1
Q
What is the function of the conducting airways?
A
Passage of air into the body
2
Q
What are the components of the conducting airways?
A
Nose, mouth, pharynx, larynx, trachea, bronchi, bronchioles, terminal bronchioles
3
Q
What prevents the walls of the trachea/bronchi from collapsing?
A
Cartilage in the walls
4
Q
What is the function of the respiratory airways?
A
Gaseous exchange
5
Q
What are the components of the respiratory airways?
A
Respiratory bronchioles, alveolar ducts, alveolar sacs
6
Q
What does a single respiratory cycle consist of?
A
One inspiration and one expiration
7
Q
Define ventilation
A
Drop in alveolar pressure causes bulk entry of air during inspiration
8
Q
What are the pleural sacs and how are they involved in expansion of the lungs?
A
- Fluid filled sacs surrounding the lungs
- Inner membrane is attached to lung and outer membrane is attached to diaphragm and thoracic wall by connective tissue
- Contraction of the diaphragm and intercostal muscles pulls on the sacs and causes the lungs to expand
9
Q
What makes up connective tissue?
A
Collagen and elastic fibres
10
Q
What makes up the thoracic wall?
A
Spinal column, ribs and intercostal muscles
11
Q
What are the additional functions of the conducting airways?
A
- Speech (larynx)
- Efficient O2/CO2 movement due to warming/moistening of air
- Infection defence (macrophages and mucus)
12
Q
How does mucus production affect infection control?
A
- Epithelial cells secrete mucus to trap dust and bacteria
- Mucus wafted towards pharynx by cilia to be swallowed, destroying the pathogens
13
Q
How does the Cystic Fibrosis Transmembrane Regulator affect mucus movement?
A
- Allows movement of Cl- out of the epithelial cells
- Watery fluid is secreted as a result which prevents mucus from becoming thick and sticky
14
Q
What is Cystic Fibrosis?
A
- Defective CFTR channel
- Decreased fluid secretion results in mucus build up
- More susceptible to infections as pathogens are not removed
15
Q
What is a pneumothorax?
A
Air enters the chest cavity due to a breakage in the pleural sac, external pressure causes lung to collapse and chest wall to expand
16
Q
What adaptation prevents damage to both lungs at any one time?
A
Pleural cavities isolate each lung, damage to one side is contained
17
Q
What disease could cause a spontaneous pneumothorax?
A
- Pneumonia
- Emphysema
18
Q
How is a pneumothorax treated?
A
- Let body absorb air and monitor by x-ray
- Remove air from chest using a needle and tube
- Surgically repair lung
- Remove lung if damage is severe
19
Q
Define:
- Tidal Volume
- Residual Volume
- Vital Capacity
A
- Tidal Volume: The amount of air inhaled/exhaled in a single breath
- Residual Volume: The amount of air left in the lungs after a forced exhalation
- Vital Capacity: Total vol. - Residual vol.
20
Q
What is the approximate total volume/volume of inspiration?
A
- Total volume ~2.5L
- Volume of Inspiration ~0.5L
21
Q
What are the two different ways of measuring ventilation and what are the equations?
What are the units?
A
- Minute Ventilation: Tidal vol. x Resp. rate
- Alveolar Ventilation: (Tidal vol. - Dead Space) x Resp. rate
- Units: ml/min
22
Q
What volume of the airways in anatomical dead space?
A
About 150ml
23
Q
Why are there two measurements for ventilation?
A
Difference between the two can highlight respiratory issues (e.g. air may not actually be reaching respiratory airways)
24
Q
What are the different lung function tests?
A
- Spirometry
- Peak Flow
25
Define FVC and FEV1
- FVC: Forced Vital Capacity, max amount of air exhaled in a forced breath
- FEV1: Forced Expiratory Volume (in 1 sec), max amount of air exhaled in a forced breath in 1 sec
26
What observations would be seen in obstructive lung disease?
- FEV1 less than 80%, FVC same as normal
| - Airways are obstructed so eventually the same volume of air will come out as the lungs can still expand as well
27
What observations would be seen in restrictive lung disease?
- Reduced FEV1 and FVC
| - Lung capacity is reduced (e.g. due to stiffening of the lung or infiltration)
28
Define lung compliance
Ease of expansion of the lungs and thorax
29
What does lung compliance depend on?
Transpulmonary pressure (difference between alveolar pressure and intrapleural pressure) and lung volume
30
What is the equation for working out compliance?
Cl = Change in vol/Change in pressure
31
What are the observations of normal, high and low compliance?
