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Medicine Year 3 > Week 0/15 - GP > Flashcards

Week 0/15 - GP Flashcards

1
Q

What should be asked when taking a psychosexual history?

A
  • Sexual function - onset + duration of erectile problems (able to manage full/partial erection)
  • Quality of erections - nocturnal and morning spontaneous erections?
  • Situations present - attempted intercourse w/ regular partner or different, self or erotic stimuli?
  • Previous history of ED, treatments?
  • Sexual orientation/gender identity
  • Past/current sexual relationships
  • Current emotional status
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2
Q

What questions should be asked when a patient presents with ED?

A
  • Psychosexual history
  • CVS/diabetes - detailed history of CV symptoms or symptoms suggestive of diabetes e.g. thirst, polyuria, polydipsia
  • Genitourinary - clarify there are no lower urinary tract symptoms which may be linked e.g. hesitancy, urgency, haematuria etc.
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3
Q

What resources are available for taking a history for ED?

A

Downloadable questionnaires available e.g. International Index of Erectile Dysfunction, Sexual Inventory for Men

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4
Q

What examinations would be performed in a patient presenting with ED?

A
  • General - BP, pulse, BMI (assess cardiac risk factors)
  • External genitalia -
    • Penile abnormalities - premalignant or malignant conditions
    • Phimosis (foreskin too tight to be pulled back over glans penis)
    • Peyronie’s disease (scar tissue plaque forms inside penis, causes bent erect penis)
    • Signs of secondary sexual characteristics - testicular size/testicular consistency
  • Digital rectal examination
    • Prostate exam in older men (>50)
    • History of prostate cancer
    • Prostate symptoms
    • Ejaculatory dysfunction - caused by enlarged prostate
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5
Q

What investigations should be done in a patient presenting with ED?

A
  • Fasting glucose or HbA1c - assess glycaemic control
  • Fasting lipids - calculate 10yr CVD risk
  • LFTs including GGT
  • Total testosterone - requires sample between 8am-11am
  • Additional tests - LSH, FH, prolactin, thyroid function tests - if testosterone low
  • Consider PSE if >50/enlarged prostate on DRE
    • Check level prior to initiating testosterone therapy
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6
Q

How common is erectile dysfunction?

A

50-55% of men 40-70 y/o

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7
Q

Define erectile dysfunction

A

Inability to achieve/maintain a penile erection adequate for satisfactory sexual intercourse

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8
Q

How is CVD linked to ED?

A

Endothelial dysfunction in CVD leads to impaired smooth muscle relaxation within the penis

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9
Q

What does the Princeton consensus propose?

A

Assessing men with CVD for exercise ability to ensure they can meet the demands of sexual activity

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10
Q

List the causes of ED

A

Classified as psychogenic or organic, commonly has overlap

  • Psychogenic - no physiological or neurovascular condition identified
    • About 10% of ED cases
    • Due to stress in a relationship, performance anxiety, psychological problem
  • Organic - 90% of men attributed to central mechanism of endothelial dysfunction
    • CVD - 40%
    • Diabetes - 33%
    • Hormonal/drugs - 11%
    • Neurological disorders - 10% e.g. MS, Parkinson’s, spinal cord trauma
    • Pelvic surgery/trauma - 3-5%
    • Anatomical abnormalities in 1-3% e.g. phimosis, Peyronie’s disease, short frenulum
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11
Q

List common drugs which cause ED

A
  • Antidepressants - SSRIs (citalopram/fluoxetine), MAOIs (phenelzine), TCAs (amitriptyline)
  • Antihypertensives - beta-blockers, verapamil, methyldopa, clonidine
  • Antiarrhythmics - digoxin, amiodarone
  • Diuretics - spironolactone, thiazide
  • Hormonal - anti-androgens (cyproterone acetate), LHRHs (goserelin), 5 alpha reductase inhibitors (finasteride), corticosteroids, ketoconazole
  • H2 receptor antagonists - cimetideine, ranitidine
  • Recreational drugs - alcohol, marijuana, cocaine
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12
Q

How can psychogenic causes of ED be differentiated from organic causes of ED?

A
  • Symptoms suggestive of psychogenic causes of ED
    • Younger age, lack of medical history/risk factors
    • Sudden onset
    • Decreased libido
    • Spontaneous erections
    • Symptoms present at specific time e.g. with partner
    • Major life events
    • Relationship changes
    • Previous psychological history
  • Symptoms suggestive of organic cause of ED
    • Older age
    • Gradual onset
    • Normal libido
    • Loss of nocturnal and early morning erections
    • Present in all situations - with partner/or stimuli
    • Risk factors for CVD/DM
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13
Q

What is the management plan for a patient with ED?

A
  • Identify and treat reversible causes of ED
    • Testosterone deficiency - establish cause of hypogonadism
    • Hyperthyroid/hyperprolactinaemia
    • Drug induced- change or withdraw medicine, caution in those on anti-psychotics as this requires psychiatric review
    • Sexual problems - consider patient referral to psychosexual counselling or relationship counselling for couples
  • Lifestyle modifications
    • Dietary changes
    • Smoking cessation
    • Reduction in alcohol - encourage ‘drink free’ nights
    • Increase exercise as BMI raised/systolic BP elevated
    • Suggest counselling or mindfulness to help w stress due to work
  • If had pre-existing CVD need to assess risk of sexual activity (Princeton consensus) - requires same effort as gardening
  • Drug therapy?
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14
Q

What is the first line drug-therapy for ED

A
  • PDE-5 inhibitors are first-line treatment for ED except if there are contraindications
  • E.g. Sildenafil (Viagra)
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15
Q

Describe the mode of action of PDE-5 inhibitors

A
  • Selective inhibitors of phosphodiesterase type 5 (PDE5)
  • Inhibit cGMP-specific PDE5 (breaks down cGMP)
    • cGMP promotes smooth muscle relaxation, increased blood flow to penis, leading to compression of the subtunical venous plexus resulting in penile erection
    • Inhibiting PDE5 maintains concentrations of cGMP necessary for achieving and maintaining erections
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16
Q

What are the contraindications for PDE-5 inhibitors

A
  • Nitrates and guanylate cyclase stimulators e.g. Riociguat (for pulmonary arterial hypertension)
  • Severe/unstable heart disease
  • Non-arteritic anterior ischaemic optic neuropathy (NAION)
  • Hypotension (systolic below 90/50 mmHg)
  • Unstable angina or angina occurring during sexual intercourse
  • Recent stroke or MI
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17
Q

What are the cautions when prescribing PDE5 inhibitors?

A
  • CVD risk stratify according to Princeton consensus II
  • Left ventricular outflow obstruction e.g. aortic stenosis
  • Anatomical penile abnormalities e.g. Peyronie’s
  • Predisposition to priapism e.g. Sickle-cell disease
  • Varendafil - elderly men and men with active peptic ulceration, bleeding disorders, long QT interval
  • Sildenafil and Avanafil - active peptic ulceration or bleeding disorders
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18
Q

Describe the dosing regimen of commonly prescribed PDE5 inhibitors

A
  • Sildenafil ‘viagra’
    • 50mg taken as needed approximately one hour before sexual activity
    • Max dose 100mg daily
    • Duration of action - 4-5 hours
  • Tadalafil ‘cialis’
    • 10mg (with or without food) taken at least 30 minutes prior to sexual activity
    • Max dose 20mg daily.
    • Frequent sexual activity (more than twice weekly) can be prescribed at doses of 2.5 and 5mg tablets for daily use
    • Duration of action - up to 36 hours
  • Vardenafil ‘levitra’
    • 10mg taken as needed, 25-60 minutes before sexual activity
    • Max dose is 20mg
    • Duration of action 4-5 hours
  • Avanafil ‘spedra’
    • 100mg dose 15-30 minutes prior to sexual activity
    • Max dose is 200mg
    • Duration of action - up to 6 hours
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19
Q

List the common and uncommon side effects of PDE5 inhibitors

A

Common

  • Backpain, dyspepsia, flushing, migraine, myalgia, nasal congestion, dizziness, nausea, vomiting

Uncommon

  • Visual disturbances, including non-arteritic anterior ischaemic optic neuropathy, stop with immediate effect if sudden visual impairment occurs
  • Sudden hearing loss
  • Priapism (persistent erection). Warn to seek advice if erection lasts longer than 4 hours.
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20
Q

Should patients buy ED therapy on the internet?

A
  • Advise extreme caution - many counterfeit medications in circulation
  • Overuse of medication to improve sexual performance is common and it is important to monitor prescription requests from patients
  • Can be purchased directly from a pharmacy
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21
Q

Which patients are exempt from payment for PDE5 inhibitors on the NHS?

A
  • Diabetics
  • Parkinson’s disease
  • MS
  • Polio
  • Single-gene neurological disease e.g. Huntington’s
  • Spinal cord injury
  • Spina bifida
  • Renal dialysis
  • Radial pelvic surgery
  • Prostate cancer
  • Treatment initiated before 1998
  • Severe stress secondary to ED - as judged by specialist
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22
Q

If symptoms of ED do not improve following prescription of a PDE5 inhibitor and lifestyle modification, what should be done next?

