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Pharmacy Year 2 > TBL Knowledge > Flashcards

TBL Knowledge Flashcards

1
Q

What is the function of the conducting airways?

A

Passage of air into the body

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2
Q

What are the components of the conducting airways?

A

Nose, mouth, pharynx, larynx, trachea, bronchi, bronchioles, terminal bronchioles

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3
Q

What prevents the walls of the trachea/bronchi from collapsing?

A

Cartilage in the walls

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4
Q

What is the function of the respiratory airways?

A

Gaseous exchange

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5
Q

What are the components of the respiratory airways?

A

Respiratory bronchioles, alveolar ducts, alveolar sacs

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6
Q

What does a single respiratory cycle consist of?

A

One inspiration and one expiration

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7
Q

Define ventilation

A

Drop in alveolar pressure causes bulk entry of air during inspiration

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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
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9
Q

What makes up connective tissue?

A

Collagen and elastic fibres

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10
Q

What makes up the thoracic wall?

A

Spinal column, ribs and intercostal muscles

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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)
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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

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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

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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
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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

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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

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17
Q

What disease could cause a spontaneous pneumothorax?

A
  • Pneumonia

- Emphysema

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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
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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.
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20
Q

What is the approximate total volume/volume of inspiration?

A
  • Total volume ~2.5L

- Volume of Inspiration ~0.5L

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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
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22
Q

What volume of the airways in anatomical dead space?

A

About 150ml

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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)

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24
Q

What are the different lung function tests?

A
  • Spirometry

- Peak Flow

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25
Q

Define FVC and FEV1

A
  • 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
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26
Q

What observations would be seen in obstructive lung disease?

A
  • 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

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27
Q

What observations would be seen in restrictive lung disease?

A
  • Reduced FEV1 and FVC

- Lung capacity is reduced (e.g. due to stiffening of the lung or infiltration)

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28
Q

Define lung compliance

A

Ease of expansion of the lungs and thorax

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29
Q

What does lung compliance depend on?

A

Transpulmonary pressure (difference between alveolar pressure and intrapleural pressure) and lung volume

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30
Q

What is the equation for working out compliance?

A

Cl = Change in vol/Change in pressure

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31
Q

What are the observations of normal, high and low compliance?

A
  • 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
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32
Q

What condition causes high lung compliance?

A

Emphysema

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33
Q

What conditions cause low lung compliance?

A

Pulmonary oedema, pneumonia, fibrosis

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34
Q

What are the two types of cells of the lungs and what are their functions?

A
  • Type 1 - Adapted for gaseous exchange

- Type 2 - Cuboidal cells, responsible for surfactant production

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35
Q

What is the effect of a lack of surfactant and why?

A
  • Causes alveoli to collapse on expiration

- Surfactant reduces surface tension in the lungs

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36
Q

What is Newborn Respiratory Distress Syndrome?

A
  • Underdeveloped cuboidal cells results in a lack of surfactant, causing lungs to collapse
  • Common in premature babies
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37
Q

What other disorders reduce lung compliance?

A

Disorders affecting rib/spinal column articulation

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38
Q

Why do ventilation and perfusion need to be matched?

A

Inequality results in reduced O2 entry

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39
Q

What is Emphysema?

What causes it?

How are patients treated?

A
  • 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
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40
Q

What is asthma?

A

Inflammation of conducting airways due to exposure to environmental allergens

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41
Q

What causes the inflammation (physiological)?

A

Excess mucus production and airway smooth muscle contraction

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42
Q

How are beta agonists used to treat asthma?

A
  • Mimic adrenaline
  • Adenylate cyclase enzyme activated, ATP to cAMP
  • Causes smooth muscle relaxation
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43
Q

How are phosphodiesterase inhibitors used to treat asthma?

A
  • Prevent breakdown of cAMP

- Smooth muscle relaxation is maintained

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44
Q

How are corticosteroids used to treat asthma?

A
  • 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
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45
Q

What cytokines cause inflammation in the airways?

A
  • Tumour necrosis factor alpha

- Interleukin 1

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46
Q

Give an example of a corticosteroid used to treat asthma

A

Beclomethasone

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47
Q

What is the allergic component of asthma?

A

Overproduction of IgE antibody

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48
Q

How does IgE production cause inflammation?

