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Phase 3A > GP, Sexual Health + Public Health > Flashcards

GP, Sexual Health + Public Health Flashcards

1
Q

What is the pathophysiology behind acne vulgaris?

A

caused by chronic inflammation, which can be combined with or without localised infection, in pockets within the skin known as pilosebaceous unit (contain the hair follicles and sebaceous glands)

acne results from increased production of sebum, trapping of keratin and blockage of the pilosebaceous unit leading to swelling and inflammation in the pilosebaceous unit

proprionibacterium acnes bacteria colonise the skin and it’s thought that excessive growth of this bacteria can exacerbate acne

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2
Q

What are macules, papules, pustules and comedomes in the context of acne lesions?

A

macules = flat marks on the skin
papules = small lumps on the skin
pustules = small lumps containing yellow pus
comedomes = skin coloured papules representing blocked pilosebaceous units

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3
Q

What are blackheads, ice pick scars, hypertrophic scars and rolling scars in the context of acne?

A

blackheads = open comedomes with black pigmentation in the centre
ice pick scars = small indentations in the skin which remain after acne lesions heal
hypertrophic scars = small lumps in the skin which remain after acne lesions heal
rolling scars = irregular wave-like irregularities of the skin which remain after acne lesions heal

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4
Q

What are some of the treatments used to treat acne vulgaris?

A

no treatment if mild

topical benzoyl peroxide reduces inflammation, helps unblock the skin and is toxic to the P. acnes bacteria

Topical retinoids (slow sebum production)

Topical antibiotics e.g. clindamycin

Oral antibiotics e.g. lymecycline

Oral contraceptive pill to stabilise hormones and slow sebum production (co-cyprindiol = most effective CCP)

oral retinoids e.g. isotretinoin for severe acne (highly teratogenic)

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5
Q

What are some potential side effects of isotretinoin for acne?

A

dry skin and lips
photosensitivity
depression, anxiety, agression and suicidal ideation
Stevens-johnson syndrome and toxic epidermal necrolysis (rare)

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6
Q

What is an acute stress reaction?

A

when a person experiences certain symptoms following a particularly stressful event e.g. a serious accident, sudden bereavement, traumatic event

usually resolves within 2-3 days

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7
Q

What are the symptoms of an acute stress reaction?

A

psychological symptoms e.g. anxiety, low mood, poor sleep

recurrent dreams or flashbacks

avoidance of memory triggers

reckless or aggressive behaviours

emotional numbness and detachment

physical symptoms e.g. palpitations, nausea, chest pain, breathing difficulties (result of adrenaline)

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8
Q

When does an acute stress reaction become a mental health problem?

A

if symptoms of an acute stress reaction last longer than 3 days but less than a month it is called an acute stress disorder

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9
Q

What is the treatment for an acute stress reaction?

A

treatment may not be needed as symptoms usually resolve quickly but it is important for patients to understand and process what has happened and why

if symptoms persist couselling, CBT and rarely medications can be used

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10
Q

What is generalised anxiety disorder?

A

marked symptoms of anxiety which persist for at least several months, for more days than not, manifested by either general apprehension or excessive worry focussed on multiple everyday events, together with additional symptoms like muscular tension, lack of concentration, irritability or sleep disturbance

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11
Q

What are some risk factors for GAD?

A

female
lower education level
poor health
presence of life stressors
divorce or separation from partner
living alone
single parent

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12
Q

What are some differential diagnoses for GAD?

A

panic disorder
PTSD
OCD
phobias
acute stress disorder
schizophrenia
dementia
anxiety and depression
alcohol dependency
physical illness e.g. thyrotoxicosis

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13
Q

What is the stepped-care model for management of GAD?

A
  1. identify, assess, engage and monitor (for all known and suspected presentations of GAD)
  2. low intensity psychological support, non-facilitated or guided self-help, psycho-educational groups (diagnosed GAD which has not improved with education and active monitoring)
  3. CBT/applied relaxation or drug treatment (GAD with an inadequate response to step 2 interventions or marked functional impairment)
  4. specialist drug and/or psychological treatment, multi-agency teams, crisis intervention, outpatient or inpatient care (complex treatment-refractory GAD and very marked functional impairment, such as self-neglect or a high risk of self-harm)
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14
Q

What is obsessive compulsive disorder?

A

characterised by obsessions and compulsions which are present on a daily basis and are not something the person will enjoy or do willingly

obsessions = unwanted and uncontrolled thoughts and intrusive images that the person struggles to ignore

compulsions = repetitive actions the person feels they must do, generating anxiety if they are not done

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15
Q

How is OCD managed?

A

mild OCD may be managed with education and self-help resources

more significant OCD may require:
Referral to CAMHS
Patient and carer education
Cognitive behavioural therapy
SSRIs medications (under the guidance of a CAMHS specialist)

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16
Q

What are phobias and how can they be treated>

A

Phobias = strong fear or dread of a thing or an event, which is out of proportion to the reality of the situation

Most effective treatment = CBT
antidepressant medication can also help in some cases

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17
Q

What are the 4 types of hypersensitivity reaction?

A

Type I: Classical allergy, mediated by the inappropriate production of specific IgE antibodies to harmless antigens

Type II: Caused by IgG and IgM antibodies that bind to antigens cells or tissues leading to cell or tissue damage

Type III: Caused by antibody-antigen complexes being deposited in tissues, where they activate the complement system and cause inflammation

Type IV: A delayed type hypersensitivity reaction caused by T helper cells traveling to the site of antigens, recruiting macrophages and causing inflammation

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18
Q

What are some examples of conditions caused by IgE mediated allergy? x5

A

food or drug allergy
asthma
allergic rhinitis
hayfever
eczema

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19
Q

What happens in the process of sensitisation leading to specific IgE antibodies being developed for that allergen?

A

CD4 cells recognise the allergen

They proliferate and differentiate into T helper 2 cells

These Th2 cells release IL-4 which stimulates the production of IgE by B cells specific to that allergen

Then IgE circulates in the blood and binds to mast cells.

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20
Q

What happens in the allergic response in type I hypersensitivity reactions?

A

On re-exposure to the allergen, it binds to the IgE attached to mast cells causing them to degranulate, releasing cytokines including histamine and TNF-a.

Histamine causes vasodilation, increased vascular permeability and bronchoconstriction, causing symptoms of allergy. This happens within minutes of exposure to the allergen.

TNF-a causes a localised inflammatory process at the site of exposure. This takes a few hours and is called the late phase reaction.

The allergic reaction can vary from mild reactions (involving itch, mild swelling and hives) to anaphylaxis which can lead to systemic shock (from severe vasodilation) and complete airway closure from bronchconstriction and oedema.

Allergic responses to allergens tend to get worse on repeat exposures due to increased sensitisation

Mast cell tryptase can be measured to confirm the diagnosis of anaphylaxis, and will be raised after an anaphylactic reaction.

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21
Q

What are some examples of Type II hypersensitivity reactions?

A

blood transfusion reactions (antibodies in the recipients blood attack donor blood causing haemolysis of the donor red blood cells)

haemolytic disease of the newborn (a rhesus negative mother has a rhesus positive baby, exposure to the babies blood during birth will cause the mother to produce IgG to rhesus. If she has another rhesus positive baby, that IgG will cross the placenta into the babies bloodstream and cause haemolysis of the babies red blood cells.)

goodpastures syndrome (antibodies specific to a type of collagen in the GBM in the kidneys and lungs lead to inflammation and destruction of the GBM leading to pulmonary haemorrhage and kidney failure)

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22
Q

What happens in type III hypersensitivity reactions?

A

where IgG and IgM antibodies bind to antigens forming immune complexes which are deposited in tissues and activate the complement system and cause inflammation.

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23
Q

What is the difference between type II and type III hypersensitivity reactions?