A
  • Referral to secondary care specialist ED clinic - genitourinary or sexual health - to discuss other management options
  • Second line therapy for ED - synthetic prostaglandin E1 analogue - alprostadil
    • Acts by increasing cGMP levels thus increasing smooth muscle relaxation and penile blood dlow
    • Can be given directly into the penis by
      • Muse - small pellet inserted directly into urethral opening of penis
      • Caverject - direct intravernosal injection into penis
  • Secondary care treatments =
    • Vacuum erection device - cylinder placed over penis, air removed with pump causing vacuum, increased blood flow to penis = erection
      • Caution needed - constriction ring placed at base of penis to maintain erection, must not stay on longer than 30 minutes
    • Can cause pain, bruising, penile numbness, skin necrosis
  • Third line therapy - penile prosthesis surgery, only suitable for patients with severe organic erectile dysfunction which has not responded to drug treatments
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23
Q

When there is a family who are not known well by the practice with potential welfare concerns, which questions should be asked?

A
  • Which family members are registered at practice?
  • What are the exact relationships within the family?
  • Why did they move from previous residency?
  • What nursey/schools do the children attend?
  • Are there any previous concerns about the family? E.g. child protection, social work
  • Do the children have any existing medical problems?
  • Do the adults have any medical/social problems in their history which would put children at risk e.g. alcohol/substance misuse?
  • What family/friends/support is available or in place for the family?
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24
Q

Where can further information be gained about a family by their GP who are potentially at risk of welfare problems?

A
  • Healthcare system
    • Medical notes - contact previous GP
    • Access to parents medical files - appropriate to access them if a concern is raised about the child
      • Must document if this has been done in parent’s notes and whether consent was gained or not
  • Child protection GP lead
    • Specific GP usually assigned role of CP - gain their advice and ask if they are aware of other information shared by other agencies/have attended meetings about the family
  • Health visitor
  • Child protection unit
    • NHS agency, could contact directly to discuss concerns or find out if any information is available locally/nationally
  • Social work services
    • Part of Health and Social Care Partnership, run by local authority
    • May have information regarding family - HV would usually know anyway
  • Education system
    • School nurse - takes over care from health visotr when child enters school system
    • Nursery nurse/teacher - ask if they have any concerns
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25
Q

Why is it important to contact health visitors, social work, teachers etc. as a GP if you have concerns about a child/family?

A

As a doctor it is your duty to share info w/ other professionals and agencies to safeguard children.

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26
Q

What risk factors/vulnerabilities are associated with child protection cases?

A
  • Domestic abuse
  • Parental alcohol and drug misuse
  • Child/adolescent mental health difficulties
  • Parental mental health difficulties
  • Children with disabilities
  • Non-engaging families
  • Female genital mutilation
  • Harmful or problematic sexual behaviour
  • Honor based violence and forced marriage
  • Fabricated or induced illness
  • Child trafficking
  • Hidden children
  • Under-age sexual activity
  • Children or young people who are missing
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27
Q

What is the next step if there are child protection concerns with sufficient evidence to back this up in a specific family?

A
  • Initiate a Notification of Concern
    • If there is enough info at time of consult and concern other professionals and agencies to do so
    • Be open and honest with parents about the notification
    • Main reasons for NOC - children may come to significant harm from domestic abuse and neglect if the appropriate intervention is not sought
  • Used to guide health care staff on how to raise a concern
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28
Q

How is a notification of concern raised?

A
  • All initial referrals regarding NOC should be made to social work by telephone - allows for discussion of case with team leader, decide appropriate action
  • If child or children are felt to be in danger - contact the police on 999
  • NOC referral form must be made electronically to the CPU and social work
    • Sent via secure email and a copy should be appended to each of the children’s medical files - all concerns recorded chronologically
  • Written documentation needs to be submitted within 48 hours of a notification being raised
  • Family should be discussed at practice in CP meeting, liaise with CP lead in practice - all children coded as ‘vulnerable’ until further information is accrued
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29
Q

Define child abuse

A

Abuse - form of maltreatment of a child

  • Somebody may abuse or neglect a child by inflicting harm or by failing to act to prevent harm
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30
Q

List the types of child abuse

A
  • Physical abuse
    • Deliberate act to harm a child which causes bruises, cuts, burns or broken bones
    • Babies - shaking or hitting them can cause non-accidental head injuries
    • Can have serious consequences for children - can grow up and cause long lasting harm
  • Sexual abuse
    • Age of consent is 16 years old, below that age young person cannot consent to sexual acts
    • Forcing or enticing a child or young person to take part in sexual activities
  • Emotional abuse
    • Psychological abuse
    • Ongoing emotional maltreatment - deliberately trying to scare or humiliate a child, isolating or ignoring a child
    • Often happens at the same time as neglect or other abuse
  • Neglect
    • Persistent failure to meet a child’s basic physical and/or psychological needs, likely to result in serious impairment of child’s health or development
    • Can occur during pregnancy e.g. through maternal substance abuse and after birth through a variety of mechanisms
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31
Q

What is the definition of child protection and what is child protection register?

A
  • When a child requires protection from child abuse or neglect
  • Not required that abuse/neglect has taken place, but a risk assessment has identified a likelihood or risk of significant harm from abuse or neglect
  • Child protection register - central register of all children, including unborn children held and maintained by local authorities
  • Has no legal status - administrative system
  • Can be accessed 24 hours a day by concerned professionals
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32
Q

What legislation in Scotland protects the rights of children?

A
  • UN convention on the Rights of the Child (UNCRC) - one of the core international human rights treaties
    • Universally agreed set of minimum child rights standards from birth to age 18 years, came into force in 1992 in the UK
  • In Scotland, children’s rights are protected under Children + Young People (Scotland) Act 2014 - implements the UNCRC
  • Scottish government produced GIRFEC - Getting it Right for Every Chuld
    • Outlines the principles and values to support children and young people, national approach to encourage the wellbeing of children in Scotland, based on UNCRC
  • Child Protection Improvement Plan implemented by Scottish government in 2016 to review CP procedures and legislation
    • Main focus is to raise awareness of emotional abuse and child neglect
    • Resulted in revision of Section 12 of Children and Young Persons (Scotland) Act 1937 - child cruelty provision
  • The legal responsibility to investigate child protection concerns is the remit of social work and police
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33
Q

Describe information sharing regarding child protection issues

A
  • When information is shared a record must be made of who the information has been shared with, the reasons for doing so and if informed consent was gained or not
  • If decision is made not to share information this also needs to be recorded
  • If families move between authority areas (temporarily or permanently) then immediately the original authority will notify the receiving authority, must be followed up in writing
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34
Q

What is the GMC guidance regarding disclosure of information with regards to children?

A
  • All doctors must take action if they believe a young person may be being abused or neglected
  • You must tell an appropriate agency e.g. local authority children’s services, NSPCC or police promptly if you are concerned that a child/young person is at risk of/is suffering abuse or neglect, unless it is not in their best interest to do so
  • You do not need to be certain - the possible consequences of not sharing relevant information will, in the overwhelming majority of cases, outweigh any harm that sharing concerns with an appropriate agency may cause
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35
Q

When can confidential information be shared about a person?

A
  • You must do so by law or in response to a court order
  • The person the information relates to has given you their consent to share the information (or a person with parental responsibility has given consent if the information is about a child who does not have the capacity to give consent)
  • It is justified in the public interest - if the benefits to a child or young person that will arise from sharing the information outweigh both the public and the individual’s interest in keeping the information confidential
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36
Q

Describe the components of the innate and adaptive immune system

A
  • Innate - genetically pre-programmed
    • Soluble factors
      • Antibacterial factors
      • Complement system
    • Cellular factors
      • Scavenger phagocytes
  • Adaptive - immunological memory
    • Humoral
      • B cells
    • Cellular
      • CD4 T cells
      • CD8 T cells
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37
Q

Describe the antibacterial factors of the innate immune system

A
  1. Lysozyme
  • Enzyme present at mucosal surfaces e.g. resp/GI tract
  • Active in breaking down the Gram +ve cell wall
  1. Lactoferrin
  • Protein found at mucosal surfaces
  • Bacteria need soluble iron for growth - lactoferrin chelates iron > less soluble iron in GI/resp tract > inhibited growth of bacteria
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38
Q

List the pathways which activate complement

A
  • Classical pathway - antigen:antibody complexes
  • MB-lectin pathway - lectin binding to pathogen surfaces
  • Alternative pathway - pathogen surfaces
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39
Q

Describe the complement pathway

A
  • Initiation of complement activation – alternative, classical or MB-lectin pathway
  • Early steps – C3 binding to pathogen surface
    • C3a – inflammation
    • C3b – opsonisation and phagocytosis
    • C5a – inflammation
  • Late steps – complement protein form membrane attack complex à lysis of microbe (lesions form)
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40
Q

Why is the complement pathway not always successful in preventing infection by pathogens?

A

Pathogenic bacteria are often resistant to complement

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41
Q

Describe the types of tissue specific macrophages

A
  • Monocyte (blood) –> macrophages (tissue)
  • Tissue specific functions e.g. Kupffer cells in liver, microglia in CNS, alveolar macrophages, sample and destroy small numbers of pathogens they come into contact with
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42
Q

What is the function of macrophages? How do they achieve this?

