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GP Flashcards

1
Q

what is the pathophys of acne vulgaris 3

A

formation of acne lesions due to three contributing factors:
1. follicular hyperkeratinization: formation of keratinous plug due to an abnormal keratinization process= skin cells do not shed as normal leading to the proliferation of P. acnes
2. increased sebum production: sebum acts as a nutrient for P.acne and forms a favourable anaerobic environment
3. Propionibacterium acnes colonization: this bacteria contributes to inflammation by releasing pro inflammatory mediators eg chemokines, cytokines and reactive oxygen species

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2
Q

Where does acne act? 1

A

on pilosebaceous unit

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3
Q

What are the different types of acne lesions seen in acne vulgaris pts 4

A

comedones= dilated sebaceous follicle (whitehead is closed and blackhead is open)
inflammatory lesions= papules and pustules
due to excessive inflammatory response= nodules and cysts
scars: ice-pick scars and hypertrophic scars

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4
Q

How is acne vulgaris classified 3

A

mild: open and closed comedones with or without sparse inflammatory lesions
moderate acne: mild + numerous papules and pustules
severe acne: extensive inflammatory lesions, which may include pitting, and scarring

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5
Q

How is acne vulgaris treated?

A

Mild/ moderate:
12 week topical combination therapy: any 2 of the following in combination:
Topical benzoyl peroxide.
Topical antibiotics (clindamycin)
Topical retinoids (tretinoin/adapalene)

Mod/ severe:
12 week course of one of the following:
-> a fixed combination of topical adapalene with topical benzoyl peroxide + either oral lymecycline or oral doxycycline
-> a topical azelaic acid + either oral lymecycline or oral doxycycline

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6
Q

When can patients be referred with acne? 6

A
  1. Acne fulminans.
  2. Mild-moderate acne not responding to two 12 week courses of treatment as above.
  3. Moderate-severe acne not responding to one 12 week course of treatment as above, including an oral antibiotic.
  4. Psychological distress/mental health disorder contributed to by acne.
  5. Acne with persistent pigmentary changes.
  6. Acne with scarring.
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7
Q

What is a specific complication of long term abx use in acne, causes and what treatment can be given?

A

Gram-negative folliculitis (caused by e.coli/ kleb/ proteus/ pseudomonas)
high dose oral trimethoprim

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8
Q

What is acute bronchitis and timeline

A

inflammation of trachea and bronchi
resolves in 3 week but can have persistant cough

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9
Q

Presentation of acute bronchitis 3

A
  1. cough
  2. wheeze
  3. sore throat
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10
Q

How can acute bronchitis be differentiated from pneumonia 2

A

no focal chest signs apart from wheeze in acute bronchitis
systemic features are more indicative of pneumonia

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11
Q

What is the management of acute bronchitis 2

A
  1. supportive (fluids and analgesia at home)
  2. only consider abx (doxycyline) if systemic unwell, co-morbidities or CRP of over 100
    -> cannot use doxycycline in children/ pregnant so use amoxicillin instead
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12
Q

What is acute stress reaction and features 4

A

occurs in first 4 weeks after a traumatic event
features: flashbacks, dissociation, hyper vigilance and sleep disturbance
(imagine a person sleeping then suddenly waking with hypervigilance, looking around the rooms- they dissociate whilst looking at the drawers in the room and get flashbacks looking at the floor)

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13
Q

What is the mangement for acute stress reaction 3

A

1st line: CBT
2. benzodiazipines: ONLY for acute anxiety, not recommended by WHO
3. encourage sleep hygeine and relaxation techniques

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14
Q

What are anal fissures and classification and features

A

tears in the distal anal canal
acute less than 6 weeks, chronic if over 6 weeks
very severely painful and bright red rectal bleeds

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15
Q

how to differentiate between anal fissures and haemorrhoids 2

A

fissures are more more painful during bowel movements and bleed more than haemorrhoids

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16
Q

What is the management of acute and chronic anal fissures (5,3)

A

acute:
1. high fibre diet and high fluid intake
2. bulk forming laxatives (isphagula husk)
3. analgesia
4. lubricants eg petroleum jelly before defecation
5. topical anaesthetic eg lidocaine gel

chronic:
1. topical GTN
2. diltiazem cream (CCB) for second line to GTN
3. referral for Sphincterotomy/ botox

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17
Q

What is the pathophys of bacterial vaginosis, is it an STI?

A

overgrowth of anaerobic organisms eg gardnerella vaginalis, leading to the increase of vaginal pH
not an STI, but seen mostly in sexually active women

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18
Q

What is the diagnosis criteria of bacterial vaginosis and what is this criteria called

A

Amsel’s criteria for diagnosis of BV - 3 of the following 4 points should be present
-> thin, white homogenous discharge
-> clue cells on microscopy: stippled vaginal epithelial cells (from high vaginal swab)
-> vaginal pH > 4.5 (swab on pH paper)
-> positive whiff test (addition of potassium hydroxide results in fishy odour)

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19
Q

What is the management for bacterial vaginosis 2

A
  1. asymptomatic= no tx required
  2. symptomatic= oral metronidazole for 5-7 days
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20
Q

What are the main risk factors of benign prostatic hyperplasia 2

A
  1. age: around 80% of 80-year-old men have evidence of BPH
  2. ethnicity: black > white > Asian
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21
Q

What is the presentation of BPH 8

A

LUTS symptoms:
issues with both storage and voiding (voiding is more common)
storage: frequency, urgency, nocturne, incontinence
voiding: poor stream, hesitancy, incomplete emptying, dribbling

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22
Q

What are the Ix for BPH 5

A
  1. DRE (rectal exam)- smooth enlarged- prostatic cancer is hard and irregular
  2. PSA (for ruling out prostate cancer but can be raised in both)
  3. urine dipstick
  4. international prostate symptom score (IPSS) to assess impact of LUTSon QOL-
    Score 20-35: severely symptomatic
    Score 8-19: moderately symptomatic
    Score 0-7: mildly symptomatic
  5. transrectal ultrasound to determine size (can determine tx options)
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23
Q

What is the management for BPH 5

A
  1. lifestyle changes and watchful waiting: decrease caffeine intake
  2. 1st line- alpha 1 antagonist eg tamsulosin which relaxes bladder neck
  3. 2nd line- 5 alpha reductase inhibitor eg finasteride which decreases testosterones production and therefore decreases prostate size
  4. combination therapy of 2 & 3
  5. surgery (last resort): transurethral resection of prostate (main complication= retrograde ejaculation)
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24
Q

What is vaginal candidiasis, cause 2 and risk factors 4

A

‘vaginal thrush’
mostly candida albicans and rest by other candida species
long term abx/ steroids, diabetes mellitus, immunocompromised

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25
Q

What is the normal vaginal flora compromised of and how does this maintain a healthy environment. What happens when this is lacking?

A

lactobacillus- releases lactic acid + HPO to maintain low ph= prevents growth of bacteria

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26
Q

What is the presentation of vaginal candidiasis 2

A

cottage cheese but non-offensive discharge
vulvitis- itching and vulval erythema

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27
Q

What are the investigations for vaginal candidiasis

A

swab not indicated if consistent clinical features with candidiasis

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28
Q

What is the management of recurrent vaginal candidiasis 4 and what is classed as recurrent

A

classified as 4+ episodes a year
1. check compliance with treatment
2. confirm candidiasis with high vaginal swab for microscopy and culture
3. glucose test to exclude diabetes
4. induction-maintenance regime
-> induction: oral fluconazole every 3 days for 3 doses
-> maintenance: oral fluconazole weekly for 6 months

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29
Q

What is the management vaginal candidiasis 3

A
  1. first line: oral fluconazole 150 mg as a single dose
  2. if allergy/ pregnant: clotrimazole 500 mg intravaginal pessary
  3. if vulval sx then add topical imidazole in combination with oral/ intravaginal antifungal
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30
Q

What is the cause of Chlamydia and why is it relevant in the UK

A

Chlamydia trachomatis
the most prevalent sexually transmitted infection in the UK

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31
Q

What is the presentation of chlamydia 3

A
  1. asymptomatic in around 70% of women and 50% of men
  2. women: cervicitis (discharge, bleeding), dysuria
  3. men: urethral discharge, dysuria
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32
Q

How is chlamydia diagnosed 4

A

test done 2 weeks after exposure
women: low vaginal swab is first-line
men: the urine test is first-line (first morning void urine sample)
both of these samples are tested via NAATs

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33
Q

What is the screening for chlamydia

A

National Chlamydia Screening Programme for 15-24 years, open to all sexually active pts

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34
Q

What is the Mx for chlamydia 3

A
  1. 7 days doxycycline 100mg BD
  2. if CI or pregnant, then azithromycin
  3. all contacts (men in 4 weeks before sx and women in 6 months before) can be offered support/ referral with GUM- if pt has confirmed chlamydia case then treat their contacts with doxycycline before testing them
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35
Q

What are the complications of chlamydia? 4

A

infertility (both)
PID (f)
epididymo-orchitis (m)
reactive arthritis (both)

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36
Q

What is chronic fatigue syndrome

A

3 months of disabling fatigue affecting mental and physical function more than 50% of the time with no other diseases causing this

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37
Q

What are the features of chronic fatigue syndrome 5

A
  1. fatigue (main one)
  2. sleep problems
  3. muscle/ joint pains
  4. headaches
  5. cognitive dysfunction (inability to concentrate, difficulty with thinking and word-finding)

(Feeling Sleepy, Might Just Head (c)Out)

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38
Q

What is the ix for chronic fatigue syndrome and diagnostic criteria?