A

in type II it is the antibodies binding to the target that causes inflammation and damage to the target, whereas in type III, the antibodies bind to antigens and its the antibody-antigen complexes which travel to their target organs where they cause inflammation and damage.

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24
Q

What are 2 examples of type III hypersensitivity reactions?

A

rheumatoid arthritis (Rheumatoid factor is IgM antibody that recognises IgG antibodies as an antigen, specifically the Fc portion. It is IgM against IgG. This leads to formation of antibody-antigen complexes in the blood. These become deposited in joints, skin, lungs and other organs where they activate the complement system and lead to chronic inflammation.)

farmers lung
( Mould and hay spores are breathed into the lungs. Antibodies against the mould or hay antigens form antibody-antigen complexes. These are deposited in the lung tissues and alveoli where they activate the complement system and lead to inflammation of the lung tissue.)

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25
Q

What happens in a type IV hypersensitivity reaction?

A

Antigens enter tissues
They get picked up by dendritic cells which deliver the antigens to the relevant CD4 cell.

CD4 cells proliferate and differentiate into T helper cells
which travel to the tissues where the original antigen presented.

T helper cells release cytokines that recruite macrophages and both cells release proinflammatory cytokines that result in localised inflammation

In skin this presents as a contact dermatitis

(this takes place over 24-72 hours)

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26
Q

What are some examples of type IV hypersensitivity reactions?

A

poision ivy

nickel and gold (chemicals from the metal enter the skin and turn proteins into antigens)

mantoux test (for TB contact)

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27
Q

What are the key symptoms of anaphylaxis? x6

A

SOB
Wheeze
Stridor (caused by swelling of the larynx)
Tachycardia
Lightheadedness
Collapse

alongside allergic signs like urticaria, ithcing, angioedema, abdo pain

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28
Q

What is the management for anaphylaxis?

A

A-E assessment - management by senior paediatrician needed
Intramuscular adrenaline, repeated after 5 mins if required

Antihistamines, e.g. chlorphenamine or cetirizine

Steroids usually IV hydrocortisone

Risk of biphasic reaction so children require post-reaction monitoring

Anaphylaxis can be confirmed by measuring the serum mast cell tryptase within 6 hours of the event

Family and patient education to prevent future attacks

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29
Q

What is an anal fissure?

A

painful tear in the squamous lining of the lower anal canal

often accompanied by a sentinel pile or mucosal tag at the external aspect if chronic

acute <6 weeks
chronic >6 weeks

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30
Q

What are some causes of anal fissures?

A

can be primary with no apparent cause

hard faeces/constipation
rarely: syphilis, herpes, trauma, anal cancer, Crohn’s, psoriasis

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31
Q

What are the presenting symptoms of anal fissures

A

anal pain on defaecation (feels like passing shards of glass) which often persists after passing stool

bleeding on defaecation (bright red blood on the stool or toilet paper)

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32
Q

What are some differentials for anorectal pain? x5

A

haemorrhoids,
abscess
proctitis
perianal sepsis
proctalgia fugax

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33
Q

What is the management for anal fissures?

A

Stool softening measures:
- plenty of fluids
- dietary fibre increase
- laxatives e.g. ispaghula husk

Analgesia
- paracetamol/ibuprofen
- warm baths
- GTN ointment
- lidocaine ointment for extreme pain

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34
Q

What are the causes of microcytic anaemia?

A

T - Thalassaemia
A - Anaemia of chronic disease
I - Iron deficiency anaemia
L - Lead poisoning
S - Sideroblastic anaemia

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35
Q

What are the causes of normocytic anaemia?

A

A - Acute blood loss
A - Anaemia of Chronic Disease
A - Aplastic Anaemia
H - Haemolytic anaemia
H - Hypothyroidism

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36
Q

What are the causes of megaloblastic macrocytic anaemia?

A

Folate deficiency
B12 deficiency

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37
Q

What is anaemia?

A

A condition in which the number of red blood cells or the haemoglobin concentration within them is lower than normal.
Defined as Hb <120g/l in females and <140 g/l in males

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38
Q

What are the normal serum haemoglobin levels?

A

female 110-147g/l, male 131 – 166g/l

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39
Q

What is the normal RBC count in blood?

A

men – 4.0 to 5.9 x 1012/L. women – 3.8 to 5.2 x 1012/L.

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40
Q

What are the causes of normoblastic macrocytic anaemia?

A
  • Alcohol
  • Reticulocytosis (usually from haemolytic anaemia or blood loss)
  • Hypothyroidism
  • Liver disease
  • Drugs such as azathioprine
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41
Q

What are the symptoms of anaemia?

A
  • Tiredness
  • SOB
  • headaches
  • dizziness
  • palpitations
  • worsening of other conditions like angina, heart failure or peripheral vascular disease
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42
Q

What are the signs of anaemia?

A
  • pale skin
  • conjunctival pallor
  • tachycardia
  • raised respiratory rate
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43
Q

What are the investigations for anaemia?

A

Haemoglobin
Mean cell volume (MCV)
B12
Folate
Ferritin
Blood film
Oesophago-gastroduodenoscopy (OGD) and colonoscopy to investigate for a gastrointestinal cause of unexplained iron deficiency anaemia (for suspected GI cancer)
Bone marrow biopsy if cause is unclear

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44
Q

What are the causes of iron deficiency anaemia?

A

Blood loss = most common cause in adults
Dietary insufficiency is the most common cause in growing children
Poor iron absorption
Increased requirements during pregnancy
Coeliac/Crohn’s diseases

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45
Q

What are the risk factors for iron deficiency anaemia?

A

Pregnancy
Vegetarian /vegan diet
Menorrhagia
Hookworm infestation
CKD
Coeliac disease
Gastrectomy
NSAIDs

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46
Q

What are the key presentations of iron deficiency anaemia?

A

fatigue ,

dyspnoea on exertion,

pica (abnormal craving for non-food substances e.g. soil, clay),

restless leg syndrome,

nail changes (e.g. koilonychya),

dysphagia,

impaired muscular performance,

dyspepsia,

pallor,

hair loss

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47
Q

What are the investigations for IDA?

A

Transferrin Saturation = Serum Iron/Total iron binding capacity (15-50%)
Ferritin (41-400ug/L)
Serum iron (12-30 umol/L)
Total iron binding capacity (45-80 umol/L)

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48
Q

What is the management for IDA?

A

Treat underlying cause and correct anaemia:
- blood transfusion
- iron infusion
- oral iron e.g. ferrous sulphate 200mg TD

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49
Q

What is sideroblastic anaemia?

A

defective Hb synthesis within mitochondria where there is increased iron but the body is unable to use it in haemoglobin synthesis.

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50
Q

What are the causes of sideroblastic anaemia?

A
  • alcoholism
  • B6 deficiency
  • lead poisoning
  • congenital
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51
Q

What are the treatment aims for sideroblastic anaemia?

A
  • remove toxic agents
  • administration of pyridoxine (vitamin B6), thiamin or folic acid
  • bone marrow or liver transplantation
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52
Q

What is shown in iron studies of patients with sideroblastic anaemia?

A

Increased serum iron, ferritin and transferrin
Decreased TIBC (total iron blood capacity)

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53
Q

What is acute bronchitis?

A

a lower respiratory tract infection (like pneumonia) which causes inflammation in the bronchi and bronchioles

usually bacterial in origin

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54
Q

What are the key signs/symptoms of acute bronchitis?

A

productive cough
fever
d + v
general malaise and chest pain
dyspnoea and cyanosis
sore throat
runny nose
headache
muscle aches
extreme fatigue

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55
Q

What investigations are used in acute bronchitis?

A

full blood count
procalcitonin levels (distinguish between bacterial/nonbacterial infections, higher in severe bacteroal infections and low in viral infections)
sputum cytology
blood culture
CXR
bronchoscopy
viral swabs

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56
Q

What are the 4 cardiac arrest rhythms? shockable/non-shockable?