A

Macrophage Functions:

  • Clearance of micro-organisms
  • Getting help – when overwhelmed sends hormonal signals to summon more immune cells

How do they do this:

  • Phagocytosis
    • Specialised in destruction of pathogens, also removed harmless debris e.g. tattoo pigment
  • Antigen presentation
    • Process engulfed particles, travels to draining lymph nodes and presents to T cells in MHC II
  • Cytokine production
    • M1 – inflammatory e.g. TNF alpha
    • M2 – regulatory e.g. IL-10
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43
Q

What is the function of pattern recognition receptors?

A
  • Genetically hardwired
  • Recognise molecules found commonly in micro-organisms
  • Able to recognise extracellular and intracellular threats
  • Respond to bacteria, fungi and yeasts
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44
Q

What is the function of toll-like receptors?

A
  • Toll-like receptors e.g. TLR1, 2, 6 etc. bind to peptidoglycans (gram +ve), lipoteichoic acids (gram -ve)
  • Initiate NF-kapaB, IRF and MAPK signalling, leads to IL-1B and TNF-alpha release
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45
Q

Why does the innate immune system fail?

A

Innate fails due to highly pathogenic bacteria and/or structural failure e.g. renal stones

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46
Q

What is the role of neutrophils in the immune system?

A
  • ‘Foot soldier’ of the immune system
  • 50-70% of WBC
  • Rapid response to infection
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47
Q

Describe the functions of neutrophils

A
  • Chemotaxis – migrate towards bacterial products e.g. lipopolysaccharide, chemokines and ‘danger’ signals e.g. complement components
  • Degranulate – release toxic granules + hydrogen peroxide extracellularly (principal method of bacteria destruction)
  • Phagocytic – will ingest and destroy pathogens using proteases, reactive oxygen species, lysozyme etc.
  • Die locally producing characteristic pus
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48
Q

What is the role of eosinophils in the immune system?

A
  • Classically respond to parasites
  • 1-6% of WBC
  • Pathological role in allergy
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49
Q

Describe the functions of eosinophils

A
  • Chemotaxis – migrate in response to chemokines e.g. eotaxin
  • Degranulation – release toxic substances onto the surface of parasites e.g. major basic protein, eosinophil cationic protein, eosinophil peroxidase
  • Cytokine production – drives inflammation e.g. IL-1, 2, 4, 8, TNF-alpha

Irritant toxin proteins released cause pruritis

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50
Q

What is the role of basophils/mast cells in the immune system?

A
  • Basophils (blood) à mast cells (tissues)
  • ‘Border guard’ of immune system, guard mucosal sites
  • Important role in allergy
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51
Q

Describe the functions of basophils/mast cells

A
  • Degranulation – rapid release pre-formed granules containing cytokines and mediators e.g. histamine (triple response wheal + flare reaction)
  • Cytokine release – store many pre-formed cytokines ready for release to attract + drive immune response
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52
Q

What is the role of dendritic cells in the immune system?

A
  • Typical branching structure e.g. Langerhans’s cells in epidermis
  • Derived from monocytes
  • ‘Sentinel’ of immune system – sample tissues looking for stranger/danger
  • Prototype antigen presenting cell
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53
Q

Describe the functions of dendritic cells

A
  • Phagocytosis – unlike macrophages not specialised in destruction of pathogens, mainly function as antigen presenting cells
  • Migration – in tissues constantly sampling environment, when active will travel to draining lymph nodes
  • Antigen presentation – presents to CD4 T cells and can initiate an adaptive immune response
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54
Q

Describe the stranger and danger models seen in dendritic cell function

A
  1. Dendritic activation
  • Stranger model – pathogen associated molecular pattern recognised by pattern recognition receptor on dendritic cell
  • Danger model – necrotic cell death causes release of danger associated molecular patterns, recognised by DAMP receptor on dendritic cell
  1. Dendritic cell maturation
  2. Conformational change from sampling to presenting - peptide-MHC complex forms, CD80 and/or CD86 co-stimulatory molecule needed
  3. Migration to draining lymph node
  4. Dendritic cell binds to T-cell receptor, activates T cell
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55
Q

Describe the organisation of adaptive immunity

A
  • Humoral
    • B cells –> antibodies (immunoglobulins) - extracellular pathogens e.g. bacteria
  • Cellular
    • CD4 T cells
      • Helper T cells
      • Directs B cells and CD8 T cells
      • Cytokine secretion
    • CD8 T cells
      • Killer or cytotoxic T cells
      • Targets intracellular pathogens e.g. viruses
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56
Q

Describe the general structure of antibodies

A
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57
Q

Describe the functions of antibodies

A
  • Opsonise for phagocytosis
  • Activate complement for lysis
  • Neutralise toxins and pathogen binding sites
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58
Q

Describe production of antibodies by B cells

A
  • Antibody expressed on cell surface = B cell receptor
  • Following stimulation, antibodies released into circulation
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59
Q

Describe the antibody isotypes

A
  • Differ in Fc regions

IgM

  • Main antibody of primary immune response
  • Low affinity, many binding sites
  • Activates complement

IgG

  • Main antibody of secondary immune response
  • Higher affinity as part of secondary response - memory
  • Activates complement, binds Fc-gamma receptor on phagocytes (opsonises)
  • Crosses placenta

IgA

  • ‘Antiseptic paint’
  • Present in secretions and lines epithelial surfaces
  • Neutralises by blocking binding of pathogens

IgE

  • High affinity binding to mast cells through Fce receptor
  • Role in allergy
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60
Q

Describe the function of B cells

A
  • Antigen recognition
  • Activation due to helper T cells, other stimuli
  • Clonal expansion, differentiation
    • Effector cells - antibody-secreting plasma cells
    • IgG expressing B cell (isotype switching)
    • High affinity Ig-expressing B cell
      • Affinity maturation - high affinity IgG
      • Memory B cell
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61
Q

Describe the production of Ig isotypes as the immune response progresses

A
  • Initial immune response – lots of IgM produced, low affinity binding
  • As immune response progresses isotype switching occurs, more IgG, higher affinity
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62
Q

Compare the primary and secondary B cell response

A
  • Primary response
    • 5-10 day lag after immunisation
    • Peak response smaller
    • Antibody type usually IgM > IgG
    • Antibody affinity - lower average affinity, more variable
  • Secondary response
    • 1-3 day lag after immunisation
    • Peak response larger
    • Relative increase in IgG and, under certain situations, in IgA and IgA (heavy chain isotype switching)
    • Antibody affinity - higher average antibody affinity (affinity maturation)
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63
Q

Why does B cell response require T cell help?

A

Optimal B cell response requires T cell help for:

  • Clonal expansion of specific B cells
  • Progression to antibody secreting (plasma) cells
  • Progression to memory B cells
  • Isotype switching to IgG, IgA and IgE
  • Affinity maturation
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64
Q

Describe the fucntion of T cell receptors

A
  • Receptor on surface of T cells, recognises antigen when presenting in MHC molecule
  • Recognises short peptide lengths, not whole 3D molecules (antibodies can recognise whole 3D macromolecules)
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65
Q

How are T cell receptors formed?

A
  • Gene splicing and recombination leads to formation of many unique T cell receptors
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66
Q

How is autoimmunity prevented?

A
  • B cells
    • Develop in bone marrow
    • If B cell receptor binds strongly to ‘self’ antigen in bone marrow – B cell dies by apoptosis
  • T cells
    • Originate in bone marrow à thymus
    • If T cell receptor binds strongly to ‘self’ antigen in thymus – T cell dies by apoptosis
  • Activation of both cell types requires presence of danger signals to activate
  • If antibody/TCR engaged in absence of ‘second signal’ cell likely to become anergic
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67
Q

What is required for T cells to recognise antigens?

A
  • T cells only see antigen in context of MHC
  • Class 1 MHC
    • Presents to CD8 T cells - causes death of infected cell
    • On all nucleated cells
    • Presents intra-cellular antigen via endoplasmic reticulum
    • Alpha 1, 2, 3 and Beta 2 microglobulin chains
  • Class 2 MHC
    • Presents to CD4 T cells - causes cytokine release
    • Presents extra-cellular derived antigen (phagocytosed - endocytosis into vesicle)
    • Found on antigen presenting cells - dendritic cells, macrophages, B cells
    • Alpha 1 and 2 and Beta 1 and 2 chains
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68
Q

Describe the function of CD4 T cells following activation by an antigen presenting cell

A
  • TH1 cells - IFN-gamma secretion, host defense against intracellular microbes, inflammation
  • TH2 cells - IL-4, 5, 13 secretion, host defense against helminths, allergic reactions
  • TH17 cells - Il-17 secretion, host defense against some bacteria, inflammatory disorders
  • T regulatory cells - act to regular function of other immune cells, in particular T cells
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69
Q

List the organs of the adaptive immune system

A
  • Primary organs
    • Thymus – T cell maturation
    • Bone marrow – B cell maturation
  • Secondary organs
    • Lymph nodes
    • Spleen
    • Mucosal associated lymphoid tissue of GI tract and bronchial tract
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70
Q

Describe the structure of a lymph node

A
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71
Q

How does a lymph node change in structure if infection is detected?

