas exchange between alveolus and artery.

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34
Q

What is the alveolar gas equation?

A

PAO2 = PiO2 - PACO2/RQ (approximately)

Use ~150 for room air PiO2 = partial pressure of inspired oxygen
RQ = Respiratory Quotient= Ratio of CO2 production to O2 consumption

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35
Q

What are the characteristics of Respiratory epithelium? (i.e. what type of epithelium? Which cells are involved?)

A 
30% ciliated columnar cells - move mucus
Goblet cells (30%) - Secrete mucus
Basal (stem) cells (30%) - renew epithelium
Brush cells with microvilli (3%)
Serous cells (3%) - secretory
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36
Q

How many rings of hyaline cartilage in the trachea?

A

10-12

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37
Q

What is found int he submucosa of the trachea?

A

Glandular structures that produce mucous -> glands and connective tissue

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38
Q

What layers make up the Trachea and what are these layers composed of?

A

Adventitia: cartilage + outer connective tissue
Submucosa: Glands + connective tissue
Mucosa: Lamina propria + epithelium

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39
Q

What are the structural differences between the bronchi and the trachea?

A

Thinner walls

Cartilage ring breaks down into individual plates in the intrapulmonary bronchi

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40
Q

What are the distinguishing features of bronchioles?

A

No cartilage
No goblet cells in epithelium
No ciliated columnar cells
Clara cells present

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41
Q

Why will you find ciliated cells further down the respiratory tract than you will find goblet cells?

A

Because goblet cells produce mucus and cilia are required to move mucus out of the respiratory tract.

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42
Q

What are Clara cells?

A

Columnar to cuboidal cells with short microvilli.
Present in bronchioles
Secrete surfactant to destroy surface tension.

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43
Q

What is the difference between Terminal and respiratory bronchioles?

A

Terminal: final level of conducting system. Cuboidal epithelium
Respiratory: Cuboidal to squamous epithelium. Contain some alveoli.

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44
Q

What will you find in the interalveolar septa?

A

Elastin fibres: pull apart alveoli
Pores: allow air to equilibrate
Type I and II pneumocytes
Intra-alveolar macrophages

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45
Q

What are the characteristics of type I pneumocytes?

A

Epithelial cells of alveoli
Simple squamous
Tight junctions limit ECF leakage
prominent basal lamina

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46
Q

What are the characteristics of type II pneumocytes?

A 
Cuboidal, chunky, big
Short microvilli
Lamellar bodies
Secrete surfactant
more common than Type I (but only 5% of area)
Can divide and give rise to Type I or II
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47
Q

What will you find between the lumen of an alveolus and an erythrocyte in the lumen of a pulmonary capillary?

A

Surfactant - alveolar epithelium - fused basal laminae - endothelium

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48
Q

What drains into the interpleural space? What is the significance of this?

A

Lymphatics.

Cancer can spread via this route.

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49
Q

What is anaphylaxis caused by?

A

Complete Mast cell degranulation

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50
Q

What does Histamine acting on H1 cause in an allergic reaction?

A

Pain and itch
Vascular ‘leak’
Mucous secretion
Bronchospasm

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51
Q

What is the effect of cysteinyl leukotrienes in asthma?

A

mucous
oedema
airway smooth muscle shortening

52
Q

What factors are involved in the immediate phase of Type I hypersensitivity?

A

Vasoactive amines

Lipid mediators: Leukotrienes, prostaglandins

53
Q

What factors are involved in the late phase of type I hypersensitivity?

A

Cytokines: IL-1; TNF

54
Q

What is Omalizumab?

A

Stops IgE binding to chain of FcER on Mast cell

55
Q

What is Montelukast?

A

Cysteinyl Leukotriene receptor antagonist

56
Q

What role to Glucocorticoids play in treating allergies?

A

Inhibit Phospholipase A2: prevent conversion of Phospholipases to Arachidonic acid.

57
Q

What are the endogenous inhibitors of mast cell activation?

A

PGE2, Adrenaline, Cortisol

58
Q

What are Coxibs?

A

Selective COX-2 inhibitors.

59
Q

What is thought to be the reason that 10% of asthmatics will have symptoms provoked by NSAIDs and coxibs?

A

It is thought that Arachidonic acid is pushed into leukotriene pathway due blockage of the prostaglandin synthesis pathway (Via COX inhibition).

60
Q

Why are H1 receptor antagonists not useful in treating asthma?

A

Because more than just H1 is involved in asthma. Many cells and cellular elements involved.