A

The 4 possible rhythms in a pulseless patient:

shockable rhythms:
- ventricular tachycardia
- ventricular fibrillation

non-shockable rhythms:
- pulseless electrical activity (all electrical activity except VF/VT, including sinus rhythm without a pulse)
- asystole

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57
Q

What is narrow complex tachycardia?

A

a fast heart rate with a QRS complex duration of less than 0.12 seconds

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58
Q

What are the 4 main differentials for narrow complex tachycardia?

A

sinus tachycardia
supraventricular tachycardia
atrial fibrillation
atrial flutter

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59
Q

What is the stepwise approach for asthma management in adults?

A
  1. SABA
  2. SABA + low-dose ICS
  3. SABA + Ld-ICS + LTRA
  4. SABA + Ld-ICS + LABA (continue LTRA depending on pt’s response)
  5. SABA +/- LTRA and switch ICS/LABA for MART
  6. SABA +/- LTRA + medium-dose ICS MART (or change back to fixed dose of ICS and LABA)
  7. SABA + /- LTRA +
    - increase ICS to high-dose
    - trial of additional drug e.g. long-acting muscarinic receptor antagonist or theophylline
    - refer to asthma expert
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60
Q

What are the investigations used in asthma diagnosis?

A

spirometry
reversibility testing
fractional exhaled nitric oxide
peak flow variability
direct bronchial challenge testing

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61
Q

What are the presenting features of an acute exacerbation of asthma?

A

progressive shortness of breath
use of accessory muscles
raised respiratory rate (tachypnoea)
symmetrical expiratory wheeze on auscultation
tight-sounding chest with widespread reduced air entry

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62
Q

What is seen on arterial blood gas in acute exacerbations of asthma?

A

initially respiratory alkalosis due to tachypnoea causing a drop in CO2
A normal pCO2 or low pO2 is a concerning sign as it means they are getting tired, indicating life-threatening asthma
respiratory acidosis due to

high pCO2 is a very bad sign

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63
Q

What are the features of a moderate asthma exacerbation? x1

A

peak flow 50-75% best or predicted

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64
Q

What are the features of a severe asthma exacerbation? x4

A

peak flow 33-50% best or predicted
respiratory rate above 25
heart rate above 110
unable to complete sentences

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65
Q

What are the features of a life-threatening asthma exacerbation? x7

A

peak flow less than 33%
oxygen sats less than 92%
PaO2 less than 8kPa
becoming tired
confusion or agitation
no wheeze or silent chest
haemodynamic instability

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66
Q

What is the treatment for mild exacerbations of asthma? x5

A

inhaled beta-2 agonists via a spacer
Quadrupled dose of their inhaled corticosteroid (for up to 2 weeks)
Oral steroids (prednisolone) if the higher ICS is inadequate
Antibiotics only if there is convincing evidence of bacterial infection
Follow-up within 48 hours

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67
Q

What are the additional treatments used for moderate asthma exacerbations? x3

A

Consider hospital admission
Nebulised beta-2 agonists (e.g., salbutamol)
Steroids (e.g., oral prednisolone or IV hydrocortisone)

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68
Q

What are the additional treatments used for severe asthma exacerbations? x6

A

Hospital admission
Oxygen to maintain sats 94-98%
Nebulised ipratropium bromide
IV magnesium sulphate
IV salbutamol
IV aminophylline

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69
Q

What are the additional treatments used for life-threatening asthma exacerbations? x2

A

Admission to HDU or ICU
Intubation and ventilation

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70
Q

What is atrophic vaginitis?

A

dryness and atrophy of the vaginal mucosa related to lack of oestrogen

also known as genitourinary syndrome of menopause

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71
Q

What causes atrophic vaginitis?

A

as women enter the menopause and oestrogen levels fall, the mucosa becomes thinner, less elastic and more dry so that the tissue is more prone to inflammation

there are also changes in the vaginal pH and microbial flora which can contribute to localised infections

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72
Q

What are the symptoms of atrophic vaginitis?

A

itching
dryness
dyspareunia (pain during sex)
bleeding due to inflammation

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73
Q

What are the signs on examination of atrophic vaginitis? x6

A

pale mucosa
thin skin
reduced skin folds
erythema and inflammation
dryness
sparse pubic hair

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74
Q

What is the management of atrophic vaginitis?

A

vaginal lubricants such as Sylk, Replens and YES

tpoical oestrogen e.g. estriol cream, pessaries, estradiol tablets or ring

  • potential association of long term use of topical oestrogen with increased risk of endometrial hyperplasia and endometrial cancer so women should be monitored at least annually
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75
Q

What is bacterial vaginosis?

A

an overgrowth of anaerobic bacteria in the vagina caused by a loss of the lactobacilli (beneficial bacteria) in the vagina

these bacilli produce lactic acid and keep the vaginal pH under 4.5 which prevents anaerobic bacteria from growing

when their numbers are reduced the pH rises allowing anaerobic bacteria like gardnerella vaginalis, myoplasma hominis and prevotella species to multiply.

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76
Q

What are some risk factors for bacterial vaginosis? x5

A

multiple sexual partners
excessive vaginal cleaning
recent antibiotics
smoking
copper coil

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77
Q

What are the presenting features of bacterial vaginosis?

A

fishy-smelling watery grey or white vaginal discharge

50% of patients are asymptomatic

not usually associated with itching, irritation or pain

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78
Q

What investigations are used to diagnose bacterial vaginosis?

A

vaginal swab and pH test
vaginal swab with microscopy analysis (clue cells on microscopy)

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79
Q

What is the management for bacterial vaginosis

A

asymptomatic BV does not usually require treatment and may resolve without treatment

metrinidazole specifically targets anaerobic bacteria and is given orally or by vaginal gel (must avoid alcohol while taking)

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80
Q

What are the meibomian glands and lacrimal puncti?

A

meibomian glands are modified sebaceous glands in the posterior aspect of the eyelid which produce the lipid outer layer of the tear film

lacrimal puncti are tiny openings on the medial aspect of each eyelid which are responsible for tear drainage

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81
Q

What is blepharitis? what are the presenting symptoms?

A

inflammation of the eyelid (most common cause of dry eye disease)

typically presents as bilateral symptoms of ocular irritation, foreign body sensation, burning, redness and crusting. may be parodoxical watering of the eye due to reflex tear secretion

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82
Q

What are some possible causes of blepharitis?

A

atopic dermatitis (staphylococcal)
seborrhoeic dermatitis
acne rosacea
demodex infestation (mites)

underlying disease process involves congestion and inflammation of eyelash follicles and meibomian glands

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83
Q

How is blepharitis treated?

A

lid hygiene is key:
- warm compression of eyelids to loosen debris
- eyelid massage to empty debris
- cleaning with cotton wool to remove debris

topical antibiotic ointments such as chloramphenicol

low does oral tetracyclines and regular omega-3 fatty acid supplements

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84
Q

What is hordeolum?

A

external = staphylococcal infection of an eyelash follicle (also known as a stye) which presents as tender, red eyelash follicle swellings

internal = infection of a meibomian gland (far less common)

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85
Q

What is the management for hodeola?