A

Germinal centres and paracortical areas swell significantly

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72
Q

Describe the immune function of the spleen

A
  • Similar function to lymph nodes
  • Filters blood of senescent (old, deteriorating) cells and blood borne pathogens
  • Important in response to encapsulated organisms and blood borne pathogens
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73
Q

Describe the histological structure of the spleen

A
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74
Q

What are the functions of the adaptive immune system?

A
  • Provides specific antibodies to innate to enhance pathogen clearance
  • Provides cytokines to innate to upregulate activity
  • Finishes clearing pathogens
  • Develops memory to prevent future infection
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75
Q

Describe a secondary immune response

A
  • Memory B and T cells already present at high frequency
  • Memory lymphocytes have lower threshold for activation and actively patrol sites of previous pathogen entry
  • Preformed antigen specific IgA prevents pathogen binding
  • Preformed high affinity IgG rapidly opsonises pathogen for phagocytosis
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76
Q

Describe the overall immune response which occurs after the skin integrity has been breached by a pathogen

A
  • Innate immune response
    • ‘Danger’ signals triggered via PAMP receptors - complement activated
    • Dendritic cells and macrophages detect pathogens and are activated
    • Local mediators e.g. histamine released, chemotaxis triggered
    • Neutrophils arrive at site of infection, begin phagocytosis
    • Dendritic cells leave via lymphatics carrying antigen
  • Activation of adaptive immune response
    • Dendritic cells to local draining lymph node
    • Circulating T cell enters from high endothelial venules of lymph node and engages dendritic cell via TCR
  • Adaptive immune response
    • CD4 T cells provides cytokines to activate CD8 T cells and antigen specific B cell
    • B cell takes up antigen via BCR, presented on MHCII
    • Some B cells go to medullary cord and become antibody secreting plasma cells
    • Other B cells enter lymphoid follicle to form germinal centre + undergo affinity maturation
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77
Q

List the types of hypersensitivity

A
  • Type I
    • Immediate, atopic
    • IgE mediated
  • Type II
    • Cytotoxic, antibody dependent
    • IgM or IgG bound to cell/matrix Ag
  • Type III
    • Immune complex
    • IgM or IgG bound to soluble Ag
  • Type IV
    • Cell mediated
    • T cells (CD4 and CD8)
  • Type V
    • Receptor mediated
    • IgM or IgG bound to receptors
    • Can be considered subset of type II

All examples of adaptive immune response - sensitisation of the immune system must occur

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78
Q

Describe type I hypersensitivity and its pathological role

A
  • ‘Classic’ allergy - immune mediated noxious response to substance body is sensitized to
  • Specific characteristics
    • Response to challenge occurs immediately - if more than 24 hours post-exposure not type 1
    • Tends to increase in severity w/ repeated challenge
    • Predominantly mediated by IgE bound to mast cells - degranulate releasing toxins which cause damage
  • Responsible for most allergies - asthma, eczema, hay fever
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79
Q

Describe the pathogenesis of allergy

A
  1. Sensitization
  2. Mast cells primed with IgE
  3. Re-exposure to antigen
  4. Antigen bind to IgE associated w/ mast cells
  5. Mast cells degranulate releasing:
  • Toxins i.e. histamine
  • Tryptase
  • Pro-inflammatory cytokines
  • Chemokines
  • Prostaglandins
  • Leukotrienes
  1. Proinflammatory process stimulates and amplifies future responses
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80
Q

What are the tissue effects of allergy?

A
  • Early phase
    • Occurs within minutes of exposure to antigen
    • Occurs largely as a result of histamine and prostaglandins
      • Smooth muscle contraction
      • Increased vascular permeability
  • Late phase
    • Occurs over hours to days after exposure to antigen
    • Principally mediated through recruitment of T-cells and other immune cells to site by cytokines
      • Sustained smooth muscle contraction/hypertrophy
      • Tissue remodelling
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81
Q

Define anaphylaxis

A
  • Severe, systemic type I hypersensitivity
    • Widespread mast cell degranulation caused by systemic exposure to antigen i.e. penicillin
  • Vascular permeability is principle immediate danger - can be rapidly fatal
    • Soft tissue swelling threatening airway
    • Loss of circulatory volume causing shock
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82
Q

What causes type II hypersenstivity

A
  • Caused by binding of antibodies directed against human cells
    • IgG usually cause (+IgM, IgA)
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83
Q

What are the pathological consequences of type II hypersensitivity?

A
  • Uncommon cause of allergy - drug associated haemolysis
  • Common cause of AI disease
  • Bullosa pemphigoid common type II hypersensitivity
    • Loss of skin integrity - IgG autoantibodies bind to basement membrane
    • Characteristic skin blistering
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84
Q

List the stages in the pathogenesis of type II hypersensitivity

A
  • Sensitization
  • Opsonization of cells
  • Cytotoxicity
    • Complement activation
    • Inflammation
    • Tissue destruction
  • In some cases:
    • Direct biological activation with antigen i.e. receptor activation, impaired enzyme action
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85
Q

What causes type III hypersensitivity?

A
  • Mediated by immune complexes bound to soluble antigen
    • Multiple binding sites on antibodies, immune complexes form
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86
Q

Describe the pathological consequences of type III hypersensitivity

A
  • Cause of autoimmune disease and drug allergy
  • Aggregate in small blood vessels e.g. glomerular capillaries
    • Direct occlusion
    • Complement activation
    • Perivascular inflammation
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87
Q

What causes type IV hypersensitivity?

A
  • Also known as delayed type hypersensitivity
    • Presents several days after exposure
    • E.g. nickel allergy to jewellery
  • Mediated by the action of lymphocytes infiltrating area - CD4/8 cells
    • Thickened epidermis
  • External substance enters body and alters conformation of self-cells (contact sensitizing agent)
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88
Q

Describe the pathogenesis of type IV hypersensitivity

A
  1. Contact-sensitizing agent penetrates the skin and binds to self proteins, which are taken up by Langerhans cells (DC)
  2. Langerhans cells present self peptides haptenated with the contact sensitizing agent to TH1 cells, which secrete IFN-gamma and other cytokines
  3. Activated keratinocytes secrete cytokines such as IL-1 and TNF-alpha and chemokines such as CXCL8, CXCL11 and CXCL9
  4. The products of keratinocytes and TH1 cells activate macrophages to secrete mediators of inflammation
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89
Q

Define autoimmune disease

A
  • Inflammatory response directed against ‘self’ tissue by the adaptive immune response
    • Organ specific
    • Systemic
  • Most don’t fit into one category of hypersensitivity
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90
Q

Give examples of organ specific AI diseases

A
  • Type 1 Diabetes
    • Selective, AI destruction of pancreatic B cells
      • Often mix of type II/IV
    • Causes profound insulin deficiency and death if not treated w/ insulin replacement
    • Inflammation of Islets of Langerhans precedes symptoms by many years
  • Myasthenia Gravis
    • Syndrome of fatigable muscle weakness
      • Limbs
      • Respiratory
      • Head and neck
    • Caused by IgG against Ach receptor - antibody blocks receptor and prevents signal transduction
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91
Q

Give examples of systemic AI diseases

A

Many varieties of systemic AI disease e.g.

  • Rheumatoid arthritis
  • Systemic lupus erythematosus
  • Inflammatory bowel disease
  • Connective tissue disease
  • Systemic vasculitis
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92
Q

What factors contribute to the pathogenesis of AI disease?

A
  • Genetic predisposition
  • Environmental factors
  • Recognition of self antigens by the immune system as foreign
  • Persistence of inflammatory response to develop chronic disease
93
Q

Which genes are involved with the genetic predisposition to AI disease?

A
  • MHC-I and II (HLA locus)
  • Cytokines and receptors i.e. TNF-alpha
  • Other immune associated genes e.g. transcription factors, cell adhesion molecules
94
Q

How do environmental factors contribute to the pathogenesis of AI disease?

A
  • Infection
    • Molecular mimicry
      • Pathogenic antigens so similar to self-antigens they get confused – antibodies produced on infection
      • E.g. S pyogenes similar to epitopes on cardiac myotome = myocarditis, valvular heart disease
  • Geographical factors
    • Vitamin D levels mediated through sunlight exposure
  • Modifiable personal risk factors
    • Smoking
95
Q

How does smoking predispose to RA?

A
  • Presence of antibodies of citrullinated proteins strongly predicts RA
  • Citrullinated proteins develop due to action of enzymes induced during inflammation
  • Smoking associated with conversion of alanine to citrulline
  • Combination of smoking history and genotype = high risk of RA
96
Q

What is MSE?

A
  • Psychiatric equivalent of physical exam
  • Objective observations by clinician and subjective descriptions by patient
  • Should link to patient’s history – cultural, education etc., what is normal for the patient
97
Q

Why is MSE important?

A
  • Snap shot of point in time
  • Help with diagnosis
  • Change over time e.g. in response to treatment
  • Describe patient to another doctor who doesn’t know them
98
Q

Which areas are covered in the MSE?

