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Phase 3a Jemima > GP part 2 > Flashcards

GP part 2 Flashcards

1
Q

what is irritable bowel syndrome

A

it is recurrent abdominal pain or discomfort which is associated with a change in stool frequency or form
the pain or discomfort may be relieved by defecation

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2
Q

what are symptoms of IBS

A

intestinal discomfort - pain, bloating, worse after eating, improved by opening bowels
bowel habit abnormalities - fluctuating
stool abnormalities - diarrhoea, constipation, passing mucus

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3
Q

what can IBS symptoms often be triggered or worsened by

A

Anxiety
Depression
Stress
Sleep disturbance
Illness
Medications
Certain foods
Caffeine
Alcohol

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4
Q

what are risk factors for IBS

A

physical or sexual abuse
PTSD
age <50
female sex
previous enteric infection
family history
family and job stress

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5
Q

how do you diagnose IBS

A

thorough history and examination to exclude red flags or any other pathology
FBC - anaemia
inflammatory markers
coeliac serology
faecal calprotectin
CA125 for ovarian cancer

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6
Q

what are the NICE clinical guidelines for a diagnosis of IBS

A

differentials need to be excluded and the patient should have at least 6 months of abdominal pain or discomfort with at least one of:
- pain or discomfort relieved by opening the bowels
- bowel habit abnormalities
- stool abnormalities
for a diagnosis the patients also require at least two of:
- straining, an urgent need to open bowels or incomplete emptying
- bloating
- worse after eating
- passing mucus

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7
Q

what lifestyle advice is given to patients who are diagnosed with IBS

A

drink enough fluids
regular small meals
adjusting fibre intake according to symptoms
limit caffeine, alcohol and fatty foods
low FODMAP diet, guided by dietician
probiotic supplements may be considered over the counter
reduce stress where possible
regular exercise

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8
Q

how is IBS treated

A
  1. first line is lifestyle management
  2. medications depend on symptoms - loperamide for diarrhoea, bilk forming laxatives for constipation, antispasmodics for cramps (mebeverine, alverine, hyoscine butylbromide)
  3. Linaclotide is a specialist secretor drug for constipation in IBS when first line laxatives are inadequate
  4. where symptoms remain uncontrolled think about other options: SSRI, low dose tricyclic antidepressants, CBT and specialist referral
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9
Q

what is a soft tissue injury

A

this is damage to muscles tendons and ligaments which may lead to pain, swelling and restricted mobility

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10
Q

what are types of soft tissue injury

A

sprains: stretching or tearing of ligaments
strains: muscle or tendon damage often occurring to the hamstring
contusions: bruises resulting from blunt force trauma that squashes muscle fibres underneath the skin without breaking the skin barrier
tendinitis: irritation or inflammation in a tenon that occurs due to overuse
bursitis: inflammation and swelling in the bursae

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11
Q

what are symptoms of a sprain

A

swelling
bruising
pain
inflammation
limited range of motion

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12
Q

what are symptoms of a strain

A

pain
muscle spasms and weakness
swelling
inflammation

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13
Q

what are symptoms of a contusion

A

pain and skin discolouration

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14
Q

what are symptoms of tendinitis

A

swelling
pain that worsens during activity

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15
Q

what are symptoms of bursitis

A

pain
swelling

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16
Q

what are causes of soft tissue injury

A

trauma - sudden impact or forceful movements can lead to soft tissue injury which might occur due to a fall, slip or sharp change in direction
overuse - repetitive movements or excessive strain on a particular muscle or joint
overloading - sudden increase in exercise intensity

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17
Q

how is soft tissue injury diagnosed

A

clinical history and examination
Xray
MRI

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18
Q

how are soft tissue injuries treated

A

rest, ice, compression and elevation
medications - analgesia
physical therapy
bracing or splinting
torn muscles, tendons, or ligaments may need surgery depending on how much of the tendon has torn and how severe it is

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19
Q

what is the classification of sprains

A

graded on severity
Grade 1: slight stretching and some damage to the fibres of the ligament
grade 2: partial tearing of the ligament. there is abnormal looseness in the joint when it is moved in certain ways
grade 3: complete tear of the ligament. may cause significant instability

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20
Q

what is lyme disease

A

it is an infection transmitted to humans following a bite from an infected tick

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21
Q

what causes lyme disease

A

a group of bacteria - Borrelia burgdoferis which is a spiral shaped bacteria

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22
Q

what are risk factors for Lyme disease

A

occupational and recreational exposure to woodland and fields
increased duration of tick attachment (over 36-48 hours)

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23
Q

what are complications of Lyme disease

A

severe neurological symptoms - chronic meningitis, encephalomyelitis, radiculopathies, peripheral neuropathy
facial palsy
lyme arthritis
persisting non specific symptoms such as fatigue, aches and pains, cognitive difficulties

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24
Q

How is Lyme disease diagnosed

A

clinical diagnosis of lyme disease in people with erythema migrans:
- spreading erythema with well defined edges
- round or oval shape
- red/purple in colour
- bulls eye appearance
in those without erythema migrans clinical presentation and laboratory testing will guide diagnosis

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25
Q

how will Lyme disease present

A

bulls eye rash
cognitive impairment ]fatigue
fever and sweats
headache
malaise
migratory joint or muscle aches and pain
neck pain or stiffness
paraesthesia
swollen glands
uveitis
facial palsy or other nerve palsies
unexplained radiculopathy

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26
Q

when does erythema migrans appear after being bitten by an infected tick

A

1-2 weeks post exposure typically and lasts several weeks untreated

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27
Q

what is the treatment for lyme disease

A

adults and children aged 12 and over:
- doxycycline 100mg twice daily for 21 days
- amoxicillin 100g three times daily for 21 days if doxycycline isnt suitable
- azithromycin 3rd line
in younger children still use doxycycline but it in dependent on body weight

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28
Q

what is a Jarisch - herxheimer reaction

A

it is a reaction that can present in 15% of people in the first 24 hours of treatment with any antibiotic for lyme disease. symptoms include fever, chills, muscle pains and headache

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29
Q

what is obesity defined as

A

it is a metabolic disease defined as an excessive accumulation of body fat that poses a risk to an individuals health

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30
Q

what are risk factors for developing obesity

A

poor diet and lack of physical activity
underlying medical conditions - cushings, PCOS, hypothyroidism, GH deficiency
medications - antidepressants and corticosteroids
socio-economic status
mental health - depression, eating disorders
genetics - Prader Willi syndrome, Bardet Bieldl syndrome

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31
Q

what are clinical features of obesity

A

excess body fat
weight above average for individuals height
breathlessness
sleep apnoea
skin issues
osteoarthritis
hypertension
diabetes
hyperlipidaemia

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32
Q

what examinations should be done in practice in someone with obesity

A

measure BMI - weight divided by height squared
central obesity by measuring waist to height ratio or waist circumference

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33
Q

what investigations should be done in a patient that is overweight

A

fasting blood glucose - obesity
lipid profile - hyperlipidaemia
LFT - non alcoholic fatty liver disease
TSH - hypothyroidism
U+E - chronic kidney disease
dexamethasone suppression test for cushings
ultrasound for PCOS

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34
Q

what is non surgical management for obesity

A

weight loss: target of 5 - 10% reduction
lifestyle changes: healthy eating, alcohol recommendations, smoking cessation, therapy
medications

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35
Q

what medications are offered to patients who are obese

A

Orlistat and liraglutide are the only medications approved by NICE for weight loss in the UK
- Orlistat prevents absorption of dietary fat
- Liraglutide is a GLP-1 analogue and delays gastric emptying and induces early satiety

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36
Q

what are side effects of liraglutide

A

nausea and vomiting
diarrhoea
pancreatitis
thyroid cancer

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37
Q

what surgical measures are there for people who are obese

A

weight loss surgery in those who are severely obese (BMI > 40 or between 35-40 with co-morbidities)
Bariatric surgery - Roux-en-Y gastric bypass, sleeve gastrectomy and gastric bypass

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38
Q

what is dumping syndrome

A

a group of symptoms caused by food rapidly emptying or being ‘dumped’ from the stomach into the small intestines. this results in undigested food within the small intestine that the body finds difficult to absorb
symptoms include sweating, bloating, abdominal cramps, diarrhoea, nausea