A

they usually resolve spontaneously but patients should be encourage to perform warm compression of the eyelid several times daily to reduce swelling

removal of eyelash (external)
incision of the hordeolum with a sterile needle
topical antibiotics (chloramphenicol)
oral antiobiotics like co-amox if severe or recurrent

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86
Q

What is a chalazion? presentation + management

A

a granulomatous inflammatory lesion which forms in an obstructed meibomian gland

non-infectious and often associated with blepharitis and acne rosacea

present as painless red eyelid cysts in the internal eyelid (if infected they become internal hordeolum)

often resolve spontaneously
patients advised to apply warm compression and eyelid massage
persistent chalazion need referral to ophthalmology for incision and curettage consideration

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87
Q

What is an entropion? cause, presentation and management

A

inward turning of the eyelid

*inward turning eyelashes may irritate the cornea causing ulceration and risking sight loss

most common cause is age-related degenerative change to the lower lid
irritation and scarring are also potential causes

management includes lubricants (to reduced risk of corneal abrasions)
referral to ophthalmology for surgical correction

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88
Q

What is an ectropion? causes, presentation, management

A

outward turning of the eyelid

mostly caused by age-related degenerative changes
facial nerve palsy (risk factor for the development of exposure keratopathy, which is damage to the cornea due to ocular dryness caused by inadequate lid closure)

presents with a sore red eye

conservative management with lubricating eye drops and taping the eye shut at night
severe cases may require surgery

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89
Q

What is trichiasis?
causes, management

A

when eyelashes grow inwards due to damaged eyelash follicles

inward-growing eyelashes may irritate the cornea causing corneal ulceration and risking sight loss

most cases caused by eyelid inflammation

epilation of the eyelash (recurrence may occur)
electrolysis or laser ablation can be a more permanent solution

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90
Q

What is benign paroxysmal positional vertigo?

A

a common cause of recurrent episodes of vertigo triggered by head movement

it is a peripheral cause, meaning that the problem is located in the inner ear rather than the brain

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91
Q

How does benign paroxysmal positional vertigo present?

A

vertigo attacks brought on by head movements which usually settle after around 20-60 seconds

patients are asymptomatic between attacks

no hearing loss or tinnitus

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92
Q

Briefly describe the pathophysiology behind BPPV

A

crystals of calcium carbonate called otoconia become displaced into the semicircular canals
(most often in the posterior semicircular canal)

can be displaced by a viral infection, head trauma, ageing or without a clear cause

the otoconia disrupt the normal flow of endolymph through the canals, confusing the vestibular system

head movement creates the flow of endolymph in the canals, triggering episodes of vertigo

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93
Q

Which manoeuvres and exercises are used to diagnose and treat BPPV?

A

Dix-Hallpike manoeuvre is used to diagnose BPPV as it causes movement of endolymph through the semicircular canals triggering vertigo in BPPV patients and rotational beats of nystagmus towards the affected ear

Epley manouevre is used to move the crystals in the semicircular canal into a position that does not disrupt the endolymph flow

Brandt-Daroff exercises can be performed at home for symptomatic relief

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94
Q

What is benign prostatic hyperplasia?

A

Non-malignant prostate hyperplasia, normal with ageing and usually presents with lower urinary tract symptoms (LUTS).

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95
Q

What is the aetiology of benign prostate hyperplasia?

A

Caused by hyperplasia of the stroma and epithelial cells of the prostate

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96
Q

What are the risk factors for benign prostate hyperplasia?

A

Older age (50+ yrs)
Ethnicity
FHx
Smoking
Metabolic syndrome

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97
Q

What is the pathophysiology of BPH?

A

BPH involves hyperplasia of both epithelial and stromal prostatic components which overtime causes bladder outlet obstruction. Obstruction has both a prostatic component due to increased epithelial tissue, particularly in a transition zone and a dynamic component due to increases in stromal smooth muscle tone.

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98
Q

What are the key presentations of BPH?

A

LUTS:
Hesitancy, urgency, frequency, intermittency, weak flow
Terminal dribbling
Incomplete emptying
nocturia

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99
Q

What are the investigations for BPH?

A

PSA (unreliable), urine dipstick, urine frequency volume chart
DRE (rectal exam) - smooth enlarged prostate (in cancer is hard and irregular) (GS)
Abdominal examination

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100
Q

What are the differential diagnoses for BPH?

A

Overactive bladder, prostatitis, prostate cancer, UTI, bladder cancer

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101
Q

What is the management for BPH?

A

Lifestyle changes
Decrease caffeine
Consider catheter if acute
a- blocker (tamsulosin)
5a reductive inhibitors (finasteride) - decreased testosterone production → ↓prostate size
Surgery last resort (TURP - transurethral resection of prostate, TUVP/TEVAP - transurethral electrovaporization of the prostate, Holmium laser enucleation of the prostate (HoLEP), open prostatectomy)

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102
Q

What is prostate cancer?

A

Neoplastic , malignant proliferation of the outer zone of the peripheral prostate.

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103
Q

What is the epidemiology of prostate cancer?

A

2nd most common cancer
5th leading cause of cancer mortality in men worldwide

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104
Q

What are the risk factors for prostate cancer?

A

Genetic - BRCA2, HOXB13
↑age
Afrocaribbean ethnicity
FHx
High dietary fat levels

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105
Q

What is the pathophysiology of prostate cancer?

A

High-grade prostatic intraepithelial neoplasia is considered to be the most likely precursor of invasive prostate cancer. Characterised by cellular proliferation with pre-existing ducts and glands with cytological changes that mimic neoplasm. Prostate cancer tends to spread along the capsular surface of the gland and may invade the seminal vesicles, periprostatic tissue and eventually the bladder neck.

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106
Q

What are the key presentations of prostate cancer?

A

LUTs but with systemic cancer symptoms + bone pain
Nocturia, urinary frequency, hesitancy, urgency, dysuria, haematuria
Weight loss/anorexia, lethargy, palpable lymphnodes
Nodular and asymmetric enlarged prostate on DRE

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107
Q

What are the investigations for prostate cancer?

A

Serum prostate-specific antigen, pre-biopsy multiparametric MRI
Prostate biopsy
Testosterone, bloods, bone scan, CT/MRI

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108
Q

What is the management for prostate cancer?

A

Local → prostatectomy
Metastatic → hormone therapy (↓testosterone = ↓cancer growth/even death)
*bilateral orchiectomy (surgical removal of testes)
* GNRH receptor agonist e.g. Goserelin
radio/chemotherapy

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109
Q

What is a breast abscess and what are the types?

A

a collection of pus within an area of the breast, usually caused by a bacterial infection

could be a:
- lactational abscess (associated with breastfeeding)
- non-lactational abscess (unrelated to breastfeeding)

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110
Q

What is mastitis?

A

inflammation of breast tissue which is often related to breastfeeding although it can be caused by infection

bacteria can enter at the nipple and back-track into the ducts, causing infection and inflammation

this may precede abscess development

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111
Q

What are some risk factors for infective mastitis/breast abscesses?

A

smoking
damage to the nipple e.g. nipple eczema, candidal infection or piercings
underlying breast disease e.g. cancer

112
Q

What are the most common causative bacteria in mastitis/breast abscesses?

A

Staph aureus (MC)
Streptococcal species
Enterococcal spp
Anaerobic bacteria e.g. bacteroides

113
Q

What breast changes are associated with mastitis with infection? x8

A

nipple changes
purulent nipple discharge
localised pain
tenderness
warmth
erythema (redness)
hardening of the skin or breast tissue
swelling

114
Q

What features of a breast lump suggest that it is an abscess? x3

A

swollen
fluctuant (fluid can be moved around within the lump on palpation)
tenderness

115
Q

What is the management for lactational mastitis?

A

conservative management with continued breastfeeding, expressing milk and breast massage

heat packs, warm showers and simple analgesia for symptom control

antibiotics (flucloxacillin or erythromycin) if infection is suspected

116
Q

What is the management for non-lactational mastitis?

A

analgesia
broad-spectrum antibiotics (co-amoxiclav or erythromycin and metronidazole)
treatment of underlying cause e.g. eczema treatment

117
Q

WHat is the management for a breast abscess?

A

antibiotics
USS
drainage - needle aspiration or surgical incision and drainage
microscopy, culture and sensitivities of the drained fluid

118
Q

What is bursitis? what is a bursa?

A

inflammation of a bursa resulting in thickening of the synovial membrane and increased fluid production, causing swelling

a bursa is a sac created by synovial membrane and filled with a small amount of synovial fluid which are found at bony prominences and reduce friction between the bones and soft tissues during movement

119
Q

What are some potential causes of bursitis?

