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Pharmacy Year 2 > The Patient - Semester 2 > Flashcards

The Patient - Semester 2 Flashcards

1
Q

What are the conducting airways and what are the components?

A

Anatomic dead space

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

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2
Q

What adaptation prevents the trachea and bronchi from collapsing?

A

Cartilage in the walls

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3
Q

What are the respiratory airways and what are the components?

A

Sites of gas exchange

Respiratory bronchioles, alveolar ducts, alveoli

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4
Q

What does one respiratory cycle consist of?

A

One inspiration and one expiration

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5
Q

Define ventilation

A

Bulk air entry caused by a drop in pressure as a result of increased lung volume

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6
Q

What are the pleural sacs and what are they connected to?

A

Fluid filled sacs surrounding the lungs

Inner membrane is connected to the lung and outer membrane is connected to the thoracic wall (spinal column, ribs and intercostal muscles) and diaphragm by connective tissue

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7
Q

How do the lungs expand?

A

Contraction of the diaphragm and intercostal muscles pulls on the pleural sacs which subsequently pulls on the elastic lung tissue, causing them to expand

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8
Q

What are the functions of the conducting airways?

A
  • Low resistance airflow pathway
  • Speech (larynx)
  • Efficient O2/CO2 exchange - Warms and moistens air entering
  • Infection defence by macrophages
  • Mucus secretion - immune defence
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9
Q

How does mucus provide a barrier to infection in the conducting airways?

A

Mucus traps dust and microorganisms, cilia then wafts mucus towards pharynx where it can be swallowed to kill bacteria

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10
Q

How is movement of the mucus maintained?

A

Cl- moves out of epithelial cells through CFTR channel in apical membrane, watery fluid follows by osmosis

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11
Q

What is cystic fibrosis?

A

Defective CFTR results in inefficient Cl- movement and therefore a build up of mucus, increasing chances of infection as pathogens are not removed

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12
Q

What is a pneumothorax?

A

Breakage of pleural sac as a result of disease or injury - this results in air entering the chest cavity

The external air pressure causes the chest wall to expand and the lungs to collapse

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13
Q

How is injury to the lung contained to one side?

A

Lungs are isolated in pleural cavities so damage to one side prevents both lungs collapsing

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14
Q

What diseases can cause a pneumothorax?

A

Pneumonia and emphysema

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15
Q

What are the treatments for a minor, moderate and severe pneumothorax?

A
  • Minor: Monitor by x ray and let body absorb air
  • Moderate: Remove external air using a needle and tube
  • Severe: Surgically repair lung or remove if damage is too severe
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16
Q

Define tidal volume, residual volume and vital capacity

A
  • Tidal volume is the amount of air inhaled and exhaled during normal breathing
  • Residual volume is the amount of air left in the lungs even after a forced exhalation
  • Vital capacity = total volume - residual volume, can be worked out by measuring air expelled after taking a deep breath and and then a forced exhalation
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17
Q

What is the volume of an approximate inhalation/exhalation?

A

~500ml

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18
Q

What are the two ways of measuring ventilation and why are they important?

A
  • Minute ventilation: Tidal vol. x Resp. Rate (ml/min)
  • Alveolar Ventilation: (Tidal vol. - Dead Space) x Resp. Rate (ml/min)

Differences can highlight respiratory issues (e.g. shallow breathing which would result in inefficient gas exchange)

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19
Q

What is the volume of anatomical dead space?

A

~150ml

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20
Q

What are the lung function tests and what measurements are taken?

A

Spirometry, peak flow meter

FVC: Forced vital capacity
FEV1: Forced expiratory volume (in 1 sec) - Usually about 80% of FVC

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21
Q

What observations are made in Obstructive Lung Disease?

Give examples of conditions

A
  • Normal FVC but FEV1 less than 80% due to resistance in airways

Asthma, COPD, CF

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22
Q

What observations are made in Restrictive Lung Disease?

Give examples of conditions

A
  • Reduced FVC and FEV1 but FEV1 still ~80% due to poor expansion of the lungs

Fibrosing alveolitis, malignant infiltrations (e.g. tumours)

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23
Q

What is lung compliance?

How is it worked out?

A

Ease of expansion of the lungs - depends on relationship between transpulmonary pressure (difference in pleural and alveolar pressure) and lung volume

Cl = Change in vol/Change in pressure

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24
Q

Describe what would be seen in normal, low and high compliance

List conditions that may alter compliance

A

Normal: Increase in TP causes increase in lung volume
High: Small increase in TP causes large increase in lung volume (emphysema)
Low: Large increase in TP causes small increase in lung volume (fibrosis, pneumonia, oedema)

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25
Q

What are the two types of cells in the lungs?

A

Type 1: Gaseous exchange cells

Type 2: Cuboid cells, surfactant producers

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26
Q

What is the purpose of surfactant in the lungs?

A

Reduces lung surface tension to prevent alveoli collapsing

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27
Q

What is Newborn Respiratory Distress Syndrome?

A

Underdeveloped type 2 cells result in less surfactant production so lungs cannot stay open

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28
Q

What other conditions (generic) can cause low lung compliance?

A

Disorders affecting rib/spinal column articulation as the pleural sacs are connected to these

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29
Q

Why do ventilation and perfusion need to be matched?

A

Inequality results in reduced O2 entry to body

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30
Q

What is emphysema?

What causes it and how is it treated?

A

Degeneration of alveolar/bronchiole walls by proteases (produced by leukocytes), surrounding capillaries may also be affected

Usually caused by smoking and insufficient oxygen intake results in patient being put on O2

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31
Q

What is asthma? What causes it?

A

Inflammation of the conducting airways due to excess mucus and contraction of smooth muscle

Caused by environmental allergens

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32
Q

How are bronchodilators used to treat asthma?

A
  • Beta receptors agonists: Mimic action of adrenaline by activating adenylate cyclase so ATP is converted to cAMP, cAMP caused relaxation of smooth muscle
  • Phosphodiesterase inhibitors: These inhibit cAMP breakdown, maintaining relaxation of the airway smooth muscle
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33
Q

How are corticosteroids used to treat asthma?

A
  • Corticosteroid binds to glucocorticoid receptor in epithelial cell cytoplasm
  • Heat shock proteins dissociate from the receptor, allowing the receptor-drug complex to move to the nucleus where is binds to regions of DNA that transcribe for cytokines
  • Reduction of cytokines results in reduced inflammation
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34
Q

What is the allergic component of asthma?