A
  1. bloods to exclude pathology: FBC, U&E, LFT, TFT, CRP, ESR, ferratin, coeliac, calcium, CK, glucose
  2. nice criteria to diagnose- fatigue not caused by any other condition, post-exertional malaise that is disproportionate to activity and with a prolonged recovery time, sleep disturbance, cognitive dysfunction for more than 3 months
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39
Q

What is the Mx for chronic fatigue syndrome 4

A
  1. refer to specialist chronic fatigue syndrome service
  2. energy management to stay within energy limit (strategy supported by CFS specialist)
  3. cognitive behavioral therapy
  4. do not encourage exercise unless part of programme with CFC specialist team
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40
Q

What are the two types of conjunctivitis

A

allergic
infective (split into bacterial and viral)

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41
Q

What are the features 2 and mx of allergic conjunctivitis 2

A

features:
->bilateral conjunctival erythema and swelling
-> itching

Mx:
first line: topical/ oral antihistamines eg cetirizine
2nd line: topical mast cell stabilisers eg sodium cromoglicate

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42
Q

Compare the sx of bacterial and viral conjunctivitis

A

bacterial: purulent discharge, eyes stuck together in morning
viral: serous discharge, recent URTI

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43
Q

How is infective conjunctivitis managed 2

A
  1. topical abc chloramphenicol eye drops, 2/3 hourly
  2. topical fusidic acid eye drops or pregnant women BD
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44
Q

What classifies as constipation

A

unsatisfactory defecation due to :

infrequent stools (<3 times weekly)
difficult stool passage (with straining or discomfort)
seemingly incomplete defecation

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45
Q

What is the management of constipation 5

A

1 month of increased fibre, fluids and exercise
2 months of bulk forming laxative eg isphagula husk
2 months of osmotic laxartive eg lactulose/ macrogol
2 months of stimulant laxative eg senna/ sodium picosulfate
if still constipated, stop all laxatives and take prucalopride 1mg

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46
Q

What is contact dermatitis types, which is more common, locations of each

A

irritant contact dermatitis: inflammation of skin due to direct contact with irritants (more common)
-> on hands/ where contact was with irritant

allergic contact dermatitis: inflammation of skin due to a type 4 hypersensitivity reaction (less common)
-> expands to area past contact with trigger

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47
Q

what r the best readings to quantify CKD 2

A

eGFR and albumin: creatinine ratio

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48
Q

what is CKD

A

eGFR of <60mL/min/1.73m2 for 3 or more months

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49
Q

what are the stages of CKD 5 and their values

A

stage 1: >90mL/min eGFR
stage 2: 60-89 mL/min eGFR
stage 3A: 45-59mL/min eGFR
stage 3B: 30-44mL/min eGFR
stage 4: 15-29mL/min eGFR
stage 5: less than 15mL/min eGFR (end stage CKD)

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50
Q

what is the pathophys of CKD 4 and explain why proteins and blood can get into urine

A

low GFR= lots to damaged nephrons
this increases burden on remaining nephrons
this also increases RAAS activation to increase GFR but this increases pressure
this causes loss of basement membranes selective permeability= blood and protein in urine

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51
Q

what are the 2 most common risk factors for CKD

A

diabetes mellitus
hypertension

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52
Q

why is CKD initially asymptomatic 1 and why does CKD become symptomatic 1

A

asymptomatic- lots of nephrons as a reserve
symptomatic- due to substance accumulation

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53
Q

What are the Ix for CKD 3

A
  1. FBC (CKD= kidnyes produce less EPO= less RBC made= anaemia) and U&Es
  2. Urinalysis - haematuria, proteinuria, glycosuria, albumin: creatine ratio
  3. Renal ultrasound: shows bilateral small atrophied kidneys
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54
Q

treatment for CKD 4
(what is the aim of treatment, example, when to refer and last resort treatment)

A

Irreversible so treat to prevent progression of disease and symptom control:

eg Oedema - fluid and sodium restriction furosemide

Referral to nephrology if eGFR < 30 (stage 4) or A:CR>70
last resort- renal replacement therapy

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55
Q

what is gout’s pathophysiology 3

A
  1. uric acid build up
  2. leads to monosodium urate monohydrate crystal deposition along joints
  3. =joints symtoms in gout
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56
Q

risk factors for gout 2

A
  1. purine rich food: high meat, seafood, alcohol diet
  2. middle aged overweight man
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57
Q

What are the medicines that increase risk of gout

A
  1. low dose aspirin eg 75mg
  2. thiazide like diuretics
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58
Q

presentation of gout 2 and what joint is usually affected 1

A
  1. sudden onset
  2. painful swollen red joint
  3. usually big toe (metatarsophalangeal joint)
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59
Q

investigations for gout 2 and result

A
  1. joint aspiration and polorised light microscopy showed needle shaped negatively birefringent crystals
  2. bloods: high uric acid
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60
Q

treatment for acute gout 3

A

1st line NSAIDs eg diclonefac PLUS PPI
2nd line colchicine (alternative to NSAIDs for patients on anticoagulants)
3rd line IM corticosteroid injection

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61
Q

prophylactic treatment for gout 2

A
  1. allopurinol
  2. lifestyle changes: decrease meat, seafood and alcohol
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62
Q

how does allopurinol prevent gout 2

A

it is a xanthine oxidase inhibitor which reduces uric acid production

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63
Q

what is the crystal composition for gout and pseudogout?

A

gout= monosodium urate monohydrate crystals
pseudogout= calcium pyrophosphate crystals

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64
Q

What is pseudogout

A

calcium pyrophosphate crystals deposits along joint capsule

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65
Q

risk factors for pseudogout 3

A
  1. hypercalcaemia
  2. hyperparathyroidism
  3. hyperthyroidism
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66
Q

investigations for pseudogout 3

A
  1. joint aspiration and polarised light microscopy shows positively birefringent, rhomboid shaped crystals
  2. bloods show high calcium
  3. joint x-ray to differentiate from rheumatoid/ osteoathritis
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67
Q

presentation of pseudogout 2

A
  1. swollen red hot joint
  2. multiple widespread joints affected (MC is the knee)
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68
Q

treatment for pseudogout 2

A
  1. same acute management as gout- NSAIDs, colchicine and corticosteroids
  2. joint aspiration in severe cases
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69
Q

What is the prophylactic treatment for pseudogout 1

A

daily low dose colchicine if no SE

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70
Q

what type of disease is type 1 diabetes mellitus, what does it cause destruction of and what is the consequence of this (3)

A

autoimmune disease
causes destruction of beta cells in pancreas
causes absolute insulin deficiency

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71
Q

what type of reaction is T1DM

A

type 4 hypersensitivity

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72
Q

what are the causes of T1DM 2

A

combination of genetics and environmental triggers

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73
Q

what are the consequences of the body not making insulin in T1DM (4 steps), start with body being unable to produce insulin to digest carbohydrates

A
  1. cells cannot take in glucose so the body thinks it is being fasted
  2. gluconeogenesis occurs in liver
  3. causing more hyperglycaemia
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74
Q

when does T1DM usually manifest and what does it present in the form of

A

in childhood
diabetes ketoacidosis

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75
Q

what are 5 symptoms of T1DM

A

polyuria, polydipsia, lethargy, thursh, sudden weight loss

(thirst, toilet, tired, thrush, weight loss)

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76
Q

explain polyuria in diabetes 1 reason only

explain polydipsia in diabetes

A

glucose excretion in urine draws water with it because glucose is osmotically active

extreme thirst due to fluid loss via urine

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77
Q

explain sudden weight loss in T1DM

A

due to breakdown of adipose and muscle tissue as an alternative energy source to glucose

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78
Q

Explain recurrent thrush in diabetics

A

due to high sugar levels which is an optimal environment for candida

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79
Q

what is the max reabsorption value for glucose in the kidneys

A

10mmol/L

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80
Q

what is required for a diagnosis of T1DM 2

A

one abnormal glucose value and symptoms or two abnormal glucose values in asymptomatic

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81
Q

what is fasting glucose value determines diabetes mellitus and units

A

> =7mmol/L

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82
Q

what is fasting glucose value determines pre diabetes and units

A

> 6mmol/L

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83
Q

what HbA1c value determines diabetes mellitus and units

A

> =48mmol/mol

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84
Q

what HbA1c value determines pre diabetes and units

A

> 41mmol/mol

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85
Q

what is the gold standard investigation test for diabetes mellitus

A

HbA1c test

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86
Q

what random glucose value/ glucose tolerance test value determines diabetes mellitus and units

A

> =11.1mmol/L

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87
Q

what is the GS treatment for T1DM (2)

A

combination of long lasting 12-24 hour basal insulin dose and a short acting bolus injected 30 mins before meals

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88
Q

what is vital for treating T1DM patients 2

A

patient education- to monitor dietary glucose intake
TREATMENT IS LIFELONG

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89
Q

what can diabetic ketoacidosis be classed as

A

a life threatening medical emergency

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90
Q

explain the pathophysiology of DKA starting with insulin deficiency

A

glucose not able to be absorbed
alternative sources of energy is to break down free fatty acids from adipose tissue
this is oxidised to acetyl coA to produce ketones
ketones are acidic and cause blood acidosis

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91
Q

what is the compensation for DKA and what is this due to/ countering

A

respiratory compensation
due to metabolic acidosis

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92
Q

symptoms of DKA (3)
signs of DKA (2)

A

nausea, vomiting, dehydration, acetone-smelling breath, Kaussmal’s breathing

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93
Q

what 3 things are required for a DKA diagnosis (not specific values)

A
  1. symptoms
  2. hyperglycaemia
  3. blood gas sample showing metabolic acidosis with respiratory compensation
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94
Q

what value dictates acidosis in the blood

A

pH <7.3

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95
Q

what test can be done to identify ketone levels and what value is DKA

A

blood ketone test
>3mmol/L

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96
Q

what is treatment for DKA (4 steps)

A
  1. ABC
  2. 0.9% NaCl infusion
  3. give insulin and glucose simultaneously
  4. correct hypokalaemia if this occurs
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97
Q

what are the three complications of DKA treatment

A
  1. cerebral oedema
  2. hypokalaemia (insulin treatment for DKA causes intracellular shift of K+ which can cause muscle weakness)
  3. hypoglycaemia (insulin treatment can cause glucose levels to drop rapidly into hypoglycaemia)
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98
Q

Name 4 non modifiable and 4 modifiable risk factors for T2DM

A

Non: age, family history, male, ethnicity

modifiable: obesity, hypertension, sedentary lifestyle, high carb diet

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99
Q

what is T2DM’s insulin deficiency and how does T2 cause hyperglycaemia

A

relative insulin deficiency
insulin resistance in liver and muscle cells causes hyperglycaemia

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100
Q

what are the diagnosis and investigations for T2DM

A

exactly the same as T1DM

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101
Q

explain the pathophysiology of T2DM starting with hyperglycaemia, including the role of the pancreas

A

hyperglycaemia causes increased insulin resistance in cells
pancreas compensates by producing large volumes of insulin but is damaged by overworking and toxic glucose levels

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102
Q

what are the 4 lines of treatment for T2DM (1,1,4,1)

A

1st: lifestyle modifications eg lose weight
2nd: metformin
3rd: add sulfonylurea, PIOGLITAZONE, DPP-4 inhibitor or SGLT-2 inhibitor
4th: insulin

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103
Q

What is the second line medication for T2DM after metformin

A

ifno co-morbidiites= solfonylurea-gliciazide
if CV co-morbidiity= SGLT2- dapagloflozin as it is cardioprotective

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104
Q

how does the SGLT2 inhibitor work? and name examples

A

inhibits reabsorption of glucose in the proximal tubule via the sodium-glucose transporter, resulting in more glucose to be excreted eg empagliflozen/ dapagliflozen

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105
Q

how does the DPP4 inhibitor work? and name an example

A

DPP4 inhibitor blocks DPP4 enzyme which prevents inhibition of GLP1. Overall effect= increased insulin production in response to a meal being sensed by the body (eg chewing) eg sitagliptin

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106
Q

how do sulfonylureas work and give an example

A

sulfonylurea binds to bind to K+ channels on beta pancreatic cells, reducing K+ efflux which causes depolarisation of the cell. There is a Ca2+ influx due to the action potential which stimulates insulin release from vesicles in the cell eg Gliciazide