A
  1. Appearance and behaviour
  2. Mood and affect
  3. Thought (form and content) and speech (RISK)
  4. Perception
  5. Cognition
  6. Insight and judgement
99
Q

Describe what might be observed in the appearance and behaviour section of the MSE

A
  • Appearance
    • Gender, ethnicity, build, dress, posture, grooming, prominent physical abnormalities
  • Rapport
    • Established or not
  • Level of alertness
    • Drowsy, alert (delirium, intoxicated)
  • Attitude
    • Co-operative, aggressive, abusive, over-familiar (e.g. manic) etc.
  • Eye-contact
    • Good, poor, intense
  • Psychomotor activity
    • Retardation, agitation
  • Movements
    • Tremor, abnormal movements
  • Other signs
    • Tics, mannerisms (odd purposeful movement), stereotypes (non-goal directed movements)
100
Q

Define mood and affect

A
  • Mood = pervasive subjective feeling state communicated by patient (0-10) - ‘climate’
  • Affect = current observed emotional state, objective and less pervasive - ‘weather’
    • Elated
    • Apathetic
    • Angry
    • Dysphoric
101
Q

What can be obsered about affect in the MSE?

A
  • Congruence, reactivity and stability of affect - blunted, flat, labile
  • Range of reactivity
102
Q

List common abnormalities of mood and affect

A
  • Schizophrenia – incongruent, blunt, restricted
  • Mania – euphoric, ecstatic, expansive, labile
  • Major depressive disorder – sad, low, restricted
103
Q

What can be observed about speech in the MSE?

A
  • Quantity – talkative, spontaneous, expansive, paucity, poverty
  • Rate – fast, slow, normal, pressured
  • Volume (tone) – loud, soft, monotone, weak, strong
  • Fluency and rhythm – slurred, clear, w/ appropriately placed inflections, hesitant, w/ good articulation, aphasic
104
Q

What might be observed about a manic patients thought and speech?

A
  • Form – flight of ideas
  • Content – delusions of grandeur
  • Stream and flow – pressure of speech
  • Possession – patients own thoughts
105
Q

Give examples of formal thought disorders

A
  • Clanging and punning
  • Flight of ideas
  • Loosening of association
  • Circumstantial
  • Tangentiality
  • Disorder of flow
    • Retardation of thinking – slow thought train, increased pauses
    • Pressure of speech – excessive thoughts, rapid voluminous speech
    • Perseveration – response continues even if stimulus changes
106
Q

Give examples of abnormal thought content

A
  • Overvalued ideas – high importance but shakeable belief
  • Delusions – false fixed firm belief
    • Held in spite of evidence to contrary
    • Not in keeping with cultural and educational setting
  • Paranoid – self-referential (most delusions are)
107
Q

Give examples of delusions

A
  • Delusions of persecution e.g. psychotic delusions
  • Delusions of reference – messaged from TV, radio etc directed towards individual
  • Delusions of grandeur – chosen one
  • Nihilistic delusions – severe mood disorder, part of body dead, poverty
  • Hypochondriacal delusions
  • Delusions of jealousy
108
Q

Give examples of disorders of thought possession

A
  • Thought insertion
  • Thought withdrawal
  • Thought broadcast
  • Thought blocking
  • Obsessions

Common in psychosis

109
Q

What are obsessions?

A
  • Recurrent and persistent ideas, thoughts, impulses or images
  • Intrusive, cause marked anxiety/distress – not simple excessive worries
  • Attempts to ignore/supress unsuccessful
  • Recognised as own thoughts
  • Usually ego-dystonic
110
Q

What are compulsions?

A
  • Repetitive behaviours or mental acts
    • Driven to perform
    • Response to obsession
  • Aimed at
    • Preventing/reducing distress
    • Preventing dreaded event/situation
111
Q

How is risk assessed in an MSE?

A
  • Can include in thought content/mood
  • Risk to self – suicidal ideas, plans/intent, ability to manage day-to-day needs, self-care etc
  • Risk to others – thoughts of harming others, driving risk etc.
112
Q

What is perception?

A
  • Reception and processing of sensory information
    • Visual - sight
    • Auditory - hearing
    • Tactile - touch
    • Gustatory - taste
    • Olfactory - smell
  • Can have abnormalities of perception in all 5 senses
113
Q

Describe perceptual disturbances

A
  • Hallucination - perception without stimulus
  • Distortion - quality of perception altered e.g. visual
  • Illusion - stimulus present but different objext perceived
  • Negative hallucination - stimulus present, no object perceived
114
Q

Compare true and pseudo-hallucinations

A
115
Q

Describe types of auditory hallucinations and causes of auditory hallucinations

A
  • Psychotic and affective illnesses
  • Elementary - hear noises
  • First person - unusual
  • Second person - separate person saying things
  • Third person - two people talking
116
Q

Describe types of visual hallucinations and causes of visual hallucinations

A
  • Consider underlying organic cause
  • Lilliputian
  • Charles Bonnet syndrome
  • Hypnogogic and hypnopompic - can be normal
117
Q

How is cognition assessed in the MSE?

A
  • Cognition (ORAAL - orientation, registration and recall, attention, apraxia, language)
  • How we take in information, process it and use it in our daily activities:
    • Attention
      • Ability to sustain focus
      • E.g. serial 7s
    • Orientation - T/P/P
      • Time - day, date, season, month, year
      • Place - building, place, floor, country
      • Person - name/doB
    • Memory
      • Ability to retain information
      • Verbal - remember 3 words and repeat
    • Executive function
      • Planning, abstract thinking, initiating appropriate actions, inhibiting inappropriate actions, includes judgement
      • Ask patient to problem solve - what would you do if you lost your keys/if there was a fire
    • Language and praxis
118
Q

How are insight and judgement assessed in the MSE?

A
  • Awareness of one’s symptoms
  • Attribution of symptoms to mental disorder
  • Appraisal or analysis of consequence of the disorder
  • Acceptance of treatment
  • Continuum rather than all or nothing - no, partial or full insight, can vary with mental state
    • Intellectual insight - recognise illness but no emotional understanding
119
Q

Define homelessness

A

Includes

  • Rough sleeping/street dwelling
  • Sofa surfing
  • Vulnerable housing situation e.g. living w/ domestic violence, debt
120
Q

What structural factors contribute to homelessness?

A
  • Conflict
  • Natural disasters
  • Housing provision
  • Welfare provision
121
Q

What factors contribute to multiple exclusion homelessness?

A
  • Disrupted family life (poverty, abuse, into care)
  • Poor educational attainment
  • Poverty
  • Experiences of violence
  • Addictions
  • Mental health problems
  • On-going risky relationships
122
Q

What is severe and multiple disadvantage?

A
  • 2/3 people in homelessness services in England also in criminal justice or addiction treatment services in the same year
  • Experiencing childhood adversity, alarming levels of loneliness, isolation, unemployment, poverty and mental ill-health are considerably worse for those in overlapping populations
123
Q

Define PTSD and complex PTSD

A

PTSD - symptoms >1 month

Complex PTSD - recurrent trauma (e.g. domestic abuse), symptoms worse

124
Q

What symptoms indicate trauma?

A
  • Depression, crying
  • Numbness
  • Nightmares
  • Guilt
  • Triggers
  • Hypervigilance – on edge, startled easily
  • Alcohol + drug abuse
  • Self harm
  • Dissociation – detachment from reality
125
Q

What factors create an obesogenic environment?

A
  • Individual psychology
  • Individual activity
  • Activity environment
  • Biology
  • Food production
  • Food consumption
  • Societal influences
126
Q

Give examples of drugs known to favour weight gain

A
  • Insulin, sulphonylureas, thiazolidinediones - diabetes
  • Beta blockers - hypertension
  • Corticosteroids - inflammatory disease
  • Cyprohaptadine - allergy, hayfever
  • Antipsychotics - psychosis
  • Sodium valproate - epilepsy
  • Tricyclic antidepressants - depression
  • Lithium - bipolar disorder
127
Q

Describe a population vs a high risk approach

A
  • Risk factors e.g. blood pressure levels and alcohol consumption are normally disributed throughout the population (bell curve)
  • Targeting prevention and treatment as those with the highest levels of risk will reduce individual risk but not contribute to substantial reductions in population risk
  • Adopting universal prevention measures shifts the population mean to the left, preventing disease in a large population of people at low risk and reducing the proportion of people above the treatment threshold
128
Q

Give examples of population vs high risk vs community strategies for obesity

A
  • Population Strategies for Obesity:
    • Education campaigns
    • HFSS (high fat, salt, sugar) food advertising
    • Weight stigma and discrimination
  • High Risk Individual Strategies for Obesity:
    • Education, employment and income influence obesity risk
  • Community Strategies for Obesity:
    • Cycling infrastructure
    • Opportunities for exercise
129
Q

Describe the tiered system of obesity treatment

A
  • Tier 1 - population wide intervention and prevention initiatives
    • Information and guidance on healthy eating and physical activity
  • Tier 2 - community weight management service
    • Multicomponent weight management services including primary identification, assessment and lifestyle interventions
  • Tier 3 - specialist weight management services
    • Multi-disciplinary specialist treatments, including pharmacotherapy, psychological assessment and low calorie diets
  • Tier 4 - surgical interventions
    • Pre-op assessment, bariatric surgery, post-op care
130
Q

How are targets for weight loss in obesity determined?