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39
Q

what are complications of obesity

A

cardiovascular disease
dyslipidaema
diabetes
stroke
obstructive sleep apneoa
cancer
pancreatitis
abnormal periods and infertility
arthritis
inflamed veins
gout
gallstones
liver disease
lung disease

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40
Q

what is otitis externa

A

it is inflammation of the external ear canal and can be either acute (less than 3 weeks) or chronic (more than three weeks)

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41
Q

what are infectious causes of otitis externa

A

bacterial - pseudomonal aeruginosa or staphylococcus aureus
fungal - candida albicans and aspergillus niger

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42
Q

what are non infectious causes of otitis externa

A

atopic dermatitis
psoriasis
acne

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43
Q

what are risk factors for developing otitis externa

A

hot and humid climates
swimming
older age
dermatological issues
narrow ear canals (downs syndrome)
previous ear surgery
previous radiotherapy to the head and neck
any history of immunosuppression including diabetes
previous topical treatments for otitis externa or otitis media

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44
Q

how does otitis externa present

A

ear pain
discharge
itch
hearing loss
fever

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45
Q

what is seen on examination in someone with otitis externa

A

skin changes or tenderness at the tragus or pinna
erythema, oedema and narrowing of the ear canal which may progress to complete occlusion
serous or purulent discharge
inflammation of the tympanic membrane which may be hard to visualise
regional lymphadenopathy in pre/post auricular nodes
conductive hearing loss secondary to obstruction

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46
Q

how is otitis externa diagnosed

A

clinical findings - history and exam
swabs for microbiology

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47
Q

what is general advice given to someone with otitis externa

A

strict water precautions to keep the ear dry
avoid itching or using cotton buds which further traumatise the ear canal

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48
Q

what is the medical management of otitis externa

A

topical antibiotic ear drops - antibiotic + steroid
treatment is administered for a minimum of 7 days
avoid aminoglycosides in patients with perforated tympanic membrane
analgesia prescribed based off severity of pain
ENT can do microsuction to remove infected debris from canal and insert an otowick

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49
Q

what are complications of otitis externa

A

necrotising otitis externa - infection spreads beyond the soft tissue of the ear canal resulting in osteomyelitis
pinna or peri-auricular cellulitis

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50
Q

what are risk factors for developing complications with otitis externa

A

diabetes mellitis
age over 65
recurrent otitis externa
immunosuppression
radiotherapy to head or neck

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51
Q

what is otitis media

A

it is the name given to an infection in the middle ear - space that sits between the tympanic membrane and the inner ear

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52
Q

what is the cause of otitis media

A

bacterial infection which enters from the back of the throat through the eustachian tube

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53
Q

what bacteria cause otitis media

A

streptococcus pneumoniae - most common
haemophilus influenzae
morazella catarrhalis
staphylococcus aureus

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54
Q

how does otitis media present

A

ear pain
reduced hearing in the affected ear
general symptoms of upper airway infection: fever, cough, coryzal symptoms, sore throat, general malaise
balance issues and vertigo
if tympanic membrane is perforated there can be discharge

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55
Q

what is seen on examination in otitis media

A

bulging, inflamed red tympanic membrane
if there is perforation you may see discharge in the ear canal and a hole in the tympanic membrane

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56
Q

what is the management of otitis media

A

refer for specialist assessment and admission in infants younger than 3 months with a temp above 38, or 3-6 months with a temp higher than 39
most cases resolve without antibiotics - normally within 3 days but can last a week
give simple analgesia to help with pain and fever

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57
Q

what are the options for prescribing antibiotics in otitis media

A
  1. immediate antibiotics - initial presentation with significant co-morbidities, systemically unwell or immunocompromised
  2. delayed antibiotics - collected and used after 3 days if the symptoms havent improved or have gotten worse
    first line choice of antibiotic is amoxicillin 5 days
  3. no antibiotics
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58
Q

what are complications of otitis media

A

Otitis medial with effusion
Hearing loss (usually temporary)
Perforated eardrum
Recurrent infection
Mastoiditis (rare)
Abscess (rare)

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59
Q

what is fibromyalgia

A

it is a chronic health condition that causes pain and tenderness throughout the body which occurs in flares. It causes musculoskeletal pain and fatigue

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60
Q

who is more likely to be diagnosed with fibromyalgia

A

people assigned female at birth
people older than 40

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61
Q

what are symptoms of fibromyalgia

A

muscle pain or tenderness
fatigue
face and jaw pain - temporomandibular joint disorders
headaches and migraines
digestive issues including diarrhoea and constipation
bladder control issues
memory issues
anxiety
depression
insomnia and other sleep disorders

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62
Q

what are risk factors for fibromyalgia

A

age - over 40
sex - more common in women
living with other chronic illnesses
infections
stress
trauma

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63
Q

what can trigger a fibromyalgia flare up

A

emotional stress - job, finance, social life
changes in daily routing
changes in diet or nutrition
hormonal changes
not getting enough sleep or change in sleep
weather or temperature changes
illness
starting new medication or treatments

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64
Q

how is fibromyalgia diagnosed

A

history and examination
diagnosis of exclusion - may do bloods and other tests to rule out other causes of fatigue

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65
Q

how is fibromyalgia treated

A

over the counter or prescription pain medication
exercises like stretches or strength training
sleep therapy
cognitive behavioural therapy
stress management
antidepressants

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66
Q

what are the four stages of treating fibromyalgia

A

non pharmacological treatments - exercise and strength training
psychological treatments
pharmacological treatments
daily functioning - occupational therapist

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67
Q

what is osteoarthritis

A

it is progressive degenerative joint disorder, referred to as a dysfunctional wear and repair process within a joint

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68
Q

what are the most common joints affected by osteoarthritis

A

knees
hips
hands

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69
Q

what is the pathophysiology of osteoarthritis

A

chondrocytes are responsible for maintaining the homeostasis between synthesis and degradation of the extracellular matrix within articular cartilage. Over time, continuous wear or trauma to the joint causes local inflammation and stimulation of chondrocytes to release degradative enzymes. these enzymes break down collagen and proteoglycan and ultimately destroy the articular cartilage

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70
Q

what are risk factors for developing osteoarthritis

A

increasing age
female sex
obesity
less commonly articular congenital deformities or trauma to the joint

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71
Q

what are symptoms of osteoarthritis

A

joint pain
stiffness: typically worse after activity and at the end of the day
limitation in day to day activities
in some cases patients will experience referred pain

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72
Q

what would you find on examination in someone with osteoarthritis

A

reduced active and passive range of movement secondary to pain
tenderness of the the joint lines
crepitus on movement

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73
Q

how does osteoarthritis of the hand present

A

sparing of the metacarpophalangeal joints
bony enlargements of the proximal interphalangeal joints known as bouchards nodes
bony enlargement of the distal interphalangeal joints known as heberdens nodes
squaring of the first carpometacarpal joint (base of the thumb)
reduced functional movement

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74
Q

what investigations should be done for someone with osteoarthritis

A

bodyweight and BMI
labs - serum CRP/ESR
imaging - Xray

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75
Q

what are the Xray changes seen in osteoarthritis

A

loss of joint space
osteophytes
subchondral sclerosis
subchondral cysts

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76
Q

When does NICE advise that osteoarthritis be diagnosed clinically

A

if a person meets the criteria:
over 45 and
has activity related joint pain and
has either no morning joint related stiffness or morning stiffness that lasts no longer than 30 minutes

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77
Q

what is the conservative management for osteoarthritis

A

education and advice about the condition
exercise: muscle strengthening and general aerobic fitness
weight loss (if overweight or obese)

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78
Q

what is the medical management of osteoarthritis

A

First line: topical NSAIDS
second line: paracetamol and topical analgesia
third line: NSAID, paracetamol and topical capsaicin
fourth line: opioid, NSAID, paracetamol and topical capsaicin
intra-articular corticosteroid injection can be offered for acute exacerbation of pain despite regular use of analgesia

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79
Q

what is the surgical management of osteoarthritis

A

joint replacement - arthroplasty
fusion of the joint - arthrodesis

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80
Q

what is peripheral arterial disease

A

this refers to the narrowing of the arteries supplying the limbs and the periphery, reducing the blood supply to these areas. It usually refers to the lower limbs, resulting in symptoms of claudication