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107
Q

how does metformin work

A

inhibits the AMPK enzyme in the liver which inhibits gluconeogensis, decreases intestinal glucose absorption and increases insulin sensitivity

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108
Q

what are the 3 microvascular complications of DM

A

retinopathy
peripheral neuropathy
nephropathy

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109
Q

what are the 4 macrovascular complications of DM

A

stroke
hypertension
peripheral artery disease
coronary artery disease

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110
Q

explain retinopathy associated with diabetes and what can this lead to

A

high blood pressure and glucose levels damages retina= blindness/ cotton wool spots

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111
Q

explain peripheral neuropathy associated with diabetes and what can this lead to

A

high glucose levels damage blood vessels supplying nerves= pain/ numbness

can lead to HTN as more likely to get atherosclerosis which can narrow blood vessels and cause hypertension

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112
Q

explain coronary artery disease associated with diabetic hypertension

A

hypertension caused by diabetes causes increased force exerted on artery walls which can damage them= atherosclerosis and embolism

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113
Q

what can hyperosmolar hyperglycaemic state be classed as and who typically presents with hyperosmolar hyperglycaemic state 2

A

a life threatening medical emergency
elderly with T2DM

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114
Q

explain the pathophysiology of hyperosmolar hyperglycaemic state starting with hyperglycaemia and ending with what this does to the blood

A

hyperglycaemia causes osmotic diuresis and the volume depletion in the body increases the serum osmolarity causing hyperviscosity of blood

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115
Q

how can you diagnose hyperosmolar hyperglycaemic state (3)

A
  1. severe hyperglycaemia (>30mmol/L)
  2. hyperosmolarity (>320mosmol/kg)
  3. no acidosis or ketosis
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116
Q

what is the presentation of hyperosmolar hyperglycaemic state (6) 2 signs and 3 symptoms

A

nausea, vomiting, dehydration, HYPOTENSION, TACHYCARDIA

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117
Q

what is osmotic diuresis and how does it cause electrolyte imbalances

A

increased urination in response to hyperglycaemia: excreted glucose in urine takes water with it so sodium and potassium follow the water and are excreted in the urine

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118
Q

what are the 3 haematological complications of hyperviscosity of blood and what condition does this occur in

A

MI, stroke, peripheral arterial thrombosis
hyperosmolar hyperglycaemic state

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119
Q

what is the treatment for hyperosmolar hyperglycaemic state (4)

A
  1. fluid replacement with saline
  2. venous thromboembolism prophylaxis eg LWMH like enoxaparin
  3. give insulin if glucose levels do not decrease
  4. give K+ if K+ levels aren’t naturally corrected
    SLIK
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120
Q

what are the two complications related to treatment of hyperosmolar hyperglycaemic state

A
  1. insulin related hypoglycaemia (due to excessive high-dose insulin therapy)
  2. treatment related hypokalaemia (due to high-dose insulin therapy)
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121
Q

what is fibromyalgia and two risk factors

A

chronic widespread MSK pain for 3+ months
1. females
2. stress

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122
Q

presentation of fibromyalgia 3

A

widespread pain
fatigue
sleep difficulties

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123
Q

investigations of fibromyalgia 2 and how is it diagnosed

A

pain or tenderness in 11 or more out of 18 sites palpated
bloods for exclusion: FBC, UE, LFT, TSH, CRP, calcium, glucose, B12 folate, urine dip (all normal in fibromyalgia)

Diagnosis criteria:
1. more than 3 months
2. generalised pain
3. fibromyalgia pain of 12+/31 (consists of widespread pain index and symptom severity score)

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124
Q

treatment for fibromyalgia 2

A
  1. encourage exercise, CBT
  2. tricyclic antidepressants for severe pain
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125
Q

what is GORD and what does it stand for
what causes the reflux

A

LOS relaxation causes reflux of gastric contents into the oesophagus

Gastro-Oesophageal Reflux Disease

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126
Q

risk factors for GORD 3 and which sex is more likely to get this by how much and why

A
  1. increased abdo pressure eg obesity & pregnancy
  2. Sliding Hiatus hernia (LOS slides up into chest)
  3. LOS relaxants: Caffeine Alcohol

Males x2 risk than females (eostrogen is protective)

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127
Q

signs and symptoms 2 of GORD including 3 red flags and 3 extra-oesophageal signs GORD

A
  1. Heartburn (main symptom) which is exacerbated when lying down as reflux more easily occurs
  2. Dyspepsia (indigestion)
  3. Extra-oseophageal signs: cough, asthma, dental erosion (due to acid eroding teeth)
  4. Red flags: dysphagia, weight loss, haematemesis
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128
Q

investigations for GORD 2

A
  1. GS and diagnostic: 24 hour pH monitoring (abnormal if pH <4 more than 4% of the time)
  2. Endoscopy to look for Barrett’s, especially in those with chronic heartburn symptoms
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129
Q

treatment for GORD 2

A

1st line: PPI
Lifestyle changes: smaller meals, avoid food from 3 hours before bed

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130
Q

1 complication for GORD and show the disease pathway

A

Gastric adenocarcinoma
GORD-> barretts-> oesophageal adenocarcinoma

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131
Q

what is barretts oesophagus and where does this occur, Ix 1 and Mx 2

A

Metaplasia from stratified squamous to simple columnar epithelium (has to occur within 1cm of the gastro-oesophageal junction)

Ix: Endoscopy with biopsy which should show metaplasia within 1cm of the GOJ

Tx: PPI + regular endoscopic surveillance

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132
Q

what is diverticular disease and where do they usually form

A

multiple outpouches of the colon wall with symptom

sigmoid colon

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133
Q

explain the pathophysiology of diverticulitis 2 steps

A
  1. high pressure in colon/ weak wall= diverticula formed
  2. inflammation if bacteria/ faecal matter gathers in diverticula
    (diverticular disease with infection)
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134
Q

signs and symptoms of diverticular disease 3

A

divertiCuLaR
constipation, lower left quadrant pain, rectal bleeding (haematochezia)

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135
Q

investigation for diverticular disease (GS)

A

CT abdomen and pelvis with contract GS

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136
Q

treatment for diverticular disease (2, GS)

A

bulk forming laxative eg isphagula husk and antibiotics (if signs of infection)
GS= surgery

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137
Q

what value is defined to be hypertension and define malignant HTN and value

A

140/90+

very high blood pressure that develops quickly and causes organ damage
180/110+

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138
Q

what are the categories of hypertension and how many cases are in each category and describe the difference between the two

A

primary 90%
secondary 10%
primary has no known cause and secondary has known causes

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139
Q

what are the causes of secondary hypertension (6)
3 Cs, 2Ps, 1R

A

renal disease (MC)
pregnancy
phaechromocytoma
cushings
conns
coarctation of the aorta (congenital narrowing of the aorta)

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140
Q

what are the 4 main areas that malignant hypertension has symptoms in and how can this be assessed

A

brain (cerebral oedema, stroke), eye (papilloedema/ cotton wool spots), heart (HF, MI) and kidneys (AKI)

fundoscopy= for papilloedema
urinalysis= for renal function
Echo/ECG= assesses left ventricular hypertrophy

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141
Q

if the bp is measured at GP and is 140/90 then what is the next step

A

check ambulatory blood pressure at home

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142
Q

how is hypertension staged and what are the actions for each stage (3)

A

stage 1: 135/85 (assess risks- including assessing organ damage)
stage 2: 150/95 (lifestyle changes + medications)
stage 3: 180/110 (malignant- same day admission and start antihypertensive medication ASAP)

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143
Q

what is the treatment approach for stage 1 hypertension 1

A

BP monitored every 5 years

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144
Q

what two things are offered to a person who has been diagnosed with hypertension

A

assessment of Cv risk
investigation for secondary hypertension

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145
Q

what is the treatment for under 55s and not of African/ Caribbean origin (2)

A

ace inhibitor or angiotensin receptor blocker

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146
Q

what is the treatment for over 55s and of African/ Caribbean origin (1)

A

calcium channel blocker

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147
Q

what is the 2nd step if one drug is not controlling hypertension for the two categories of people to treat

A

<55 not A/C origin= CCB or thiazide like diuretic eg indapamide can be added
>55 of A/C origin= ACEi or ARB or thiazide like diuretic eg indapamide can be added

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148
Q

if a patient is on ACEi and CCB and indapamide already but still symptomatic what should be given to them 1 (and normal potassium levels)

A

low dose spironolactone

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149
Q

what is a side effect of ACEi and what can be given instead

A

dry long term cough
ARB- losartan

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150
Q

give an example of an ARB, ACEI, beta blocker, calcium channel blocker

A

losartan, ramipril, bisoprolol, amlodipine

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151
Q

what is ACEi contradicted in 3

A

asthma and pregnancy and renal stenosis

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152
Q

side effect of beta blockers 1 and what can this cause 1

A

postural hypotension which cause cause loss of consciousness

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153
Q

SE of CCB

A

ankle swelling

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154
Q

what is the first line medication for diabetics with hypertension

A

ACEi

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155
Q

what happens when hypertension persists even when multiple medications are prescribed (2)

A
  1. talk about adherence
  2. add a beta blocker (potassium above 4.5) or spironolactone (potassium below 4.5)
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156
Q

what are haemorrhoids

A

enlarged veins around anus

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157
Q

3 causes of haemorrhoids and main cause

A

MC: constipation
obesity
pregnancy

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158
Q

What are the two types of haemorrhoid

A

External
originate below the dentate line
prone to thrombosis, may be painful

Internal
originate above the dentate line
do not generally cause pain

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159
Q

grades of haemorrhoids 4

A
  1. No prolapse
  2. Prolapse when straining and return on relaxation
  3. Prolapse when straining and can be manually pushed back in
  4. Prolapse permanently
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160
Q

signs and symptoms of haemorrhoids 2

A

painless haematachezia (fresh bleeding from rectum)
Puritis anus

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161
Q

What is the mx of haemorrhoids 3, 2

A

symptom mx:
1. high fibre diet and high fluid intake
2. bulk forming laxatives (isphagula husk)
3. topical treatment eg hydrocortisone cream (anusol)

escalation:
1. rubber band ligation (outpt tx) for internal only
2. haemorrhoidectomy (for large symptomatic haemorrhoids that do not respond to outpt tx)

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162
Q

what are rolling hiatal hernias

A

where the lower gastro-osophageal junction remains the the abdomen but a bulge of stomach (typically fundus) herniates up into the chest via the oesophageal hiatus

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163
Q

what is a hiatal hernia and what r the two types of hiatal hernias and which is MC

A

stomach hernia through diaphragm aperture

sliding (MC) and rolling

164
Q

what r sliding hiatal hernias and what is a consequence of this

A

where the lower gastro-osophageal junction slides up into the chest, above the diaphragm

acid reflux

165
Q

investigations for hiatal hernia

A

barium swallow + x-ray for diagnosis

166
Q

Mx for hiatal hernia 3

A
  1. conservatives: encourage weight loss, treat heartburn with gaviscon
  2. PPI
  3. laproscopic hiatal hernia repair
167
Q

what is hypothyroidism and what does is generally cause

A

thyroid hormone deficiency
generalised slowing of processes

168
Q

what are the two types of hypothyroidism and how do they each cause hypothyroidism