A

Overproduction of IgE - IgE binds to Fce region on mast cells, basophils and dendritic cells which causes release of histamine, cytokines, prostaglandins and leukotrienes

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35
Q

How are monoclonal antibodies used to treat asthma?

Give an example of one

A
  • MAbs bind to Fc region on IgE to prevent binding to inflammatory cells
  • Release of inflammatory markers inhibited

Omalizumab

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36
Q

What structures control breathing?

A

Pons and Medulla in the brainstem

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37
Q

What neurones are involved in breathing control and how do they have this effect?

A

Inspiratory, expiratory and mixed neurones from the pontine respiratory group

Impulses from neurones cause contraction of diaphragm and intercostal muscles

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38
Q

Where are central chemoreceptors found and what do they monitor?

A
  • Brain stem medulla

- pH and pCO2 of cerebrospinal fluid

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39
Q

Where are peripheral chemoreceptors found and what do they monitor?

A
  • Carotid and aortic bodies

- pH, pCO2 and pO2 of arterial blood

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40
Q

Why is high CO2 dangerous and how is it controlled?

A

High CO2 is toxic to respiratory neurones in the medulla

High levels detected by receptors which results in increased contraction of intercostal muscles and diaphragm

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41
Q

What causes reversible bronchospasm in asthma?

A

Release of cytokines by T-lymphocytes

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42
Q

What are the symptoms of asthma?

A

Shortness of breath, cough, dyspnoea, wheeze

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43
Q

What are the aims of asthma treatment?

A

Symptom control, prevent exacerbations and requirement of rescue pack, improve lung function, promote self care, minimise side effects

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44
Q

How can asthma be managed without medicines?

A 
Avoid trigger
Avoid cold air exposure
Lifestyle changes (weight, smoking)
Avoid use of NSAIDs and beta-blockers 
Buteyko breathing technique - slow, gentle breathing through nose to prevent drying airways
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45
Q

What routes can be used for administration of asthma drugs?

A

Oral or inhaled

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46
Q

What are the types of inhaled formulations?

A

Inhalers as relievers (SABAs), controllers (LABAs) and preventers (ICS)
Nebulisers in cases where coordination cannot be controlled

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47
Q

How are beta-2 agonists used in asthma treatment?

A

Relaxation of bronchial smooth muscle and enhanced mucus clearance by cilia

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48
Q

What are the side effects of b-2 agonists?

A

Tremor, nervous tension, headache, peripheral vasodilation, tachycardia, hyperkalaemia

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49
Q

What are the different types of corticosteroid treatment in asthma?

A
  • Inhaled for prevention (beclometasone)
  • 40-50mg orally for 5 days post-acute attack (prednisolone)
  • IV in case of inability to take orally (hydrocortisone)
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50
Q

When is an ICS used as a preventer in asthma treatment?

A
  • Exacerbation in the last 2 years
  • Experiencing symptoms and use of b-agonist more than 3 times weekly
  • Experiencing waking frequently
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51
Q

What are the side effects of an ICS?

A

Dysphonia, oral thrush, adrenal suppression, hypertension, osteoporosis, skin thinning, hyperglycaemia, moon face, acne

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52
Q

How are leukotriene antagonists used in asthma treatment?

A
  • Given orally

- Prevention of bronchoconstriction, oedema and mucus production

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53
Q

Give two examples of leukotriene antagonists

A

Montelukast, Zafirlukast

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54
Q

What are the side effects of leukotriene antagonists?

A

Abdominal pain, headache, thirst, rash, sleep disturbance, effects on the CNS

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55
Q

How are methylxanthines used in asthma treatment?

A

Phosphodiesterase inhibitors - maintain bronchodilation (cAMP)
Prevent synthesis of leukotrienes

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56
Q

Give two examples of methylxanthines and their RoA

A

Theophylline - Oral

Aminophylline - Oral/IV

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57
Q

What are the issues with methylxanthines?

A

Narrow therapeutic index

CYP450 metabolism - drug interactions

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58
Q

What are the side effects of methylxanthines?

A

Nausea, diarrhoea, nervousness, headache, vomiting, insomnia, arrhythmia, hyperglycaemia, convulsions, death by overdose

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59
Q

What factors can reduce clearance of methylxanthines?

A

Congestive heart failure
Liver disease
Obesity
Enzyme inhibition

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60
Q

How are cromones used in asthma treatment? Give an example

A

Inhibit histamine release from mast cells

Nedocromil

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61
Q

What are the side effects of cromones?

A

Nausea and vomiting, bitter taste, indigestion (dyspepsia)

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62
Q

Give some examples of immunosuppressants used in asthmas treatment

A

Methotrexate
Ciclosporin
Gold

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63
Q

How are MAbs administered and how long is treatment?

A

Subcutaneously for 2-4 weeks

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64
Q

What are the steps for managing chronic asthma in adults?

A
  • SABA prn
  • Low dose ICS for prevention
  • Add LABA if required
  • If still uncontrolled, increase ICS dose
  • Stop LABA and increase ICS further
  • Trial LTA, SR theophylline or long-acting muscarinic antagonist (LAMA)
  • Consider fourth drug
  • Specialist referral
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65
Q

What factors affect Peak Expiratory Flow? What percentage of expected should it be?

A

Effort, age, height, sex

At least 80% of expected

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66
Q

What characterises acute severe asthma?

A

PEF <50%, dysphonia, RR >25, HR >110

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67
Q

What characterises acute life threatening asthma?

A

Severe PLUS silent chest, cyanosis, bradycardia, confusion, exhaustion, coma, inability to speak full sentences, PEF <33%

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68
Q

What drugs would be given if a patient is hospitalised for acute asthma?

A
  • Nebulised b2-agonist, IV/oral steroid

- Possibly ipratropium nebuliser, IV MgSO4, IV aminophylline/salbutamol

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69
Q

What are the monitoring requirements in acute asthma?

A

PEF, O2 saturation, ABGs, HR, RR, theophylline level, K+ level, glucose level, hydration, WCC, CRP

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70
Q

What should be checked before discharging an asthma patient?

A

Inhaler technique

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71
Q

What is COPD?

A 
Parenchymal damage (damage to functional parts of airways)
Progressive airway obstruction
Treatable but not curable
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72
Q

At what age is COPD a more likely diagnosis than asthma?

A

Above 35 years

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73
Q

What are the symptoms of COPD?

A

Chronic cough, mucus production, breathlessness

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74
Q

How is COPD diagnosed?

A

Spirometry, chest xray and FBC

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75
Q

What are the systematic effects of COPD?