- Normal: Increase in TP causes increase in volume
- High: Small increase in TP causes big increase in volume
- Low: Big increase in TP causes small increase in volume
32
What condition causes high lung compliance?
Emphysema
33
What conditions cause low lung compliance?
Pulmonary oedema, pneumonia, fibrosis
34
What are the two types of cells of the lungs and what are their functions?
- Type 1 - Adapted for gaseous exchange
| - Type 2 - Cuboidal cells, responsible for surfactant production
35
What is the effect of a lack of surfactant and why?
- Causes alveoli to collapse on expiration
| - Surfactant reduces surface tension in the lungs
36
What is Newborn Respiratory Distress Syndrome?
- Underdeveloped cuboidal cells results in a lack of surfactant, causing lungs to collapse
- Common in premature babies
37
What other disorders reduce lung compliance?
Disorders affecting rib/spinal column articulation
38
Why do ventilation and perfusion need to be matched?
Inequality results in reduced O2 entry
39
What is Emphysema?
What causes it?
How are patients treated?
- Degeneration of the alveolar/bronchiole walls and the surrounding capillaries
- Generally due to protease action
- Caused by smoking
- Results in oxygen treatment because patient cannot get enough oxygen
40
What is asthma?
Inflammation of conducting airways due to exposure to environmental allergens
41
What causes the inflammation (physiological)?
Excess mucus production and airway smooth muscle contraction
42
How are beta agonists used to treat asthma?
- Mimic adrenaline
- Adenylate cyclase enzyme activated, ATP to cAMP
- Causes smooth muscle relaxation
43
How are phosphodiesterase inhibitors used to treat asthma?
- Prevent breakdown of cAMP
| - Smooth muscle relaxation is maintained
44
How are corticosteroids used to treat asthma?
- Bind to glucocorticoid receptors in cytoplasm of epithelial cells
- Heat shock proteins that hold the receptor in place dissociate so receptor-drug complex moves to nucleus
- In the nucleus it binds to regions of DNA that are responsible for transcribing cytokine molecules
- Cytokines not produced therefore no inflammation
45
What cytokines cause inflammation in the airways?
- Tumour necrosis factor alpha
| - Interleukin 1
46
Give an example of a corticosteroid used to treat asthma
Beclomethasone
47
What is the allergic component of asthma?
Overproduction of IgE antibody
48
How does IgE production cause inflammation?
- Allergen binds to IgE causing it to bind to Fce receptor on mast cells, basophils and dendritic cells
- This causes release of histamine, cytokines, prostaglandins and leukotrienes
49
How are monoclonal antibodies used as treatment for asthma?
- Antibody binds to Fc region of IgE antibody
| - Antibody can't bind to inflammatory cells so inflammatory markers are not released
50
Which neurones are involved in breathing control?
Where are they found?
- Inspiratory neurones
- Expiratory neurones
- Mixed neurones
- Pons (brain stem)
51
How do neurones affect breathing?
Cause contraction of diaphragm and intercostal muscles
52
What do central chemoreceptors monitor and where are they found?
- pH and pCO2 of cerebrospinal fluid
| - Present in brain stem medulla
53
What do peripheral chemoreceptors monitor and where are they found?
- pH, pCO2 and pO2 of arterial blood
| - Found in carotid and aortic bodies
54
Why is high CO2 dangerous and how is it controlled?
- Toxic, inhibits respiratory neurones of the medulla
| - When high CO2 is detected, contraction of intercostal muscles and diaphragm is increased
55
What is the GI tract specialised for?
Digestion and absorption
56
What are the components of the GI tract?
Mouth, pharynx, oesophagus, stomach, small intestine (duodenum, jejunum, ileum), large intestine (colon), rectum, anus
57
What are the functions of the salivary glands?
- Amylase/lipase secretion
| - Mucin production (glycoprotein - lubricates for swallowing)
58
What are the three sets of salivary glands?
- Sublingual
- Submandibular
- Parotid (cheek)
59
What virus affects the parotid salivary glands and what are its effects in post-adolescent men?
Mumps - may cause sterility
60
What other organ can the mumps virus attack?
Pancreas - May cause temporary or permanent diabetes
61
How is swallowing coordinated?
Food bolus sensed by tactile receptors in throat and send a signal to medulla oblongata, impulses sent to throat muscles which cause contraction (swallowing)
62
What types of nerves are involved in the coordination of swallowing? (6)
- Trigeminal
- Facial
- Glossopharyngeal
- Vagus
- Spinal Accessory
- Hypoglossal
63
What is dysphagia?