A

primary- issue with thryoid gland, lack of T3/4 (one i in thyroid= 1)
secondary- issue with pituitary, lack of TSH (two i in pituitary= 2)

169
Q

what are the causes of primary hypothyroidism (4) and secondary (1)

A

Hashimotos thyroiditis, De Quervain’s thyroiditis, dietary iodine deficiency, carbimazole

pituitary adenoma

170
Q

6 symptoms of hypothyroidism

A

weight gain, lethargy, cold intolernace, loss of lateral aspect of eyebrow, constipation, fluid retention

171
Q

what three diseases are associated with hypothyrodism

A

downs and turners syndrome and coeliac disease (DOWN the stairs, TURN the corner and you’ll SEE it)

172
Q

what are the investigations for hypothyroidism (3)

A

1st line: thyroid function test
2. antithyroid peroxidase antibody levels for autoimmune causes
3. fasting blood glucose in patients with non-specific fatigue and weight gain due to association with T1DM

173
Q

what are the thyroid function test results for primary and secondary hypothyroidism

A

primary: low T3, high TSH
secondary: low T3, low TSH

174
Q

treatment for hypothyroidism and how does this work

A

levothyroxine
synthetic T4

175
Q

what is hashimotos thyroiditis, what does it lead to and what type of hypothyroidism does it cause

A

thyroid gland is attacked by immune system via antithyroid antibodies and leads to loss of function

primary hypothyroidism

176
Q

what is the presentation of hashimotos like 2 and what does this progress to

A

same as hypothyroidism
plus goitre of thyroid gland which progresses to atrophy

177
Q

what is the gold standard investigation for hashimotos

A

antithyroid peroxidase antibodies test should be positive (anti-TPO)

178
Q

What are the two strain of herpes simplex virus that affects humans, how does each spread and what is particular to note about herpes virus?

A

HSV-1, HSV-2
1= orally (more likely to be responsible for cold sores)
2= sexual contact (more likely to be responsible for genital ulceration)
can be latent and reinfect body

179
Q

What are the features of HSV infection.

A
  1. cold sores
  2. painful genital ulceration (can happen repeatedly but first is worst)
  3. severe gingivostomatitis
180
Q

What is the ix for a HSV genital ulcer

A

swab + NAAT test

181
Q

What is the mx for herpes simplex virus?

A
  1. for gingivostomatitis: oral aciclovir, chlorhexidine mouthwash
  2. for cold sores: topical aciclovir
  3. for genital herpes: oral aciclovir, especially if multiple episodes
182
Q

What is the appearance of HSV on a pap smear? 3

A

3 Ms
Multinucleated giant cells
Margination of the chromatin
Molding of the nuclei

183
Q

What is the cause and acute infection location of gonorrhoea

A

Gram-negative diplococcus Neisseria gonorrhoeae
on any mucous membrane surface, typically genitourinary but also rectum and pharynx

184
Q

Features of gonorrhoea

A

males: urethral discharge, dysuria
females: cervicitis e.g. leading to vaginal discharge
rectal and pharyngeal infection is usually asymptomatic

185
Q

Why can we not immunise or prevent reinfections of gonorrhoea

A

due to antigen variation of type IV pili (proteins which adhere to surfaces) and Opa proteins (surface proteins which bind to receptors on immune cells)

186
Q

What is the Mx of gonorrhoea

A

1st line single dose 1g ceftrioxone IM

187
Q

What is Blepharitis, features, progression and mx

A

inflammation of the eyelid margins with lots of crusting at the base of eyelids
features: dry and itchy eyes
this can lead to styes and chalazions
mx: warm compresses and gentle cleaning of eyelid margins

188
Q

What are styes, pathophys and mx

A

infection of sweat glands on eyelid, mc staph aureas
mx: warm compresses and analgesia, chloramphenicol if conjunctivitis sx/ persist

189
Q

What is a chalazion and difference to styes. Mx

A

blocked and swollen meibomian gland
typically on inside of eyelid
mx: warm compresses and gentle massaging towards eyelashes

190
Q

What is entropian and mx

A

when eyelid turns inwards, causing lashes to press against the eye
Mx: taping eyelid down, lubricating eye drops and surgical resolvement

191
Q

What is Ectropion

A

when the eyelid turns outwards, exposing the conjunctiva and means the eyeball is not adequately lubricated and protected

192
Q

What is the mx for any benign eyelid disorders that cause a risk to sight

A

same-day referral to ophthalmology

193
Q

What is thrichiasis and Mx

A

inward growth of eyelashes which causes corneal damage and ulceration
mX; remove affected eyelashes

194
Q

What is periorbital cellulitis, features and mx

A

infection in front of the orbital septum (in front of the eye)
features: swollen, red, hot skin around the eyelid and eye
Mx: urgent referral to opthamology, CT to distinguish from orbital cellulitis, systemic oral abx

195
Q

What is orbital cellulitis

A

infection of tissues behind the orbital septum
features: pain with eye movement, reduced eye movements, vision changes, abnormal pupil reactions, and proptosis (bulging forward of the eyeball)
Mx: emergency opthamology admission, IV abx
LIFE THREATENING

196
Q

What is atrophic vaginitis, who does it affect 1, features, tx 3

A

atrophy (thinning, drying and inflammation of vaginal walls)
post-menopausal women
vaginal dryness, dyspareunia and occasional spotting
Tx: vaginal lubricants and moisturisers, if these do not help then topical oestrogen cream can be used

197
Q

define IBS 3

A

Chronic functional bowel disorder characterised by abdominal pain and change in bowel habits

198
Q

3 risk factors for IBS

A

Stress/ anxiety
Female
Younger age (peak at 20-30 year olds)

199
Q

5 investigations for IBS and what is the general investigation aim for IBS

A

Exclude coeliacs with serology (anti-tTG or anti-EMA)
Exclude IBD with faecal calprotectin
Exclude infections with ESR/CRP/ blood cultures
Exclude colorectal cancer with FIT test
Exclude hyperthyroidism with tfts

Process of exclusion of other conditions

200
Q

diagnosis checklist for IBS 3

A

Diagnosis checklist=
1. recurrent abdominal pain for at least 1 day weekly for past 3 months
2. symptoms from 6 months ago
3. one of the following
-Symptoms relieved by defecation
-Change in bowel appearance
-Change in bowel frequency

201
Q

conservative treatment for IBS 2

A

Reassure patient
Advise to avoid trigger foods eg caffeine/ alcohol and short chain carbohydrate

202
Q

mild treatment of IBS 2

A

Anti mobility eg Loperamide for diarrhoea
Laxatives eg Senna for constipation

203
Q

severe treatment of IBS 3

A

Tricyclic antidepressants eg amitriptyline
CBT
GI referral

204
Q

what is osteoarthritis 1 and what happens 1

A

degenerative disease of joint due to mechanical erosion of the cartilage in the joint

205
Q

symptoms of osteoarthritis 2

A
  1. painful joints (typically high usage joints- worse towards end of day/ after usage)
  2. morning stiffness for less than 30 mins
206
Q

state and explain two clinical signs of osteoarthritis

A

Bouchards nodes (bony growths on PIP joints= proximal)
Heberdens nodes (bony growths on DIP joints=distal)

207
Q

2 investigations into osteoarthritis and results

A

bloods= normal
x-ray of joint (LOSS- loss of joint space, osteophytes (bony growths on joints), subchondral sclerosis (increased density bone along joint line), subchondral cysts (fluid filled holes in bone)

208
Q

what is the treatment of osteoarthritis 3

A

lifestyle changes: physio, weight bearing
pain relief: NSAIDs
last resort: joint replacement

209
Q

what is rheumatoid arthritis and what happens

A

inflammatory disease
autoimmune destruction of synovium (soft tissue of the joints)

210
Q

compare the symmetry and number of joints affected for rheumatoid arthritis and osteoarthritis

A

osteoarthritis= asymmetrical, affects few joints
rheumatoid= symmetrical, affects many joints

211
Q

risk factors of rheumatoid arthritis 2

A

HLADR4/1
women

212
Q

symptoms of rheumatoid arthritis 2 and clinical signs of RA 4

A

painful swollen joints
morning stiffness lasting more than 30 mins

rheumatoid skin nodules
boutinniere deformity
swan neck thumb
ulnar deviation

213
Q

treatment for R arthritis 3

A
  1. Disease modifying anti rheumatic drugs- methotrexate/ hydroxychloroquine/ sulfsalazine
  2. analgesia- NSAIDs/ steroid injections
  3. biologics
    -> 1st line: TNF alpha inhibitor infliximab (given with methotrexate)
    -> 2nd line: B cell inhibitor (CD20 target)- rituximab
    RADAB
214
Q

What is a differential for fibromyalgia

A

polymalgia rheumatica

215
Q

investigations for R arthritis 4 and results

A
  1. bloods: high ESR/CRP
  2. serology: positive rheumatoid factor, positive anti-CCP antibodies
  3. genetic test for HLA DR1/4
  4. X-ray (LESS- lost joint spaces, bony erosion, soft tissue swelling, periarticular osteopenia)
216
Q

compare polymyalgia rheumatica anad fibromyalgia 3

A

fibromyalgia at any age but PR over 50 Y/O
PR= concentrates pain in shoulder and hips, onsest over a few days with joint stiffness
PR resolves within 2 years, fibromyalgia is chronic and lifelong

217
Q

What is syphillis and cause

A

STI
caused by the gram negative bacteria Treponema pallidum

218
Q

What is the disease progression for syphyilis

A

primary stage:
chancre (painless ulcer at site of sexual contact/ where direct contact occured)

secondary stage: 1 week after primary
> systemic symptoms: fevers, lymphadenopathy
> non itchy maculopapular rash on trunk, palms and soles
> buccal ‘snail track’ ulcers (30%)
> condyloma lata (painless, white lesions on the genitalia)

tertiary features: type 4 hypersensitivity reaction (severe immune response) and organ damage
> gummas (granulomatous lesions formed from WBC)
> ascending aortic aneurysms due to aortitis
> weakness and paralysis and loss of sensation (T. pallidum affects anterior spinal cord)
> tabes dorsalis (T.pallidum damages dorsal column-medial lemniscus nerve pathway= loss of vibration and proprioception)
> Argyll-Robertson pupil (pupil loses light reflex but does have accomodation reflex)

219
Q

Explain the latent stage of syphillis

A

Latent phase happens after secondary phase of syphillis infection (basically an asymptomatic stage)

early latent phase: within a year of infection- T. pallidum mostly found in capillaries of organs/ tissues finds its way back into bloodstream= secondary symptoms again

late latent phase: after a year of infection- T. pallidum stays in capillaries of organs/ tissues finds its way back into bloodstream