A
  • Targets for weight loss based on comorbidities and risks rather than weight alone (SIGN) - target those at highest risk.
    • In patients with BMI 25-35kg/m2 obesity-related comorbidities are less likely to be present
    • In patients with BMI >35kg/m2 obesity-related comorbidities are more likely to be present
  • 5-10% weight loss (approximately 5-10kgs) is required for cardiovascular disease and metabolic risk reduction.
131
Q

Describe the multicomponent interventions for obesity

A
  • Diet: 600 kcal deficit; higher protein/ lower carb = better adherence (Larsen NEJM 2010)
  • Physical activity: 45-60 mins moderate intensity/day
    • ~2000 kcal/ week
  • Behaviour change: Self monitoring; stimulus control; goal setting; relapse prevention
  • Additional interventions considered where appropriate
    • Psychological support
    • Specialised liquid diet
    • Medication
    • Surgery
132
Q

Describe the primary care referral criteria for obesity

A
  • BMI >25 (22.5*) + impaird fasting glucose/impaired glucose tolerance/high risk of T2DM, T2DM
  • BMI >30 (27.5)* + T1DM/T2DM/existing CVD/mobility issues/weight loss required pre-surgery
  • BMI >40 no co-morbidity required
  • >180kg no co-morbidity required

* patients with South Asian/Chinese/Middle Eastern ethnicity have a lower BMI threshold

133
Q

What are the barriers to access to obesity management services for patients and practitioners?

A
  • Patients
    • Location/timing of classess
    • Lack of awareness of service
    • Delay between referral - assessment - classes
    • Lack of cultural awareness
  • Practitioners
    • Lack of awareness of nearest centre
    • Lack of confidence in service
    • Lack of knowledge of what service involves
    • Opt-in process felt to be a barrier
    • PNs better placed to discuss weight than GPs
134
Q

What is people first language?

A

The standard for respectfully addressing people with chronic disease, rather than labelling them by their illness

135
Q

Define treatment burden

A

Workload of healthcare for individuals managing long-term health conditions and the impact on wellbeing

Arises as a Consequence of:

  • Workload volume
  • Care deficiencies
136
Q

Define illness work and treatment work

A

Illness Work = the ‘work’ that the patients and their families do to understand and ‘live with’ a chronic illness

Treatment work = tasks that need to be performed to manage health and follow treatments set by healthcare providers

137
Q

What are the potential consequences of high levels of treatment burden?

A
  • Poor adherence
  • Disengaging from health services
  • Poorer quality of life

A self-perpetuating cycle - treatment burden high –> poor adherence –> worse health oucomes –> escalated treatments from healthcare providers –> higher treatment burden

138
Q

What are the components of treatment burden?

A
  • Sense making work
    • Understanding treatments/disease
  • Relationship work
    • Interact w/ wide range of HCP
    • Interact w/ family and friends - help with getting to appointments, picking up prescriptions
  • Enacting work
    • E.g. intense regular physiotherapy
  • Reflective work
    • How are they progressing?
    • What do they need to do going forward?
139
Q

How many international migrants were there in 2018?

A

258 million

  • 4.8 million students
  • 150.3 million migrant workers
  • 25.4 million registered refugees
140
Q

Has the international migrant population changed in the past 30 years?

A

International migrant population globally has increased in size but remained relatively stable as a proportion of the world’s population

141
Q

Why do international migrants migrate?

A
  • Family reasons
  • Work
  • Education
  • Other
142
Q

Define candidacy

A

What shapes people’s knowlege of, and access to, services

143
Q

Describe the role of structure in the risk of poor health in migrants

A
  • Asylum process
  • Refugee experience
  • Language
  • The environment
  • Experiences of racism
  • Cultural norms about meanings of health
  • Access to social resources
  • Access to financial resouces
144
Q

Describe the portrayal of migrants in the media

A
  • Reporting on migration and migrants a constant presence in UK (English-based) media
  • Many “voices” reported – politicians predominated
  • Right leaning papers draw on anti-migrant think tanks
  • Often more sympathetic to individual migrants, than to migration per se
  • Less sympathetic when group “faceless” – unclear or mixed group
  • Fairly sympathetic towards ASR women – individuals stories

Major themes:

  • Migrants are a threat to UK culture
  • Migrants are over-running the NHS
  • UK citizens are disadvantaged by migration
145
Q

How can migrants be encouraged to engage in health services?

A

Safe surgeries - nationality or immigration status does not affect right to register at a GP practice

  • Offer interpreter if difficult to communicate in English
  • Receptionists don’t ask about immigration status
  • Offer advice if worried about giving address - confidentiality
146
Q

Define pharmacokinetics

A

The science of the rate of movements of drugs within biological systems, as affected by the absorption, distribution, metabolism and elimination of medications.

‘What your body does to the drug’

147
Q

Define pharmacodynamics

A

Study of the underlying biochemical and physiologic processes underlying drug action

  • Mechanism of drug action
  • Drug-receptor interaction
  • Efficacy
  • Safety profile

‘What the drug does to your body’

148
Q

Define bioavalability

A

Fraction of the administered dose of drug that reaches the systemic circulation, expressed as letter F.

149
Q

Give examples of factors that effect bioavailability

A
  • Drug factors
    • Molecular weight/localisation
  • Absorption
    • Gastric pH/health of GI tract
  • First pass metabolism (hepatic)
    • Phenytoin may reduce F
    • Grapefruit juice may increase F
150
Q

Define the apparent volume of distribution

A

Theoretical volume that drug is spread out in

  • Smaller volume if stay intravascular
  • Larger volume if interstitial
151
Q

Define clearance

A

Volume of plasma ‘cleared’ of drug per unit time (e.g. ml/min or L/h)

152
Q

Define half life

A

Time required for serum plasma concentration to decrease by half

153
Q

What determines half life?

A

Determined by clearance and volume of distribution

  • VD is the volume in which the amount of drug would need to be uniformly distributed to produce observed blood concentration
154
Q

Why is half life clinically relevant?

A

4-5 half lives to reach steady state

Loading doses often used for drugs with long half-life

155
Q

Define elimination half life

A

Time for concentration to fall to half

156
Q

What determines elimination half life?

A

Clearance and volume of distribution

T1/2 = 0.693 x V/CL

157
Q

How is elimination half life used clinically?

A
  • Time to eliminate drug
  • Time to reach steady state
  • Dosage interval
158
Q

Describe the features of linear pharmacokinetics

A

Concentration that results from a dose is proportional to the dose

  • Double the dose, double the concentration

Rate of elimination is proportional to the concentration

  • 50% of drug will be eliminated in a given time frame
159
Q

Describe the features of non-linear pharmacokinetics. Give examples

A
  • Concentration that results is not proportional to dose
  • Rate of elimination is constant regardless of amount of drug present
  • Dosage increases can saturate binding sites and result in non-proportional increase in drug levels
  • Or opposite in dose decrease

E.g. alcohol, phenytoin

160
Q

What is the influence of age on pharmacokinetics?

A
  • Decrease in total body water (due to decrease in muscle mass) and increase in total body fat affects volume of distribution
  • Water soluble drugs - lithium, aminoglycosides, alcohol, digoxin
    • Serum levels may go up due to decreased volume of distribution
  • Fat soluble - diazepam, thiopental, trazadone
    • Half life increased with increase in body fat
  • Absorption - not highly impacted by aging
  • Variable changes in first pass metabolism due to variable decline in hepatic blood flow
    • Typically reduced with age but variable
161
Q

How does the function of the liver in drug metabolism change with age?

A
  • Acetylation and conjugation do not change appreciably with age
  • Oxidative metabolism through cytochrome P450 system does decrease with aging, resulting in a decreased clearance of drugs
  • Hepatic blood flow variable
162
Q

How does excretion and elimination of drugs change with age?

A
  • GFR generally declines with aging, but is extremely variable
    • 30% have little change
    • 30% have moderate decrease
    • 30% have severe decrease
  • Serum creatinine is an unreliable marker
    • If accuracy needed, do Cr Cl
163
Q

Describe the methods of calculating creatinine clearance

A

Biochemistry use MDRD equation to calculate eGFR - done on U&E results

Pharmacists usually use Cockroft and Gault

Cr Cl = 140-age(yrs) x wt (kg) x.85 for women

Cr (mg/100ml) x 72

May overestimate Cr Cl, especially in frail elderly people

164
Q

How do pharmacodynamics change with age?