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81
Q

what is intermittent claudication

A

it is a symptoms of ischaemia in a limb, occurring during exertion and relieved by rest. It is typically a crampy, achy pain in the calf, thigh or buttock muscles associated with muscle fatigue when walking beyond a certain intensity

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82
Q

what is critical limb ischaemia

A

it is end stage peripheral arterial disease, where there is an inadequate supply of blood to a limb to allow it to function normally at rest. there is a significant risk of losing the limb

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83
Q

what are the features of critical limb ischaemia

A

pain at rest
non healing ulcers gangrene
pain is worse at night when the leg is raised as gravity no longer helps to pull blood into the foot

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84
Q

what is acute limb ischaemia

A

it refers to a rapid onset of ischaemia in a limb, typically it is due to thrombosis blocking the arterial supply of a distal limb, similar to a thrombus blocking a coronary artery in myocardia infarction

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85
Q

what do atheromatous plaques lead to in vessels

A

stiffening of artery walls leading to hypertension and strain on the heart
stenosis leading to reduced blood flow
plaque rupture resulting in a thrombus

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86
Q

what are non modifiable risk factors for atherosclerosis

A

older age
family history
male

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87
Q

what are modifiable risk factors for atherosclerosis

A

smoking
alcohol consumption
poor diet
low exercise/sedentary lifestyle
obesity
poor sleep
stress

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88
Q

what are medical co-morbidities which can increase the risk of atherosclerosis

A

diabetes
hypertension
chronic kidney disease
inflammatory conditions such as rheumatoid arthritis
atypical antipsychotic medications

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89
Q

what are the features of acute limb ischaemia

A

pain
pallor
pulseless
paralysis
paraesthasia
perishingly cold

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90
Q

what is Leriche syndrome

A

it occurs with occlusion of the distal aorta or proximal common iliac artery. There is a clinical triad of:
thigh/buttock claudication
absent femoral pulses
male impotence

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91
Q

what peripheral pulses may be weaker in someone with peripheral arterial disease

A

radial
brachial
carotid
abdominal aorta
femoral
popliteal
posterior tibial
dorsalis pedis

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92
Q

what are signs of arterial disease on inspection

A

skin pallor
cyanosis
dependent rubor (deep red colour when limb is lower than the rest of the body)
muscle wasting
hair loss
ulcers
poor wound healing
gangrene

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93
Q

when examining someone with peripheral arterial disease what may you see

A

reduced skin temperature
reduced sensation
prolonged capillary refill time (>2 seconds)
changes during buergers test

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94
Q

what are arterial ulcers typically caused by

A

ischaemia secondary to an inadequate blood supply

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95
Q

what are the features of an arterial ulcer

A

smaller than venous
deeper than venous
well defined borders
punched out appearance
occur peripherally
have reduced bleeding
are painful

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96
Q

what are venous ulcers typically caused by

A

impaired drainage and pooling of blood in the legs

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97
Q

what are the features of venous ulcers

A

occur after a minor leg injury
are larger than arterial ulcers
more superficial than arterial ulcers
irregular, gently sloping borders
affect the gaiter area of the leg (mid-calf down)
less painful than arterial ulcers
occur with other signs of chronic venous insufficiency

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98
Q

what investigations should be done on someone with peripheral arterial disease

A

ankle-brachial pressure index
duplex ultrasound
angiography

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99
Q

what is the conservative management for someone with peripheral arterial disease

A

lifestyle changes - manage modifiable risk factors
exercise training

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100
Q

what medical treatments are there for peripheral arterial disease

A

atorvastatin 80mg
clopidogrel 75mg once daily
naftidrofuryl oxalate (5-HT receptor antagonist that acts as a peripheral vasodilator)

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101
Q

what surgical options are there for peripheral arterial disease

A

endovascular angioplasty and stenting
endarterectomy - cutting vessel open and removing the atheromatous plaque
bypass surgery

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102
Q

what is the management of critical limb ischaemia

A

urgent referral to the vascular team
- endovascular angioplasty and stenting
- endarterectomy
- bypass surgery
- amputation

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103
Q

what are risk factors or chronic venous insufficiency

A

age
immobility
obesity
prolonged standing
deep vein thrombosis

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104
Q

what is chronic venous insufficiency

A

this occurs when blood does not efficiently drain from the legs back to the heart. Usually this is a result of damage from the valves inside the legs

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105
Q

what are symptoms of chronic venous insufficiency

A

skin changes - haemosiderin staining
venous eczema due to chronic inflammatory response in the skin
lipodermatosclerosis
atrophie blanche - porcelain white scar tissue on skin
cellulitis
poor healing after injury
skin ulcers
pain

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106
Q

what is the management for chronic venous insufficiency

A
  1. keeping the skin healthy - monitor skin health, regular use of emollients, topical steroids to avoid flares of venous eczema, very potent topical steroids to treat flares of lipodermatosclerosis
  2. improving venous drainage - wt loss, keeping legs elevated and compression stockings
  3. management of complications- antibiotics, analgesia and wound care
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107
Q

what is polymyalgia rheumatica

A

it is an inflammatory condition that causes pain and stiffness in the shoulders, pelvic girdle and neck
there is often a strong association with giant cell arteritis

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108
Q

how does polymyalgia rheumatica present

A

may have relatively rapid onset of symptoms from days to weeks
pain and stiffness of the shoulders, pelvic girdle and the neck
worse in the morning
worse after rest or inactivity
interferes with sleep
can take at least 45 minutes to ease in the morning
somewhat improves with activity
can have systemic symptoms - wt loss, fever, fatigue
muscle tenderness
carpel tunnel syndrome
peripheral oedema

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109
Q

what are differential diagnosis for polymyalgia rheumatica

A

Osteoarthritis
Rheumatoid arthritis
Systemic lupus erythematosus
Statin-induced myopathy
Myositis (e.g., polymyositis)
Cervical spondylosis
Adhesive capsulitis (frozen shoulder)
Hyperthyroidism or hypothyroidism
Osteomalacia
Fibromyalgia
Lymphoma or leukaemia
Myeloma

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110
Q

how is polymyalgia rheumatica diagnosed

A

based on clinical presentation, its response to steroids and excluding differentials
labs - FBC, U+E, LFT, calcium, serum protein electrophoresis (myeloma), TSH, creatinine kinase (myositis), rheumatoid factor, urine dip
also consider:
antinuclear antibodies for SLE
anti-cyclic citrullinated peptide (CCP) for RA
urine bence jones for myeloma
chest X ray

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111
Q

how is polymyalgia rheumatica treated

A

steroids:
15mg prednisolone daily initially and then follow up after 1 week (patients with PR should have a dramatic improvement in a week)
treatment with steroids usually lasts for 1-2 years and then follow the reducing regime of prednisolone

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112
Q

what is the reducing regime of prednisolone that NICE suggests following

A

15mg until symptoms are fully controlled then
12.5mg for 3 weeks then
10mg for 4-6 weeks then
reducing by 1mg every 4-8 weeks

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113
Q

what are the additional managements for patients on long term steroids

A

Dont STOP
Dont - steroid dependence occurs after three weeks of treatment, and abruptly stopping risks adrenal crisis
S- sick rules, steroids doses need to be increased if the patient becomes unwell
T- treatment card, patients should carry a card which tells others they are steroid dependent
O- Osteoporosis prevention may be required with bisphosphonates and calcium and vit D
P- proton pump inhibitors are considered for gastro protection

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114
Q

what is the blood supply of the prostate gland

A

the inferior vesical (primary), middle rectal and internal pudendal arteries

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115
Q

what is the nervous innervation of the prostate gland

A

sympathetic = hypogastric nerve
parasympathetic = pelvic nerve

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116
Q

what are risk factors for the development of prostate cancer

A

age over 50
black ethnicity
family history of prostate cancer
family history of other heritable cancers such as breast or colorectal
high levels of dietary fat

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117
Q

where does prostate cancer spread to

A

lymph nodes and bones

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118
Q

what are symptoms of prostate cancer

A

Lower urinary tract symptoms - frequency, urgency, nocturia, hesitancy, dysuria, post void dribbling
haematuria
haematospermia
systemic symptoms - weight loss, weakness, fatigue
bone pain