220
Q

What are the Ix for syphilis 3

A
  1. Dark-field microscopy from swab of chancre/ secondary lesions (+ is presence of T. pallidum)
  2. serology testing: treponemal eg florescent treponemal antibody (more specific and sensitive so used for diagnosis) and non-treponemal tests eg Rapid Plama Reagin blood test (screening and monitoring tx response)
  3. CSF examination: Should be considered in tertiary syphilis to evaluate for CNS involvement.
221
Q

Explain serology test results for syphilis 4 and action for 1

A

both positive= active/ recent syphilis infection

Positive non-treponemal test + negative treponemal test= no syphilis, false positive due to other causes eg SLE/ pregnancy

Negative non-treponemal test + positive treponemal test = primary/ latent syphillis/ previously having treated or untreated syphilis

both negative= no syphilis or incubating syphilis (should repeat after 3 months, as syphilis has an incubating time period of 3 months)

222
Q

What is the mx for syphilis 5

A
  1. 1st line IM benzathine penicillin once confirmed
  2. needs referral to GUM, with follow up at 3,6, and 12 months
  3. if CI then doxycycline (14 days if early syphillis, 28 dys if late)
  4. should monitor nentroponemal titres to assess response (fourfold decline in titres seen as an adequate response to treatment)
  5. avoid sex until fully treated

IBANG (ive been a nasty girl)
(C)I then doxycycline- 14 for early, 28 dys for late
benpen IM injection once + results
avoid sex until fully treated
Non treponemal titres to assess response (fourfold decline in titres= adequete response)
GUM referral with 3,6,12 month follow up

223
Q

What is a SE of syphilis mx and mx of this

A

Jarisch- Herxheimer reaction:
fever, rash and tachycardia several hours after treatment
no treatment apart from antipyretics

224
Q

What are the causes of otitis externa and features

A

causes: recent swimming, staph aureaus, p.aerginosa, dermatitis
features: ear pain, itch, discharge

225
Q

Mx of otitis externa 3

A
  1. topical antimicrobial (acetic acid) plus with steroid (eg ciprofloxacin and dexamethasone combined-otomize spray)
  2. oral flucox if cellulitis expanding past ear or immunocompromised/ diabetes
  3. refer to ENT if do not respond to topical abx
226
Q

What is Trichomonas vaginalis and cause

A

STI
caused by Trichomonas vaginalis: a highly motile, flagellated protozoan parasite

227
Q

What are the features of Trichomonas vaginalis 5

A
  1. vaginal discharge: offensive, yellow/green, frothy
  2. vulvovaginitis
  3. strawberry cervix
  4. pH > 4.5
  5. in men is usually asymptomatic but may cause urethritis

4 Vs (1-4)

228
Q

What is the Ix for Trichomonas vaginalis 2

A

NAAT swab (same as chlamydia + g)
microscopy of a wet mount shows motile trophozoites

229
Q

What is the mx of microscopy of Trichomonas vaginalis 1

A

oral metronidazole 5-7 days

230
Q

What is Sinusitis

A

inflammatory disorder of paranasal sinuses and linings of the nasal passages

231
Q

What are the features of sinusitis 4

A
  1. facial pain: typically frontal pressure pain which is worse on bending forward
  2. nasal discharge: usually clear if allergic or vasomotor. Thicker, purulent discharge suggests secondary infection
  3. nasal obstruction: e.g. ‘mouth breathing’
  4. post-nasal drip: may produce chronic cough
232
Q

What are the red flags for sinitis 3 and action for these

A

unilateral symptoms
persistent symptoms despite compliance with 3 months of treatment
epistaxis
referral to ENT

233
Q

How is acute and chronic sinusitis managed 2 and what is the timeline for this

A

acute: supportive as it is self limiting, NICE avoids antibiotics

chronic: 3+ months

  1. intranasal corticosteroids
  2. nasal irrigation with saline solution
234
Q

risk factors for prostate cancer 4

A

genetic BRCA1/2 and HOXB13 and lynch syndrome
elderly
family history
A/C origin

235
Q

what is prostate cancer

A

proliferation of outer peripheral zone of prostate (adenocarcinoma)

236
Q

presentation of prostate cancer 2

A

LUTS like BPH (voiding and storage issues) but with systemic cancer symptoms eg weight loss, fatigue, night pain and bone pain

237
Q

investigations for prostate cancer 3

A

DRE is hard and irregular
PSA in community
multiparametric MRI-influenced prostate biopsy

238
Q

where does prostate cancer typically metastasise to and what is the effect of this

A

typically metastasises to bone= sclerotic lesions, typical lumbar back pain
also metastasises to liver, lung and brain

239
Q

what determines if multiparametric MRI is offered to someone with suspected prostate cancer?

A

If the Likert scale is >=3 a multiparametric MRI-influenced prostate biopsy is offered

If the Likert scale is 1-2 then NICE recommend discussing with the patient the pros and cons of having a biopsy.

240
Q

3 treatment approaches for prostate cancer

A

radical prostatectomy
radiotherapy
hormone therapy: only for T3/T4 and metastatic malignancy

241
Q

explain hormone therapy treatment for prostate cancer (example name, how does it work and 2 side effects)

A

GnRH agonist eg goserelin
increases LH and FSH but results in suppression of HPG axis= less testosterone
side effects= libido loss, erectile dysfunction

242
Q

What is vasovagal syncope and fully explain a vasovagal syncopal episode

A

transient loss of consciousness due to global cerebral hypoperfusion with rapid onset, short duration and spontaneous recovery trigerred by emotion, pain or stress

EPISODE:
prodrome: lightheadedness, visual disturbances, muffled hearing, nausea, pallor

event: loss of postural tone and consciousness up to a minute

recovery: may show signs of confusion, weakness and can recollect prodromal period but has amnesia for actual syncopal event

243
Q

What are the ix for vasovagal syncope

A
  1. BP readings: fall BP >20 mmHg is diagnostic for postural hypotension
  2. ECG
244
Q

What are the other types of syncope apart from vasovagal and explain each

A

REFLEX SYNCOPE: carotid sinus + vasovagal + situational
situational: specifically associated with certain situations eg coughing, defecation, post-exercise

carotid sinus: hypersensitivity of carotid sinus baroreceptors which stimulate bradycardia/ vasodilation when stimulated eg turning head/ tight collars. Mostly affects elderly

OTHER SYNCOPE TYPES:
orthostatic: due to postural BP drop eg Parkinsons and Lewy body (nervous system unable to regulate BP changes well), diarrhoea/ diuretics/ vasodilators (volume deplation)

cardiac: bradycardias and arrythmias

245
Q

What is lyme disease caused by and how does it spread?

A

caused by the spirochaete Borrelia burgdorferi and is spread by ticks

246
Q

How does lyme disease present?

A
  1. early features within 30 days
    - ‘bulls-eye’ rash is typically at the site of the tick bite which slowly increases in size
    -systemic features eg lethargy and fever
  2. later features after 30 days
    - myocarditis/ heart block (CV)
    - facial nerve palsy, radicular pain, meningitis (Neuro)
247
Q

What is the mx of lyme disease 3

A
  1. if asymptomatic tick bite just ensure you remove tick if still present with tweezers and wash area thoroughly after. no other tx
  2. suspected/ confirmed lyme disease- doxycycline if early disease and ceftrioxone if disseminated disease
248
Q

What are the Ix for lyme disease

A

1st line ELISA for Borrelia burgdorferi
if negative, repeat after 1 month
if positive, do a immunoblot test for lyme disease

249
Q

What is infectious mononucleosis caused by and what is its alternative name

A

Epstein-Barr virus
glandular fever

250
Q

What are the features of infectious mononucleosis 7

A

triade: pharyngitis (with exudative tonsils), lymphadenopathy, sore throat
other: palatal petechiae, maculopapular pruritic rash when being treated with amoxicillin/ penicillins (although this is not part of mx when it is known to be infectious mono, hepatitis (high ALT)

LISTENING TO PEALSH FM
pharyngitis (struggling to swallow)
Exudate on tonsils
antibiotics cause MP rash
Lymphadenopathy (cervical)
Sore throat
Hepatitis (high ALT)

FBC (haemolytic anaemia)
Monospot test (2 weeks in)

if pt treated for tonsillitis with abs and gets a rash, then its infectious mononucleosis

251
Q

How is infectious mononucleosis dx 3

A

NICE guidelines suggest FBC (can show haemolytic anaemia) and Monospot test in the 2nd week of the illness to confirm a diagnosis of glandular fever, otherwise clinical

252
Q

What is the mx for infectious mononucleosis 2

A
  1. rest, analgesia, drink fluids
  2. avoid contact sports for 4 weeks after symptoms to reduce risk of splenic rupture
253
Q

What is folliculitis

A

infection from a single hair follicle, causing pustule/ papule formation (pimples) which can form anywhere on the body except for hands and feet

254
Q

Causes of folliculitis 4

A

bacterial: staph aureus MC or hot tub folliculitis (caused by pseudo. aeruginosa) or any gram neg bacteria after a long course of abx (eg after acne tx)
yeast: malassezia (yeast from skins normal flora infecting hair follicles)

255
Q

What is the mx of folliculitis 2

A
  1. topical antimicrobial (benzyl peroxide) + antibacterial soaps (Hibiscrub)
  2. Oral antibiotics (trimethoprim for gram neg due to long term abx use for acne mx) may also be required in more severe cases or cases that don’t respond to topical treatments
256
Q

What is another name for atopic dermatitis and features

A

eczema
pruritic, dry, erythemous patches on skin, in a typical distribution pattern in fleuxural areas (inner elbows, behind knees, armpits)

257
Q

What can cause exacerbation of atopic dermatitis 3

A

stress, irritants, allergens

258
Q

How is atopic dermatitis diagnosed

A
  1. An itchy skin condition in the last 12 months

Plus three or more of
Onset of some sx below 2 years* (not used for kids under 4)
History of flexural involvement
History of generally dry skin
Personal history of other atopic disease
Visible flexural dermatitis

259
Q

How is atopic dermatitis managed 6, 3 community, 3 specialist

A
  1. emollients to be liberally applied
  2. topical corticosteroids for acute flares/ severe eczema (hydrocortisone 1 for face/ genitals, betamethasone valerate 0.1 for thicker areas like palms/ soles or in severe cases)
  3. chloramphenamine (sedating antihistamine) to short term releive itch adn help with sleep disturbance, otherwise cetirizine if non sedating more appropriate

SPECIALIST MX:
4. immunosuppressants eg tacrolimus by a specialist dermatologist
5. phototherapy in unresponsive cases
6. biologics eg dupilomab for severe unresponsive cases

260
Q

what is the MC arrythmia

A

atrial fibrillation

261
Q

what is the atrial firing rhythm of atrial fibrillation

A

irregular irregular atrial firing rhythm

262
Q

causes of atrial fibrillation (4)