What patients commonly experience it?
Difficulty swallowing
Stroke patients if they suffer nerve damage
64
Describe the journey of a food bolus
Mouth -> Oesophagus -> Stomach
Passes through oesophageal hiatus to enter stomach
65
What is a hiatus hernia?
- Stomach pushes through diaphragm
| - Acid reflux experienced
66
What cells line the oesophagus?
Squamous cells
67
How is the oesophagus protected from acid and digestive enzymes?
Sealed by oesophageal sphincter
68
What is Barrett's Oesophagus?
- Squamous cells damaged by acid/enzyme contact
- Replaced with abnormal columnar cells (pre-cancerous)
- Not exchanged even when reflux stops
- Patients at risk of adenocarcinoma
69
What are the 4 gastric cell types and where are they found?
- Mucus cells
- G-Cells (Antrum)
- Chief Cells (Fundus/Body)
- Parietal Cells
70
What is the function of G-Cells?
Secrete gastrin, therefore responsible for acid secretion
71
What are the functions of Chief Cells?
- Secrete pepsinogen (inactive pepsin - protease), cleaved by HCl (and later pepsin as well)
- Secrete gastric lipase, conversion of short chain triglycerides to monoglycerides
72
What are the functions of Parietal Cells?
- Release of HCl:
1) Acetylcholine released after activation of food receptors
2) Gastrin binds to parietal cell
3) Histamine released after stomach stretching (distension)
73
How do H2 antagonists prevent acid reflux?
Give 2 examples
- Prevent release of HCl by blocking histamine receptors
| - Cimetidine and ranitidine
74
How do PPIs work?
- HCl formed from H+ that parietal cells pump into stomach lumen
- PPI irreversibly binds to H+/K+ ATPase
- H+ can't enter stomach so HCl cannot be formed
75
How are drugs degraded in the stomach and how is this prevented?
Give 2 examples of drugs like this
- Degraded by HCl
- Can be enteric coated to prevent this
Pencillin G and erythromycin
76
What drugs are best absorbed in the GI tract and why?
Lipid soluble, weakly acidic drugs - they remain unionised
77
What is the main site of drug absorption in the GIT?
- Small intestine
78
What are the protective adaptations of the stomach?
- Protected from digestion by secretion of pepsinogen rather than pepsin
- Mucus barrier produced by foveolar cells, neutralise HCl
- Tight junctions connect epithelial cells so acid and pepsin cannot reach deeper tissues
- Quick cell renewal (2-3 days)
79
How are gastric/duodenal ulcers formed?
Mucus barrier breaks down and stomach tissue is exposed to acid and pepsin
80
What is a perforated ulcer?
Damage completely erodes GIT wall so stomach contents (chyme) enters peritoneal cavity
May lead to inflammation (peritonitis)
81
What are the effects of Helicobacter pylori and how is an infection treated?
- Infects gastric mucosa, reducing barrier efficacy
- May lead to gastric ulcers
- Treated with two antibiotics (clarithromycin+amoxicillin/metronidazole) and a PPI (omeprazole, esomeprazole)
82
What are the doses of treatment for a H. pylori infection?
- C+A = 500mg+1g BD
- C+M = 250mg+400mg BD
- PPI = 20mg BD
83
How is a food bolus moved along the intestine?
Peristalsis
- Circular muscle contraction prevents backwards movement
- Longitudinal muscle contraction pushes bolus along intestine
84
What causes diarrhoea (physiological), what is the effect and how is it treated?
- Excess longitudinal contraction
- Excess ion/fluid loss
- Loperamide - Opioid receptors of myenteric plexus targeted, contact time of bolus increased so more water/ions reabsorbed
85
What is the function of bile acids and how are they synthesised?
- Emulsify lipids to allow them to be absorbed
| - Produced in liver using cholesterol and stored in gall bladder
86
What vitamins enhance fat absorption?
A, E, K and D
87
How are gastric surgeries a treatment for weight loss?
- Reduce stomach size and therefore calorific intake
- Severe cases
- Procedures: Gastric sleeve, gastric bypass, gastric band
88
What is sepsis?
Infection with systemic manifestations (causes an inflammatory response)
89
What are the common symptoms of sepsis?
- Pyrexia
- Drop in BP
- Ill feeling
- Pallor
- Tachycardia
- Raised CRP
- Raised WBC
90
What is severe sepsis?
