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PHASE 3A > PRIMARY CARE - cardio, resp, endocrine, GI, MSK, neuro, infection > Flashcards

PRIMARY CARE - cardio, resp, endocrine, GI, MSK, neuro, infection Flashcards

1
Q

define primary and secondary HTN

A

primary - high BP that doesn’t have a known secondary cause (lifestyle, age, genetics)

secondary - high BP caused by another medical condition e.g. Conn’s, kidney disease, hyperthyroidism

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2
Q

describe the pathophysiology of HTN

A

plaque build up > thickening of vessel wall > narrowing of lumen > builds up vascular pressure

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3
Q

risk factors for hypertension

A
  • diabetes mellitus
  • metabolic syndrome
  • old age
  • physical inactivity
  • tobacco + alcohol
  • obesity
  • diet
  • genetics/FMHx
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4
Q

how does HTN present?

A

normally asymptomatic, found incidentally

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5
Q

1st line investigation for HTN

A

clinical BP monitoring
1. if BP >140/90 in clinic, recheck on 2-3 occasions
2. if persistently high, offer ABPM (24hr) or HBPM if ambulatory not tolerated
3. if stage 1 - QRISK to decide tx
4. if stage 2 - start antihypertensive tx

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6
Q

investigations once ABPM has confirmed high blood pressure

A

look for target organ damage…
1. ECG
2. urine - ACR and dip for haematuria
3. bloods - U&Es, HbA1c, cholesterol, HDL
4. fundoscopy

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7
Q

what is assessed once BP readings and further investigations have been completed?

A

CV risk - with QRISK

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8
Q

what are the stages of hypertension (ABPM/home average)?

A

stage 1 (prehypertension) - between 135/85 and 140/90

stage 2 - between 150/95 and 160/100

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9
Q

what is normal BP?

A

90/60 - 120/80

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10
Q

QRISK
1) what is it?
2) what does it involve?
3) what score is low, medium and high risk?

A

1) calculates a person’s risk of developing a heart attack OR stroke in the next 10 years

2) RFs like age, sex, smoking, diabetes, angina/heart attack in 1st degree relative, CKD, AF, HTN, BMI, RA

3) low risk = <10%, medium risk = 10-20%, high risk = >20%

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11
Q

management of a patient with a QRISK score of:
a) moderate
b) high

A

a) lifestyle advice changes e.g. stop smoking, diet, reduce alcohol, exercise

b) start tx e.g. statins

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12
Q

hypertension treatment pathway if patient is <55 and not of black African/African-Caribbean family origin

A
  1. ACEi or ARB
  2. ACEi/ARB + CCB OR thiazide-like diuretic
  3. ACEi or ARB + CCB + thiazide-like diuretic
  4. confirm resistant hypertension, seek advice or add low-dose spironolactone/alpha blocker/beta blocker
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13
Q

hypertension treatment pathway if patient is >55 or of black African/African-Caribbean family origin

A
  1. CCB
  2. CCB + ACEi/ARB OR thiazide-like diuretic
  3. ACEi/ARB + CCB + thiazide-like diuretic
  4. confirm resistant hypertension, seek advice or add low-dose spironolactone/alpha blocker/beta blocker
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14
Q

1st line hypertension medication if the patient has diabetes (regardless of age/ethnicity)

A

ACEi/ARB

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15
Q

target BP after HTN treatment for <80y in
a) clinic
b) ABPM/home avg

A

a) <140/90
b) <135/85

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16
Q

target BP after HTN treatment for >80y in
a) clinic
b) ABPM/home avg

A

a) <150/90
b) <145/85

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17
Q

angiotensin-converting enzyme inhibitors (ACEis)
a) examples
b) mechanism
c) side-effects
d) contraindications

A

a) ‘-IL’ e.g. ramipril
b) blocks angiotensin-converting enzyme from converting angiotensin I to angiotensin II (a vasoconstrictor hormone)
c) hypotension, dry cough
d) pregnancy

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18
Q

angiotensin receptor blockers (ARBs)
a) examples
b) mechanism
c) side-effects
d) contraindications

A

a) ‘-sartans’ e.g. candesartan
b) bind to and inhibit the angiotensin II type 1 receptor > block formation of angiotensin II (vasoconstrictor)
c) hypotension, hyperkalaemia
d) pregnancy

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19
Q

calcium-channel blockers (CCBs)
a) examples
b) mechanism
c) side-effects
d) contraindications

A

a) ‘-pine’ e.g. amlodipine, felodipine
b) blocks calcium channels in heart and arteries > prevents Ca2+ causing strong contractions > allows vessels to dilate
c) peripheral vasodilation: flushing, headache, oedema. Negatively chronotropic (slows heart): bradycardia. Constipation (gut CCs)