61
Q

What processes in asthma lead to airway obstruction?

A

ASM shortening
Bronchial wall oedema
mucous hypersecretion

62
Q

What is the mechanism of Short-acting Beta-2 adrenoceptor Agonists?

A

Bind beta-2-adrenoceptor
increase cAMP/PKA
inhibit IP3R
Increased uptake of Ca2+ via SERCA

63
Q

Why are LABAs combined with Glucocorticosteroids?

A

Because monotherapy is associated with increased morbidity/mortality.

64
Q

To which class of drugs does Salbutamol belong?

A

Short Acting Beta-2-drenoceptor Agonists.

65
Q

What is the mechanism of action of Short Acting Muscarinic-receptor Antagonists?

A

Less Target M3 muscarinic receptors on Airway Smooth Muscle. To prevent manifestations of reflex airway obstruction.

66
Q

Is there more or less bronchodilation in S/LABAs compared to S/LAMAs?

A

More.

67
Q

W/r/t respiratory tract viral infections, what does droplet size determine?

A

The initial site of virus deposition.

i.e. the greater the droplet, the deeper into the RT the virus will be deposited.

68
Q

What are three viruses causing URTI?

A

Rhinovirus, coronavirus, adenovirus

69
Q

Which virus causes pharyngitis?

A

Adenovirus

70
Q

Which viruses can cause an influenza-like illness?

A

Influenza virus, Respiratory Syncitial Virus

71
Q

What virus causes Croup?

A

Parainfluenza

72
Q

What viruses can cause bronchiolitis

A

Respiratory Syncitial virus, parainfluenza 3

73
Q

Which viruses can cause pneumonia?

A

Respiratory Syncitial virus, parainfluenza 3, influenza virus, adenovirus

74
Q

What are the usual characteristics of viruses that infect the intestinal tract?

A

Acid and bile resistant

Do NOT have an envelope

75
Q

What is the role of Type 1 interferon (IFN-alpha/beta)?

A

Inhibits viral replication
Activates NK cells
MHC class I expression

76
Q

What is the role of Type II interferon (IFN-gamma)?

A

Inhibits viral replication
Activates Macrophages
Enhances MHCI and II expression
Produced by NK cells

77
Q

In what ways can viruses reduce antigen presentation?

A
  • bind Transporter of Antigenic Peptide (TAP) - (HSV and CMV)
  • Decrease production of class I gene (many)
  • Bind MHC peptide complex and retain in ER (Adenovirus)
  • Endocytosis of MHC I (HIV)
  • Encoding an MHC I - like molecule that doesn’t actually work properly
78
Q

What are the histological features of asthma?

A

Goblet cell metaplasia (epithelia replaced)
Subepithelial collagen thickening (fibrosis)
Infiltration of inflammatory cells
Mucosal vascularity (exudate, oedema, mucous)

79
Q

What is PKR?

A

Protein Kinase R. Stops the translation of proteins and protects cells against viral infection.
Activated by the presence of dsRNA.
Produced in an inactive form when Interferon binds its receptor.

80
Q

Usual bacterial cause of Pharyngitis/tonsilitis/sinusitis.

A

Group A Strep.

81
Q

Bacterial cause of otitis media.

A

Pneumococci, H. influenzae

82
Q

Bacterial cause of epiglottitis.

A

H. influenzae type B

83
Q

Under what circumstances should Otitis Media be treated?

A

if <2y.o. or prolonged or severe.

84
Q

What are bacterial causes of an acute exacerbation of chronic bronchitis?

A

Pneumococci and H. influenzae.

85
Q

Most likely cause of acute pneumonia?

A

Pneumococci.

86
Q

Likely causes of Atypical pneumonia?

A

Mycoplasma

Chlamydia

87
Q

What is the treatment for pneumonia?

A

Penicillin G/amoxycillin + doxycyclan/macrolide

88
Q

What are the usual bacterial causes of lung abscess?

A

Staph aureus (IVDU)
Klebsiella (Alcoholics)
* not always, but common.

89
Q

What happens to the pressure of pulmonary arteries during exercise?

A

It stays the same, because of the dilation and recruitment of pulmonary vessels that are not normally perfused during rest.

90
Q

Why does blood pressure decrease during inspiration?

A

Because inspiration causes:
Decreased venous return to left atrium
reduced CO
(relates to size of interpleural negative pressure)

91
Q

How does Left heart failure cause Pulmonary oedema?

A

Decreased LV output - increased LV pressure - increased LA pressure - increased PVP - increased PCP - pulmonary oedema.