A

heart failure
hypertension
secondary to mitral stenosis
sometimes idiopathic

263
Q

explain the pathophysiology of atrial fibrillation and how it increases the risk of thromboembolic events (3)

A
  1. rapid firing rate 300-600 bpm causes atrial spasm (not co-ordinated contraction like normal)
  2. blood is not efficiently pumped to ventricles
  3. this decreases cardiac output and increases the risk of thromboembolic events
264
Q

symptoms of A fib (6)

A

palpitations
irregularly irregular pulse
thromboemboli eg ischaemic stroke
chest pain
SYNCOPE
HYPOTENSION

6 Ps- palpitations, pulse, pain in chest, (hy)potension, (P)FAINTING and thromPoemboli

265
Q

what are the 3 types of atrial fibrillation and what are their patterns

A

paroxysmal (episodic)
persistant (longer than 7 days)
permanent (sinus rhythm unrestorable)

266
Q

diagnostic investigation for atrial fibrillation (1, 3)

A

ECG is diagnostic:
irregularly irregular pulse
narrow QRS (less than 120ms
no p waves (fibrillatory squiggles instead)
acronym= PIQ

267
Q

acute treatment for atrial fibrillation

A

synchronised cardioversion DC (shock heart back into normal rhythm)

268
Q

long term treatment for atrial fibrillation 4

A
  1. start anticoagulant (justify with ChadsVasc stroke risk score and ORBIT bleeding risk score)
  2. offer rate control first line: eg beta blocker/ CCB (only first line if not causing HF/ new onset). Can also give digoxin for non paroxysmal, not exercising person when other rate drugs ruled out)
  3. offer rhythm control: eg amiodarone (when pts have worse symptoms and HF)
  4. surgical: radio frequency ablation which
    intends to prevent future episodes
269
Q

what is atrial flutter firing rhythm (2) and compare it for atrial fibrillation (2)

A

regularly irregular atrial firing
less common and less severe than atrial fibrillation

270
Q

pathophysiology of atrial flutter 2

A
  1. fast atrial ectopic firing 120-350 bpm
  2. this causes atrial spasm
271
Q

symptoms of atrial flutter (2)

A

shortness of breath
palpitations

272
Q

investigation for atrial flutter (1) and results (2)

A

ECG diagnostic: f wave ‘saw tooth’ pattern, often with a 2:1 blocker (2 p waves for every QRS)

273
Q

what is the wolff parkinson white AVRT and explain the pathophysiology and inheritence

A

accessory pathways for conduction= bundle of Kent

pre-excitation syndrome (excite ventricle faster than typical pathwa)

autosomal dominant

274
Q

treatment for atrial flutter that is acutely unstable

treatment for atrial flutter that is stable (2) and what is the purpose of these treatments

A

acute: DC synchronised cardioversion

stable:
1. rhythm/ rate control with beta blocker and oral anticoagulation
2. radio frequency ablation to prevent future episodes

275
Q

what are the symptoms of wolff parkinson white (3)

A

palpitations
dizziness
dyspnoea

276
Q

what are the ECG changes seen in Wolff parkinson white (3)

A

slurred delta waves
short PR interval
wide QRS complex
acronym= QuPiD

277
Q

what is the treatment for wolff parkinson white (3)

A
  1. valsalva manoeuvre and carotid massage
  2. IV adenosine (temporarily ceases conduction- warn patient it feels like dying)- 6mg then 12mg, then 12 mg and additional doses if unsuccessful
  3. radiofrequency ablation of bundle of Kent
278
Q

what is long QT syndrome and what type of arrythmia does this lead to? What is the interval

A

congenital channelopathy disorder where mutation affects cardiac ion channels
=ventricular taachycardia

QT interval is 480ms +

279
Q

what are the 4 causes of long QT syndrome

A
  1. Romano Ward syndrome (autosomal dominant)
  2. Jerrell Lange Nelson syndrom (autosomal recessive)
  3. hypokalaemia and hypocalcaemia (not inherited)
  4. drugs eg amiodarone
280
Q

what are two examples of long QT syndrome

A

torsades de pointes
ventricular fibrillation

281
Q

what is torsades de pointes, what does this look like on an ECG, what can this progress to

A

polymorphic ventricular tachycardia in patients with prolong QT

rapid irregular QRS completes which ‘twist’ around baseline

ventricular fibrillation

282
Q

what does ventricular fibrillation look like on ECG and what can happen with ventricular fibrillation

A

shapeless rapid oscillations on ECG

patient becomes pulseless and goes into cardiac arrest (no effective cardiac output)


283
Q

what is the first line of treatment for ventricular fibrillation

A

electrical defibrillation

284
Q

what is primary AV block

A

PR interval prolongation (200ms +) and every P followed by QRS

285
Q

what is the treatment for asymptomatic and symptomatic primary AV block (1, 3)

A

if asymptotic then no treatment
symptomatic treatment= beta blocker eg atenolol, CCB eg verapamil, digoxin to block AVN conduction

286
Q

what are the two types of secondary AV block and explain what each are

A

Mobitz type 1 and 2

1: PR prolongation until a QRS is dropped (PR progressively elongates)

2: PR interval is consistently prolonged at the same length
with random dropped QRS

287
Q

What is the tx for 2 AV block

288
Q

what is a tertiary AV block and explain pathophys

A

AV dissociation (complete heart block so atria and ventricles beat independantly of each other)

ventricular escape rhythm is sustaining the heartbeat
(ventricle pacemakers take over which is bad (firing rate= 20-40bpm))

289
Q

tx for tertiary AV block

A

IV atropine and permanent pacemaker

290
Q

what is a bundle branch block and what are the two types and explain each

A

blocked bundles of His

RBBB: right ventricle is activated later than left ventricle
LBBB: left ventricle is activated later than right ventricle

291
Q

what is the heart sound and ECG pattern in RBBB

A

wide physiological S2 splitting heart sound
MARROW: M in V1 (R wave), W in V6 (S wave)

292
Q

what is the heart sound and ECG pattern in LBBB

A

WILLIAM: W in V1 (r wave), M in V6 (s wave)

293
Q

What is MART, its use and example

A

combined ICS and LABA treatment in one inhaler and this inhaler is used both for daily maintenance and to relieve symptoms
eg formoterol

294
Q

How much is a low and high dose of inhaled corticosteroids?

A

<= 400 micrograms budesonide or equivalent = low dose
400 micrograms - 800 micrograms budesonide or equivalent = moderate dose
> 800 micrograms budesonide or equivalent= high dose

295
Q

How is asthma diagnosed in adults 3

A
  1. FeNO test (40+ ppb is positive, 35+ in kids)
    PLUS
  2. spirometry + bronchodilator reversibility test (positive if improvement of FEV1 by 12+% and increase in volume of 200ml+ (childrne just need 12% improvement in FEV1)
  3. spirometry (FEV1:FVC less than 0.7= obstructive)
296
Q

What is balanitis and most common causes 3

A

inflammation of glans penis
1. candidiasis (candida albicans)
2. contact/ allergic/ eczema (look for hx of eczema elsewhere on body)/ psoriasis dermatitis
3. bacterial (staph)

297
Q

What are the clinical features of balanitis? 3

A

itching
white/ clear non-urethral discharge
if bacterial: painful, itchy and yellow non-urethral discharge

298
Q

What is the mx for balanitis?

A
  1. gentle and thorough saline washes
  2. 1% hydrocortisone for irritation and dermatitis causes
  3. topical clotrimzole 2 weeks if candiasis
  4. if bacterial then oral flucoxacillin
299
Q

What is Chancroid and symptoms 2

A

tropical disease caused by Haemophilus ducreyi
-> painful genital ulcers
-> unilateral painful inguinal lymph node enlargement

300
Q

What are the classifications of heart failure? Explain each

A

systolic (heart unable to pump properly = reduced ejection fraction)
diastolic (heart unable to relax properly= preserved ejection fraction)

acute HF (new onset or acute deterioration of chronic HF)
chronic HF= gradual progression and takes years to develop

301
Q

Explain the classification for HF

A

New York Heart Association (NYHA) Classification of HF

  1. Class 1 - no limitation in physical activity, and activity does not cause undue fatigue, palpitations or dyspnoea.
  2. Class 2 - slight limitation of physical activity, and comfort at rest. Ordinary physical activity causes fatigue, palpitations and/or dyspnoea.
  3. Class 3 - marked limitation in physical activity, but comfort at rest. Minimal physical activity causes fatigue (less than ordinary).
  4. Class 4 - inability to carry on any physical activity without discomfort, with symptoms occurring at rest. If any activity takes place, discomfort increases.
302
Q

What are two clinical signs of HF 2

A
  1. orthopnoea (SOB when lying flat, releived by sitting/ standing up)
  2. paroxysmal nocturnal dysponoea (sudden onset SOB whilst a person is sleeping, causing them to wake up from sleep)
303
Q

symptoms of left sided HF (8)

A

respiratory crackles (due to bilateral pleural effusions)
pink-tinged sputum
tachycardia
fatigue
CYANOSIS
EXERTION DYSPNOEA
cough
PULMONARY oedema due to vessel backflow

lungs: 4 cough, pulmonary oedema, resp crackles, cyanosis
systemic: 2 tachy, fatigue, exertional dyspnoea
specific: 1 pink tinged sputum

304
Q

symptoms of right sided HF (5)

A

ASCITES
hepatosplenomegaly
WEIGHT GAIN
raised JVP (due to increased pressure in right atrium)
PERIPHERAL OEDEMA due to systemic venous backflow

305
Q

What are the ix for HF

A
  1. first line is NT-pro-BNP
    ->400-2000 refer to cardio and TTE within 6 weeks
    -> 2000+ urgent referral to cardio and TTE within 2 weeks
    -> TTE (echo) confirms ventricular dysfunction= dx
  2. 12 lead ECG
  3. CXR:
    A: Alveolar oedema (with ‘batwing’ perihilar shadowing)
    B: Kerley B lines (caused by interstitial oedema)
    C: Cardiomegaly (cardiothoracic ratio >0.5)
    D: dilated upper lobe vessels
    E: Pleural effusions (typically bilateral transudates)
    F: Fluid in the horizontal fissure
306
Q

What are the causes of HF? 5

A

uncontrolled HTN
MI
coronary heart disease
valve abnormalities
Arrythmias eg AF

307
Q

What is the conservative advice for HF 5

A
  1. Weight loss if BMI >30.
  2. Smoking cessation
  3. Salt and fluid restriction (improves mortality)
  4. Supervised exercise-based group rehabilitation programme for people with heart failure.
  5. Offer annual influenza and one-off pneumococcal vaccinations for patients diagnosed with heart failure.
308
Q

What is the main symptom management for HF?