A

Weight loss, skeletal muscle loss, osteoporosis, depression, increased risk of CVD

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76
Q

What increases the risk factor for COPD?

A

Smoking, age, gender (male) occupational hazards, previous lung impairment

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77
Q

Name a genetic risk factor for COPD

A

Alpha-1 antitrypsin deficiency

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78
Q

What are the aims of COPD treatment?

A

Improve day-to-day symptoms, prevent acute infective exacerbations, slow progression of disease, maintain nutritional intake, improve quality of life, smoking cessation

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79
Q

How do antimuscarinics reduce airway constriction?

A

Acetylcholine stimulates M3 receptors which cause bronchoconstriction, antimuscarinics prevent the action of acetylcholine

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80
Q

What are the side effects of antimuscarinics?

A

Dry mouth, blurred vision, urinary retention, constipation, hypotension

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81
Q

When are corticosteroids used in treatment of COPD?

A

If patient has FEV <50% and SABA has little or no effect

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82
Q

What should be avoided if patient is on oxygen therapy?

A

Smoking due to flammability

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83
Q

When is oxygen therapy used in COPD?

A

if FEV <35%

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84
Q

What oxygen concentration is used to prevent respiratory depression and why?

A

24-28% to prevent hypoxic drive (body responds to low O2 rather than high CO2 - oxygen treatment then takes away requirement to breath as body registers O2 levels as high)

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85
Q

How are infectious exacerbations prevented and how are they treated?

A

Administration of influenza and pneumococcal vaccines

Chest infections are treated with antibiotics

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86
Q

What are mucolytics and when are they used in COPD treatment?

A

Reduce viscosity of mucus so it is easier to expel from the airways

Used when patient has a chronic productive cough

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87
Q

How are LAMAs/LABAs used in COPD treatment?

A

Unmanaged COPD, if FEV <80% give combination inhaler of LABA/ICS

If still unmanaged give LAMA + combination inhaler

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88
Q

What lifestyle changes can be made to improve COPD symptoms?

A

Smoking cessation, exercise, nutrition management

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89
Q

How often is COPD reviewed and what parameters and checked?

A

Annually

FEV, dyspnoea, BMI, depression, inhaler technique and medication review

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90
Q

What is the danger of using steroids in COPD treatment?

A

Steroid increase susceptibility to infection so infective exacerbations (chest infections) are more likely

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91
Q

What antibiotics are used to treat a chest infection?

A

Amoxicillin 500mg TDS, tetracycline, doxycycline 200mg STAT then 100mg OD

May use broad spectrum cephalosporin or macrolide

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92
Q

What is cor pulmonale?

A

Right side heart death due to damage to the pulmonary circuit as a result of hypertension

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93
Q

What is polycythaemia?

A

RBC and haematocrit level rises due to hypoxia, blood viscosity increases

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94
Q

What are the functions of the tissues and organs in the GIT?

A

Specialised for digestion and absorption

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95
Q

Define alimentary

A

Relating to nutrition

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96
Q

What are the components of the GIT?

A

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

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97
Q

What are the accessory structures to the GIT and what are their functions?

A

Salivary glands (sublingual, submandibular and parotid)

Secretion of amylase and lipase, mucin production (glycoprotein that provides lubrication for swallowing)

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98
Q

What does the Mumps virus affect and what are the symptoms?

A

Affects parotid glands

Swelling to side of face and neck

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99
Q

Describe the mechanism of swallowing

A

Food bolus sensed by tactile receptors in the back of the throat, signal sent to medulla oblongata which then sends impulses to throat musculature, causing coordination of swallowing

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100
Q

What 6 nerve groups are involved in coordination of swallowing?

A

Trigeminal, facial, glossopharyngeal, vagus, spinal accessory and hypoglossal

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101
Q

What patients may develop dysphagia?

A

Stroke patients due to nerve damage

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102
Q

Describe the journey of a food bolus

A

Mouth -> Oesophagus -> Stomach (past oesophageal hiatus)

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103
Q

What is a hiatus hernia?

A

Stomach pushes through diaphragm resulting in acid reflux

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104
Q

What is Barrett’s Oesophagus?

A

Squamous epithelial cells damaged by acid reflux and then replaced with abnormal columnar cells (pre-cancerous)

Patients at higher risk of developing adenocarcinoma

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105
Q

What adaptation prevents stomach acid from entering the oesophagus?

A

Lower oesophageal sphincter seals stomach

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106
Q

What are the four types of gastric cells?

A

Mucus cells, G-Cells, Chief Cells, Parietal Cells

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107
Q

What are the functions of G-Cells?

A

Gastrin secretion, gastrin binds to parietal cells causing HCl release

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108
Q

What are the functions of Chief Cells?

A 
Secrete pepsinogen (pepsin in inactive form)
Secrete gastric lipase
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109
Q

What are the functions of Parietal Cells?

A

HCl release (p. cell pumps H+ into stomach lumen):

Food receptors send impulses to stomach causing release of acetylcholine
Gastrin binds to parietal cells causing HCl release
Stomach distension causes release of histamine which causes release of HCl

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110
Q

How are H2 receptor antagonists used to treat acid reflux? Give two examples

A

Histamine effects reduced or abolished by blocking receptor

Cimetidine and Ranitidine

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111
Q

How are PPIs used to treat acid reflux?

A

Inhibition of H+/K+ ATPase pump, preventing H+ entering stomach so no formation of HCl

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112
Q

Why are enteric coatings used in drug formulations? Give two examples that may need enteric coatings

A

Some drugs may undergo degradation by HCl in the stomach, enteric coating protects active ingredient

Penicillin G and erythromycin

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113
Q

What structures are best absorbed in the BIT and why?

A

Lipid-soluble, weakly acidic drugs because they remain unionised and can cross the lipid membrane

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114
Q

What is the main site of absorption in the GIT?

A

Small intestine

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115
Q

What are the protective adaptations of the stomach?

A
  • Pepsin secreted as inactive pepsinogen to prevent breakdown of stomach proteins
  • Mucus layer produced by foveolar cells protects stomach epithelium - neutralises stomach acid and protects from protease digestion
  • Epithelial cells connected by tight junctions prevents exposure of epithelium to acid/pepsin
  • Cells are replaced every 2-3 days
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116
Q

How gastric/duodenal ulcers formed?

A

Breakdown of protective adaptations leads to damage of the stomach epithelium

If damage extends deep enough it can damage blood vessels and cause a haemorrhage

If damage erodes GIT wall (perforated ulcer) chyme may enter peritoneal cavity

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117
Q

What is peritonitis?