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20
Q

thiazide-diuretics
a) examples
b) mechanism
c) side-effects
d) contraindications

A

a) ‘-mide’ e.g. indapamide
b) promote diuresis (urine output) > removes excess fluid
c) hypotension, hypokalaemia, hyponatraemia, impaired glucose tolerance, hypercalcemia, postural hypotension
d) pregnancy

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21
Q

define GORD

A

complications due to the reflux of gastric contents into/beyond the oesophagus, via the lower oesophageal sphincter

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22
Q

aetiology of GORD

A

weakening of the oesophageal sphincter, due to…
1. lower oesophageal sphincter hypertension
2. hiatus hernia

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23
Q

risk factors for GORD

A
  • obesity
  • fatty foods
  • smoking + alcohol
  • coffee
  • chocolate intake
  • pregnancy
  • hiatus hernia
  • certain medications e.g. NSAIDs
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24
Q

pathophysiology of GORD

A
  1. reduced tone of lower oesophageal sphincter (LOS) > increased transient LOS relaxations
  2. LOS relaxes independently of swallowing
  3. allows gastric acid etc to flow back up
  4. reflux of acid, bile, pepsin and pancreatic enzymes
  5. oesophageal mucosal injury
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25
Q

signs and symptoms of GORD

A
  1. HEARTBURN - centre of lower chest, aggravated by bending, stooping and lying down. may be relieved by antacids
  2. belching
  3. food/acid regurgitation
  4. increased salivation (water brash)
  5. odynophagia (painful swallowing)
  6. nocturnal asthma
  7. chronic cough
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26
Q

investigations for GORD

A

usually clinical diagnosis unless red flags (weight loss, haematemesis, dysphagia)

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27
Q

non-pharmacological treatment for GORD

A

weight loss, smoking cessation, avoiding late meals, decrease alcohol intake

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28
Q

pharmacological tx for GORD

A
  1. antacids e.g. gaviscon
  2. PPI e.g. lansoprazole, omeprazole
  3. H2 receptor antagonists e.g. cimetidine
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29
Q

mechanism of action of PPIs in the tx of GORD

A

inhibits gastric H+ release > prevents the production of gastric acid

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30
Q

mechanism of action of H2 receptor antagonists in the tx of GORD

A

blocks histamine receptors on parietal cells > reduces acid release

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31
Q

surgical management for GORD

A
  1. fundoplication
  2. repair of hiatal defects
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32
Q

complications of GORD (3)

A
  1. peptic stricture
    inflammation of oesophagus > narrowing and stricture change
  2. Barrett’s oesophagus
    distal oesophageal epithelium undergoes metaplasia from squamous to columnar (cancer risk)
  3. peptic ulceration of lower oesophagus
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33
Q

define primary and secondary hypothyroidism

A

underactive thyroid gland caused by
1. thyroid gland disease (primary)
2. pituitary/hypothalamic disease (secondary)

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34
Q

epidemiology of hypothyroidism (3)

A
  1. F > M
  2. white populations
  3. 60-70 y/o
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35
Q

most common cause of congenital hypothyroidism

A

iodine deficiency during pregnancy

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36
Q

most common cause of acquired hypothyroidism

A

acquired almost always PRIMARY and due to Hashimoto’s thyroiditis (autoimmune)

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37
Q

most common cause of hypothyroidism in..
a) developing countries
b) developed countries

A

a) iodine deficiency (congenital)
b) Hashimoto’s (acquired)

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38
Q

what is postpartum thyroiditis?

A

thyroid becomes inflamed after childbirth > can proceed to permanent hypothyroidism

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39
Q

primary causes of hypothyroidism

A
  1. Hashimoto’s
  2. absence/dysfunction of thyroid e.g. surgery/iodine therapy for Grave’s/head or neck cancer
  3. drugs - iodine, lithium, antithyroid drugs
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40
Q

RFs for hypothyroidism

A
  1. white
  2. female
  3. postpartum
  4. iodine deficiency
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41
Q

symptoms of hypothyroidism

A

THINK SLOW
- up to half of pts have nonspecific sx
- weakness/lethargy
- depression
- cold sensation
- constipation
- weight gain
- brittle hair
- menorrhagia
- decreased libido

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42
Q

signs of hypothyroidism

A
  • bradycardia
  • slow reflexes
  • ataxia
  • dry hair/skin
  • yawning
  • cold hands
  • ascites
  • immobile
  • congestive cardiac failure
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43
Q

why is everything ‘slow’ in hypothyroidism?

A
  • T4 is mainly produced by the thyroid and converted to T3 in target tissues
  • T3 stimulates cellular O2 consumption and energy generation
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44
Q

investigations for hypothyroidism

A

1st line = TFTs

other = FBC and fasting glucose (if fatigue and weight gain present), thyroid biopsy and USS

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45
Q

TFT results in:
a) primary hypothyroidism
b) secondary hypothyroidism

A

a) raised TSH, low free T4 and T3
b) inappropriately low TSH for reduced T4/3 levels

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46
Q

hypothyroidism management

A

levothyroxine (synthetic T4) - start LOW and titre up

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47
Q

what is a hiatus hernia?

what are the two main types?