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119
Q

what might you find on clinical examination with prostate cancer

A

on a DRE - asymmetrical prostate, nodular prostate, indurated prostate

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120
Q

what investigations should be done in someone with suspected prostate cancer

A

Serum prostate specific antigen
U+E
FBC
testosterone levels
LFTs
MRI and biopsy
DEXA, CT and PMSA PET to look for metastasis

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121
Q

what grading system is used to grade prostate cancer

A

the gleason grading system
the TNM staging is also used for prostate cancer to help stage the cancer

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122
Q

how is the gleason score calculated

A

by adding the two most prevalent differentiation patterns together

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123
Q

what does a gleason score of under 6 mean

A

its a stage 1 tumour
low grade, sometimes clinically insignificant

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124
Q

what does a gleason score of 7 mean

A

7 (3+4) is stage 2, intermediate grade
7 (4+3) is stage three, intermediate grade tumour but less favourable outcome than 3+4

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125
Q

what does a gleason score of 8 mean

A

stage 4, high grade tumour

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126
Q

what does a gleason score of 9-10 mean

A

stage 5, highest grade tumour

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127
Q

what is used as the first line investigation for suspected localised prostate cancer

A

multiparametric MRI

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128
Q

how are the results of a multiparametric MRI used to report on prostate cancer

A

reported on a Likert scale and scored as:
1 – very low suspicion
2 – low suspicion
3 – equivocal
4 – probable cancer
5 – definite cancer

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129
Q

what are the options for getting a prostate biopsy

A

transrectal ultrasound guided biopsy
transperineal biopsy

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130
Q

what are common causes of a raised PSA

A

Prostate cancer
Benign prostatic hyperplasia
Prostatitis
Urinary tract infections
Vigorous exercise (notably cycling)
Recent ejaculation or prostate stimulation

131
Q

how is ow risk prostate cancer managed

A

PSA <10, gleason score <6, T1-2a
- watchful waiting with regular DRE and PSA tests, if anything significantly changes then palliative care may be initiated
- active surveillance with regular DRE, PSA and often biopsies annually, if anything changes then active treatment may be initiated

132
Q

how is intermediate risk prostate cancer managed

A

PSA 10-20, OR gleason score 7/T2B stage
- Active surveillance
- surgery: removal of the prostate
- radiotherapy: external beam radiotherapy, or brachytherapy

133
Q

what is the treatment for high risk prostate cancer

A

PSA >20 OR gleason score 8-10/T2c or above
- active surveillance
- surgery: radical prostatectomy
- radiotherapy: external beam radiotherapy
- Hormone therapy: GnRH therapy, androgen receptor blockers, androgen blockers targeting the adrenal glands, bilateral orchiectomy, oestrogen therapy

134
Q

what are side effects of hormone therapy for prostate cancer

A

hot flushes
decreased bone density
fractures
low libido
erectile dysfunction
altered lipids - gnaecomastia
fatigue

135
Q

what is psoriasis

A

it is a chronic autoimmune condition that causes recurrent symptoms of psoriatic skin lesions

136
Q

what are patches of psoriasis

A

they are dry, flaky, scaly, faintly erythematous skin lesions that appear in raised and rough plaques, commonly over the extensor surfaces of the elbows, knees and scalp

137
Q

what causes skin changes in psoriasis

A

rapid generation of new skin cells, resulting in an abnormal buildup and thickening of skin in those areas

138
Q

what is plaque psoriasis

A

it causes thickened erythematous plaques with silver scales, commonly seen on extensor surfaces and the scalp
this is the most common form of psoriasis in adults

139
Q

what is guttate psoriasis

A

it is common in children
it causes main raised small papules across the trunk and the limbs. They are mildly erythematous and can be scaly. Over time they can turn into plaques

140
Q

what is Guttate psoriasis often triggered by

A

streptococcal throat infection
stress
medications

141
Q

what is pustular psoriasis

A

it is where pustules form under areas of erythematous skin. the pus is non infectious
- should be treated as medical emergency and those with it should require hospital admission

142
Q

what is erythrodermic psoriasis

A

it is a rare form of psoriasis with extensive erythematous inflamed areas covering most of the surface area of the skin
the skin comes away in large patches resulting in raw exposed areas
- treated as a medical emergency and patients require admission

143
Q

what are the types of psoriasis

A

plaque psoriasis
guttate psoriasis
pustular psoriasis
erythrodermic psoriasis

144
Q

What are signs which are suggestive of psoriasis

A

Auspitz sign: small points of bleeding when plaques are scraped off
Koebner phenomenon: development of psoriatic lesions to areas of skin affected by trauma
residual pigmentation of the skin after lesions resolve

145
Q

how is psoriasis managed

A

dependent on the severity of the condition
1. topical steroids
2. topical vitamin D analogues (calcipotriol)
3. topical dithranol
4. topical calcineurin inhibitors (adults)
5. phototherapy with narrow band ultraviolet B light

146
Q

what is given in psoriasis if topical treatments fail

A

may be started in systemic treatment (unlicensed in children) which might include methotrexate, cyclosporin, retinoids or biologics
there are two products that are both a potent steroid and vitamin D analogue (not licensed in children and guided by specialist) which are dovobet and enstilar

147
Q

what is psoriasis associated with

A

nail psoriasis
psoriatic arthritis
psychosocial implications - depression and anxiety
obesity
hyperlipidaemia
hypertension
type 2 diabetes

148
Q

what organism causes syphilis

A

an organism called Treponema pallidum, a spirochete

149
Q

what is the incubation period of syphilis

A

between initial infection and symptoms is about 21 days

150
Q

how is syphilis transmitted

A

sexually transmitted infection - oral vaginal or anal sex
vertical transmission
IV drug use
blood transfusions and other transplants

151
Q

what are the stages of syphilis

A

primary
secondary
latent
tertiary
neurosyphilis

152
Q

what is primary syphilis

A

this involves a painless ulcer called a chancre at the original site of infection

153
Q

what is secondary syphilis

A

systemic symptoms, particularly of the skin and mucous membranes. These symptoms can resolve after 3 – 12 weeks and the patient can enter the latent stage.

154
Q

what is latent syphilis

A

after the secondary stage of syphilis, where symptoms disappear and the patient becomes asymptomatic despite still being infected. Early latent syphilis occurs within two years of the initial infection, and late latent syphilis occurs from two years after the initial infection onwards.

155
Q

what is tertiary syphilis

A

can occur many years after the initial infection and affect many organs of the body, particularly with the development of gummas and cardiovascular and neurological complications.

156
Q

what is neurosyphilis

A

this occurs if the infection enters the central nervous system and presents with neurological symptoms

157
Q

what are symptoms of primary syphilis

A

A painless genital ulcer (chancre). This tends to resolve over 3 – 8 weeks.
Local lymphadenopathy

158
Q

what are symptoms of secondary syphilis

A

Maculopapular rash
Condylomata lata (grey wart-like lesions around the genitals and anus)
Low-grade fever
Lymphadenopathy
Alopecia (localised hair loss)
Oral lesions

159
Q

what are symptoms of tertiary syphilis

A

Gummatous lesions (gummas are granulomatous lesions that can affect the skin, organs and bones)
Aortic aneurysms
Neurosyphilis

160
Q

what are symptoms of neurosyphilis

A

Headache
Altered behaviour
Dementia
Tabes dorsalis (demyelination affecting the spinal cord posterior columns)
Ocular syphilis (affecting the eyes)
Paralysis
Sensory impairment

161
Q

what is an Argyll-Robertson pupil

A

it is a specific finding of neurosyphilis. It is a constricted pupil that accommodates when focusing on a near object, but doesnt react to light

162
Q

how is syphilis diagnosed

A

Antibody testing for T.pallidum antibodies
referral to GUM clinic
samples from infection site can be tested to confirm presence with dark field microscopy and PCR
Rapid plasma reagin and venereal disease research laboratory tests are two non specific but sensitive tests used to assess for active syphilis - assesses the quantity of antibodies

163
Q

what is the management of syphilis

A

GUM referral - screening for other STIs, advice about avoiding sexual activity, contact tracing
single deep IM dose of benzathine benzylpenicillin is the standard treatment
- other regimes and types of penicillin are used in late and neurosyphilis. Ceftriaxone, amoxicillin and doxycycline are alternatives