A

Inflammation of the peritoneum due to contact with chyme, can lead to sepsis

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118
Q

What is the relationship between Helicobacter pylori and gastric ulcers?

A

Infections are a common cause of ulcers, eradication of H. pylori dramatically reduced incidence of ulcers

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119
Q

What are the treatments and doses of H.pylori infections?

A

Two antibiotics and PPI:

Clarithromycin (500mg BD) + Amoxicillin (1g BD) + Omeprazole/Esomeprazole (20mg BD)

Clarithromycin (250mg BD) + Metronidazole (400mg BD) + Omeprazole/Esomeprazole (20mg BD)

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120
Q

What is peristalsis?

A

Coordinated contraction of intestine to push a food bolus along the lumen

Circular muscles contract to prevent the backwards movement of a food bolus whereas longitudinal muscles contract to push the food bolus along

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121
Q

How is diarrhoea characterised and how is it treated?

A

Excessive fluid and ion loss due to excessive longitudinal contraction

Loperamide - Targets opioid receptors of myenteric plexus to reduce contraction and increase contact time of food bolus, allows reabsorption of ions and water

122
Q

Where is bile acid produced and stored?

A

Produced in the liver and stored in the gall bladder

123
Q

What is the purpose of bile acids?

A

Released into the intestine to allow lipid absorption by emulsification, then reabsorbed in ileum

124
Q

What are the lipid soluble vitamins?

A

A, D, E and K

125
Q

Why are gastric surgeries used for weight loss and how does it work?

What procedures are there?

A

Used in severe cases of weight loss

Reduce capacity of stomach so lower food intake = lower calorific intake

Gastric band, gastric sleeve, gastric bypass

126
Q

What other conditions can peptic ulcer treatment be used for and how may they differ?

A

Dyspepsia, reflux, duodenal/gastric ulcers, NSAID-related ulcers, gastro-oesophageal reflux disease

Dose, administration, treatment duration

127
Q

What is GORD and what are the symptoms?

A

Reflux with similar symptoms to chronic heartburn

Chronic cough, laryngitis

128
Q

What are the ALARMS symptoms of dyspepsia/heartburn/peptics ulcers?

A

Anaemia, Loss of weight, Anorexia, Recurrent problems, Melaena/haematemesis (blood in vomit/stools), Swallowing problems

129
Q

How are antacids used for treatment of peptic ulcer disease?

A

Neutralise stomach acid, when required and at mealtimes

Liquids are more effective

130
Q

List some effects of components of antacids

A

Mg - Laxative effect
Al - Constipation
Ca - Hypercalcaemia/Rebound acid secretion

131
Q

When are low Na+ formulations used?

A

Renal/cardiac patients, hypertension patients, pregnant patients

132
Q

When are products containing Na2CO3 contraindicated?

A

Patients with reduced salt intake

133
Q

How are H2 antagonists used in peptic ulcer disease?

A

Used at higher doses for peptic ulcer treatment

134
Q

What drugs does cimetidine interact with and what is the effect?

A

Warfarin, phenytoin, carbamazepine, valproate, theophylline, sildenafil

Inhibits metabolism

135
Q

What are the side effects of H2 antagonist interactions?

A

Headache, diarrhoea, dizziness, rash, altered LFTs

136
Q

How do Helicobacter pylori bacteria replicate?

A

Convert urea to CO2 and NH3 using water, NH3 neutralises acid

137
Q

How do Helicobacter pylori cause damage?

A

Bacterial mucinase - Mucosal damage
Gastric acid, proteases and effector molecules then cause mucosal inflammation
Cytokines and NH3 cause mucosal cell death

138
Q

How is a H. pylori infection detected?

A

Antibodies in serum, saliva and urine
Urease activity on C-13 urea may produce C-13 CO2
Mucosal biopsies
High antibody titre

139
Q

What are the treatment aims for H. pylori infections?

A

Eradication

140
Q

How does treatment differ in complicated ulceration?

A

PPI continued for 3 weeks longer

141
Q

How is GORD treated?

A

Full dose PPI for 1-2 months, lower dose then eventually stop

142
Q

How is GORD in children treated?

A

Alter frequency or volume of feed, make feed thicker, use alginate, H2 antagonist or PPI

143
Q

How can NSAIDs cause peptic ulcer disease?

A

Prevent production of mucous, bicarbonates and prostaglandins which are all protective factors for gastric acid damage

144
Q

How do prostaglandin analogues have a protective effect?

A

PGE1 has antisecretory and cytoprotective effects

Misoprostol (antagonist) increases mucus production causing ulcer healing and preventative uses

145
Q

What action should be taken in the case of continuing NSAIDs?

A

Long term PPI treatment
PPI + misoprostol after healing
PPI + Cox-2 inhibitor

146
Q

Define achlorhydria

A

Low gastric acid production

147
Q

What adaptations increase the GIT capacity for digestion and absorption?

A

Highly perfused - surrounding capillaries and lacteals Folded - large SA
Epithelium only one cell thick
Digestive enzymes convert large macromolecules into small, absorbable molecules

148
Q

Give the digestion of three sugars and the enzymes that do them

A

Lactose -> Glucose + Galactose (Lactase)
Maltose -> Glucose + Glucose (Maltase)
Sucrose -> Glucose + Fructose (Sucrase)

149
Q

Describe the absorption of glucose, galactose and fructose

A

Glucose and galactose transported into enterocytes by SGLT1, requires Na+
Fructose transported into enterocytes by GLUT5

150
Q

How are monosaccharides absorbed from enterocytes?

A

Transported into the blood by transporters in the basolateral membrane

151
Q

How are proteins digested and absorbed?

A

Digested into smaller peptides or amino acids
Small peptides transported into enterocytes by PEPT1, requires H+
Amino acids are transported using a number of different systems

152
Q

Why are drugs not well absorbed?

A

Hydrophilic, cannot pass membrane so bioavailability

153
Q

How is absorption of drugs optimised during design?

A

Designed to mimic a natural ligand so they can be transported into cells using uptake transporters

154
Q

How do efflux transporters affect drug bioavailability?

A

Drugs effluxed out of cell which is detrimental to absorption

155
Q

What efflux transporters recognise multiple drugs structures?

A

P-gp and BCRP

156
Q

Why can’t anti-cancer drugs be given orally?