A

protrusion of intra-abdominal contents through an enlarged oesophageal hiatus

  1. sliding (95% of cases) - gastroesophageal junction (GOJ) moves above the diaphragm
  2. rolling (paraesophageal) - GOJ remains below diaphragm but separate part of stomach herniates through oesophageal hiatus
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48
Q

RFs for a hiatus hernia

A
  • obesity
  • increased intraabdominal pressure e.g. ascites, pregnancy, multiparity
  • age
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49
Q

signs and symptoms of a hiatus hernia

A
  • may be asymptomatic!
  • most common presenting complaint = GORD…
  • heartburn
  • dysphagia
  • regurgitation
  • chest pain
  • weight loss
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50
Q

investigations for a hiatus hernia

A
  1. abdominal exam (rule out cancer - masses/enlarged lymph nodes)
  2. refer for upper gastro endoscopy (1st line) and barium swallow (identifies type/extent of hiatal hernia)
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51
Q

treatment for hiatus hernia

A
  • all patients: conservative e.g. weight loss, smoking cessation, reducing alcohol
  • medical: PPIs e.g. omeprazole
  • surgery IF… sx persist despite medical tx, or have symptomatic paraesophageal hernia
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52
Q

define acute bronchitis

A

a self-limiting, acute LRT infection causing inflammation in the brochial airways

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53
Q

what organisms commonly cause acute bronchitis?

A

normally VIRAL
- rhinovirus
- enterovirus
- influenza A/B

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54
Q

risk factors for acute bronchitis

A
  • viral infection exposure
  • smoker
  • pollution
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55
Q

what are the Macfarlane criteria for acute bronchitis (4)?

A
  1. acute illness (<21 days)
  2. cough is predominant symptom
  3. at least one other LRT sx e.g. sputum, wheezing, chest pain
  4. no other alternative explanation for sx
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56
Q

signs and symptoms of acute bronchitis

A
  • cough <30 days (PREDOMINANT SX)
  • productive
  • no hx of chronic resp illness
  • fever
  • wheeze
  • rhonchi (coarse rattling breathing)
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57
Q

investigations for acute bronchitis

A

none - clinical diagnosis!

if suspecting pneumonia (young/old, rust coloured sputum, dyspnoea, pleuritic chest pain, malaise) refer for CXR

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58
Q

management of acute bronchitis if…
a) cough <4 weeks
b) cough >4 weeks

A

a) 1st line = observe (self-limiting) but consider…
- paracetamol if fever
- SABA e.g. salbutamol if wheezing
- antitussive (cough med) for acute severe cough e.g. oral dextromethorphan

b) 1st line = evaluate for other causes e.g. asthma, reflux, upper airway cough syndrome
consider…
- SABA e.g. salbutamol

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59
Q

what are haemorrhoids?

A

when haemorrhoidal cushions (normal, highly vascularised areas in the anal canal) become abnormally swollen, causing sx

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60
Q

what are:
a) external haemorrhoids
b) internal haemorroids

A

a) covered by modified squamous epithelium which is richly innervated with pain fibres
b) covered by columnar epithelium which have no pain fibres

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61
Q

causes of haemorrhoids (7)

A
  1. straining on toilet
  2. constipation
  3. ageing
  4. conditions causing raised intra-abdo pressure e.g. pregnancy, childbirth, ascites, pelvic mass
  5. chronic cough
  6. heavy lifting
  7. low fibre
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62
Q

presentation of haemorrhoids

A
  • bright red painless rectal bleeding
  • perianal pain
  • pruritis
  • feeling of incomplete evacuation
  • tender palpable lesion
  • anal mass
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63
Q

investigations and findings for haemorrhoids (2)

A
  1. examination
    - inspect area, may see bluish mass
    - perform DRE
  2. anoscopic exam
    - to make diagnosis/classify severity
    - pink swellings
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64
Q

management of haemorrhoids

A
  1. advice
    - dietary and fluid intake
    - anal hygiene (clean and dry)
  2. symptom management
    - paracetemol
    - topical haemorrhoid preparation e.g. anusol
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65
Q

what are anal fissures? (primary and secondary)

A

a tear or ulcer in the skin lining the distal anal canal

primary - no clear underlying cause
secondary - underlying condition

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66
Q

causes of anal fissures (4)

A
  1. hard stool
  2. conditions e.g. IBD, STIs, cancer, skin infections
  3. anal trauma e.g. surgery, sex
  4. pregnancy/childbirth
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67
Q

presentation of anal fissures

A
  1. pain on defecation
    - “broken glass”
    - occurs every time
    - severe, sharp followed by burning for several hours
  2. tearing sensation
  3. fresh blood on stool/paper
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68
Q

investigations for anal fissures

A

clinical diagnosis with history and DRE

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69
Q

management of anal fissures (advice and medical)

A
  1. advise…
    - dietary fibre
    - keep region clean and dry
    - sit in shallow warm bath several times a day
  2. medications
    - paracetemol
    - if severe pain, short course of topical anaesthetic e.g. lidocaine 5% ointment before passing stool
    - if symptoms >1w with no improvement, consider rectal GTN 0.4% ointment (relaxes anal sphincter)
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70
Q

define anaephylaxis
what is it characterised by?