164
Q

what is acute rhinosinusitis

A

acute inflammation of the mucosal linings of the nasal passage (rhinitis) and paranasal sinuses (sinusitis)

165
Q

what causes of acute rhinosinusitis

A

most common causes are viral organisms such as rhinovirus, influenza or adenovirus however they can be caused by bacterial organisms such as s.pneumoniae, H. influenzae or M.catarrhallis
allergic precipitants that can cause rhinosinusitis are dust, pollen and cat or dog hair

166
Q

what are the paranasal sinuses

A

they are hollow spaces within the bones of the face, arranges symmetrically around the nasal cavity

167
Q

what are the 4 paranasal sinuses

A

frontal sinus - within the frontal bone, most superior of the paranasal sinuses
ethmoid sinus - in the ethmoid bone and are made up of 3 separate cavities
sphenoid sinus - in the sphenoid bone, opening out into the nasal cavity
maxillary sinus - largest, located laterally and slightly inferiorly to the nasal cavities and drain into them

168
Q

what are the main risk factors for developing acute rhinosinusitis

A

cigarette smoking exposure
air pollution
anatomical variations such as septal deviation, nasal polyps or sinus hypoplasia
atopic disease such as asthma or hayfever

169
Q

what are the clinical features of acute rhinosinusitis

A

symptoms lasting less than 12 weeks
sudden onset of two or more of the following symptoms:
nasal obstruction
discoloured nasal discharge
facial pain or pressure
altered sense of smell

170
Q

what are symptoms which might indicate bacterial rhinosinusitis

A

severe local pain
discoloured discharge
fever
worsening after initial improvement (post viral)

171
Q

what are differential diagnosis for acute rhinosinusitis

A

viral upper respiratory tract infection
allergic rhinitis
facial pain syndromes
nasal foreign body

172
Q

how is acute rhinosinusitis diagnosed

A

clinical symptoms and history
can have imaging such as CT if complications are suspected
skin prick testing for allergy may be appropriate in patients with recurrent episodes

173
Q

how is acute rhinosinusitis managed

A

most cases are managed in the community and do not require antibiotics
- for uncomplicated cases treat with simple analgesia, nasal douche and decongestants
- for those with acute bacterial rhinosinusitis antibiotics will be required
if there is no improvement after 7-14 days of treatment or the presence of red flag symptoms then refer to ENT

174
Q

what are red flag symptoms for rhinosinusitis

A

eye signs - swelling, erythema, displaced globe, visual changes, ophthalmoplegia
severe unilateral headache, bilateral frontal headache or frontal swelling
neurological signs or reduced consciousness

175
Q

what is specialist management of rhinosinusitis

A

nasal endoscopy - look at any structural abnormalities or pathology
CT scan of paranasal sinuses
severe infections may require admission with oral steroids, IV antibiotics and surgery

176
Q

what are complications of acute rhinosinusitis

A

peri-orbital cellulitis
osteomyelitis - can lead to penetration into the skull
Potts puffy tumour - osteomyelitis of the frontal sinus leading to soft boggy swelling over the overlaying tissue on the forehead

177
Q

what are the tonsils a part of in the oropharynx

A

Waldeyers ring - ring shapes lymphoid tissue in the oropharynx which consists of four main groups of tonsils: adenoid, tuba, palatine and lingual (in clinical practice tonsilitis = palatine)

178
Q

what are causes of tonsillitis

A

Viral causes
Bacterial causes
non infectious causes

179
Q

what are the common viral causes of tonsilitis

A

rhinovirus - most common
coronavirus
parainfluenza
epstein barr virus

180
Q

what are common bacterial causes of tonsilitis

A

Group A beta haemolytic strep (pyogenes) - most common
haemophilus influenzae
moraxella catarrhalis

181
Q

what are non infectious causes of tonsilitis

A

Gastroesophageal reflux disease
physical irritation (nasogastric tubes)

182
Q

what are the typical symptoms of tonsilitis

A

sore throat
cough
coryzal prodrome
dysphonia
pyrexia
pain and malaise
dysphagia
halitosis

183
Q

what would be seen on examination of someone with tonsilitis

A

fever
swollen erythematous palatine tonsils
cervical lymphadenopathy
tonsils covered with exudate
peritonsillar abscess - usually a complication of acute tonsilitis

184
Q

what are differential diagnosis for tonsilitis

A

epiglottitis
infection mononucleosis
squamous cell carcinoma

185
Q

what investigations should be done for tonsilitis

A

acute episodes can be diagnosed using clinical features alone - key to determine whether its viral or bacterial which is done using the help of the CENTOR and FeverPAIN criteria

186
Q

what is the CENTOR criteria

A

used to determine if its viral or bacterial looking at symptoms of tonsilitis
- tonsillar exudate
- tender anterior cervical lymphadenopathy
- history of fever (>38)
- absence of cough
score of 0-2 has a low probability of a bacterial infection and should be managed conservatively
score of 3-4 has a higher probability of bacterial infection and should be treated with antibiotics

187
Q

what is the FeverPAIN score

A

it is a criteria which consists of five symptoms of acute tonsilitis each scoring 1 point, indicating the likelihood of a bacterial tonsillitis

188
Q

what are the criteria of the FeverPAIN score

A

Fever (during previous 24 hours)
Purulence (pus on tonsils)
Attend rapidly (within 3 days after symptom onset)
severely Inflamed tonsils
No cough or coryza
A score of 0-2 has a low probability of bacteria infection and should be managed conservatively
a score of 3-4 has a higher change of bacterial infection and is treated with antibiotics

189
Q

what lab tests can be done for tonsilitis

A

they are not routinely performed, however they may be useful in confirming bacterial infection with other conditions such rheumatic fever and heart disease
- throat swab for culture - rapid streptococcal antigen test
- monospot test for EBV

190
Q

what is the acute management of tonsilitis

A

supportive: hydration, fluids, ibuprofen plus paracetamol and rest
prescribe antibiotics if suspected bacterial infection - phenoxymethylpenicillin for 10 days
- if allergic to penicillin clarithromycin or erythromycin for 5 days

191
Q

what is chronic management of tonsillitis

A

NICE advises that certain patients with recurrent episodes of tonsillitis can be referred for tonsillectomy:
- more than 7 documented, adequately treated, sore throat episodes in 1 year
- more than 5 episodes in 2 years
- more than 3 episodes in 3 years
- for whom there is no other explanation for recurrent symptoms

192
Q

what are complications of tonsillitis

A

otitis media - most common
sinusitis
peritonsillar abscess
scarlet fever

193
Q

what are the four muscles in the rotator cuff

A

subscapularis
supraspinatus
infraspinatus
teres minor

194
Q

what are the clinical findings in a rotator cuff injury

A

pain - insidious onset, often night pain, exacerbated by overhead activities, in traumatic tear the pain and weakness are acute
weakness - loss of active range of motion with greater passive range of motion

195
Q

what would be seen on examination of someone with a rotator cuff injury

A

additional weakness on the resisted movement of the rotator cuff muscles

196
Q

how are rotator cuff injuries diagnosed

A

clinical history and examination
imaging - X-rays to look for any tear, tendonitis etc. Ultrasound and MRI

197
Q

how is rotator cuff injury managed

A

non surgical - physiotherapy, activity modification, NDAIDs, corticosteroid injections
surgical- repair the rotator cuff +/- subacromial decompression

198
Q

what is tennis/golfers elbow

A

it is an overuse syndrome of the lateral epicondyle (tennis elbow) and medial epicondyle (golfers elbow)

199
Q

what is an overuse injury

A

it is due to eccentric overload at the common extensor tendon leading to tendinitis and inflammation at the origin of the ECRB commonly known as tennis elbow
- same happens for golfers elbow just at the flexor pronator mass origin

200
Q

what are the clinical findings of tennis/golfers elbow

A

pain - insidious onset, is localised over the medial or lateral epicondyle, worse with wrist and forearm motion and gripping

201
Q

what would you see on examination of someone with tennis/golfers elbow

A

point tenderness distal and anterior to the medial epicondyle (golfers) and tenderness at the ECRB insertion into the lateral epicondyle (tennis)
tennis elbow: resisted wrist extension with the elbow fully extended
golfers: pain with resisted forearm pronation and wrist flexion

202
Q

what is the management of tennis/golfers elbow

A

non surgical; rest, ice, physiotherapy, activity modification, bracing and NSAIDS
surgical: open debridement of the origin