A

Effluxed by P-gp transporter but inhibition increases toxicity of drugs

157
Q

Give three examples of anti-cancer drugs

A

Etoposide
Doxorubicin
Paclitaxel

158
Q

What are the concerns with giving chemotherapy IV?

A

Cell death at the injection site

Extravasation may lead to tissue necrosis

159
Q

What is the effect of P-gp inhibitors administered alongside substrates?

A

Increased plasma conc. of substrate, patient may experience substrates

160
Q

Describe the physiology of the liver

A

Largest organ in the body

2 blood supplies - hepatic artery and portal vein, 80% is from the portal vein

161
Q

What are the functions of the liver?

A

Storage of glycogen and fat-soluble vitamins
Synthesis of proteins, albumin and clotting factors
Immune functions - T cell proliferation, acute phase protein production
- Clearance and metabolism of drugs and cholesterol

162
Q

Describe the biliary system of the liver

A

Left and right hepatic ducts lead into common hepatic duct; cystic duct and common hepatic duct lead into common bile duct which then leads to duodenum

Pancreatic duct also leads into duodenum

163
Q

What parameters are included in LFTs?

A

Bilirubin
Gamma-Glutamyl Transferase (increased after alcohol)
Alanine/Aspartate Aminotransferase
Alkaline Phosphate (not liver specific)
Albumin (synthesis in liver)
Prothombin Time (synthesis of clotting factors)

164
Q

What characterises hepatocellular damage?

A

Increased ALT
Increased AST
Increased GGT
Increased total bilirubin

165
Q

What is cholestatic damage?

A

Decrease in bile flow due to blockage of drainage system

166
Q

What characterises cholestatic damage?

A

Increase conjugated bilirubin
increased alkaline phosphate
Increased total cholesterol
Pruritis (itchy skin)

167
Q

Describe acute liver disease

A

Self limiting (normally)
Hepatocyte damage or inflammation
Generally caused by drugs or acute viral infection

168
Q

To what extent can drugs damage the liver?

A

Reversible damage ranging to fatal hepatic necrosis

169
Q

What are the two types of drug reactions and what is the latent period for each?

A

Type A - Predictable and dose dependent, latent period of hours to weeks
Type B - Unpredictable, less common and independent of dose, latent period of weeks to months

170
Q

What are the two types of acute liver disease?

A

Acute hepatitis (with jaundice) - Spontaneous recovery and supportive therapy
Acute liver failure - May become hepatic failure and affect whole liver or may become chronic liver disease
- Patient may require liver transplant

171
Q

What are the causes and symptoms of chronic liver disease? What is the disease timeframe?

A

Alcohol, chronic viral hepatitis (hep C), primary biliary cirrhosis, auto-immune hepatitis, cancer

Fatigue, malaise, fever, N&V, upper right abdominal pain, pruritis, jaundice, oedema

Longer than 6 months

172
Q

What are the three types of alcoholic liver disease? How would they be diagnosed from LFTs?

A

Steatosis (excessive lipid retention), increased GGT with or without AST
Fibrosis and then cirrhosis (thickening and scarring connective tissue), high prothrombin and low albumin
Hepatitis (and cirrhosis), elevated bilirubin

173
Q

What causes itching in pruritis?

A

Bile salts collecting under the skin

174
Q

How is cholestatic disease treated?

A

If cause by gall stones, remove surgically
If cause unknown:
- Anion exchange resins bind bile acids in gut
- Antihistamines for symptom relief
- Topical creams for symptom relief

175
Q

What is Ascites and what are the causes?

A

Fluid collection in abdominal cavity

Portal hypertension, activation of renin-angiotensin system, decreased oncotic pressure (low albumin)

176
Q

What is the treatment for ascites?

A

Diuretics:

  • Spironolactone 100-600mg OD
  • Furosemide 40-160mg OD
  • Metolazone if above do not work

Reduce sodium in diet

177
Q

How is ascitic pain treated?

A

Analgesics:

  • Paracetamol (max 2g daily)
  • Tramadol
  • Opioids WITH CAUTION (decreased clearance)
178
Q

Why can’t NSAIDs or anti platelets be used in ascitic pain?

A

Bleeding risk

179
Q

What is hepatic encephalopathy?

A

Nitrogenous waste and other toxins reach the brain, causes altered mental state

180
Q

What causes exacerbations of hepatic encephalopathy?

A

Gi Bleeds
Constipation
Use of opiates
High protein diet

181
Q

How is hepatic encephalopathy treated?

A 
Low protein diet
Lactulose - prevents constipation
Neomycin - Peripheral neuropathy
Rifaxamin
Metronidazole
Enemas if unable to swallow
182
Q

How are oesophageal varices formed?

A

Intrahepatic vascular resistance causes portal hypertension along with splanchoic arteriolar vasodilation. Dilation of pre existing vessels and angiogenesis cause formation of varices in stomach and oesophagus

Further increase in portal hypertension causes increase in size of varices, eventually they rupture and bleed (large blood loss)

183
Q

How are varices treated?

A

Constrict blood flow and reduce portal hypertension

184
Q

How are alcohol and vitamin deficiencies treated?

A

Chlordiazepoxide
Oral vitamin B and thiamine (or IV pabrinex)
Water soluble menadiol (vit K)

185
Q

What are the different types of viral hepatitis?

A

Hepatitis A-E

186
Q

How are the different viral hepatitis diseases treated?

A

Hep A: Supportive treatment
Hep B: Chronic treatment with antivirals (entecavir/tenofovir) and interferon alpha-2a
Hep C: Ribavarin with interferon alpha-2b

187
Q

What is coeliac disease and what are the triggers?

A

Autoimmune disease - immune system is triggered by wheat proteins

188
Q

What are the symptoms of coeliac disease?

A

Headaches
Diarrhoea (therefore weight loss and malnutrition)
Stomach Pains
Lethargy

189
Q

How is coeliac disease managed?

A

Gluten free diet (life long), may include foods with specially modified wheat starch

190
Q

When can prescriptions be given for gluten free foods? How much are they?

A

Diagnosed with coeliac disease, dermatitis herpetiformis

Standard £8.40 prescription tax

191
Q

When are guidelines for monthly prescribed amounts of GF foods used?

A

Patients presenting with malnutrition, intractable malabsorption, difficulty swallowing, IBD, bariatric procedures, short bowel syndrome

192
Q

What are the forms of enteral nutrition?

A

Sip feeds, supplements, nasogastric feeding, PEG/PEJ tubes, distal feeding

193
Q

What are three common causes of stoma care?