A

an acute, severe allergic reaction to an antigen to which the body has become hypersensitive

characterised by rapidly developing airway and/or breathing and/or circulatory problems associated with skin and mucosal changes

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71
Q

anaphylaxis triggers

A
  1. drugs e.g. penicillin, anaesthetics, NSAIDs, aspirin
  2. contrast agents used in xrays
  3. latex and plasters
  4. foods e.g. nuts, milk, uncooked meats
  5. venom e.g. wasp and bee sting
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72
Q

what 3 criteria suggest anaphylaxis is likely?

A
  1. sudden onset and rapid progression
  2. life-threatening airway/breathing/circulation problems
  3. skin and/or mucosal changes
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73
Q

use ABCD to suggest some signs and symptoms of anaphylaxis

A

Airway
- tongue/throat swelling
- difficulty breathing and swallowing
- hoarse voice
- stridor

Breathing
- SOB
- wheeze
- tiredness
- cyanosis
- low SpO”

Circulation
- signs of shock e.g. pale, clammy
- tachycardia
- low BP
- feeling faint/collapse/decrease or loss of consciousness

Disability
- confusion, agitation

PLUS erythema/urticaria/angio-oedema

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74
Q

investigations for anaphylaxis

A

ABCDE approach

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75
Q

primary care management of anaphylaxis

A
  1. call for ambulance
  2. assess person - if unresponsive, CPR
  3. if CPR not needed, examine for airway obstruction, check pulse and BP
  4. give IM adrenaline as per age guidelines
  5. if available - O2 through mask
  6. monitor with pulse oximetry, BP, ECG
  7. consider inhaled salbutamol or ipratropium therapy
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76
Q

adrenaline dosage in anaphylaxis for age:
a) >12/adult
b) 6-12y
c) 6m-6y
d) under 6m

A

a) 500mcg
b) 300mcg
c) 150mcg
d) 100-150mcg

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77
Q

what surgical management may be considered for anal fissures if they’ve failed to respond to conservative management?

A

sphincterotomy

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78
Q

what is osteoarthritis? what 3 things is it typically characterised by?

A

degenerative arthritis due to wear and tear of the joints, resulting in loss of articular cartilage

characterised by joint pain, stiffness and functional limitation

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79
Q

who is osteoarthritis common in?

A

elderly and females (esp postmenopause)

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80
Q

causes of osteoarthritis
a) primary
b) secondary

A

a) idiopathic, no preceding injury

b) previous insult to joint e.g. congenital abnormality, inflammatory arthropathies, ongoing strenuous physical activities

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81
Q

risk factors for osteoarthritis (7)

A
  1. age
  2. female (post menopause)
  3. occupation
    - manual labour = OA in hand joints
    - farming = OA in hips
    - football = OA in knees
  4. genetics
  5. obesity
  6. previous joint trauma
  7. RA
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82
Q

signs and symptoms of osteoarthritis

A
  1. pain (ache, burning) - usually ACTIVITY related, pain at rest rare
  2. functional difficulties e.g. knee giving way
  3. bone deformities - osteophytes (bony outgrowths) leads to Bouchard’s and Heberden’s nodes
  4. limited range of motion
  5. stiffness for less than 30 mins-1hr in the morning, gets WORSE throughout the day
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83
Q

which joints are commonly affected in osteoarthritis? what joint involvement is useful for distinguishing between OA and RA?

A
  • knee, hip hand and spine
  • in hand, PIP and DIP joint affected but NOT MCP (first knuckle) unlike RA
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84
Q

where are
a) bouchard’s nodes
b) heberden’s nodes
found in OA?

A

a) proximal interphalangeal joint (PIP)
b) distal interphalangeal joint (DIP)

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85
Q

investigations for OA

A

1st line = refer for x-ray

if inflammatory/rheumatoid arthritis suspected, order serum CRP/ESR and rheumatoid factor (RF)

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86
Q

xray findings in osteoarthritis

A

LOSS
L - loss of joint space

O - osteophytes (bony lumps around joint)

S - subarticular sclerosis (hardening of bone at joint due to loss of cartilage)

S - subchondral cysts

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87
Q

non-pharmacological management options for OA

A

exercise
physio
weight loss
better footwear
walking aid e.g. stick

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88
Q

analgesic ladder for managing OA

A
  1. mild pain
    non opioid analgesic e.g. aspirin, paracetemol, NSAIDs
  2. moderate pain
    weak opioid analgesic e.g. tramadol, codeine +/- non opioids
  3. severe pain
    strong opioid analgesic e.g. morphine, fentanyl, buprenorphine, methadone +/- non opioids
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89
Q

what surgery can be done for OA? when is it indicated?