203
Q

what is urinary incontinence

A

it refers to the loss of control of urination

204
Q

what are the two types of urinary incontinence

A

urge and stress

205
Q

what is urge incontinence

A

it is overactivity of the detrusor muscle of the bladder (overactive bladder)

206
Q

what are symptoms of urge incontinence

A

sudden feeling of the urge to pass urine
having to rush to the bathroom and not arriving before urination occurs

207
Q

what causes stress incontinence

A

the pelvic floor consists of a sling of muscles that supports the contents of the pelvic floor. When the muscles of the pelvic floor are weak, the canals become lax and the organs are poorly supported

208
Q

what is stress incontinence

A

incontinence due to weakness of the pelvic floor and sphincter muscles allowing urine to leak out at times of increased pressure on the bladder such as laughing, coughing or surprised

209
Q

what is mixed incontinence

A

this is a combination of urge and stress incontinence - crucial to identify which is the bigger issue and treat that one first

210
Q

what is overflow incontinence

A

this can occur when there is chronic urinary retention due to an obstruction to the outflow of urine. Chronic urinary retention results in overflow of urine and the incontinence occurs without the urge to pass urine

211
Q

what can cause overflow incontinence

A

anticholinergic medications
fibroids
pelvic tumours
neurological conditions - MS, diabetic neuropathy, spinal cord injuries

212
Q

what are risk factors for urinary incontinence

A

Increased age
Postmenopausal status
Increase BMI
Previous pregnancies and vaginal deliveries
Pelvic organ prolapse
Pelvic floor surgery
Neurological conditions, such as multiple sclerosis
Cognitive impairment and dementia

213
Q

what modifiable risk factors can contribute to incontinence

A

Caffeine consumption
Alcohol consumption
Medications
Body mass index (BMI)

214
Q

what might be seen on examination of someone with incontinence

A

pelvic organ prolapse
atrophic vaginitis
urethral diverticulum
pelvic masses
leakage from urethra if patient is asked to cough
also look for strength of pelvic muscle contraction during bimanual and grade on the modified oxford grading system

215
Q

what are the grades of pelvic muscle contractions measured using the modified oxford grading system

A

0: No contraction
1: Faint contraction
2: Weak contraction
3: Moderate contraction with some resistance
4: Good contraction with resistance
5: Strong contraction, a firm squeeze and drawing inwards

216
Q

how is incontinence investigated

A

a bladder diary
urine dipstick testing
post void residual bladder volume
urodynamic testing - for urge incontinence not responding to treatment

217
Q

what is urodynamic testing

A

it is a way of assessing the presence and severity of urinary symptoms - a thin catheter is inserted into the bladder and another into the rectum. They measure the pressures in the bladder and rectum and compare them

218
Q

what does cystometry measure

A

measures the detrusor muscle contraction and pressure

219
Q

what does uroflowmetry measure

A

the flow rate

220
Q

what is the leak point pressure

A

point at which the bladder pressure results in leakage of urine. The patient is asked to cough, move or jump when the bladder is filled to various capacities. This assesses for stress incontinence.

221
Q

what is video urodynamic testing

A

filling the bladder with contrast and taking xray images as the bladder is emptied. Theses are only performed where necessary and not a routine part of urodynamic testing.

222
Q

how is stress incontinence managed

A

lifestyle advice: avoid caffeine, diuretics and overfilling of the bladder. Avoid excessive exercise or restricted fluid intake. Weight loss if appropriate
supervised pelvic floor exercises for at least three months before considering surgery
surgery
duloxetine - SNRI antidepressant

223
Q

what are the surgical options for treatment of stress incontinence

A

tension free vaginal tape - mesh sling under the urethra
autologous sling procedures - strip of facia from patients abdominal wall is used
colposuspention - stitches connecting the anterior vaginal wall and the pubic symphysis around the urethra
intramural urethral bulking - injections around the urethra to reduce the diameter and add support

224
Q

what surgical intervention is used where stress incontinence is caused by a neurological disorder or other surgical methods have failed

A

artificial urinary sphincter - pump inserted into the labia that inflates and deflates a cuff around the urethra allowing women to control their continence manually

225
Q

what is the management of urge incontinence

A

bladder retraining for at least 6 weeks is first line
anticholinergic medication (oxybutynin, tolterodine)
mirabegron
invasive procedures

226
Q

what are side effects of anticholinergic medication

A

dry mouth
dry eyes
urinary retention
constipation
postural hypotension
cognitive decline, memory issues and worsening of dementia

227
Q

what is Mirabegron

A

it is used as an alternative treatment for urge incontinence with less anticholinergic burden

228
Q

what condition is mirabegron contraindicated in

A

uncontrolled hypertension as it works as a beta 3 agonist leading to sympathetic nervous stimulation and raising blood pressure

229
Q

what are the invasive options for treatment of overactive bladder

A

Botulinum toxin type A
percutaneous sacral nerve stimulation
augmentation cystoplasty - using bowel tissue to enlarge the bladder
urinary diversion

230
Q

what is reactive arthritis

A

it involves synovitis in one or more joint in response to an infective trigger. Typically it causes acute monoarthritis, affecting a single joint.

231
Q

what are the most common triggers of reactive arthritis

A

gastroenteritis
STI - chlamydia and gonorrhoea (typically causes septic)

232
Q

what is the classic triad of reactive arthritis

A

bilateral conjunctivitis
anterior uveitis
urethritis
arthritis
cant see, cant pee, cant climb a tree
- can also cause circinate balanitis (dermatitis of the head of the penis)

233
Q

how is reactive arthritis diagnosed

A

1st you need to exclude septic arthritis and antibiotics may be given until septic arthritis is excluded
- require joint aspiration sent for MC+S, as well as crystal examination

234
Q

what is the management of reactive arthritis

A

treatment of the triggering infection
NSAIDS
steroid injections into the affected joints
systemic steroids may be required, particularly where multiple joints are affected

235
Q

what is urticaria

A

it is also known as hives. It is small, itchy lumps that appear on the skin. They may be associated with a patchy erythematous rash. They may be localised to a certain area or widespread

236
Q

what is the pathophysiology of urticaria

A

Urticaria are caused the release of histamine and other pro-inflammatory chemicals by mast cells in the skin. This may be part of an allergic reaction in acute urticaria or an autoimmune reaction in chronic idiopathic urticaria.

237
Q

what are causes of acute urticaria

A

Allergies to food, medications or animals
Contact with chemicals, latex or stinging nettles
Medications
Viral infections
Insect bites
Dermatographism (rubbing of the skin)

238
Q

what is chronic urticaria

A

it is an autoimmune condition where autoantibodies target mast cells and trigger them to release histamine and other chemicals. It can be sub classified depending on the cause

239
Q

what are the different types of chronic urticaria

A

Chronic idiopathic urticaria
Chronic inducible urticaria
Autoimmune urticaria

240
Q

what is chronic idiopathic urticaria

A

recurrent episodes of chronic urticaria without a clear underlying cause or trigger.

241
Q

what is chronic inducible urticaria

A

describes episodes of chronic urticaria that can be induced by certain triggers, such as:
Sunlight
Temperature change
Exercise
Strong emotions
Hot or cold weather
Pressure (dermatographism)

242
Q

what is autoimmune urticaria

A

chronic urticaria associated with an underlying autoimmune condition, such as systemic lupus erythematosus.