A

friction from repetitive movements or leaning on the elbow
trauma
inflammatory conditions (e.g gout or RA)
infection (septic bursitis)

120
Q

What are the presenting symptoms of bursitis? What signs might indicate septic bursitis?

A

swollen bursa
warm
tender
fluctuant

infective features:
hot to touch
more tender
erythema spreading to surrounding skin
fever
sepsis features (tachycardia, hypotension, confusion)

121
Q

How is septic bursitis differentiated from septic arthritis?

A

septic arthritis involves joint swelling, rather than just the bursa
there will be greater pain and reduced range of motion in the joint

122
Q

What is the management for bursitis?

A

rest
ice
compression
analgesia
protection of the joint from pressure/trauma
aspiration (can relieve pressure)
steroid injections (for problematic cases where infection has been excluded)
antibiotics for infection (fluclox then clarithromycin)

123
Q

What is candidiasis?

A

also known as thrush

a vaginal infection with a yeast of the candida family

MC candida albicans

124
Q

what are some risk factors for candidiasis? x4

A

increased oestrogen
poorly controlled diabetes
immunosuppression (e.g. using corticosteroids)
broad-spectrum antibiotics

125
Q

What are the symptoms of vaginal candidiasis?

A

thick, white discharge - usually non-smelling
vulval and vaginal itching, irritation or discomfort

more severe infection:
- erythema
- fissures
- oedema
- dyspareunia
- dysuria
- excoriation

126
Q

How is candidiasis diagnosed?

A

test vaginal pH (pH <4.5) - rules out bacterial vaginosis or trichomonas (pH>4.5)

charcoal swab with microscopy (GS)

127
Q

What is the management for candidiasis?

A

antifungal cream e.g. clotrimazole
antifungal pessary
oral antifungal tablets (e.g. fluconazole)

128
Q

What is the cause of chlamydia?

A

STI caused by the gram-ve bacteria chlamydia trachomatis - intracellular organism which enters and replicates within cells before rupturing the cell and spreading to others.

129
Q

What are the risk factors for chlamydia?

A

young adults
multiple sexual partners
sexual activity

130
Q

What are the key presentations of chlamydia in women?

A

75% are asymptomatic but can present with:
Abnormal vaginal discharge
Pelvic pain
Abnormal vaginal bleeding
Painful sex (dyspareunia)
Painful urination (dysuria)

131
Q

What are the symptoms of chlamydia in men?

A

Roughly 50% asymptomatic in men but can present with:
Urethral discharge or discomfort
Dysuria
Epididymo-orchitis (inflammation of epididymis and testicles)
Reactive arthritis

132
Q

What are the signs of chlamydia on examination?

A

Pelvic or abdominal tenderness
Cervical motion tenderness
Inflamed cervix
Purulent discharge

133
Q

What are some differentials for chlamydia?

A

Bacterial vaginosis, vaginal candidiasis, gonorrhoea

134
Q

What is the management for chlamydia?

A

Doxycycline 100mg bi-daily for a week
Abstain from sex for 7 days
Give sexual health advice

135
Q

What are the potential complications of chlamydia?

A

pelvic inflammatory disease, chronic pelvic pain, infertility, ectopic pregnancy, epididymo-orchitis, conjunctivitis, lymphogranuloma venereum, reactive arthritis

136
Q

What is the aetiology of gonorrhoea?

A

Caused by neisseria gonorrhoeae, a gram negative diplococcus bacteria which infects mucous membranes with a columnar epithelium such as the endocervix, urethra, rectum, conjunctiva and pharynx. It spreads via contact with mucous secretions from infected areas

137
Q

What are the risk factors for gonorrhoea?

A

Young adults (20-29yrs)
MSM
Black ancestry
Current or previous Hx of STI
Sexually active
Multiple sexual partners

138
Q

What are the symptoms of gonorrhoea in women?

A

50% women are asymptomatic but can present with:
Odourless purulent discharge, possibly green or yellow
Dysuria
Pelvic pain

139
Q

What are the symptoms of gonorrhoea in men?

A

90% men are symptomatic:
Odourless purulent discharge, possibly green or yellow
Dysuria
Testicular pain or swelling (epididymo-orchitis)

140
Q

What are the investigations for gonorrhoea?

A

Charcoal endocervical swab
NAAT (nucleic acid amplification testing) (GS)

141
Q

What are some differentials for gonorrhoea?

A

Chlamydia, trichomonas, other infectious causes of urethritis, cervicitis, PID, epididymitis, candidal vaginitis or bacterial vaginosis, UTI

142
Q

What is the management for gonorrhoea?

A

SIngle dose of Intramuscular ceftriaxone 1g (unknown sensitivities)
Single oral ciprofloxacin 500mg (for known sensitivities)
Sexual health advice

143
Q

What are some potential complications of gonorrhoea?

A

PID, chronic pelvic pain, infertility, prostatitis, conjunctivitis, urethral strictures, disseminated gonococcal infection, skin lesions

144
Q

What is the cause of syphilis?

A

Caused by the spirochaetal bacteria Treponema pallidum. Infection is typically acquired through direct person-to-person sexual contact with an individual who has early (primary or secondary) syphilis.

145
Q

How can syphilis be contracted?

A

It can be contracted through:
oral , vaginal or anal sex involving direct contact with infected area
Vertical transmission from mother to baby during pregnancy
Intravenous drug use
Blood transfusions and other transplants (rare)

146
Q

What are the risk factors for syphilis?

A

Sexually active
MSM
Illicit drug use
Commercial sex workers
Multiple sexual partners
HIV or other STIs

147
Q

What are the different types of syphilis?

A

Primary Syphilis = painless ulcer (chancre) at original site of infection

Secondary= systemic symptoms, particularly of the skin and mucous membranes

Latent = occurs after secondary stage where symptoms disappear and the patient becomes asymptomatic despite still being infected (early = within 2 years of infection, late = >2 years following infection)

Tertiary = multi-organ symptoms which present many years after initial infection, often includes development of gummas (granulomatous growths which can cause severe tissue damage and deformation) and cardiovascular or neurological symptoms.

Neurosyphilis occurs if the infection involves the CNS

148
Q

What are the key presentations of primary syphilis?

A

Painless genital chancre (tends to resolve over 3-8 weeks), local lymphadenopathy

149
Q

What are the key symptoms of secondary syphilis?

A

maculopapular rash, condylomata lata, low-grade fever, lymphadenopathy, alopecia, oral lesions

150
Q

What are the key symptoms of tertiary syphilis?

A

gummatous lesions, aortic aneurysms, neurosyphilis

151
Q

What are the symptoms of neurosyphilis?

A

headache, altered behaviour, dementia, tabes dorsalis, ocular syphilis, paralysis, sensory impairment, argyll-robertson pupil (constricted pupil which doesn’t react to light)

152
Q

What are the investigations for syphilis?

A

Rapid plasma reagin(RPR), venereal disease research lab test (VDRL)
Dark-field microscopy swab from lesion (GS)

153
Q

What are some differentials for syphilis?

A

Genital herpes, chancroid, HIV infection

154
Q

What is the management of syphilis?

A

Single IM dose of benzathine benzylpenicillin
Full screening for other STIs
Advice about sexual health
Contact tracing

155
Q

What is COPD?

A

Chronic obstructive pulmonary disease
= progressively worsening, irreversible airflow limitation

156
Q

What are the types of COPD?

A

chronic bronchitis
emphysema
A1AT deficiency

157
Q

What are the causes of COPD?

A

almost always due to smoking
patients are susceptible to exacerbations during which there is worsening of their lung function
exacerbations are often triggered by infections

158
Q

What are the risk factors for COPD?

A

SMOKING
air pollution
genetics
occupational exposure
age

159
Q

What are the stages of severity for COPD?