A

arthroplasty (replace some/all of joint with prosthetic)

indicated for severe unmanageable pain

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90
Q

what is atrial fib? what is it strongly associated with?

A

a type of supraventricular tachyarrhythmia
associated with co-existing heart conditions e.g. HTN, CAD, MI

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91
Q

brief pathophys of atrial fib

A
  1. uncoordinated atrial activation
  2. ineffective atrial contraction
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92
Q

what does atrial fibrillation hugely increase the risk of?

A

stroke

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93
Q

what are the triggers for a first AFib episode/worsening of current AFib? (PIRATES)

A
  1. Pulmonary embolism
  2. Ischaemia
  3. Resp disease
  4. Atrial enlargement/myxoma
  5. Thyroid disease
  6. Ethanol
  7. Sepsis and Sleep apnoea
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94
Q

signs and symptoms of AFib

A

symptoms
1. palpitations (‘fluttering’ in chest)
2. dizziness
3. dyspnoea
4. anxiety
5. chest pain
6. fatigue
7. syncope

signs
1. irregularly irregular pulse
2. tachycardia

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95
Q

primary care investigations for AFib

A
  1. auscultation - extremely irregular HR
  2. 12-lead ECG
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96
Q

ECG findings in AFib (3)

A
  1. irregularly irregular QRS complex
  2. absent p waves
  3. QRS >120ms
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97
Q

indications for hospital admission in a patient presenting with AFib

A
  1. onset within 48h
  2. haemodynamically unstable
  3. serious underlying cause e.g. stroke, TIA
  4. pre-existing or newly diagnosed structural heart disease
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98
Q

managing AFib in a stable patient not requiring admission

A
  1. assess stroke risk with CHADsVAS
  2. assess bleed risk with ORBIT
  3. oral anticoag if CHADsVASC >1 - DOAC e.g. apixaban
  4. consider tx for rate control - beta-blocker e.g. metoprolol
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99
Q

what does CHADsVAS stand for?

A

C - congestive heart failure
H - HTN
A - age (>75) (2 points)
D - diabetes
S - stroke/TIA/thromboembolism
V - vasc disease
A - age (65-74)
S - sex (female)

100
Q

what is atrial flutter? what is it commonly associated with?

A

a type of supraventricular tachycardia where the atria beat REGULARLY but FASTER than normal

associated with AFib (can degenerate into it)

101
Q

RFs for atrial flutter (2)

A
  1. atrial surgery/atrial ablation
  2. toxic and metabolic conditions
102
Q

signs and symptoms of atrial flutter

A

usually part of an acute disease process e.g. PE
- palpitations
- dizziness
- fatigue
- syncope (v uncommon)

103
Q

investigations for atrial flutter

A
  1. auscultation
  2. ECG
104
Q

what will the ECG findings be in atrial flutter? (2)

A
  1. sawtooth pattern
  2. regularly irregular QRS complex
105
Q

management for atrial flutter

A

emergency hosp admission if haemodynamically unstable

consider rate control drug (beta-blocker e.g. metoprolol) and anticoagulant

106
Q

step-wise asthma management in adults (12+) (7)

A
  1. SABA e.g. salbutamol
    • low-dose ICS e.g. budesonide
    • leukotrine receptor antagonist LRTA e.g. montelukast
    • LABA e.g. salmeterol
  5. continue SABA + LRTA, switch LABA+ICS for a combined maintenance and reliever therapy (MART) which includes ICS
  6. SABA + LRTA + medium ICS dose MART
  7. SABA + LRTA + one of the following
    - stand alone high-dose ICS
    - trial additional drug e.g. theophylline or LAMA
    - seek advice from asthma specialist
107
Q

what is a bursa? so what is bursitis?

A

bursa = jelly-like sac containing synovial fluid that lies between a tendon and either bone or skin . helps joint move smoothly

bursitis = inflammation/swelling of bursa

108
Q

where does bursitis most commonly present in GP? (5)

A

knee
subacromial (shoulder)
trochanteric (hip)
retrocalcaneal (heel)
olecranon (elbow)

109
Q

what causes bursitis? (4)

A
  • repetitive stress
  • infection
  • autoimmune disease
  • trauma
110
Q

signs and symptoms of bursitis

A
  1. pain, swelling, erythema and warmth at site of bursa
  2. tenderness to palpation
  3. decreased ROM
  4. may have low-grade temp

if subacromial - painful arc on shoulder abduction
if trochanteric - lateral hip pain

111
Q

how is bursitis investigated?