243
Q

what is the management of urticaria

A

antihistamines are the main treatment - fexofenadine
oral steroids may be considered as short courses for severe flares
in very problematic cases referral to specialist may be required and consider treatment with:
Anti-leukotrienes such as montelukast
Omalizumab, which targets IgE
Cyclosporin

244
Q

what is syncope

A

it is the event of temporarily losing consciousness due to a disruption of blood flow to the brain, often leading to a fall

245
Q

what is a vasovagal episode

A

problem with the autonomic nervous system regulating blood to the brain. When the vagus nerve receives a strong stimulus it can stimulate the parasympathetic nervous system. this leads to a drop in blood pressure and hypoperfusion of the brain tissue, causing a faint

246
Q

what are prodrome symptoms of a vasovagal syncope

A

Hot or clammy
Sweaty
Heavy
Dizzy or lightheaded
Vision going blurry or dark
Headache

247
Q

what might happen during a vasovagal episode

A

Suddenly losing consciousness and falling to the ground
Unconscious on the ground for a few seconds to a minute as blood returns to their brain
There may be some twitching, shaking or convulsion activity, which can be confused with a seizure

248
Q

what are primary causes of syncope (simple fainting)

A

Dehydration
Missed meals
Extended standing in a warm environment, such as a school assembly
A vasovagal response to a stimuli, such as sudden surprise, pain or the sight of blood

249
Q

what are secondary causes of syncope

A

Hypoglycaemia
Dehydration
Anaemia
Infection
Anaphylaxis
Arrhythmias
Valvular heart disease
Hypertrophic obstructive cardiomyopathy

250
Q

what are key details in someones history would point you towards syncope

A

Features that distinguish a syncopal episode from a seizure
After exercise? Syncope after exercise is more likely to be secondary to an underlying condition.
Triggers?
Concurrent illness? Do they have a fever or signs of infection?
Injury secondary to the faint? Do they have a head injury?
Associated cardiac symptoms, such as palpitations or chest pain?
Associated neurological symptoms?
Seizure activity?
Family history, particularly cardiac problems or sudden death?

251
Q

what examinations should be performed if someone comes in after syncope

A

Are there any physical injuries as a result of the faint, for example a head injury?
Is there a concurrent illness, for example an infection or gastroenteritis?
Neurological examination
Cardiac examination, specifically assessing pulses, heart rate, rhythm and murmurs
Lying and standing blood pressure

252
Q

what investigations should you do if someone comes in after a syncope episode

A

ECG, particularly assessing for arrhythmia and the QT interval for long QT syndrome
24 hour ECG if paroxysmal arrhythmias are suspected
Echocardiogram if structural heart disease is suspected
Bloods, including a full blood count (anaemia), electrolytes (arrhythmias and seizures) and blood glucose (diabetes)

253
Q

what is the management of vasovagal syncope

A

need to exclude other pathology
once vasovagal episode is diagnosed, reassurance and simple advice can be given:
- avoid dehydration
- avoid missing meals
- avoid standing for long periods of time
- when experiencing prodromal symptoms such as sweating and dizziness, sit or lie down and have some water or something to eat

254
Q

what are varicose veins

A

they are dilated tortuous veins which mainly occurs in the superficial venous system in the legs

255
Q

what is the pathophysiology of varicose veins

A

varicose veins develop due to the incompetence of the one way valves, leading to leakage, retrograde flow and consequently pooing of blood in the superficial venous system
additionally the thinner weaker walls of the superficial veins make them more prone to the effects of the high pressure build up of blood leading to distension and tortuosity o the affected segment, leading to bulging of the skin over the affected vein

256
Q

what are causes of varicose veins

A

mostly idiopathic
secondary causes can be due to venous outflow obstruction due to intravascular (DVT) or extravascular (pelvic mass) reasons
progesterone and oestrogen are also believed to have vasodilatory properties which can predispose or worsen varicose veins

257
Q

what are risk factors for varicose veins

A

family history of varicose veins
older age (especially 40 years and above)
pregnancy
female sex
history of DVT
obesity
prolonged standing or sitting
previous lower limb fracture
being caucasian

258
Q

what are symptoms of varicose veins

A

pain - dull ache or burning
leg fatigue, discomfort, worsening pain after prolonged standing
leg cramps
restless legs
skin discolouration over the affected areas
heaviness of the legs
itching after prolonged standing
ankle oedema
lipodermatosclerosis

259
Q

what are severe presentations of varicose veins

A

ulceration
haemorrhage especially if the variceal segments are large, traumatised or over bony prominences
thrombophlebitis

260
Q

how are varicose veins diagnosed

A

clinical features - presence of tortuous veins and history of risk factors
duplex ultrasound can confirm the diagnosis as well as ruling out DVT
ABPI can exclude peripheral artery disease

261
Q

how are varicose veins managed

A

referral to vascular services
lifestyle changes - exercise and wt loss
conservative - compression stockings using bandages or stockings however its NOT recommended by NICE unless surgical intervention is declined or inappropriate
surgery - endovenous techniques or open surgery

262
Q

what endovenous techniques are used to treat varicose veins

A

aim to block faulty veins which has the same benefit as removing them
- endothermal ablation (first line)
- ultrasound guided foam sclerotherapy
- glue, steam or mechanochemical devices

263
Q

what open surgery is done to treat varicose veins

A

ligation and stripping: incompetent veins are ties off and removed
phlebectomy: varicose veins are pulled out through small incisions

264
Q

what are the viruses that cause viral gastroenteritis

A

rotavirus
norovirus
adenovirus - tends to cause resp symptoms

265
Q

what is the primary concern with gastroenteritis

A

dehydration

266
Q

what can be used to prevent dehydration in people with gastroenteritis

A

oral rehydration salt solution (dioralyte mixed with water) that helps to replace losses. It contains glucose, potassium and sodium

267
Q

what are post gastroenteritis complications

A

Lactose intolerance
Irritable bowel syndrome
Reactive arthritis
Guillain–Barré syndrome
Haemolytic uraemic syndrome

268
Q

what are the symptoms of the stomach flu

A

diarrhoea
nausea and vomiting
loss of appetite
abdominal pain and cramping
systemic symptoms: fever, chills, fatigue, body aches, headaches, lymphoedema

269
Q

what are the stages of stomach flu

A
  1. exposure
  2. incubation - few hours to a few days
  3. acute infection - from a day to weeks
  4. recovery
270
Q

how long is viral gastroenteritis contagious for

A

most contagious during the acute phase of the infection and for a few days after

271
Q

what are causes of viral gastroenteritis

A

norovirus - leading in adults
rotavirus - leading in children
astrovirus - children younger than 3
adenovirus - affects all ages

272
Q

what is exanthem

A

it is a widespread rash that usually is accompanied by systemic symptoms such as fever, malaise and headache

273
Q

what causes exanthems

A

usually due to viral infections: varicella, measles, rubella, herpes 6B and parvovirus B19 (there are many other causes such as HIV, smallpox, hepatitis, EBV etc)
bacterial infection: staphylococcal and streptococcal toxin infections
may also be due to medications and connective tissue disease (SLE, SJA etc)

274
Q

what are the symptoms/signs of exanthemas

A

non specific exanthemas appear as spots or blotches and can be itchy. The rash is widespread and may be more extensive on the trunk or extremities
general symptoms: fever, malaise, headache, LOA, abdominal pain, irritability, muscle aches and pains

275
Q

how are exanthemas diagnosed

A

pattern of rashes and prodromal symptoms allowing for a clinical diagnosis
viral swab - culture and PCR
bloods - serology, PCR, ANA, tissue antibodies
genotyping

276
Q

what is the treatment for exanthemas

A

paracetamol/simple analgesia to reduce fever
moisturising emollients to reduce itch

277
Q

what are viruses that commonly cause exanthem rash

A

Chickenpox (varicella-zoster virus).
COVID-19 (coronavirus).
Fifth disease (parvovirus B19).
Hand, foot and mouth disease(coxsackievirus A16).
Measles (morbillivirus).
Roseola (human herpesvirus 6).
Rubella (rubella virus).
Other viruses that may cause viral exanthem rash include: Hepatitis, HIV, EBV

278
Q

what are radiculopathies

A

radiculopathies refer to the compression of irritation of a spinal nerve route causing pain with sensory changes (numbness, pins and needles etc) or motor changes (weakness, diminished deep tendon reflexes)

279
Q

what is the most common kind of radiculopathy

A

lumbar radiculopathy - tends to affect men and women in the 4th-6th decades of life

280
Q

what is the most common cause of lumbar radiculopathies

A

herniated disk
degenerative changes = 2nd

281
Q

what nerve roots are the most commonly affected in lumbar radiculopathies

A

L4-S1

282
Q

what are the two sections of a spinal nerve root

A

ventral (anterior) - motor
dorsal (posterior) - sensory

283
Q

what are causes of lumbar radiculopathy

A

herniated disc - most common cause
spinal stenosis and spondylolisthesis
pelvic or lumbar fractures
nerve root may become compromised due to peripheral nervus system syndromes (GBS) - polyradiculopathy
cancer
infection