All the normal symptoms of sepsis as well as sepsis-induced organ dysfunction
91
What causes organs dysfunction from sepsis?
Inappropriate inflammatory response, drop in BP causes organs to fail
92
What are the signs of organ failure?
- Low tissue perfusion
- Raised lactate
- Altered blood clotting
93
What is septic shock?
Persistent hypotension that is not influenced by the administration of a fluid bolus
94
What is fluid resuscitation?
Administration of a large volume of fluid quickly raises BP
95
What are the parameters for septic shock?
Systolic BP <90mmHg or mean arterial pressure of 70mmHg
96
What is an indwelling infection?
An infection caused by the fitting of a medical device
97
What are the increasing risk factors for sepsis?
- Immunocompromised patients
- Patients with chronic disease
- Neonates and infants
- Recent surgery or invasive procedures (e.g. medical device fitted)
98
What is the approximate mortality of patients with septic shock?
~50%
99
What is the main cause of death from sepsis?
Delayed diagnosis and treatment
100
Describe the deregulated inflammatory response of sepsis
- Bacterial proteins activate cellular defence mechanism
- Inflammatory cytokines (TNF-alpha, IL-1,6) are produced
- Release of nitric oxide cause vasodilation (hypotension)
- Complement mechanism activated
- Porosity of capillaries increased (hypovolaemia and oedema) - reduced tissue perfusion
101
What is the 'golden hour'?
Initial signs of sepsis displayed, mortality increases by 10% every hour after
102
What 6 actions should be undertaken in the 'golden hour'?
- Administration of oxygen
- Fluid resuscitation
- Blood cultures
- Empirical antibiotics
- Measure lactate and haemoglobin
- Measure urinary output
103
What is empirical antibiotic treatment?
- Treatment started to target likely causative organism before it is identified
- Broad spectrum at max dose and frequency
- After cultures received, treat with narrow spectrum antibiotics
104
What is used for fluid resuscitation?
0.9% NaCl infusion delivered as quickly as possible
105
What is the importance of measuring lactate in sepsis?
- Shows if glucose metabolism is being used for ATP production (stress response)
- Shows low O2 perfusion
106
What is the importance of measuring urinary output?
Tests kidney function
107
What is the role of a pharmacist in sepsis?
- Part of hospital treatment team
| - Recognise signs of sepsis and immediately refer in community pharmacy
108
What are the healthcare-associated infections? (5)
```
UTIs
RTIs
Sepsis
C. difficile
Surgical Site Infections
```
109
How do SSIs arise?
Microorganisms enter through surgical cut and multiply in surgical site tissue
110
What are the two classifications of SSIs and what do they entail?
- Incisional: Superficial, only affects skin and subcutaneous tissue
- Deep Incisional: Affects deep soft tissue (fascia and muscle)
- Organ and Space: Affects tissues separate to original surgical site
111
What are the levels of contamination for wounds?(4) Describe them
- Clean Wound: Operation avoids colonised area of body, only risk in environmental/surgical team
- Clean-Contaminated Wound: Operation reaches colonised area BUT in controlled conditions, risk generally from body's own microflora
- Contaminated Wound: Gross contamination of surgical site BUT no active infection, possibly due to unconfined spillage from injury
- Dirty Wounds: Active infection present, SSI usually caused by same pathogen as this
112
What is the most common microbial cause of SSIs?
Staphylococcus aureus
113
How can SSI incidence be reduced?
Bacterial surveillance
Prophylactic antibiotics
Aseptic techniques
Preparation of surgical site
114
What are the preparation techniques to reduce SSI chances?
- Warming of local area
- Increased blood flow to site to increase oxygenation
- Glucose control using insulin - Stress hyperglycaemia increases chances of SSI
115
When is antibiotic prophylaxis used?
Before clean, clean-contaminated and contaminated surgeries
- Only before clean if surgery involves prosthetic/implant fitting
- Given IV with anaesthetic
116
Why is hair removal done before surgery?
What are the disadvantages?
- Easier access and reduced infection rates
| - Damage from razors can increase chance of SSI therefore clippers are used instead
117
What chemicals are used in surgical antisepsis and what surgeries are they used in?
- Chlorhexidine-Alcohol
- Povidone-Iodine
- Clean-contaminated surgeries, used as paint
118
What are patient specific directions?
Written by a prescriber for a specific patient for the supply of POMs in hospital without a prescription
119
Who can supply against a patient specific direction?