A

Colon cancer
Bladder cancer
IBD

194
Q

Describe the difference between a temporary stoma or permanent stoma

A

Temporary: Diversion of faeces from surgically rejoined intestine or obstructions
Permanent: Loss of bowl/urinary function due to disease or its treatment

195
Q

How can post-surgical problems arise in stoma care?

A

Stoma itself or other conditions

196
Q

How are stoma supplies prescribed for and dispensed?

A

Stoma appliances available for prescription are on drug tariff, stock is then ordered by mail depending on amounts

197
Q

Where is a stoma bag placed?

A

Just before the section that is removed due to a colostomy procedure

198
Q

What is a common side effect in patients who have undergone a colostomy?

A

Constipation

199
Q

What are the issues surrounding MR preparations and laxatives in colostomy patients?

A

GI transit may be rapid

Laxatives should be avoided due to loss of water and electrolytes

200
Q

How is constipation in colostomy patients treated?

A

Initially fluid/dietary fibre

Low dose laxatives used with caution

201
Q

What are the issues with Mg, Al, Ca and Fe in colostomy patients?

A

Mg - Increased risk of diarrhoea
Al/Ca - Increased risk of constipation
Fe - use I/M administration to prevent loose stools

202
Q

What are the issues with compound analgesics (codeine +) or antibiotics in colostomy patients?

A

Analgesics may cause constipation

Antibiotics may cause diarrhoea

203
Q

What are the effects of potassium-sparing diuretics and digoxin in colostomy patients?

A

K+ sparing diuretic should be avoided due to K+ depletion

Digoxin may cause hypokalaemia so should be given with liquid K+ supplement to avoid osmotic diarrhoea

204
Q

What problems are associated with the use of a stoma appliance?

A

Leaking - incorrect stoma size
Skin problems - prevented by cleansing agents, protective creams and sealants
Manual dexterity - May result in reduced ability to change stoma appliance
Odours

205
Q

How can GI conditions affect absorption of other drugs?

A

May increase or decrease absorbance depending how the drug is absorbed, therefore altering the therapeutic effect
Antacids may interact with other drugs
Omeprazole may block feeding tubes

206
Q

What frequency of bowel movements characterises normal and diarrhoea?

A

Normal: 3x weekly - 3x daily
Diarrhoea: More than 300g daily, >70% water

207
Q

What are the causes of diarrhoea?

A

Poor fluid absorption due to infection, IBD
Osmotic effects of unabsorbed foods
Enzyme deficiencies
Gut motility issues from IBD, diabetes, hyperthyroidism, drugs

208
Q

What characterises acute diarrhoea?

A

3-4 unformed stools per 24 hour period
Usually self-limiting to 3 days
Caused by virus (rotavirus, norovirus, adenovirus)
May affect travellers due to destination or change in diet

209
Q

How is oral rehydration used for treatment in acute diarrhoea?

A

Replaces electrolyte deficit
Contain alkalinising agent to counter acidosis (dextrose or rice powder citrate/bicarbonate)
Continue with normal volumes of fluid in between rehydration drinks

210
Q

How is loperamide used for treatment in acute diarrhoea?

A

Decrease gut motility
Reduced opiate activity
Available OTC

211
Q

How are antispasmodics used for treatment in acute diarrhoea?

A

Symptomatic relief of abdominal cramps

212
Q

What is racecadotril and what is its mechanism?

What patient groups is it used for?

A

Oral enkephalinase inhibitor
Reduces hypersecretion of water and electrolytes
Used in children of >3months

213
Q

How is the rotavirus vaccine administered in children and why?

A

Protection against gastro-enteritis

First dose at 6-15 weeks, second dose at least 4 weeks later

214
Q

How is Kaolin used in diarrhoea?

A

Absorb toxins to bulk out stool

215
Q

When should patients with diarrhoea be referred?

A 
Symptoms lasting >1 week
Patient if young child/baby
Presenting with dehydration or fever
Dark stools/presence of blood
Severe abdominal/rectal pain
216
Q

What is pseudomembranous colitis and what causes it?

A

Swelling/inflammation of large intestine caused by C. difficile overgrowth
Generally result of poor hygiene but may be caused by antibiotic treatment

217
Q

What is the treatment for pseudomembranous colitis?

A

Cease antibiotic treatment
Patient isolation
Replace fluid and electrolytes
Metronidazole 400mg TDS/Oral Vancomycin 125mg QDS
May use newer antibiotics, probiotics or IV immunoglobulins

218
Q

What two diseases are classified as IBD? Describe them

A

Ulcerative colitis - Affects lower section of GIT, cured by total colostomy
Crohn’s - Incurable, patchy inflammation affecting whole GIT

219
Q

What are the general treatment steps for patients with IBD?

A

Local corticosteroid/aminosalicylate
Oral corticosteroid/aminosalicylate
Hospitalisation - IV steroid/immunosuppressive treatment
Sulphasalazine is used to maintain remission in UC

220
Q

What parameters should be monitored in patients with IBD?

A 
Faecal calprotectin
Stool frequency
Blood/mucus in stool
Temp
CRP
U&amp;Es
221
Q

What actions are undertaken in an IBD relapse?

A

Bed rest
Low residue diet
Monitoring
Corticosteroid use

222
Q

How is constipation classified and what should be done before treating?

A

Hard, less frequent stools
Increase fluid intake and dietary fibre
Assess cause

223
Q

What are the causes of constipation?

A 
Lack of dietary fibre and fluid
Obstructions
Motility issues
Neurological causes
Side effects of drugs
Lifestyle
224
Q

How is constipation treated? How do they work?

A

Bulking agents - Increase in mass stimulates peristalsis
Stimulants - Increase intestinal motility
Osmotic agents - Increase water in large bowel
Softening agents - Promotes bowel movements

225
Q

When may laxatives be used?

A

Expulsion of parasites
Post MI
Prior to surgery/x-ray
In liver failure

226
Q

What are the functions of the kidney?

A

Homeostasis - Blood volume and pressure, ion levels, acid-base balance
Excretion - metabolites, chemicals and drugs
Endocrine - Erythropoetin production, vitamin D3 production, Ca2+ regulation

227
Q

Where are the kidneys located?

A

Back of abdominal wall

228
Q

What are the regions and functional units of the kidneys?