A
  • 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
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49
Q

How are monoclonal antibodies used as treatment for asthma?

A
  • Antibody binds to Fc region of IgE antibody

- Antibody can’t bind to inflammatory cells so inflammatory markers are not released

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50
Q

Which neurones are involved in breathing control?

Where are they found?

A
  • Inspiratory neurones
  • Expiratory neurones
  • Mixed neurones
  • Pons (brain stem)
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51
Q

How do neurones affect breathing?

A

Cause contraction of diaphragm and intercostal muscles

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52
Q

What do central chemoreceptors monitor and where are they found?

A
  • pH and pCO2 of cerebrospinal fluid

- Present in brain stem medulla

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53
Q

What do peripheral chemoreceptors monitor and where are they found?

A
  • pH, pCO2 and pO2 of arterial blood

- Found in carotid and aortic bodies

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54
Q

Why is high CO2 dangerous and how is it controlled?

A
  • Toxic, inhibits respiratory neurones of the medulla

- When high CO2 is detected, contraction of intercostal muscles and diaphragm is increased

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55
Q

What is the GI tract specialised for?

A

Digestion and absorption

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56
Q

What are the components of the GI tract?

A

Mouth, pharynx, oesophagus, stomach, small intestine (duodenum, jejunum, ileum), large intestine (colon), rectum, anus

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57
Q

What are the functions of the salivary glands?

A
  • Amylase/lipase secretion

- Mucin production (glycoprotein - lubricates for swallowing)

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58
Q

What are the three sets of salivary glands?

A
  • Sublingual
  • Submandibular
  • Parotid (cheek)
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59
Q

What virus affects the parotid salivary glands and what are its effects in post-adolescent men?

A

Mumps - may cause sterility

60
Q

What other organ can the mumps virus attack?

A

Pancreas - May cause temporary or permanent diabetes

61
Q

How is swallowing coordinated?

A

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
Q

What types of nerves are involved in the coordination of swallowing? (6)

A
  • Trigeminal
  • Facial
  • Glossopharyngeal
  • Vagus
  • Spinal Accessory
  • Hypoglossal
63
Q

What is dysphagia?

What patients commonly experience it?

A

Difficulty swallowing

Stroke patients if they suffer nerve damage

64
Q

Describe the journey of a food bolus

A

Mouth -> Oesophagus -> Stomach

Passes through oesophageal hiatus to enter stomach

65
Q

What is a hiatus hernia?

A
  • Stomach pushes through diaphragm

- Acid reflux experienced

66
Q

What cells line the oesophagus?

A

Squamous cells

67
Q

How is the oesophagus protected from acid and digestive enzymes?

A

Sealed by oesophageal sphincter

68
Q

What is Barrett’s Oesophagus?

A
  • 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
Q

What are the 4 gastric cell types and where are they found?

A
  • Mucus cells
  • G-Cells (Antrum)
  • Chief Cells (Fundus/Body)
  • Parietal Cells
70
Q

What is the function of G-Cells?

A

Secrete gastrin, therefore responsible for acid secretion

71
Q

What are the functions of Chief Cells?

A
  • Secrete pepsinogen (inactive pepsin - protease), cleaved by HCl (and later pepsin as well)
  • Secrete gastric lipase, conversion of short chain triglycerides to monoglycerides
72
Q

What are the functions of Parietal Cells?

A
  • 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
Q

How do H2 antagonists prevent acid reflux?

Give 2 examples

A
  • Prevent release of HCl by blocking histamine receptors

- Cimetidine and ranitidine

74
Q

How do PPIs work?

A
  • 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
Q

How are drugs degraded in the stomach and how is this prevented?

Give 2 examples of drugs like this

A
  • Degraded by HCl
  • Can be enteric coated to prevent this

Pencillin G and erythromycin

76
Q

What drugs are best absorbed in the GI tract and why?

A

Lipid soluble, weakly acidic drugs - they remain unionised

77
Q

What is the main site of drug absorption in the GIT?

A
  • Small intestine
78
Q

What are the protective adaptations of the stomach?

A
  • 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
Q

How are gastric/duodenal ulcers formed?

A

Mucus barrier breaks down and stomach tissue is exposed to acid and pepsin

80
Q

What is a perforated ulcer?