284
Q

what are modifiable risk factors for lumbar radiculopathy

A

smoking
obesity
strenuous physical activity
whole body vibration

285
Q

what are non modifiable risk factors for lumbar radiculopathy

A

age
history of lower back pain
genetic factors such as variations in intragenic vitamin D receptor gene

286
Q

what are clinical features of lumbar radiculopathies

A

most common symptom in radiating pain (sharp, stabbing, shooting, throbbing etc) that spreads distally from the lumbar spine
pain is often unilateral but can be bilateral
sensory change: numbness, paraesthesia
motor change: weakness, loss of strength or power
pain is worse after periods of inactivity
can worsen with coughing or sneezing
can be acute or insidiously
can be consistent, worsening or relapsing remitting

287
Q

what medications can cause neuropathy with similar symptoms to radiculopathy

A

amiodarone
docetaxel
carbamazepine

288
Q

what might be seen on clinical examination of someone with lumbar radiculopathy

A

muscle atrophy
diminished deep tendon reflexes
gain disturbances

289
Q

what are the targeted clinical examinations for suspected lumbar radiculopathy

A

dermatomes: L1-S2
myotomes: L1-S2 using the MRC scale
reflexes: L3-S1
special tests: slump test and straight leg test

290
Q

what investigations should be done for lumbar radiculopathies

A

majority of cases managed conservatively and dont need investigations
Imaging: MRI (gold for herniation, prolapse or degenerative process), X-Ray
EMG and nerve conduction tests

291
Q

what is conservative management for lumbar radiculopathies

A

normally 1st line treatment
1. patient education: avoid triggers, information and reassurance
2. lifestyle modification
3. Paracetamol and NSAIDs. If pain persists use of steroid injections or oral steroids can be used.
4. referral to musculoskeletal physiotherapy
5. referral to psychological services if needed

292
Q

what is the surgical management of lumbar radiculopathies

A

given if conservative management ails, symptoms are worsening, if there is a serious pathology, or severe neurological deficits
- discectomy
- spinal decompression
- open laminectomy with discectomy
- microendoscopic discectomy

293
Q

what are complications of lumbar radiculopathies

A

pain: functional mobility loss, loss of independence, inability to fulfil social or occupational roles
Central sensitisation of nociplastic pain
muscle atrophy and deconditioning
progressive muscle weakness
cauda equina syndrome

294
Q

what are red flag symptoms of radiculopathy

A

cauda equina - faecal incontinence, urinary retention, saddle anaesthesia
infection - immunosuppression, IV drug use, unexplained fever
fracture - significant trauma, osteoporosis, chronic steroid use
malignancy - new onset after 50
metastatic disease - history of malignancy

295
Q

what is normally the first line prescribed treatment for radiculopathy pain

A

neuropathic pain medications - amitriptyline, or pregabalin and gabapentin as alternatives
patients who supper from muscle spasms may be managed with benzodiazepines or baclofen

296
Q

what are symptoms of cervical radiculopathy

A

pain in the neck, shoulder, upper back or arms

297
Q

what are causes of cervical radiculopathy

A

disc degeneration
spondylosis - age related arthritis of the vertebra
bone disease
cancer
herniated disc

298
Q

what is the most common site for cervical radiculopathy

A

lower cervical certebrae - C5-7

299
Q

what is a common test for cervical radiculopathy

A

the spurling’s maneuver where the individual tilts their head to the side, backwards and tries to pull their head back upright while the clinician pushes it down

300
Q

how is varicella zoster virus transmitted

A

droplet spread or direct skin contact with vesicle fluid

301
Q

what is the incubation period of varicella zoster virus

A

typically 10-14 days but can be up to 21 days

302
Q

what is the prodrome symptoms of varicella zoster virus

A

symptoms can last up to 4 days and include:
high fever
general malaise
myalgia
anorexia
headache
nausea

303
Q

what is the rash associated with varicella zoster virus

A

it begins as small erythematous macules on the scalp, face, trunk and proximal limbs
these macules develop into papules, vesicles and pustules
shallow oral and genital ulcers can occur which are painful
crusting of the vesicles and pustules usually occurs within 5 days at which point new vesicle formation has ceased

304
Q

what is the general advice given to those with chickenpox

A

adequate hydration
avoidance of scratching
avoidance of pregnant women, neonates and immunocompromised individuals

305
Q

what is symptomatic management of chickenpox

A

paracetamol for fever and discomfort
NSAIDS should be AVOIDED!
sedating antihistamines (chlorphenamine), emollients and calamine lotion for the itch
if an adolescent or adult presents within 24 hours of rash onset, oral aciclovir may be considered

306
Q

how are high risk groups treated for chickenpox

A

urgent specialist advice:
antiviral medication with aciclovir
intravenous immunoglobulin

307
Q

where in the UK is chickenpox a notifiable disease

A

scotland and northern ireland

308
Q

how long should children with VZV stay off school

A

until all the lesions have crusted over

309
Q

what are complications of chickenpox

A

dehydration
secondary bacterial infection of the lesions
scarring
viral pneumonia
encephalitis
reyes syndrome - thought to be connected to aspirin use
shingles

310
Q

what can happen if chicken pox is caught in pregnancy

A

can lead to congenital varicella syndrome if contracted before 20 weeks:
intrauterine growth restriction
microcephaly
limb hypoplasia
ophthalmological defects
cutaneous scarring

311
Q

what are screening tests

A

check done on a healthy person to pick up a condition before it develops or at a very early stage

312
Q

what criteria must apply before a national screening programme is considered

A
  1. there must be a test available which picks up a disease or condition before symptoms develop
  2. the test must be reasonably accurate. It should not be positive for too many people who do NOT have the condition and must not miss many people who DO have the condition
  3. the test must be reasonable simple to perform and acceptable to the people having the test
  4. the benefits of screening but be greater than any potential risk or harm it could cause
  5. the cost of the test, must not be more than the benefits it gives
  6. there must be a treatment at the early stage of the condition or disease which will make a difference to the outcome
  7. the condition being screened for must be important to health and wellbeing
  8. there must be an organised, efficient plan for what happens next if the test is positive
313
Q

what are the benefits of screening tests

A
  1. in picking up problems early you can treat things earlier and increase survival
  2. cancers picked up early, treatments are more likely to be successful
  3. newborn baby screening allows things to be corrected if picked up early enough
  4. screening in pregnancy helps to identify any serious abnormalities
314
Q

what are issues with screening tests

A
  1. no test can be 100% accurate
  2. some people may have treatment which wasnt needed due to a false positive
  3. tests can cause worry - if initially test is positive but further tests are normal
  4. cost: screening large numbers of healthy people is expensive
  5. for some conditions screened for, a negative result at one point in time doesnt rule out developing the condition in the future
  6. screening tests can lead to difficult decisions
315
Q

what are the current screening tests available in England

A
  1. abdominal aortic aneurysm screening programme
  2. bowel cancer screening
  3. breast screening programme
  4. cervical screening programme
  5. diabetic eye screening programme
  6. fetal anomaly screening programme
  7. infectious diseases in pregnancy screening programme
  8. newborn and infant physical examination screening programme
  9. newborn blood spot screening programme
  10. newborn hearing screening programme
  11. sickle cell and thalassaemia screening programme
316
Q

what screening is offered in pregnancy

A

screening for infectious diseases (Hepatitis B, HIV and syphilis)
screening for down’s syndrome, pataus syndrome and edwards syndrome
screening for sickle cell and thalassaemia
20 weeks screening scan
diabetic eye screening

317
Q

what screening is offered to newborn babies

A

physical examination - eyes, heart, hips and testicles
hearing screening
a blood spot test

318
Q

what ages does cervical screening go between

A

25 to 64
it is offered every 3 years for those aged 25-49
it is offered ever 5 years for those aged 50-64

319
Q

when is diabetic eye screening offered

A

from the age of 12, all people with diabetes are offered regular diabetic eye screening

320
Q

when is breast cancer screening offered

A

to women between the ages of 50-70

321
Q

when is bowel cancer screening offered

A

it is offered to everyone aged 50-74 every 2 years
if you are over 75 you can ask for a kit every 2 years by phoning

322
Q

when is the AAA screening offered

A

it is offered to men when the turn 65 to detect AAA, men over 65 fan self refer

323
Q
A

Phase 3a Jemima (16 decks)

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