92
Q

What is one potential cause of non-cardiogenic pulmonary oedema?

A

After Trauma - Inflammatory mediators circulating in the blood increase pulmonary capillary permeability.

93
Q

What is the effect of pulmonary oedema on lung function?

A

reduced lung volume
reduced lung compliance
increased airway resistance (fluid compressing conducting airways)
Increased work of breathing (elastic and resistive)

94
Q

What is the mechanism of Sulfanilamides?

A

Resembles PABA - part of folic acid synthesis pathway. Stops bacteria from making folate, so they cannot make DNA. Bacteriostatic.

95
Q

What is the mechanism and common use of Trimethoprim?

A

Inhibits dihydrofolate reductase
UTI - excreted by kidney in an active form
Bacteriostatic

96
Q

What is the mechanism of methotrexate?

A

Resembles folic acid.
Inhibits purine synthesis.
Kills rapidly dividing cells. (hence GI problems)
used for abortions.

97
Q

What is the “Triple Whammy”?

A

Diuretic
ACE inhibitor
NSAID (blocks prostaglandin-mediated vasodilation in kidneys)

98
Q

What is a pathogenicity island?

A

Block of genes found on chromosome of pathogens that is missing from non-pathogens of same species

99
Q

(GI infections) Which organisms adhere to intact epithelium?

A

Cholera, ETEC

100
Q

(GI infections) Which organisms cause brush-border damage?

A

EPEC

101
Q

How does EPEC adhere intimately to the epithelium?

A

Bundle forming pili - adhesion
Type III secretion system - “carry own receptor”
Allows intimate adhesion via intimin.

102
Q

(GI infections) Which organism is restricted to invading mucosa?

A

Shigella

103
Q

(GI infections) Which organisms can invade the submucosa?

A

Salmonella, Campylobacter

104
Q

(GI infections) Which organism can invade systemically?

A

Salmonella

105
Q

Which is the only species of shigella to produce shiga toxin?

A

Shigella dysenterii

106
Q

Which organism (GI infections) causes Haemolytic uremic syndrome?

A

EHEC

107
Q

What are the virulence determinants of GI bugs?

A

Adhesins
Invasive ability
Exotoxins
Ability to resist killing

108
Q

From which organism did EHEC evolve?

A

EPEC

109
Q

Oral rehydration takes advantage of which cotransporter in the stomach? How?

A

Solute/Na+ cotransporter.

Contain amino acids or glucose to increase Na+ uptake and water reabsorption from gut.

110
Q

What is a definitive host?

A

the host where organism reaches sexual maturity

111
Q

What is an intermediate host?

A

Host in which parasite develops but does not reach sexual maturity.

112
Q

What is a Paratenic host?

A

Host in which parasite lives but does not develop.

113
Q

What is an example of an immunomodulatory cytokine?

A

TGF-beta

114
Q

What do Omeprazole/esomeprazole do?

A

Proton pump inhibitors: Inhibits H+/K+ ATPase on the lumenal surface of parietal cells to reduce H+ release into the lumen of the stomach.

115
Q

What does Ranitidine do?

A

Inhibits H-2-receptors (Histamine) on the basal surface of parietal cells to reduce gastric acid production.

116
Q

What is the function of Promethazine

A

Histamine receptor antagonist for motion sickness

117
Q

What is the use of Hyoscine hydrobromide?

A

Muscarinic Receptor Antagonist - used to treat motion sickness

118
Q

What is the role of metoclopramide?

A

D2-receptor antagonist.
Agonist of 5HT4 Receptor -> increase ACh in gut -> gut motility
Effective anti-emetic

119
Q

What is the function of Ondansetron?

A

Anti-emetic (e.g. Chemotherapy)

5HT3-receptor antagonist

120
Q

What is Magnesium sulphate used for?

A

Osmotic laxative

121
Q

How do stimulant laxatives work?

A

By increasing stimulation of myenteric nerve plexuses to increase gut motility

122
Q

What is Loperamide used for?

A

Anti-diarrhoeal. Opioid.

123
Q

What are Adefovir and Tenofovir? What are they used to treat?

A

Nucleotide analogues. Hep B.

124
Q

What does Pegvisomant treat?

A

Acromegaly. GF antagonist.

125
Q

Where are glucocorticoids produced?

A

Zona fasciculata (little in reticularis)

126
Q

Where are sex hormones produced?

A

Zona reticularis (some in fasciculata)

127
Q

Where are mineralocorticoids produced?

A

Zona glomerulosa

Respiratory block (1 decks)

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