A

Damage completely erodes GIT wall so stomach contents (chyme) enters peritoneal cavity

May lead to inflammation (peritonitis)

81
Q

What are the effects of Helicobacter pylori and how is an infection treated?

A
  • Infects gastric mucosa, reducing barrier efficacy
  • May lead to gastric ulcers
  • Treated with two antibiotics (clarithromycin+amoxicillin/metronidazole) and a PPI (omeprazole, esomeprazole)
82
Q

What are the doses of treatment for a H. pylori infection?

A
  • C+A = 500mg+1g BD
  • C+M = 250mg+400mg BD
  • PPI = 20mg BD
83
Q

How is a food bolus moved along the intestine?

A

Peristalsis

  • Circular muscle contraction prevents backwards movement
  • Longitudinal muscle contraction pushes bolus along intestine
84
Q

What causes diarrhoea (physiological), what is the effect and how is it treated?

A
  • 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
Q

What is the function of bile acids and how are they synthesised?

A
  • Emulsify lipids to allow them to be absorbed

- Produced in liver using cholesterol and stored in gall bladder

86
Q

What vitamins enhance fat absorption?

A

A, E, K and D

87
Q

How are gastric surgeries a treatment for weight loss?

A
  • Reduce stomach size and therefore calorific intake
  • Severe cases
  • Procedures: Gastric sleeve, gastric bypass, gastric band
88
Q

What is sepsis?

A

Infection with systemic manifestations (causes an inflammatory response)

89
Q

What are the common symptoms of sepsis?

A
  • Pyrexia
  • Drop in BP
  • Ill feeling
  • Pallor
  • Tachycardia
  • Raised CRP
  • Raised WBC
90
Q

What is severe sepsis?

A

All the normal symptoms of sepsis as well as sepsis-induced organ dysfunction

91
Q

What causes organs dysfunction from sepsis?

A

Inappropriate inflammatory response, drop in BP causes organs to fail

92
Q

What are the signs of organ failure?

A
  • Low tissue perfusion
  • Raised lactate
  • Altered blood clotting
93
Q

What is septic shock?

A

Persistent hypotension that is not influenced by the administration of a fluid bolus

94
Q

What is fluid resuscitation?

A

Administration of a large volume of fluid quickly raises BP

95
Q

What are the parameters for septic shock?

A

Systolic BP <90mmHg or mean arterial pressure of 70mmHg

96
Q

What is an indwelling infection?

A

An infection caused by the fitting of a medical device

97
Q

What are the increasing risk factors for sepsis?

A
  • Immunocompromised patients
  • Patients with chronic disease
  • Neonates and infants
  • Recent surgery or invasive procedures (e.g. medical device fitted)
98
Q

What is the approximate mortality of patients with septic shock?

99
Q

What is the main cause of death from sepsis?

A

Delayed diagnosis and treatment

100
Q

Describe the deregulated inflammatory response of sepsis

A
  • 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
Q

What is the ‘golden hour’?

A

Initial signs of sepsis displayed, mortality increases by 10% every hour after

102
Q

What 6 actions should be undertaken in the ‘golden hour’?

A
  • Administration of oxygen
  • Fluid resuscitation
  • Blood cultures
  • Empirical antibiotics
  • Measure lactate and haemoglobin
  • Measure urinary output
103
Q

What is empirical antibiotic treatment?

A
  • 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
Q

What is used for fluid resuscitation?

A

0.9% NaCl infusion delivered as quickly as possible

105
Q

What is the importance of measuring lactate in sepsis?

A
  • Shows if glucose metabolism is being used for ATP production (stress response)
  • Shows low O2 perfusion
106
Q

What is the importance of measuring urinary output?

A

Tests kidney function

107
Q

What is the role of a pharmacist in sepsis?

A
  • Part of hospital treatment team

- Recognise signs of sepsis and immediately refer in community pharmacy

108
Q

What are the healthcare-associated infections? (5)

A 
UTIs
RTIs
Sepsis
C. difficile
Surgical Site Infections
109
Q

How do SSIs arise?

A

Microorganisms enter through surgical cut and multiply in surgical site tissue

110
Q

What are the two classifications of SSIs and what do they entail?