A

loop diuretic for fluid overload eg furosemide

309
Q

How is ventricular dysfucntion measured + classified in HF and how

A

Transthoracic echocardiogram (TTE)

EF <40% = HF with reduced ejection fraction (systolic dysfunction)

EF >40% but with raised BNP = HF with preserved ejection fraction (diastolic dysfunction)

310
Q

What are the surgical managements for HF 1

A
  1. Cardiac resynchronisation therapy if wide QRS and above NYHA class 3 (aims to improve QoL)
311
Q

What is the mx for reduced ejection fraction HF? 6?

A

1st line = ACE-I (if CI then ARB) and beta-blocker (bisoprolol)

if sx persist or NYHA class 3/4 then:

-> add aldosterone agonist (spironolactone)
-> Afro-Caribbean patients add hydralazine and a nitrate
-> IvAbradine if in sinus rhythm and impaired EF.
-> AF/ not sinus rhythm add digoxin
-> ACEi replacement with sacubitril valsartan once pt is stable on ACE and if ejection fraction is less than 35 (stop ACEi 36 hours beforehand before starting SV due to risk of angioedema- facial oedema)

312
Q

what are the two methods the body uses to compensate for heart failure (2) and why is this only effective short term?

A

RAAS system activation (increased salt and water reabsorption to increase bp)
sympathetic system activation (increases inotrophy and chronotrophy)
short term as high RAAS and SNS activation exacerbates fluid overload

313
Q

What is the mx for preserved ejection fraction HF? and class of drug

A

SGLT2 inhibitors dapagliflozin

314
Q

acute heart failure treatment (4)

A

oxygen, morphine, furosemide, GTN spray
OMFG

315
Q

What are the causes 2 and features 3 of innocent murmurs

A

causes: due to increased cardiac output in febrile illness/ anaemia
features: soft systolic murmur, asymptomatic, loudest left sternal edge

317
Q

What are the 3 foetal circulation shunts?

A

Ductus venosus: shunts oxygenated blood from placenta in umbilical vein towards the fetal heart (placenta to umbilical vein to ductus venosus to skip liver straight to heart via inferior vena cava then to right atria then to left atria via foramen ovale)
Foramel ovale: shunts oxygenated bloods from R to L atria to bypass lungs
Ductus arteriosus: connects pulmonary artery with aorta to shunt blood away from lungs into the aorta

320
Q

what is the tetralogy of fallots pathophysiology and is it cyanotic

A

congenital condition with four different heart problems

cyanotic due to ventricular systolic defect causes right ventricle outflow obstruction (deoxygenated blood is shunted to the systemic circulation)

321
Q

investigations for tetralogy of fallot and what do they show (2,1)

A

echo, chest x-ray shows a boot shaped heart

322
Q

what is a behavior of infants with tetralogy of fallot and why do they do this

A

infants often seen in knee to chest squatting position which increases preload and after load and improves cyanosis

get tet spells where they turn blue for short periods of time

323
Q

What are the features of tetralogy of fallot

A

PROVe
P for pulmonary stenosis
R for Right ventricular hypertrophy
O for overriding aorta
V for Ventricular Septal Defect

324
Q

treatment for tetralogy of fallot 2

A

treatment: full surgical repair within 2 years of life (this gives a good prognosis if done)
encourage knees to chest for tet spells and can give beta blockers to help with tet spells egp propanalol/ o2 in hospital

326
Q

what is coarctation of the aorta 1 and what is the pathophysiology of this

A

congenital narrowing of aorta
blood is diverted through proximal aortic arch branches= increased perfusion to upper body vs lower body

327
Q

symptoms/ signs of coarctation of aorta (5)

A
  1. upper body hypertension
  2. radio-femoral delay
  3. diminished femoral pulses but strong UL pulses
  4. systolic murmur, loudest between scapulae
  5. leg claudication during physical activities in children
328
Q

diagnostic investigation for coarctation of aorta

A

echocardiogram

329
Q

treatment for coarctation of the aorta

A

baloon angioplasty + stent insertion

330
Q

what are the cardinal signs of heart failure 3

A

orthopnea (difficulty breathing whilst lying down)
ankle oedema
fatigue

331
Q

if a patient is on ACEi and BB already for HF but still symptomatic what should be given to them 1

A

spironolactone

332
Q

what is the 1st line ix for IE and what is the GS

A

1- TTE
2- TOE

333
Q

what is a side effect of amlodipine and what alternative can be given to prevent this side effect 2

A

peripheral/ ankle oedema
ace inhibitor (if not already given) and indapamide

334
Q

what ecg leads look at the lateral aspect of the heart, anterior, inferior and septal

A

I, aVL, V5, V6
V3-4
II, III, aVF
V1-2

see mneumonic online when drawing up the ecg graph (like in iceland, like in spain, some amazing ass anal lois lane)

335
Q

what ecg leads looks at the LAD, RCA, Lcx. diagonal of LAD

A

V1-4
II, III, aVF
I, aVL, V5-6

336
Q

What is the cause of mumps and method of transmission

A

RNA paramyxovirus
resp droplets

337
Q

What are the features of mumps? 3

A
  1. fever
  2. malaise, muscular pain
  3. parotitis (= earache/pain on eating: unilateral initially then becomes bilateral in 70%
338
Q

What are the features of influenza? 6

A
  1. fever >38
  2. myalgia
  3. headache
  4. sore throat
  5. cough
  6. lethargy
339
Q

is mumps a notifiable disease?

340
Q

What is the mx for influenza?

A

only give antivirals if high risk pt presents within 48 hours from onset of sx during a flu outbreak
-> antiviral= oseltamivir (zanamivir for renal impairment/ immunocompromised)

341
Q

What are the features of acute tonsillitis? 5

A
  1. sore throat
  2. fever >38
  3. dysphagia
  4. cough, headache (indicates viral) OR cervical lymphadenopathy (indicates bacterial)
  5. white pathes on tonsils
342
Q

What is acute tonsillitis? Causes?

A

acute infection of the palatine tonsils
MC viral: MC rhinovirus, coronavirus and parainfluenza virus (MC to LC)
bacterial: group A strep MC

343
Q

How is acute tonsillitis dx?

A
  1. physical exam: inflamed tonsils, purulent tonsils (suggests bacterial), painful and large cervical lymph nodes
344
Q

What tool is used to predict likelihood of bacterial cause of tonsillitis? Explain

A

CENTOR criteria:
score 1 point for each (maximum score of 4)
presence of tonsillar exudate
tender anterior cervical lymphadenopathy or lymphadenitis
history of fever
absence of cough
3/4 points= more likely to be bacterial (32 to 56% chance of isolating strep in swab)

CENTor
Cough absent
Enlarged lymph nofes
Not normal temp (fever)
Tonsillar pus

345
Q

What is the mx for tonsillitis 2

A
  1. conservative: fluids and painkillers
  2. if 3+ on centor criteria or immunosuppressed or feverPAIN score is 4+, give abx:
    -> 1st line: Phenoxymethylpenicillin for 10 days
    -> Clarithromycin if allergy
347
Q

What is a viral exanthma and name some causes 4

A

widespread rash due to virus eg:
1. chickenpox
2. hand foot and mouth disease

348
Q

Why do people get arterial and venous ulcers

A

arterial: peripheral arterial disease (atherosclerosis= inadequate blood supply)
venous: chronic venous insufficiency (poor venous return= HTN in lower limbs)

349
Q

Compare arterial and venous ulcers

A

arterial: small, deep ‘punched out’ ulcers that do not bleed or ooze, at heel/ above foot, PAINFUL, cold, no palpable pulses

venous: large and shallow, with sloping edges, and bleed or ooze, on medial side, PAINLESS

350
Q

What are the ix for ulcers 2

A
  1. doppler US for venous ulcers
  2. ABPI for arterial
351
Q

What is the mx for arterial and venous ulcers? 3 2

A

arterial: need to improve arterial circulation
1. lifestyle changes
2. antiplatelets, statins
3. surgery: angioplasty/ peripheral bypass grafting

venous: need to compress veins to increase venous return
1. 4 layer band compression stockings
2. If fail to heal after 12 weeks or >10cm2 skin grafting may be needed

352
Q

What are varicose veins?

A

dilated superficial veins that are formed due to incompetent venous valves

353
Q

What are the rfx of varicose veins? 4

A

elderly
pregnancy (uterus compresses pelvic veins)
obesity
inactivity

354
Q

What is the ix for varicose veins + result? 1

A

venous duplex ultrasound: this will demonstrate retrograde venous flow

355
Q

What are the complications of varicose veins? 5

A
  1. varicose eczema (also known as venous stasis)
  2. haemosiderin deposition → hyperpigmentation
  3. lipodermatosclerosis → hard/tight skin
  4. DVT
  5. venous ulcers
356
Q

What is the mx for varicose veins? 4

A
  1. conservative: weight loss, elevation, graduated compression stockings
  2. referral to 2’ care if skin changes (eg eczema), ulcers or significant sx (pain/ swelling)
  3. endothermal ablation
  4. surgery: ligation of vein
357
Q

what is reactive arthritis

A

sterile inflammation of synovial membranes and tendons

358
Q

what causes reactive arthritis 3

A

reaction to a distant GI/GU infection
normally by chlamydia trachomatis or campylobacter jejuni

359
Q

presentation of reactive arthritis 2

A
  1. Reiters triad: can’t see, can’t pee, can’t climb a tree= uveitis, urethritis and arthritis
  2. occurs a month after intiial infection onset
360
Q

investigations of reactive arthritis 1

A

joint aspirate: plane polarised light microscopy is negative for crystalarthropathy

361
Q

treatment for reactive arthritis 3

A
  1. symptomatic relief: NSAIDs/ steroid injection
  2. give antibiotics until septic arthritis is ruled out
  3. methotrexate for chronic
362
Q

what is Psoariatic arthritis

A

inflammatory arthritis that 1/5 with Psoriasis get

363
Q

presentation of Psoariatic arthritis 4

A
  1. psoriatic rash on skin: hidden sites eg behind ears, scalp
  2. enthesitis (inflammation of entheses)
  3. dactylitis (sausage fingers)
  4. oncholysis (nail separation from nail bed)
364
Q

Describe the psoriasis rashes

A

well-demarcated red, scaly patches affecting the extensor surfaces and scalp

365
Q

investigations of psoariatic arthritis 1,3

A

x ray
-> osteolysis
-> dactylitis
-> pencil in cup appearance

366
Q

complication of psoriatic arthritis 1

A

arthritis mutilans

367
Q

What is guttate psoriasis cause and appearance

A

psoriatic rash frequently triggered by a streptococcal infection.
Multiple red, teardrop lesions appear on the body

368
Q

What is the mx for psoriasis? 6

A
  1. regular emollients
  2. hydrocortisone OD
  3. vit D analogue (calcitriol) OD and if it doesn’t work then vit D BD
  4. short-acting dithranol (slows down the production of new skin cells)

SECONDARY CARE REFERRAL
5. phototherapy UVB light
6. if associated joint disease, then NSAIDS and then if unresponsive: oral methotrexate