A

normally clinical diagnosis

if suspect sepsis - refer for fluid aspirate staining/culture

112
Q

how is bursitis managed? what if these initial tx don’t work?

A
  1. conservative - avoid activities that worsen sx, apply ice, use crutches/walking stick, gentle mobilisation
  2. analgesia 1st line = paracetemol

self-limiting so should settle in a few weeks
if not settling, consider corticosteroid injection

113
Q

what is COPD?

A

irreversible progressive disorder of airway obstruction

114
Q

most common cause of COPD

A

SMOKING

115
Q

types of COPD

A

chronic bronchitis and emphysema

116
Q

brief pathophysiology of:
a) chronic bronchitis
b) emphysema

A

a) long-term inflammation of bronchi, increased mucus production

b) alveoli permanently enlarge and lose elasticity > can’t recoil and expel air

117
Q

general signs and symptoms of COPD

A

SIGNS
- dyspnoea (persistent, progressive, worse on exertion)
- tachypnoea
- oedema
- clubbing

SX
- SOB
- chronic cough
- recurring chest infections
- reduced exercise tolerance

118
Q

classic presentation of chronic bronchitis

A

BLUE BLOATERS
- daily productive cough for >3 months in at least 2 consecutive years
- chronic resp infection
- overweight
- cyanotic
- peripheral oedema
- hypoxemia and hypercapnia
- crackles and wheezing

119
Q

classic presentation of emphysema

A

PINK PUFFERS
- exhaling slowly through pursed lips
- dyspnoea
- tachypnoea
- weight loss
- minimal cough!
- barrel chest
- quiet chest

120
Q

what are the 5 grades on the MCR dyspnoea scale?

A
  1. not troubled by breathlessness unless strenuous exercise
  2. SOB when hurrying/walking up slight hill
  3. walks slower than contemporaries due to breathlessness/has to stop for breath when walking at own pace
  4. stops for breath after walking for about 100m/few mins
  5. too breathless to leave house or breathless when dressing/undressing
121
Q

when should A1AT deficiency be suspected?

A

in YOUNG patients with COPD and deranged LFTs/other liver signs like ascites and jaundice

122
Q

what is the most common causative organism of infective exacerbations of COPD?

A

Haemophilus influenzae

123
Q

primary care investigations for COPD (3)

A
  1. FBC - may have anaemia
  2. spirometry - FEV1/FVC ratio <0.7
  3. refer for CXR
124
Q

general management for patients with COPD (4)

A
  1. SMOKING CESSATION - nicotine replacement therapy
  2. annual flu vaccine
  3. one-off pneumococcal vaccine
  4. pulmonary rehabilitation (if MRC grade 3 or above)
125
Q

stepwise medical tx for COPD (4)

A
  1. first line = SABA (salbutamol) or SAMA (ipratropium bromide)
  2. if not steroid responsive then add LABA (salmeterol) + LAMA (tiotropium)

if steroid responsive then LABA (salmeterol) + ICS (budesonide) - can be given in symbicort inhaler

  1. triple therapy - LABA + LAMA + ICS
  2. referral for add-on tx e.g. long-term O2 therapy
126
Q

key complication of COPD and tx

A

cor pulmonale (oedema, raised jug venous pressure, systolic parasternal heave)

give loop diuretic

127
Q

signs of an acute exacerbation of COPD

A
  • increase in dyspnoea, cough and wheeze
  • increased sputum
  • may be hypoxic/confused
128
Q

management of an acute exacerbation of COPD if:
a) can manage in primary care

b) need admission to hosp

A

a)
1. increase frequency of bronchodilator use, consider nebs
2. prednisolone 30mg for 5 days
3. can give abx (amoxicillin/clarithromycin/doxycycline)

b)
1. oxygen therapy
2. nebulised bronchodilator e.g. salbutamol or ipratropium
3. oral pred/IV hydrocortisone
4. IV theophylline if not responding to bronchodilators

129
Q

what is crystal arthropathy (gout)?

A

a type of arthritis caused by monosodium urate crystals forming inside/around joints

130
Q

list some a) under excretion of uric acid and b) over production of uric acid causes of gout

A

a) diabetes (nephropathy), CKD, drugs e.g. aspirin, diuretics, dehydration

b) high purine diet (alcohol, red meat, shellfish, fructose sweetened drinks), increased cell turnover (leukaemia, lymphoma, psoriasis)

131
Q

pathophysiology of gout

A
  1. uric acid produced from breakdown of purines
  2. normally excreted by kidneys
  3. if levels in blood too high > deposits as urate crystals in joints
132
Q

RFs for gout

A
  1. comorbidities - CKD, HTN, DM, hyperlipidaemia, osteoarthritis, psoriasis
  2. diet
  3. obesity
  4. family hx
  5. male sex
  6. post-menopause
  7. older age
  8. medications - aspirin, diuretics, ciclosporin
133
Q

presentation of gout

A

RAPID ONSET SEVERE joint pain (often overnight)
joint = painful, swollen, tender, erythematous
may have fever

134
Q

what is a sign of longstanding untreated gout?