A

Cortex, medulla and nephrons

229
Q

Describe the functional units of the kidneys and their functions

A

Glomerulus -> Bowman’s Capsule -> PCT -> PST -> LoH -> DCT -> CCD -> MCD -> Bladder

Filtration of the blood - high hydrostatic pressure maintained by different diameter of the afferent and efferent arteriole

230
Q

Describe glomerular filtration

A

Blood filtered through three layers into bowman’s space, where it then enters nephron - capillary endothelium, basement membrane, podocytes of the bowman’s capsule

231
Q

How is the rate of glomerular filtration altered? What does it show?

A

Increases with blood pressure
Defined as volume of fluid entering bowman’s capsule with unit time
Can be used to reflect kidney function

232
Q

What is secretion?

A

Some molecules may be secreted from the vasa recta and enter the nephron further along

Blood may also enter at this point

233
Q

What is reabsorption?

A

Molecules are reabsorbed from the nephron filtrate into the vasa recta
Includes glucose, amino acids and some drugs

234
Q

What factors influence renal function and how?

A

Age, disease
Reduced kidney function may reduce rate of elimination
Patients may require lower drug doses

235
Q

What two ways is eGFR measured?

A

Inulin clearance - Administered IV and freely filtered, not metabolised by kidney therefore amount filtered into Bowman’s capsule is amount in urine
Creatinine clearance - Creatinine produced in muscles but freely filtered, ~10% is secreted by nephron BUT does not require IV administration

236
Q

What is the definition of renal clearance and how is it measured?

A

Volume of plasma completely cleared of a substance with unit time
Cx = [Ux]V/[Px]

237
Q

How are substances secreted from the vasa recta into the nephron tubule?

A

Uptake transporters in the basolateral membrane removes substances from the blood
Efflux transporters in the apical membrane transport these into the filtrate

238
Q

How is glucose reabsorbed from the kidney filtrate?

A

Uptake via glucose transporter and reabsorbed into vasa recta

239
Q

Give an example of diabetes treatment and how it works

A

Dapagliflozin - Blocks SGLT2, preventing glucose reabsorption

240
Q

Give 5 uptake and elimination examples of drugs

A

Methotrexate - Uptake: OAT1 and OCT1, Efflux: MRP2 and P-gp
Pituvastatin - Uptake: OAT3, Efflux: BCRP
Rosuvastatin - Uptake: OAT3, Efflux: BCRP
Fexofenidine - Uptake: OAT3, Efflux: P-gp
Digoxin - Uptake: OATP1, Efflux: P-gp

241
Q

How is water reabsorbed in the kidneys?

A

~70% of Na+ is reabsorbed in PCT, some reabsorbed in collecting ducts. Water follows by passive diffusion

242
Q

How is Na+ reabsorbed?

A

Co-transported with organic molecules (e.g. glucose)

Coupled with H+ secretion (acid-base balance)

243
Q

Describe the mechanism of acid-base balance in the kidneys

A

Dissociation of carbonic acid forms H+ and HCO3-, anitporter protein effluxes H+ by uptake of Na+ and HCO3- moves into blood to act as a buffer

244
Q

How is the acid-base balance regulated in the lungs?

A

Excretion of CO2 from the body

245
Q

What is acidosis and how is it prevented?

A

H+ build up due to inefficient lung function (due to fibrous tissue formation and inefficient CO2 removal)
Kidneys compensate by increasing H+ secretion to prevent build up and restore normal levels

246
Q

What is the CO2/H+ equilibrium?

A

CO2+H2O H2CO3 H+ + HCO3-

247
Q

What equation defines the proportion of acid to dissociated acid?

A

pH = pKa + log([A-]/[HA])

248
Q

How is aldosterone secreted?

A

Renin-Angiotensin system
Low Na+ sensed by kidney juxtaglomerular cells -> Renin production -> Conversion of angiotensinogen to ATI -> Conversion of ATI to ATII by ACE -> ATII stimulates aldosterone production and secretion from adrenal cortex

249
Q

How does aldosterone increase Na+ levels?

A

Increased Na+ channels in apical membrane and increased Na+/K+ ATPase in basolateral membrane of cells in collecting duct

250
Q

How do ACE inhibitors prevent sodium reabsorption?

What conditions are they used in?

A

Prevent conversion of ATI to ATII so no aldosterone secretion
Heart failure and hypertension

251
Q

Give two examples of diuretics and how they prevent water retention

A

Spironolactone - Aldosterone analogue, prevents Na+ reabsorption by preventing extra channels in collecting duct cell membranes
Amiloride - Binds to and blocks Na+ channels

Both result in Na+ excreted in urine, water is not reabsorbed without sodium due to osmosis

252
Q

How much of the glomerular filtrate is reabsorbed?

A

~99% - 120L of blood filtered but only 1.5L urine produced every 24 hours

253
Q

What factors affect the number of nephrons?

A

Age

Hypertension

254
Q

Describe the different parts and processes of the nephron

A

Proximal Tubule - Tight junctions between epithelia cells (leaky), secretion of organic acids/bases
Descending LoH - Hypertonicity of interstitial fluid causes water to diffuse out
Ascending LoP - Low water permeability, active transport of Na+ into interstitial fluid
Distal tubule - Impermeable to water, some Na+ reabsorption
Collecting Duct - Water reabsorbed via aquaporins

255
Q

How is water reabsorption in the collecting duct mediated?

A

Release of ADH from pituitary gland binds to vasopressin receptors, aquaporins in vesicles are inserted into membrane

256
Q

What are the actions of diuretics?

A

Increase urinary output
Decrease oedema
Reduced plasma volume

257
Q

How do loop diuretics work and what effect do they have on ion reabsorption?

A 
Inhibition of Na+/K+/Cl- carrier (ALoH) but Na+/H+ exchanger remains unaffected
K+, Cl-, Ca2+, Mg2+ excreted in urine
Plasma conc. of HCO3- increases
Less uric acid excretion
Vasodilation before diuresis
258
Q

How do NSAIDs interact with loop diuretics?

A

PGE2 inhibits absorption of Na+/Cl-
NSAIDs prevent PGE2 production so opposite diuretic effect
Also competes with diuretic for OAT

259
Q

What are the indications for loop diuretics?

A 
Acute pulmonary oedema
Chronic heart failure
Liver cirrhosis
Nephrotic syndrome
Renal failure
Hypertension
Hypercalcaemia
260
Q

What are the side effects of loop diuretics?

A 
Hypertension
Hypokalaemia
Metabolic alkalosis
Gout
Hearing Loss
261
Q

Describe the pharmacokinetics of loop diuretics

A

Absorbed in GIT
Effect <6hours
Half life 90mins
Albumin binding

262
Q

How do Thiazide and Thiazide-like diuretics work and what effect to they have on ion reabsorption?