369
Q

what is peripheral arterial/ vascular disease

A

ischaemia of lower limb arteries

370
Q

general symptoms of PVD 2 and test and positive result for it 1

A

skin changes: pale colour, cold and ulcers
pulses: weak/ absent
buerger test positive: elevate leg 45 degrees for 1 min= pallor, pt to sit up with legs hanging off on the coach= blue then reactive hyperaemia (red)

371
Q

why does chronic ischaemic pain occur at night (2) and what can this lead to (2)

A

due to elevation of limb which can further reduce blood supply to the distal part of the limb which can cause ulcers and gangrene

372
Q

intermittent claudification: when is there pain, how occluded is the lumen and what is the cause of the occlusion

A

intermittent claudification
pain on exertion, relieved by rest
partial lumen occlusion
atherosclerotic

373
Q

critical limb ischaemia: when is there pain, and what is there a risk of getting 2

A

pain at rest
gangrene and infection

374
Q

ix for PVD 3

A
  1. ABPI
  2. colour duplex ultrasound imaging- assesses degree of stenosis
  3. CT angiography if surgery is considered
375
Q

what does ABPI stand for, what is it what is classed as normal and explain what the value for results means

A

ankle brachial pressure index
compares blood pressure in upper and lower limbs as a ratio
0.5-0.9= intermittent claudication
less than 0.5= critical limb ischaemia
absent/0= risk of acute limb threatening ischaemia

376
Q

treatment for intermittent claudification (5)

A
  1. reduce risk factors eg stop smoking
  2. exercise programme for intermittent which trains through the pain to stimulate collateral blood supply growth
  3. meds: 80mg highest dose statin, clopidogrel is 1st line for PAD
  4. according to NICE, can give naftidrofuryl oxalate: vasodilator (for pt with poor QOL)
  5. if severe: percutaenous transluminal angioplasty +/- stent placement
377
Q

treatment for critical limb ischaemia (1)

A

surgical emergency requires revascularisation within 4-6 hours otherwise there is an increase amputation risk via percutaenous transluminal angioplasty +/- stent

378
Q

what are the 6 Ps and how can they assess the severity of the acute limb ischaemia

A

6 Ps: pulselessness, pallor, pain, persistently cold, paralysis, parasthesia
->the more of these 6 Ps that you have, the more severe the ischaemia

379
Q

How is BMI calculated and state the classifications

A

BMI = weight (kg) / height (m) squared

Underweight < 18.49
Normal 18.5 - 25
Overweight 25 - 30
Obese class 1 30 - 35
Obese class 2 35 - 40
Obese class 3 > 40

380
Q

What is the mx for obesity 4

A
  1. conservative: diet, exercise
  2. orlistat
    -> pancreatic lipase inhibitor
  3. liraglutide injections
    -> GLP1
  4. types of bariatric surgery:
    -> laparoscopic-adjustable gastric banding
    -> sleeve gastrectomy
    -> Roux-en-Y gastric bypass surgery
381
Q

What are the NICE guideline criteria for medical mx of obesity

A

orlistat:
-> BMI of 28 kg/m^2 or more with associated risk factors, or
-> BMI of 30 kg/m^2 or more
-> continued weight loss e.g. 5% at 3 months
->orlistat is normally used for < 1 year

liraglutide (SC daily injection)
-> person has a BMI of at least 35 kg/m²
-> prediabetic hyperglycaemia (e.g. HbA1c 42 - 47 mmol/mol)

382
Q

What is classed as obesity in pregnancy

A

BMI >= 30 kg/m² at the first antenatal visit

383
Q

What is the mx for obesity in pregnancy?

A
  1. obese women should take 5mg of folic acid, rather than 400mcg
  2. screened for gestational diabetes with an oral glucose tolerance test (OGTT) at 24-28 weeks
  3. if the BMI >= 35 kg/m² women should give birth in a consultant-led obstetric unit (as obesity increases risk of complications at birth and fetal complications)
  4. if the BMI >= 40 kg/m² should have an antenatal consultation with an obstetric anaesthetist and a plan made (“ “)

543O

384
Q

What is the ix 1 and mx 4 for bursitis?

A

ix: joint aspiration for when septic bursitis/ crystal arthropathy is suspected

  1. modify activities to ensure not putting pressure on affected joint
  2. conservative: ice and elevation
  3. NSAIDs
  4. corticoid injections for chronic bursitis
385
Q

What is bursitis? What are the symptoms of bursitis? 3

A

Inflammation of the bursa (fluid filled sacs in joints) that become inflammed due to repetitive trauma
1. dull achy pain
2. swelling over area
3. redness

386
Q

What are the five types of bursitis?

A
  1. prepatellar (knee)
  2. olecranon (elbow)
  3. trochanteric (hip)
  4. subacromial (shoulder)
  5. retrocalcaneal bursitis (back of heel)
    only one joint is affected usually on presentation
387
Q

Explain screening for AAA

A

all men aged 65 offered US screening for asymptomatic AAA
-> women only screened 70+ with existing co-morbidities eg fhx or CV disease
-> done via abdo US
-> if aorta diameter 3cm+ then refer to vascular team (urgent referral if 5.5+)

388
Q

Explain screening for bowel cancer

A

FIT tests sent every 2 years for people between 60-74
-> if FIT is postiive then sent for colonoscopy
-> people with rfx eg FAP, HNPCC or IBD are offered a colonoscopy at regular intervals to screen for bowel cancer

389
Q

Explain screening for diabetic eyes and results

A

yearly eye checks, if last 2 tests were clear then in 2 years
-> tropicamide put into eyes to make pupils large so photo can be taken of back of eye
results:
STAGE : background retinopathy means small changes but vision unaffected, non-proliferative
STAGE 2: pre-proliferative retinopathy means widespread changes in the retina, including bleeding= more frequent screening
STAGE 3: proliferative retinopathy= retinal detachment, risk of vision loss, needs referral for treatment
DIABETIC MACULOPATHY: leaky/ blocked blood vessels supplying macula, risk of vision, needs more frequent testing and treatment

390
Q

What are the different types of diabetic eye disease 4

A
  1. diabetic retinopathy (haemorrhages, cotton wool spots, aneurysm)
  2. diabetic macular odema (leaky BV cause fluid build up in macula= blurry vision)
  3. cataracts (high sugar levels over time damage the eye lens= less flexible and less transparent= cloudy vision and sensitivity to light/ glares)
  4. glaucoma (damaged retina BV= abnormal collaterals= block fluid from draining out of eye= increased eye pressure= blurry vision)
391
Q

What is the care after newborn birth 5

A
  1. clamp the umbilical cord
  2. skin to skin, keeping baby warm
  3. vitamin K injection (baby’s have deficiency so this prevents bleeds and stimulates baby to cry to open up lungs)
  4. measure baby’s weight and length
  5. screening:
    -> NIPE within 72 hours
    -> blood spot test
    -> newborn hearing test
392
Q

Expain the newborn spot test

A

-> test on day 5 with parental conset screenign for 9 congenital conditions:
eg sickle cell disease, cystic fibrosis, congenital hypothyroidism, Maple syrup urine disease

4 Ss: (S for Spot) SIckle, Systic, Slow (cong hypothyroid), Syrup

393
Q

Explain screening done in NIPE

A
  1. oxygen sats (should be 94+)
  2. head: circumference, fontanelle, red reflex, cleft lip/ palate, suckling reflex, tone
  3. shoulder/ hand: shoulder symmetry for clavicle fracture, check all digits are present
  4. chest: heart and breath sounds
  5. abdo: check umbilicus for healing, check for hernias
  6. genitals: descended testes, patent anus, check it is being cleaned well, ask if baby opened bowel yet
  7. legs: check digits, symmetry of legs, Barlows (to dislocate (Dr Barlow= bad)- involves addution and putting pressure down) and Ortolani manouveres, femoral pulse
  8. back: spina bifida
  9. reflexes: Moro (startle), rooting (turning head towards the direction where something touched their mouth), grasp, stepping
  10. any abnormalities, refer (undescended testes) or US (hip clicking)
394
Q

What are the MC causes of COPD 2

A

smoking
alpha 1 antitrypsin deficiency

395
Q

What are COPD CXR signs 3

A

barrel chest
flat hemidiaphragm
hyperinflation bullae
(big fat heart- meaning chest)

396
Q

What are the sx of an acute exacerbation of COPD 3

A
  1. increased green sputum
  2. increase in cough
  3. increase inSOB
397
Q

What are the causes of acute exacerbation of COPD 2

A
  1. haemophilus influenza (MC)
  2. strep pneumoniae
398
Q

What is the tx for acute exacerbation of COPD 3

A
  1. pred 30mg for 5 days
  2. abx only if sputum is purulent or clinical signs of pneumonia (amoxicillin)
  3. admisison if severe SOB, O2 sats less than 90: give 02 with venturi mask at 4L/min with target sats of 88-92
399
Q

What is the risk for patients with acute exacerbation of COPD and how is this risk managed?

A

risk of developing type 2 resp failure
non invasive ventilation

400
Q

What are the ix for COPD diagnosis and how does the severity scale work?

A

spirometry to demonstrate airflow obstruction: FEV1/FVC ratio less than 70%

FEV1 is used to rank severity:
>80= stage 1 mild (symptoms need to be present to diagnosed COPD in these patients)
50-79= stage 2 moderate
30-49= stage 3 severe
<30= stage 4 very severe

401
Q

What is the mx for stable COPD? 5

A
  1. lifestyle: stop smoking
  2. vaccinations: annual influenza, one off- pneumococcal vaccine
  3. first line SABA
  4. if asthmatic features/ features that suggest steroid responsiveness then add regular LABA + ICS, otherwise LABA + LAMA
  5. prophylactic azithromycin (ECG needs to be done as azithromycin can prolong QT interval)
  6. pulmonary rehabilitation for MRC 3+ individuals
402
Q

What are the extra tests for COPD? 5

A
  1. FBC to exclude polycythaemia, anaemia and infection
  2. CXR to exclude lung cancer
  3. BMI (weight loss can occur in severe disease)
  4. sputum culture (for recurrent infections)
  5. Serum alpha-1 antitrypsin to look for alpha-1 antitrypsin deficiency
403
Q

What are the MRC scale grades

A

Grade 1: Breathless on strenuous exercise
Grade 2: Breathless on walking uphill
Grade 3: Breathlessness that slows walking on the flat
Grade 4: Breathlessness stops them from walking more than 100 meters on the flat
Grade 5: Unable to leave the house due to breathlessness

404
Q

SABA, LAMA, LABA, ICS, LRA: what does each stand for and examples for each

A

SABA: short acting brochodilator agonist, salbutamol
SAMA: short acting muscarinic agonist, ipratropium bromide
LAMA: long acting muscarinic agonist, tiotropium bromide
LABA: long acting brochodilator agonist, salmetorol
ICS: inhaled corticosteroids, beclomethasone dipropionate
LRA: leukotriene receptor antagonist, montelukast

405
Q

What is infa

3a content (6 decks)

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