A

tophi - hard cutaneous nodules

135
Q

investigations for gout

A

bloods - serum urate is diagnostic (>360 mol/L)

136
Q

management for gout:
a) acute
b) prophylactic

A

a) first line = NSAIDs e.g. naproxen
- if NSAIDs contraindicated then colchicine
- paracetamol can be adjunct
- ice packs

b) first line = allopurinol
- lifestyle changes: weight loss, less alcohol, hydration, dairy products, alter risky meds

137
Q

what is constipation? what is the Rome IV diagnostic criteria?

A
  • problematic defecation due to infrequent and/or hard stools
  • ROME IV = bowel movements < 3 a week
138
Q

what timeframe defines chronic constipation?

A

constipation persisting for > 3 months

139
Q

RFs for constipation (social, psych and physical)

A

social
- diet
- reduced mobility
- socioeconomic deprivation
- family hx
- change in routine

psych
- anxiety/depression
- eating disorders
- hx of sexual abuse

physical
- female sex
- older age
- dehydration
- pyrexia

140
Q

secondary causes of constipation (medications, organic, neuro, structural)

A

medications
- opiates
- antidepressants
- antipsychotics
- antimuscarinics
- CCBs
- diuretics

organic
- DM
- hypercalcemia
- hypokalaemia
- hypothyroidism

neuro
- MS
- parkinson’s
- spinal cord injury
- Hirschsprungs

structural
- haemorrhoids
- diverticulitis
- IBD
- cancer
- postnatal damage

141
Q

presentation of constipation in
a) adults
b) elderly

A

a) <3 a week, may be daily but symptoms e.g. excessive straining, abdominal pain, distension/bloating

b) confusion/delirium, nausea or loss of appetite, overflow diarrhoea, urinary retention

142
Q

red flags for constipation (5)

A
  1. sudden change in bowel habit
  2. bleeding
  3. weight loss
  4. fe deficiency anaemia
  5. abdominal pain
143
Q

first line tx for constipation

A

LIFESTYLE MEASURES
- diet high in grains, fruit, veg, sorbitol e.g. apples, apricots, pears
- fluids
- increase activity levels
- improve toilet routine e.g. regular, unhurried, respond immediately, appropriate access

144
Q

management for constipation if <3 months and lifestyle measures haven’t worked

A

first line = ispaghula (bulk-forming laxative)
second line = macrogol

145
Q

management for constipation if >3 months and lifestyle measures haven’t worked
what are some last resort options?

A
  • same as if <3m (first line ispaghula, second line macrogol)
  • consider prucalopride (laxative) IF 2 laxatives of different classes haven’t worked
  • last resort = invasive tx e.g. suppositories, enemas, irrigation
146
Q

define
a) diverticulosis
b) diverticular disease
c) diverticulitis

A

a) outpouchings (herniation) of colonic mucosa and submucosa through the muscular layer of the colonic wall (can be asymptomatic)

b) clinical state caused by symptoms pertaining to diverticular

c) inflammation of diverticulum/diverticula

147
Q

RFs of diverticular disease/diverticulitis (4)

A
  1. low fibre
  2. decreased physical activity
  3. obesity
  4. NSAIDs
148
Q

presentation of diverticular disease and diverticulitis

A
  1. intermittent abdo pain in LLQ (sigmoid) - may be triggered by eating and relieved by passage of stool
  2. constipation/diarrhoea
  3. occasional rectal bleeds

in diverticulitis > severe, more constant pain, fever

149
Q

1st line investigation for diverticulitis

A

bloods: FBC - polymorphonuclear leukocytosis, raised CRP

150
Q

imaging options for diverticulitis and their findings (3)

A
  1. erect CXR - may show pneumoperitneum if perforation
  2. abdo x-ray - may show dilated bowel loops, obstruction/abscesses
  3. abdo CT
151
Q

management of mild diverticulitis

A
  1. oral abx
  2. liquid diet
  3. analgesia e.g. paracetemol
152
Q

when should a patient with diverticulitis be admitted to hospital for IV abx?

A

if symptoms don’t settle within 72h
if initially presenting very severe

153
Q

diagnostic investigation options for diverticular disease (3)

A
  • colonoscopy
  • CT cologram
  • barium enema
154
Q

management of diverticular disease (4)
what meds should be avoided?

A
  1. high fibre diet
  2. if diet not working - bulk-forming laxatives
  3. paracetemol
  4. avoid NSAIDs and opioids (risk of perforation)
155
Q

what is a normal eGFR?

A

125ml/min

156
Q

what are the diagnostic criteria of CKD? what are some markers of kidney damage?