A

Stage 1 - mild: FEV1 >80%
Stage 2 - Moderate: FEV1 50-79%
Stage 3 - severe: FEV1 30-49%
Stage 4 - very severe: FEV1 <30%

160
Q

What is the pathophysiology of chronic bronchitis?

A
  1. hypertrophy and hyperplasia of mucous glands in response to toxic or infectious stimuli
  2. chronic inflammation cells infiltrate bronchi + bronchioles –> luminal narrowing
  3. mucous hypersecretion, ciliary dysfunction, narrowed lumen –> infection risk + airway trapping
161
Q

What is the pathophysiology of emphysema?

A
  1. destruction of the elastin layer in alveolar ducts/sacs/respiratory bronchioles
  2. elastin keeps the walls open during expiration (Bemouli principle)
  3. decreased elastin –> air trapping distal to blockage
162
Q

What are the different types of emphysema?

A

centriacinar (respiratory bronchioles affected only)
panacinar (rib, alveoli, alveolar sacs)
distal acinar
irregular

163
Q

What are the clinical manifestations of COPD?

A

Chronic cough with often purulent sputum (infection risk due to mucus hypersecretion + stasis)
Blue bloater (chronic bronchitis) - chronic purulent cough, dyspnoea, cyanosis, obesity
Pink puffer (emphysema) - mimics cough, pursed lip breathing, cachectic (muscle wasting), barrel chest, hyperresonant, percussion
Most patients a mix of BB/PP

164
Q

What are the investigations for COPD?

A

clinical exam/history
GS: spirometry (FEV1/FVC ratio <0.7)
reversibility testing with B-2 agonists like salbutamol during spirometry testing, CXR, FBC sputum, ECG/echo, serum A1AT

165
Q

What are the differential diagnoses for COPD?

A

lung cancer, fibrosis, heart failure, asthma

166
Q

What is the management for COPD

A

first smoking cessation + vaccines for flu + pneumococcal
1. short acting bronchodilators - B-2 agonists (SABA) (salbutamol/terbutaline) or short acting antimuscarinics (ipatropium bromide)
2. Long acting beta agonist (LABA) + long acting muscarinic antagonist (LAMA)

for more severe cases:
+ nebulisers, oral theophylline, oral mucolytic therapy
+ long term oxygen therapy is used for severe COPD

167
Q

What is conjunctivitis?

A

inflammation of the conjunctiva which is a thin layer of tissue which covers the inside of the eyelids and the sclera

can be unilateral or bilateral

168
Q

What are the key presenting features of conjunctivitis?

A

red, bloodshot eye
itchy or gritty sensation
discharge

does NOT cause pain, photophobia or reduced visual acuity

169
Q

What are the similarities/differences between bacterial and viral conjunctivitis?

A

bacterial presents with a purulent discharge which typically sticks the eyelids together in the morning, usually starts in one eye and can spread to the other

viral is common and presents with a clear discharge, often associated with other viral symptoms and there may be tender pre-auricular nodes

both very contagious (bacterial more so than viral)

170
Q

What are some differentials for an acute and painful red eye?

A

acute angle-closure glaucoma
anterior uveitis
scleritis
corneal abrasions or ulceration
keratitis
foreign body
traumatic or chemical injury

171
Q

What are some differentials for an acute painless red eye

A

conjunctivitis
episcleritis
subconjunctival haemorrhage

172
Q

What is the management for conjunctivitis?

A

usually self-resolving within 1-2 weeks

hygiene measures to reduce spreading e,g. avoid towel sharing and wash hands regularly

chloramphenical or fusidic acid eye drops for bacterial conjunctivitis

173
Q

What is osteoarthritis?

A

Degenerative joint disorder involving the entire joint and characterised by joint pain, stiffness and functional limitation.

174
Q

What is the aetiology of osteoarthritis?

A

result of mechanical and biological events which destabilise the normal process of degradation and synthesis of articular cartilage chondrocytes, extracellular matrix, and subchondral bone

175
Q

What are the risk fators osteoarthritis?

A

obesity
age
occupation
trauma
being female
family history

176
Q

What is the pathophysiology of osteoarthritis?

A

Imbalanced cartilage breakdown > repair; ↑chondrocyte metalloproteinase secretion
Bone attempts to overcome this w/ T1 collagen; abnormal bony growths (osteophytes)

177
Q

What are the key presentations of osteoarthritis?

A

Joint pain
Stiffness
Deformity, instability and reduced joint function
Heberden nodes (affects DIP joints)

178
Q

What are the investigations for osteoarthritis?

A

NICE suggests that diagnosis can be made without any investigations if the patient is >45yrs, has typical activity related pain and no morning stiffness or stiffness lasting less than 30 minutes

179
Q

What are the XR signs for osteoarthritis?

A

Loss of joint space
Osteophytes
Subchondral sclerosis
Subchondral cysts

180
Q

What are some differentials for osteoarthritis?

A

Bursitis
Gout
Pseudogout

181
Q

What is the management for osteoarthritis?

A

Pt education and lifestyle advice
Physiotherapy and occupational therapy +/- orthotics
Analgesia for symptomatic relief:
Oral paracetamol and topical NSAIDs
Add oral NSAIDs and consider also prescribing a PPI
Consider opiates such as codeine and morphine
Intra articular steroid injections provide temporary inflammation and pain reduction
Joint replacement in severe cases

182
Q

What are the most commonly affected joints in osteoarthritis?

A

hips, knees, sacro-iliac joints, distal-interphalangeal joints in the hands (DIPs), carpo-metacarpal joint at the base of the thumb, wrist, cervical spine

183
Q

What is rheumatoid arthritis?

A

autoimmune condition causing chronic inflammation of the synovial lining of the joints, tendon sheaths and bursa

184
Q

What is the epidemiology of RA?

A

3 times more common in women than men
Affects around 1% of the population
Most common inflammatory arthritis seen by physicians

185
Q

What are the risk factors for RA?

A

Age 30-50 yrs
Female
FHx
Smoking

186
Q

What are the key presentations of RA?

A

symmetrical distal polyarthopathy
key symptoms: pain, swelling, stiffness of the joint (often worse in the morning and eases as day goes on)

187
Q

What are some signs of RA?

A

Swan neck deformity
Boutonniere’s deformity (flexion at PIP joint)
Ulnar deviation
Rheumatoid nodules
Vasculitic lesion

188
Q

What are some associated symptoms of RA?

A

fatigue, weight loss, flu-like illness, muscle aches and weakness

189
Q

What are the investigations for RA?

A

Usually clinically diagnosed
Bloods = ↑ESR/CRP, normocytic normochromic anaemia (mc as can also cause microcytic and macrocytic)
Serology = +ve anti-CCP (80% specific), +ve RF (70% non-specific)
Radiographs
ultrasonography

190
Q

What are the XR signs of RA?

A

LESS
Loss of joint space
Eroded bone
Soft tissue swelling
Soft bones (osteoporosis)

191
Q

What are some differentials for RA?

A

Psoriatic arthritis
infectious arthritis
Gout
SLE
Osteoarthritis

192
Q

What is the management of RA?

A

Short course of steroids at first presentation and during flare-ups to settle disease
DMARD (disease modifying antirheumatic drugs)- methotrexate
NSAID analgesia
Intra-articular steroid injection if very painful
Biologics 1st line- TNF-a inhibitor (infliximab
2nd line - B cell inhibitor - Rituximab

193
Q

What are the commonly affected joints in RA?

A

the small joints of the hands and feet, the wrist, ankle, MCP and PIP

194
Q

What are the extra-articular effects of RA?

A

lungs (PE, pulmonary fibrosis), heart (↑IHD risk), eyes (episcleritis, keratoconjunctivitis sicca), spinal cord compression, kidney (CKD), rheumatoid skin nodules

195
Q

What is gout

A

Type of crystal arthropathy associated with chronically high blood uric acid levels

196
Q

What is the aetiology of gout?

A

Urate crystals are deposited in the joint causing it to become hot, swollen and painful

197
Q

What are the risk factors for gout?