Appropriate practitioners can supply according to a drug chart
- Doctors
- Dentists
- Supplementary Prescribers
- NIPs
- PIPs
120
Do patient specific directions have to be in writing?
Can be verbal but good practice to have in writing - hospital may have its own policy which must be adhered to
121
What are the legal requirements for a CD prescription?
- Indelible ink
- Prescriber: Signature, address
- Patient: Name, address, age (if <12yrs)
- Date
- Specific dose
- Formulation
- Strength
- Quantity (numbers and words)
- Total quantity
- Dental/Instalment wording where appropriate
122
When can a Pharmacist still dispense a CD prescription if there is an error?
What should be done?
- Minor spelling error but still easy to interpret
- Numbers OR words of quantity missing
- Add details and endorse with initials, date, reg no. and signature
123
What standardised form is used for CD2/CD3 private prescriptions?
What is an additional legal requirement?
FP10PCD
Private prescriber number has to be on the prescription to dispense in the community
124
What is the fate of a FP10PCD form?
NHSBSA
125
What records are kept for each schedule of CD?
- CD2: CD Register
- CD3: No register but keep invoice for 2 years, if private make POM register
- CD4: No invoice or register, if Sativex Spray CD register is good practice (cannabis derivatives)
- CD5: No register, keep invoice for 2 years
126
What requirements are necessary for CD supply against hospital bed charts?
All requirements for a CD prescription in community pharmacy
127
What requirements are necessary for CD administration against hospital bed charts?
Does not require prescription requirements but should have all appropriate for correct administration of medicine
128
How long is a CD prescription valid for?
28 days
129
How many days treatment can be prescribed on a CD instalment prescription?
14 days
130
What is the maximum amount of CD medication to be prescribed under good practice?
Ideally no more than 30 days supply
131
Who can prescribe for the addiction of cocaine, dipipanine and diamorphine?
Only doctors, requires authorisation by secretary of state
132
When is ID required to collect a CD prescription?
If collected by HCP on behalf of a patient whilst acting in their profession
Requires name, address and confirmation of profession
133
What are the limitations of achieving steady-state plasma concentrations?
- Concentration of drugs fluctuates at different dosing intervals
- Frequent doses required if drug has a short half life
- Doses may be forgotten
- No doses taken overnight
134
What characterises an ideal dosage regimen?
Immediate acceptable therapeutic concentration which is then maintained at the site of action
135
Why are MR dosage forms used?
Drug release characteristics accomplish therapeutic or convenience objectives that cannot be achieved by conventional dosage forms
136
What are the advantages of MR dosage forms?
- Steady therapeutic levels
- Lower frequency dosage regimen improves patient compliance
- Less side effects
- Less drug used overall
- Less monitoring
- Shorter treatment plan
- Less dispensing required
137
What are the main disadvantages of MR doses?
- 'Dose dumping' - Exaggerated, premature drug release
- Drug instability
- More costly
138
What are the different delivery systems? (6) Describe them
- Delayed Release: Not released immediately after administration
- Repeat Action: Single doses released at intervals after one immediate release
- Prolonged Release: Drug absorbed over a longer period of time, drug released slowly from dosage form
- Sustained Action: Initial release to provide immediate therapeutic dose, then gradual release to maintain
- Extended Release: Drug released slowly, plasma conc. maintained for 8-12 hours
- Controlled Release: Drug released at constant rate, plasma concentration remains constant
139
How are repeat action drugs differentiated from sustained action?
Two separate doses released, generally done by layers - inner are enteric coated for later release
140
What are the plasma conc. aims for an MR dosage?
- Remain constant for a prolonged period of time
OR
- Decline at a rate which causes the plasma conc. to remain within therapeutic range for a prolonged time
141
How is the release of a drug from a dosage form controlled?
Use of a chemical or physical barrier
142
What properties make a drug suitable for MR formulation? (5)
- Biological half life of 2-8 hours
- High therapeutic window
- LogP = ~2.2-3.3
- Uniformly absorbed and not too unstable throughout GIT
- Moderately potent
143
What are the four BCS classifications of drugs?
- Class 1: High solubility and permeability
- Class 2: High permeability but low solubility
- Class 3: High solubility but low permeability
- Class 4: Low solubility and permeability
144
What needs to be balanced to achieve constant plasma levels?
Release rate with patient clearance rate
145
How does the balance between release and clearance provide an issue when achieving an ideal release rate?
- Variability between conditions of the GIT
- Clearance rate depends on patient
- Disease state of patient may affect drug absorption and clearance
- Food and diet may affect drug release and absorption