A
  • Some effects are increased
    • Alcohol
    • Opiates
    • Sedatives
    • Theophylline
  • Some effects are decreased
    • Diminished HR response to isoproterenol and beta-blockers
165
Q

Describe the prevalence and cause of adverse drug reactions in the elderly

A
  • About 15% of hospitalisations in elderly related to adverse drug reactions
  • More medications a person is on, higher risk of drug-drug interactions or adverse drug reactions
  • More medications a person is on, higher the risk of non-adherence
166
Q

Give examples of common drug-drug interactions in the elderly

A
  • Statins and clarithromycin and other antibiotics
  • Verapamil and beta-blockers – complete heart block
  • Warfarin and multiple drugs (incl aspirin)
  • ACE inhibitors increase hypoglycemic effect of sulfonylureas
167
Q

Give examples of common drug-disease interactions in the elderly

A
  • Patient with PD have increased risk of drug induced confusion
  • NSAID (and COX-2’s) s can exacerbate CHF
  • Urinary retention in BPH patients on decongestants or anticholinergics
  • Constipation worsened by calcium, anticholinergics, calcium channel blockers
  • Neuroleptics and quinolones lower seizure thresholds
168
Q

Give examples of undertreatment of the elderly

A
  • CAD
    • Beta blockers
    • Aspirin
  • Anticoagulation in AF
  • HTN, especially systolic HTN
  • Pain
    • Particular fear of narcotics in the elderly
169
Q

Give examples of common prescribing cascades which occur in the elderly

A
  • NSAID -> HTN -> antihypertensive therapy
  • Metoclopramide -> parkinsonism -> Sinemet
  • Dihydropyridine -> oedema -> frusemide
  • HCTZ -> gout-> NSAID -> 2nd antihypertensive
  • Sudafed -> urinary retention -> alpha blocker
  • Antipsychotic -> akathisia -> BDZ
170
Q

What is the effect of renal impairment on pharmacokinetics?

A
  • Decreased elimination
    • Aminoglycosides
    • Lithium
    • Digoxin
    • Methotrexate
    • Penicillins
  • Decreased protein binding
  • Decreased hepatic metabolism
171
Q

What is the effect of renal impairment on pharmacodynamics?

A
  • Altered sensitivity to drug effect
    • Increased sensitivity to sedatives
  • Adverse effects
  • ? Altered BBB permeability
172
Q

How should drug prescription be done in renal impairment?

A

Determination of renal function –> alteration of dosing schedule –> monitoring drug concentrations

173
Q

What is the effect of renal impairment on protein binding? What is the clinical relevance of this?

A
  • Renal failure leads to acid retention
  • “Acidic” drugs less bound to albumin:
    • Conformational change in albumin, less ionised drug to bind
    • Increased free (active) drug in plasma
  • Usually of little clinical relevance;
    • Phenytoin (acidic)
    • Less bound drug (more free drug)
    • Target concentration lower in renal failure
    • Increased clearance by HD
174
Q

Describe hepatic drug metabolism in renal failure

A
  • Hepatic metabolism of some drugs is slower in renal failure
  • ? Endogenous inhibitor in uraemic plasma
  • Normalised by HD
175
Q

Give examples of drugs which can have adverse effects in renal impairment

A
  • Nephrotoxins - amphotericin, gentamicin
  • Fluid retention - NSAIDs
  • Increasing uraemia - tetracyclines
  • Electrolyte disturbance - amiloride, digoxin
176
Q

List the drugs which should be avoided/dose adjusted in renal disease

A
  • Antibiotics (reduce dose)
  • LMWH (reduce dose)
  • Metformin (avoid)
  • NSAIDs (avoid)
  • Digoxin (reduce dose)
  • Phenytoin (reduce dose)
  • ACE Inhibitors (caution)
177
Q

How should dosing interval be altered in renal disease?

A
  • Same hepatic metabolism
  • Same/increased VD and prolonged elimination (T1/2 increased)
  • Thus, increased dosing interval
178
Q

What is the effect of hepatic impairment on pharmacokinetics?

A
  • First pass metabolism
  • Activation of prodrugs
  • Decreased protein binding
  • Decreased elimination
  • Difficult to predict, many factors involved
    • No simple test (compared to Cr Cl in renal impairment)
179
Q

What is the effect of hepatic impairment on pharmacodynamics?

A

Altered sensitivity to drugs

  • Sensitivity to sedatives
  • Sensitivity to oral anticoagulants
  • Precipitation of encephalopathy
  • Fluid retention
  • Hepatorenal syndrome
180
Q

List the drugs which have altered metabolism/activation in hepatic impairment

A
  • Profound changes in bioavailability
    • Chlormethiazole (1000% increase)
    • Verapamil (140% increase)
    • Paracetamol (50% increase)
  • First pass activation reduced:
    • Enalapril, perindopril etc. (prodrugs)
181
Q

Compare high and low extraction drugs and the effect hepatic impairment has on their metabolism

A
  • High extraction
    • Metabolised at high rate by liver
    • Rate varies with delivery
    • Affected by changes in blood flow
    • Morphine, verapamil, lignocaine
  • Low extraction
    • Metabolised at low rate by liver
    • Independent of blood flow
    • Sensitive to changes in liver enzyme activity
    • Chloramphenicol, theophylline
182
Q

How should the effect of hepatic impairment on pharmacokinetics be managed?

A

Start w/ low dose, therapeutic drug monitoring

183
Q

Give examples of drugs whose prescription should be altered in liver disease

A
  • Some antibiotics
  • Valproate
  • Warfarin
  • Sedatives
  • Verapamil
184
Q

How should the dosage interval be altered in hepatic impairment?

A
  • Same renal elimination
  • Same/increased VD and slower rate of enzyme metabolism (T1/2/F increased)
  • Thus dosage reduced, dosing interval increased
185
Q

What effect does congestive cardiac failure have on pharmacokinetics/dynamics

A

Altered:

  • Absorption
  • Hepatic elimination
  • Renal elimination
186
Q

Give examples of GI diseases which can alter pharmacokinetics/dynamics

A
  • Achlorrhydria
  • Crohn’s disease
  • Post-operative issues
187
Q

What symptoms should be asked about in a dementia history?

A
  • A history from an informant is necessary as often the patient cannot give a full history.
  • Cognitive – clarify duration of onset and progression
    • Memory problems, repetitive questions
    • Any difficulties with activities of daily living ADLs - washing, dressing, toileting, cooking.
    • Executive ADLS- shopping, paying bills, managing money, travelling
  • Behavioural- agitation, aggression, wandering, inappropriate behaviour, delusions and hallucinations
  • Psychological –mood/anxiety/sleep pattern-early morning wakening/concentration/lack of interest and motivation
188
Q

What investigations should be done in suspected dementia?

A
  • FBC, ESR, CRP - anaemia, vasculitis
  • TFTs - hypothyroidism
  • Bone profile - hypercalcaemia or hypocalcaemia
  • U&Es - renal failure, dialysis dementia
  • LFTs - alcoholism, metastatic disease
  • Glucose - diabetes
  • Vitamin B12 and folate - vitamin deficiency dementia
  • Lipid prolife - vascular dementia
  • HIV and syphilis not routinely checked for unless specific indication
  • Midstream specimen of urine - UTI

ECG/CXR dependent on clinical history and examination findings

189
Q

What is the differential diagnosis for dementia?

A
  • *Delirium
  • *Depression
  • Alzheimer’s Disease
  • Vascular (multi-infarct) dementia
  • Dementia with Lewy bodies
  • Dementia secondary to an acute event, e.g. head injury/subdural haematoma
  • Pick’s disease
  • Chronic alcoholism
  • Hypothyroidism
  • Brain tumour
  • Hydrocephalus and normal pressure hydrocephalus
  • Creutzfeldt-Jacob disease
  • Huntington’s chorea
  • Syphilis
  • Vitamin B12 deficiency
  • ’Dialysis dementia’ secondary to aluminium intoxification

*most common differentials for suspected dementia - important to exclude

190
Q

Give examples of medications which could cause a dementia-like presentation

A

Anticholinergics

Benzodiazepines

Antipsychotics

191
Q

Describe personal care services in Scotland

A
  • Contact social care if patient consents for assessmen of package of care - member of social care team visit patient at home to discuss what assistance they may require
    • Useful if family member or friend present to give collaborative history
  • Personal care for >65s free in Scotland, under 65 standard charges apply
  • First line of support is usually local council but some patients and families utilise private home care for a fee
192
Q

When is the result of an MMSE invalid?

A

Patient acutely confused or has an affective disorder

193
Q

What is the next step in management if dementia is suspected?

A
  • Referral to memory clinic led by old age psychiatry team in patients over 65
    • Patient assessed for dementia by specialist nurse and psychiatrist
  • Under 65 - referral to neurologist for further investigation
  • If dementia rapidly progressive an urgent referral should be made to the neurology service to exclude an organic illness e.g. tumour/CJD
194
Q

How should a patient with mild cognitive impairment be advised about driving?

A
  • Patient must inform DVLA of diagnosis, if they are not able to do so then the GP must as soon as practically possible
    • Must be documented in patient’s clinical notes
  • Mild cognitive decline - can have performance assessed annually
    • Free service, patients can be referred by GP or hospital consultant
    • Sometimes referred directly by DVLA
195
Q

What is Alzheimer’s disease?

A
  • Progressive neurodegenerative disease
  • Accounts for >50% dementia seen in Western society
  • Predominantly affects elderly population
196
Q

Describe the progression of Alzheimer’s disease

A
  • Normally insidious onset and develops slowly but progressively over a number of years
  • First symptom usually forgetfulness - memory impairment
  • Life expectancy lowered by 3x that of population without AD
197
Q

List the risk factors associated with Alzheimer’s disease

A
  • Advancing age >65
  • Smoking
  • Excess alcohol
  • Head injury
  • High cholesterol
  • Low physical activity
  • Mental inactivity
  • Genetic link - variant of apolipoprotein E on chromosome 19
198
Q

How is Alzheimer’s disease diagnosed?