A

Male
Obesity
High purine diet (meat and seafood)
Alcohol diuretics
Existing cardiovascular or kidney disease
Family history

198
Q

What are the key presentations of gout?

A

Monoarticular and typically big toe
Sudden onset, severe swollen big toe - can’t put weight on it!

199
Q

What are the investigations for gout?

A

can be diagnosed clinically or using joint fluid aspirate (no bacteria + needle shape crystals, negatively birefringent of polarised light, monosodium urate crystals)

200
Q

What is the management for gout

A

Diet changes - ↓purines, ↑dairy
NSAIDs then consider colchicine, then steroid injection
prevention : allopurinol (xanthine oxidase inhibitor)

201
Q

Which joints are most commonly affected by gout?

A

Most commonly seen in the metatarsophalangeal joints (base of big toe), wrists and carpometacarpal joints (base of thumb)

202
Q

What is pseudogout?

A

calcium pyrophosphate crystals deposit along joint capsule
Also known as chondrocalcinosis

203
Q

What are the risk factors for pseudogout?

A

Elderly females (70+)
Diabetes
Metabolic diseases
osteoarthritis

204
Q

What are the key presentations for pseudogout?

A

Often polyarticular with knee commonly involved
Swollen hot red joint

205
Q

What are the investigations for pseudogout?

A

Joint aspiration + polarised light → +vely birefringent, rhomboid shaped crystals

206
Q

What are the XR signs for pseudogout?

A

chondrocalcinosis (thin white line in the middle of joint space caused by calcium deposition)
+ LOSS

207
Q

What is the management for pseudogout?

A

Only acute management - NSAIDS, then colchicine, then steroid injection (no prevention drug here)

208
Q

What is osteoporosis?

A

reduced bone density

209
Q

What is osteopenia

A

reduction in bone density like osteoporosis but less severe

210
Q

What are the risk factors for osteoporosis?

A

Steroids
Hypothyroid/hyperparathyroid
Alcohol + smoking
Thin (↓BMI)
Testosterone↓
Early menopause (↓oestrogen)
Renal /liver failure
Erosive + inflammatory disease
DMT1 or malabsorption

211
Q

What are the key presentations of osteoporosis?

A

Fractures (proximal femur (falls), Colles’ forked wrist; fall on outstretched wrist), compression vertebral crush (may cause kyphosis))

212
Q

What are the investigations for osteoporosis?

A

DEXA scan (produces T score 1<T≤2.5)
FRAX score

213
Q

What is the management for osteoporosis?

A

Bisphosphonates (alendronate, risedronate, inhibit RANK-L signalling —> osteoclast inhibition)
mAB denosumab (inhibit RANK-L)
HRT - oestrogen, testosterone
Oestrogen receptor modulator -raloxifene
Recombinant PTH - teraparatide

214
Q

What is the pathophysiology of RA?

A

arginine –> citrulline mutation in T2 collagen => anti-CCP formation
IFN-a causes further pro-inflammatory recruitment to synovium
- synovial lining expands and tumour -like mass (pannus) grows past joint margins
- pannus destroys subchondral bone + articular cartilage

215
Q

What are the 4 clinical phases of gout when left untreated?

A

asymptomatic

hyperuricaemia - uric acid is building up in the blood and starting to form crystals around joints

acute/recurrent gout - symptoms start to occur, causing a painful gout attack

inter-critical gout - periods of remission between gout attacks

chronic tophaceous gout - frequent gout pain and tophi form in jointsf

216
Q

What is the pathophysiology of gout?

A

↑uric acid/CKD –> impaired excretion of uric acid –> monosodium urate

217
Q

What is fibromyalgia?

A

Chronic widespread musculoskeletal pain for 3+ months with all other causes ruled out

218
Q

What are the risk factors for fibromyalgia?

A

Females
Depression
Stress
20-60 yrs
FHx

219
Q

What is the pathophysiology of fibromyalgia?

A

The primary pathology in fibromyalgia is in the CNS and involves pain and/or sensory amplification
A hallmark of these conditions is diffuse hyperalgesia (increased pain in response to normally painful stimuli) and/or allodynia (pain in response to normally non-painful stimuli)

220
Q

What are the key presentations of fibromyalgia?

A

Chronic pain
Diffuse tenderness on exam
Fatigue unrelieved by rest
Sleep disturbance
Mood disturbance
Cognitive dysfunction
Headaches
Numbness /tingling sensations
Stiffness
Sensitivity to sensory stimuli such as bright lights, odours, noises

221
Q

What are the investigations for fibromyalgia?

A

Clinical diagnosis - all other possible causes ruled out

222
Q

What are the differentials for fibromyalgia?

A

Polymyalgia Rheumatica = large cell vasculitis presenting as chronic pain syndrome (↑ESR+CRP is diagnostic and treatment is prednisolone)
Myofascial pain syndrome
Chronic fatigue syndrome
Rheumatoid arthritis
Vitamin D deficiency

223
Q

What is the management for fibromyalgia

A

Education + physiotherapy
Antidepressant for severe neuropathic pain (e.g. TCAs; amitriptyline) + CBT

224
Q

What is polymyalgia rheumatica?

A

Inflammatory condition which causes pain and stiffness in the shoulders, pelvic girdle and neck

225
Q

What are the risk factors for polymyalgia rheumatica?

A

Older age (50+)
Female
Caucasian heritage
Strong association with GCA

226
Q

What are the key presentations of polymyalgia rheumatica?

A

Bilateral shoulder pain which can radiate to the elbow
Bilateral pelvic girdle pain
Worse on movement
Interferes with sleep
Stiffness for at least 45 mins in the morning

227
Q

What are the investigations for polymyalgia rheumatica?

A

Inflammatory markers (ESR, plasma viscosity and CRP) usually raised
FBC, U+Es, LFTS, calcium, etc. to exclude differentials
Based on clinical presentation and response to steroids

228
Q

What are some of the differential diagnoses for polymyalgia rheumatica?

A

Osteoarthritis, RA, SLE, myositis, cervical spondylosis

229
Q

What is the management for polymyalgia rheumatica?

A

Steroids: initially prednisolone 15mg per day, stopped if no response, can reduce if good response after 4 weeks

230
Q

What is psoriatic arthritis?

A

Inflammatory arthritis associated with psoriasis which is variable in severity

231
Q

What are the risk factors for psoriatic arthritis?

A

Psoriasis
FHx
HX of joint or tendon trauma
HIV infection

232
Q

What is the mpst severe form of psoriatic arthritis?

A

Most severe form - arthritis mutilans which occurs in the phalanxes
Osteolysis leads to progressive shortening of the digit
Skin then folds as the digit shortens giving “telescopic finger” appearance

233
Q

What are the key presentations of psoriatic arthritis?

A

Has several patterns of affected joints:
Symmetrical polyarthritis (affects wrists, ankles and DIP joints but MCP less commonly affected)
Asymmetrical pauciarthritis (affecting mainly digits and feet, pauci- = few)
Spondylitic pattern (back stiffness, sacroiliitis, atlanto-axial joint involvement) - more common in men
The spine, achilles tendon and atlanto-axial joint can also be involved

234
Q

What are the signs of psoriatic arthritis

A

Plaques of psoriasis on the skin
Nail pitting
Onycholysis (separation of the nail from the nail bed)
Dactylitis (inflammation of the full finger)
Enthesitis (inflammation of the entheses)

235
Q

What are the x-ray changes in psoriatic arthritis?

A

Periostitis (results in thickened and irregular outline of bone)
Ankylosis (bones join together)
Osteolysis
Dactylitis (inflammation of whole digit)
Pencil-in-cup appearance (bone seems pointed and wears away at surface making it cup-like)

236
Q

What are the investigations for psoriatic arthritis?