A

Na+/Cl- co-transporter in DCT inhibited
Vasodilation
Same mechanism as loop diuretics
Ca2+ excretion decreased - used in those with a risk of osteoporosis

263
Q

Why does chronic use of thiazide-like diuretics have a limited hypotensive effect?

A

Decreased blood volume causes increased activity of renin-angiotensin system

264
Q

What are the indications for thiazide-like diuretics?

A

Hypertension, heart failure, oedema, nephrogenic diabetes

265
Q

What are the side effects of thiazide-like diuretics?

A

Increased urination frequency
Erectile dysfunction
Hypokalaemia
Impaired glucose tolerance

266
Q

How is hypokalaemia prevented when using diuretics?

A

Increase dietary intake
K+ supplements
K+ sparing diuretics

267
Q

What type of diuretic is Spironolactone?

A

K+ sparing diuretic

268
Q

What are the indications of K+ sparing diuretics?

A 
Hyperaldosteronism
Ascites
Oedema
Severe heart failure 
Left ventricular failure post MI
269
Q

What are the side effects of K+ sparing diuretics?

A

Hyperkalaemia
GI upsets
Menstrual disorders
Testicular atrophy

270
Q

How do osmotic diuretics work?

A

Filtered to increase osmolarity of filtrate, Na+ reabsorption prevented by dilution

271
Q

What are the varying levels of renal impairment?

A

Pre dialysis
Haemodialysis/Peritoneal dialysis
Requiring kidney transplant

272
Q

What characterises kidney disease?

A

Damage for > 3months and GFR >60ml/min/1.73m2
GFR <60ml/min/1.73m2 with or without damage
Function or structure abnormal
Generally alongside other conditions
Not always symptomatic

273
Q

What markers are used to assess renal function or rate of change?

A 
Albuminuria
Urine sediment abnormalities
Electrolyte abnormalities
Cellular abnormalities
Structural abnormalities 
Previous kidney transplantation
274
Q

How is serum creatinine influenced?

A

Proportional to muscle mass and can be influenced by drugs/diet

275
Q

What is considered when working out eGFR?

A

Gender, age, creatinine levels, ethnicity (correction factors)

276
Q

When is Cystatin C-based GFR used?

A

If eGFR (creatinine) is 45-60ml/min for more than 90days and no other marker of CKD

277
Q

What does a urine dipstick test for

A

Haematuria

Proteinuria/Albuminuria

278
Q

What are risk factors for CKD?

A 
Diabetes
Hypertension
Kidney injury
CVD
Family history
Haematuria detection
279
Q

What medications slow disease progression or reduce risk of another disease as a result of CKD?

A

Glycaemic control
BP control
Statins to prevent development of CVD

280
Q

What are the different stages of CKD and what do they refer to?

A

Stages 1-4: drop in eGFR

Stage 5: Consider replacement therapy

281
Q

What are some complications of CKD?

A 
Anaemia
Disordered bone metabolism
Osteoporosis
High phosphate
Pruritis
Acidosis
Hypertension
282
Q

What causes nausea in CKD?

A

Build up of toxins

283
Q

What is the main cause of death in acute kidney injury?

A

Delay in recognition and treatment

284
Q

What is an acute kidney injury?

A

Rapid reduction in renal excretory function characterised by increased creatinine and reduced urinary output

285
Q

What are the risk factors for acute kidney injuries?

A

Clinical factors
Co-morbidities
Nephrotoxic drugs

286
Q

How is an acute kidney injury detected?

A

Increase in serum creatinine by >26mml/L in 48hrs or 50% in 7 days
Urine output <0.5ml/kg/hour for 6hours(adults) or 8hours(children)
Decrease in eGFR by 25% within 7days

287
Q

What are the causes of AKI?

A

Pre renal - Issues with perfusion
Renal - Affects function of kidney
Post renal - Obstruction of fluid leaving kidney

288
Q

What is the SADMAN check when a patient presents with AKI?

A 
Checking for medicines that may cause AKI
Sulphonylureas
ACE/ARB
Diuretics
Metformin
Aldosterone antagonist 
NSAIDs
289
Q

When should haemodialysis be considered for an AKI patient?

A 
In cases of:
Fluid overload
High K+
Pericardial rub
uraemia/encephalopathy
Metabolic acidosis
290
Q

List some common nephrotoxic drugs

A 
Antibiotics
Chemotherapy
Immunosuppressants
Heavy metals
Statins
Abused drugs
291
Q

What is dialysis and what is the difference between haemodialysis and peritoneal dialysis?

A

Diffusion of molecules across a semi permeable membrane along an electrochemical conc. gradient
Haemodialysis uses semi synthetic membrane
Peritoneal dialysis uses peritoneum

292
Q

How is the gradient maintained in dialysis?

A

Dialysate flow is in opposite direction to blood flow

293
Q

What is the aim of dialysis and what are the side effects?

A

Aim is removal of electrolytes

Anaemia, hypertension, time consuming, infections, clotting problems, pain

294
Q

What are the advantages and disadvantages of peritoneal dialysis?

A

Slower decline in kidney function but not as efficient removal of electrolytes

295
Q

What are the benefits and disadvantages of organ transplantation?

A

Better quality of life
Lower morbidity and mortality
Cheaper than dialysis

Requires an organ donor
Immunosuppression from point of transplantation
Chance of organ rejection

296
Q

What combination treatments for immunosuppression are used?

A

Ciclosporin/Tacrolimus +/-
Prednisolone +/-
Mycophenolate/Azathioprine

297
Q

What are the issues surrounding ciclosporin/tacrolimus/sirolimus?

A

Narrow TI

Many drug interactions

298
Q

How does kidney disease affect pharmacokinetics?

A

Altered GI absorption
Altered 1st pass metabolism
Increased volume from renal failure results in increased volume of distribution - Lower plasma concentration
Drug metabolites may not be excreted

299
Q

What affects the filtration, secretion and reabsorption of the drug?

A

Water solubility
Protein binding
Molecular size
Distribution

300
Q

What factors affect adherence in kidney disease?

A

Amount of medicine to take
Cost of medicines
Treatment duration
Side effects

301
Q

Why should opioids and codeine be used with caution in kidney disease?

A

Morphine renal excreted

Codeine metabolised to morphine

302
Q

How are patients with kidney disease immunocompromised?

A

Susceptible to infections

BP may affect immunity

Pharmacy Year 2 (9 decks)

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