A

Clinical diagnosis, confirmation histologically on post-mortem of neurofibrillary tangles and senile amyloid plaques in brain

199
Q

List the symptoms of Alzheimer’s disease

A
  • Cognitive
    • Problems carrying out ADLs e.g. washing, dressing, toileting, making meals
    • As disease progresses executive ADLS e.g. travelling, handling money, paying bills, remembering medications
    • Over time will likely require increasing care, either at home or in supported living arrangement e.g. care home
  • Non-cognitive symptoms
    • Behavioural and psychological symptoms of dementia
    • Affect >80% of patients with dementia over course of disease
    • Often become worse as disease progresses
    • Include
      • Agitation
      • Wandering
      • Aggression - verbal and physical
      • Jealousy
      • Depression
      • Delusions
      • Hallucinations
200
Q

Describe the pharmacological treatment of Alzhiemer’s disease

A
  • Drug treatments shown to slow cognitive decline, dependent on severity of disease
  • Mild-moderate
    • Acetylcholinesteriase inhibitors (AchEI drugs) e.g. donepezil, rivastigmine, galantamine
  • Moderate-severe (or intolerant of AChEI drugs)
    • NMDA receptor antagonist - memtantine
201
Q

Describe the main side effects, contraindications and dosage of acetylcholinesterase inhibitors

A
  • Main side effects - syncope, bradycardia, GI upset
  • Contraindications - cardiac conduction abnormalities (need ECG before commencing)
  • Dosge - rivastigmine twice daily, donepezil and galantamine once daily
202
Q

Describe the main side effects, contraindications and dosage of NMDA receptor antagonists

A
  • Main side effects - constipation/hypertension/dizziness
  • Contraindications - renal impairment
  • Dosage - daily
203
Q

How are the behavioural and psychological symptoms of dementia managed?

A
  • Some evidence that both AChEI and memantine may delay the emergence of BPSD
  • Important to rule out stimulis that may be causing distress e.g. pain, ensure there is no reversible clinical cause
  • Environmental cause e.g. change of career may also be attributable
  • Treat depression in dementia w/ antidepressants, first line SSRIs e.g. sertraline
  • Consider antipsychotics for patients with dementia who are either:
    • At risk of harming themselves or others
    • Experiencing agitation, hallucinations or delusions that are causing them severe distress
204
Q

What non-pharmacological management is available for mild-moderate Alzheimer’s disease?

A
  • Group cognitive stimulation therapy
  • Group reminiscence therapy
  • Cognitive rehabilitation or occupational therapy which supports functional ability
205
Q

What social support is available for patients with dementia and their carers?

A
  • Home care provision as discussed
  • Occupational therapist
  • Voluntary organisations e.g. Alzheimer’s society - with 24hr helpline AD support
  • Day care centre
  • Drop in centre
  • Support groups
206
Q

What financial support is available for patients with dementia and their carers?

A
  • Not uncommon for relative to reduce working hours or stop work altogether to care for a family member with dementia - has consequences on their QOL
  • Support and advice through social services or citizens advice bureau (CAB)
  • Access to benefits for patient and carer(s) include
    • Attendance allowance
    • Carer’s allowance
    • Council tax exemption
207
Q

What forward planning should be done by a GP for a patient with dementia?

A
  • Annual GP review - chronic disease management of dementia
  • Information sharing - discuss with patient at time of diagnosis who they wish to share information with (relative/carer or other services), should be documented in notes
  • Care plan - electronic log of patient wishes of care, need consent of the patient
  • Have discussion about advanced directes with the patient and family around the time of diagnosis - power of attorney
208
Q

What is a POA and how is it put in place?

A
  • POA is a legal document put in place for another person, known as an attorney to look after a patient’s welfare and/or financial affairs
  • Preferably drawn up with patient still has capacity to make decisions
  • Must be certified by a medical practitioner, most commonly signed by their GP
  • Patient and appointed attorney (usually a family member) are interviewed before a POA is certified to ensure the patient has capacity and is not influenced by the attorney
  • Having a POA in place allows the patient’s affairs to be looked after as their disease progresses and they inevitably start to lose capacity
209
Q

How should bisphosphonates be taken?

A

Take 30 mintes before breakfast or another oral medicine, stand upright for 30 minutes after ingestion

210
Q

What is dyspepsia?

A

Dyspepsia = epigastric pain or discomfort which may occur with early satiety, postprandial fullness, heartburn and regurgitation

Group of symptoms not a diagnosis

211
Q

What is the differential diagnosis for dyspepsia?

A
  • Peptic Ulcer Disease (PUD)
  • GORD
  • Gastric Carcinoma * important to exclude given age if weight loss present
  • Pancreatic carcinoma
  • Gallstones
  • Acute/Chronic Pancreatitis
  • Drug-induced gastritis
  • Ischaemic bowel- mesenteric angina
  • Non-ulcer dyspepsia
  • Malabsorption syndromes
  • Intestinal Parasites
  • Systemic Diseases- DM/Hyperthyroidism/hyperparathyroidism/Connective Tissue Disease
212
Q

What are the possible ADRs of apixaban?

A

Bleeding risk

213
Q

What are the possible ADRs for amlodipine?

A

Ankle swelling

GI upset

214
Q

What are the possible ADRs of alendronic acid?

A

GI upset, jaw necrosis, atypical femoral fractures

215
Q

What are the possible ADRs of bisoprolol?

A

Bradycardia, lethargy

216
Q

What are the possible ADRs of accrete D3?

A

Nausea, GI upset

217
Q

What are the possible ADRs of sertraline?

A

GI bleed

218
Q

What are the possible ADRs of paracetamol?

A

Potential overdose

219
Q

In which patients should caution be taken with gaviscon use?

A
  • Gaviscon = alginate therapy for GORD
  • Contain sodium carbonate and caution should be taken in patients on salt restriction e.g. cardiac failure
220
Q

List common drugs which cause GI upset

A
  • NSAIDs
  • Anticoagulants - warfarin, DOACs
  • COX2 inhibitors - celecoxib
  • Corticosteroids
  • SSRIs - sertraline, fluoxetine, citalopram
  • Calcium channel blockers - amlodipine, verapamil
  • Nitrates - ISMN
  • Antibiotics - doxycycline
  • Bisphosphonates
  • Nicorandil/digoxin/potassium chloride/levodopa/colchicine
  • Theophylline/aminophylline
221
Q

Define polypharmacy

A

Polypharmacy - multiple medications, commonly recognised as five or more medications which are prescribed to a patient at any one time

222
Q

Why is there a rise in polypharmacy in the UK?

A
  • Ageing population
  • Chronic disease burden (multi-morbidity)
  • Preventative medications in line with national guidelines e.g. anticoagulation in AF
223
Q

What is the impact of polypharmacy?

A
  • Multiple medications prescribed to optimise patient care
  • Polypharmacy can be detrimental to patient
    • Can lead to hospital admission and poor clinical outcomes
    • Adverse drug reactions occur when co-prescribing
  • Considerable cost to NHS and medication waste
224
Q

Describe the types of polypharmacy

A
  • Appropriate polypharmacy - prescribing for a patient with multiple conditions whereby their medication regime can optimised and aligned with best evidence.
  • Inappropriate/Problematic polypharmacy - prescribing of multiple medications inappropriately or when the intended benefit of the medication is not realised.
225
Q

What should be considered when performing a medication review?

A

Is it:

  • The right medication
  • For the right reason
  • At the right dose
  • By the right route (pill, liquid etc.)
  • At the right frequency
  • At the right time
  • At the right place
226
Q

What patient population is most vulnerable to adverse outcomes of polypharmacy?

A
  • Increasing age
  • Increasing frailty
  • Increased number of medications
  • Resident in a care home
  • High risk medicines
  • Approaching end of their lives
  • Deprivation
227
Q

How can you identify patients most at risk from polypharmacy?

A
  • Toolkits identify medications that may cause ADRs.
  • Several tools have been developed for prescribing in the elderly.
  • Beer’s Criteria, revised in 2012, mainly used in USA Hospitals.
  • STOPP/START is a common screening tool used in UK.
  • Recommended by NICE for optimisation of prescribing medicines safely and effectively.
  • A toolkit used within primary care in Scotland ‘7 steps to Appropriate Polypharmacy’. It involves an in-depth medication review with the patient (and carer) with a HCP - which can be GP or pharmacist.
228
Q

How can health care professionals help to tackle inappropriate polypharmacy?

A
  • Advanced Pharmacists - experienced pharmacists working in GP now taking on polypharmacy reviews instead of GPs
  • Social Carers - with consent – carry out medication prompts
    • Write down when patient refuses medications or takes late.
    • If carers cannot access home - consider key safe
    • Locked cabinet to prevent patient accessing medication when not required to prevent overdose
  • District Nurses often attend patients with chronic disease condition.
    • Weight/HR and BP checked
    • Blood monitoring as required
    • E.g. Check Hb improving /dropping.
    • Renal function for apixaban
  • Health care assistants (HCAs) – increasingly taking on roles previously performed by district nurses.
  • Practice staff
    • Ensure patients are recalled for chronic health reviews

Medicine Year 3 (15 decks)

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