A

PEST screening (questionnaire re joint pain, swelling, arthritis hx), ESR + CRP, RF, ACCP, lipid profile, uric acid
Xray

237
Q

What is the management for psoriatic arthritis?

A

NSAIDs
DMARDS (methotrexate, leflunomide, sulfasalazine)
Anti-TNF meds (etanercept, infliximab or adalimumab)
Ustekinumab is last line

238
Q

What is reactive arthritis?

A

Synovitis in the joints as a reaction to a recent infective trigger
Previously known as Reiter Syndrome

239
Q

What are the risk factors for reactive arthritis?

A

Gastroenteritis (C. jejuni, salmonella, shigella)
STIs (chlamydia)
HLA B27 gene
Male
BCG immunotherapy

240
Q

What are the key presentations of reactive arthritis?

A

Acute, warm, swollen, painful joint
Reiter’s triad - uveitis, urethritis/balanitis, arthritis + enthesitis
Fever
Peripheral and axial arthritis
Dactylitis
Conjunctivitis and iritis
Skin lesions including circinate balanitis and keratoderma blennorrhagicum
Bilateral conjunctivitis
Anterior uveitis
Circinate balanitis (dermatitis of head of penis)

241
Q

What is the management for reactive arthritis?

A

NSAIDs
Steroid injections into affected joint/s
Systemic steroids in multi-joint presentations

242
Q

What are haemorrhoids?

A

Swollen veins around anus disrupt anal cushions causing prolapse of parts of the anal cushions through the anal passage

243
Q

what is the classification of haemorrhoids?

A

1st degree: no prolapse
2nd: prolapse when straining and return on relaxing
3rd: prolapse when straining, do not return on relaxing, but can be pushed back
4th: prolapsed permanently

244
Q

What are the risk factors for haemorrhoids?

A

constipation
anal sex
age 45-65
pregnancy
pathological pelvic lesions

245
Q

What are the 2 types of haemorrhoid presentation?

A

Internal - originate above internal rectal plexus (dentate line), less painful as has decreased sensory supply
external - originate below dentate line, so painful patient can’t sit down

246
Q

What are the key presentations of haemorrhoids?

A

bright red fresh PR bleeding + mucousy bloody stool
bulging pain
pruritis ani

247
Q

What are the investigations for haemorrhoids?

A

PR exam for external
protoscopy for internal

248
Q

What is the management for haemorrhoids?

A

topical treatments for symptomatic relief
scleropathy (injection of phenol oil)
rubber band ligation

249
Q

What is IBS?

A

Irritable Bowel Syndrome = functional chronic bowel disorder which can be characterised by constipation, diarrhoea or mixed symptoms

250
Q

what is the aetiology of IBS?

A

thought to be multifactorial with a variety of possible causes which include:
- food poisoning/gastroenteritis triggers
- stress
- irregular eating or abnormal diet
- certain medications
- interaction between the brain and gut

251
Q

What are the risk factors for IBS?

A

Physical + sexual abuse
PTSD
Age <50 yrs
Female
Previous enteric infection
FHx
family/job stress

252
Q

What are the key presentations of IBS?

A

Abdo pain + bloating (relieved by defecation)
Altered stool form + frequency

253
Q

What are the investigations for IBS?

A

Diagnosis is by ruling out other conditions e.g. coeliac which is done through serology, faecal calprotectin, ESR/CRP/blood cultures

254
Q

What are the differentials for IBS?

A

coeliac, IBD, colorectal cancer, ovarian cancer

255
Q

What is the management for IBS?

A

Conservative = patient education (diet changes) + reassurance
Moderate = IBS-C → laxatives (e.g. senna), IBS-D → antimotility drug (loperamide)
Severe = TCA (tricyclic antidepressants e.g. amitriptyline) + consider CBT/GI referral

256
Q

What is diverticular disease?

A

Outpouching of colonic mucosa
Diverticulum = outpouching at perforating artery sites
Diverticulosis = asymptomatic outpouching
Diverticular disease = symptomatic outpouch
Diverticulitis = inflammation of outpouch (infection)

257
Q

What are the risk factors of diverticular disease?

A

> 50 yrs
Low dietary fibre
Diet high in salt, meat, sugar
Obesity (BMI>30)
NSAID and opioid use
smoking

258
Q

What is the pathophysiology of diverticular disease?

A

A low fibre diet increases intestinal transit time and decreases stool volume resulting in increased intraluminal pressure and colonic segmentation, which predispose to diverticular formation. Precise mechanism is not fully understood.

259
Q

What are the key presentations of diverticular disease?

A

LLQ pain, guarding, tenderness
Constipation
Fresh rectal bleeding
Leukocytosis
Fever
bloating

260
Q

What is the gold standard investigation for diverticular disease?

A

CT abdo pelvis

261
Q

What is the management for diverticular disease?

A

Diverticulosis = nothing, watch and wait
Diverticular disease = bulk forming laxatives, surgery (gold standard)
Diverticulitis = antibiotics (co-amoxiclav) and paracetamol. IV fluid + liquid food, rarely surgery

262
Q

What are the ABC symptoms which indicate IBS consideration in diagnosis?

A

Abdominal pain/discomfort
Bloating
Change in bowel habit

263
Q

What is gastroenteritis?

A

inflammation affecting the stomach and intestines which presents with pain, nausea, vomiting and diarrhoea

264
Q

What are the most common viral causes of gastroenteritis?

A

rotavirus
norovirus
adenovirus

265
Q

What is GORD?

A

Gastroesophageal reflux disease = reflux of gastric contents into the oesophagus resulting in symptoms and/or complications

266
Q

What is the pathophysiology of GORD?

A

Abnormally frequent occurrences of transient lower oesophageal sphincter relaxation causing reflux of gastric contents into the oesophagus.
This causes damage to the oesophageal mucosa of varying severity depending on the duration of contact.

267
Q

What are the risk factors for GORD?

A

FHx
Older age
Hiatus hernia
obesity
Pregnancy
Drugs e.g. antimuscarinics
Scleroderma (scarring of lower oesophageal sphincter)

268
Q

What are the key presentations for GORD?

A

Heartburn
Regurgitation
*symptoms worse lying down as acid can reflux more easily
Dysphagia
Chronic cough + nocturnal asthma
bloating /early satiety

269
Q

What are the investigations for GORD?

A

Clinical diagnosis if no red flags
Red flags = dysphagia, haematemesis, weight loss
→ endoscopy (oesophagitis or Barrett’s oesophagus), oesophageal manometry (measures LOS pressure + gastric acid pH)

270
Q

What is the management for GORD?

A

Conservative = lifestyle changes (smaller meals, 3+ hrs before bed)
PPI, antacids, alginates (gaviscon)
Last resort = surgical tightening of LOS (Nissen fundoplication = wrapping of fundus around LOS externally to increase pressure)

271
Q

What are the potential complications of GORD?

A

Oesophageal sphincters: usually 60+ patients, progressively worsening dysphagia, Tx: oesophageal dilation + PPI
Barrett’s Oesophagus: 10% GORD patients develop, always involves hiatal hernia, metaplasia of oesophageal lining (SSNKE → simple columnar), ↑risk of adenocarcinoma

272
Q

WHat is a hiatus hernia? what are the 4 types?

A

herniation of the stomach up through the diaphragm so that the contents of the stomach can reflux into the oesophagus

1- sliding
2- rolling
3- combination of sliding and rolling
4- large opening with additional abdo organs entering the thorax

273
Q

How do hiatus hernias present?

A

dyspepsia
heartburn
acid reflux
reflux of food
burping
bloating
halitosis

274
Q

What investigations are used to identify hiatus hernia?

A

can be intermittent and so not seen on investigations
CXR
CT endoscopy
barium swallow testing

275
Q

What is the treatment for hiatus hernia

A

conservative (medical treatment of GOR)
surgical repair if high risk of complications or resistant symptoms (laparoscopic fundoplication)

Phase 3A (10 decks)

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