A
  • 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
Q

What are the levels of contamination for wounds?(4) Describe them

A
  • 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
Q

What is the most common microbial cause of SSIs?

A

Staphylococcus aureus

113
Q

How can SSI incidence be reduced?

A

Bacterial surveillance
Prophylactic antibiotics
Aseptic techniques
Preparation of surgical site

114
Q

What are the preparation techniques to reduce SSI chances?

A
  • Warming of local area
  • Increased blood flow to site to increase oxygenation
  • Glucose control using insulin - Stress hyperglycaemia increases chances of SSI
115
Q

When is antibiotic prophylaxis used?

A

Before clean, clean-contaminated and contaminated surgeries

  • Only before clean if surgery involves prosthetic/implant fitting
  • Given IV with anaesthetic
116
Q

Why is hair removal done before surgery?

What are the disadvantages?

A
  • Easier access and reduced infection rates

- Damage from razors can increase chance of SSI therefore clippers are used instead

117
Q

What chemicals are used in surgical antisepsis and what surgeries are they used in?

A
  • Chlorhexidine-Alcohol
  • Povidone-Iodine
  • Clean-contaminated surgeries, used as paint
118
Q

What are patient specific directions?

A

Written by a prescriber for a specific patient for the supply of POMs in hospital without a prescription

119
Q

Who can supply against a patient specific direction?

A

Appropriate practitioners can supply according to a drug chart

  • Doctors
  • Dentists
  • Supplementary Prescribers
  • NIPs
  • PIPs
120
Q

Do patient specific directions have to be in writing?

A

Can be verbal but good practice to have in writing - hospital may have its own policy which must be adhered to

121
Q

What are the legal requirements for a CD prescription?

A
  • 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
Q

When can a Pharmacist still dispense a CD prescription if there is an error?

What should be done?

A
  • 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
Q

What standardised form is used for CD2/CD3 private prescriptions?

What is an additional legal requirement?

A

FP10PCD

Private prescriber number has to be on the prescription to dispense in the community

124
Q

What is the fate of a FP10PCD form?

125
Q

What records are kept for each schedule of CD?

A
  • 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
Q

What requirements are necessary for CD supply against hospital bed charts?

A

All requirements for a CD prescription in community pharmacy

127
Q

What requirements are necessary for CD administration against hospital bed charts?

A

Does not require prescription requirements but should have all appropriate for correct administration of medicine

128
Q

How long is a CD prescription valid for?

129
Q

How many days treatment can be prescribed on a CD instalment prescription?

130
Q

What is the maximum amount of CD medication to be prescribed under good practice?

A

Ideally no more than 30 days supply

131
Q

Who can prescribe for the addiction of cocaine, dipipanine and diamorphine?

A

Only doctors, requires authorisation by secretary of state

132
Q

When is ID required to collect a CD prescription?

A

If collected by HCP on behalf of a patient whilst acting in their profession

Requires name, address and confirmation of profession

133
Q

What are the limitations of achieving steady-state plasma concentrations?

A
  • 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
Q

What characterises an ideal dosage regimen?

A

Immediate acceptable therapeutic concentration which is then maintained at the site of action

135
Q

Why are MR dosage forms used?

A

Drug release characteristics accomplish therapeutic or convenience objectives that cannot be achieved by conventional dosage forms

136
Q

What are the advantages of MR dosage forms?

A
  • 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
Q

What are the main disadvantages of MR doses?

A
  • ‘Dose dumping’ - Exaggerated, premature drug release
  • Drug instability
  • More costly
138
Q

What are the different delivery systems? (6) Describe them

A
  • 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
Q

How are repeat action drugs differentiated from sustained action?

A

Two separate doses released, generally done by layers - inner are enteric coated for later release

140
Q

What are the plasma conc. aims for an MR dosage?

A
  • 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
Q

How is the release of a drug from a dosage form controlled?

A

Use of a chemical or physical barrier

142
Q

What properties make a drug suitable for MR formulation? (5)

A
  • 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
Q

What are the four BCS classifications of drugs?

A
  • 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
Q

What needs to be balanced to achieve constant plasma levels?

A

Release rate with patient clearance rate

145
Q

How does the balance between release and clearance provide an issue when achieving an ideal release rate?

A
  • 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

Pharmacy Year 2 (9 decks)

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