A

EITHER of the following for a MINIMUM of 3 months:
1. impaired GFR (<60)

  1. markers of kidney damage
    - albumin : creatinine ratio >3mg/mmol
    - urine sediment abnormalities e.g. RBCs, WBCs, renal tubular epithelial cells
    - electrolyte abnormalities
    - structural abnormalities identified by imaging
157
Q

GFR categories (1-5)

A
  1. > 90 (normal)
  2. 60-89 (mildly decreased)

3a. 45-59 (moderately decreased)

3b. 30-44 (moderate-severe)

  1. 15-29 (severe)
  2. <15 (kidney failure)
158
Q

ACR categories (3) (mg/mmol)

A

A1 - <3 (normal-mildly increased)

A2 - 3-30 (moderately increased)

A3 - >30 (severely increased)

159
Q

using the eGFR and ACR categories, what stage CKD would a person with an eGFR of 25ml/min and an ACR of 15mg/mmol have?

A

CKD G4A2

160
Q

what 3 things are used to classify CKD?

A
  1. underlying cause
  2. GFR category
  3. proteinuria category
161
Q

prerenal, intrarenal and postrenal causes of CKD

A

PRERENAL
- heart failure
- liver cirrhosis

INTRARENAL
- HTN
- diabetes
- renal artery stenosis
- systemic disease e.g. SLE, RA, HIV, vasculitis
- glomerular disease
- long term NSAIDs
- nephrotoxic substances e.g. lead, tobacco

POSTRENAL
- BPH
- repeated pyeloneph
- structural renal tract disease e.g. tumour
- recurrent urinary calculi

162
Q

CKD may be asymptomatic in the early stages. what incidental findings may cause you to suspect it? (5)

A
  • raised serum creatinine
  • serum eGFR <60
  • proteinuria
  • haematuria
  • urine sediment abnormalities
163
Q

signs and symptoms of early CKD

A
  • polyuria, nocturia, oliguria
  • lethargy
  • pruritis
  • cramps (often worse at night)
  • sleep disturbance
  • poor appetite, weight loss
  • N&V
164
Q

signs and symptoms of progressive CKD

A
  • malnutrition
  • cognitive impairment
  • dehydration
  • dyspnoea
  • frothy urine
  • HTN
  • pallor (renal anaemia)
  • bladder/flank mass
  • peripheral oedema
  • peripheral neuropathy
  • rash
  • uraemic odour e.g. ammonia breath
165
Q

investigations for CKD (3)

A
  1. bloods - serum creatinine (raised), eGFR (<60)
  2. urine sample - albumin-creatinine ratio raised (>3mg/mmol)
  3. urine dipstick - haematuria (persistent)
166
Q

how is CKD monitored?

A

eGFR and ACR

167
Q

how is CKD managed?

A

manage cause… e.g. if HTN/diabetes
- 1st line for HTN is ACEi e.g. lisinopril
- 1st line for hyperlipidaemia is a statin
- 1st line for diabetes is SGLT-2 e.g. dapagliflozin

immunisations e.g. flu, pneumococcal

168
Q

how is end stage renal disease managed?

A

renal replacement therapy e.g. haemodialysis, kidney transplant, peritoneal dialysis

169
Q

which cells secrete insulin? where?
how does insulin decrease blood glucose?

A

beta cells
in islets of langerhans in pancreas
moves glucose from blood into cells

170
Q

which genes are associated with DM1?

A

HLA-DR and HLA-DQ

171
Q

what sort of insulin deficiency is DM1 characterised by?

A

absolute insulin deficiency

172
Q

signs and symptoms of DM1

A

3 Ps - poluria, polydipsia, polyphagia (increased appetite)

weight loss, blurred vision

173
Q

1st line investigations for DM1 and DM2 and their results

A
  1. random plasma glucose >11.1mmol/L
  2. fasting glucose (>7mmol/L)
  3. Hba1c (>48mmol/l)
174
Q

how often should HbA1c be monitored in diabetics?

A

every 3-6 months

175
Q

insulin therapy for DM1 - what is 1st line and what are other options?

A

1st line = multiple daily injection basal-bolus insulin regimen

other options
- short-acting soluble (start working within 30-60 hours, last 4-6 hours)
- short-acting analogues (faster onset, shorter duration)
- long-acting (can last >12 hours)

176
Q

what is DM2 characterised by? (3)

A
  1. hyperglycaemia
  2. insulin resistance
  3. relative lack of insulin
177
Q

pathophys of DM2 - what is it caused by a combo of?

A

insulin resistance (body unable to respond to normal insulin levels) and insulin deficiency (pancreas unable to secrete enough insulin to compensate for resistance)

178
Q

RFs for DM2

A
  • obesity
  • racial groups e.g. african, asian
  • pancreatic trauma/cancer
  • hyperthyroidism
  • pregnancy
  • acromegaly
  • cushing’s
  • age
  • physical inactivity
  • family hx
  • genetics
179
Q

signs and symptoms of DM2 (6)

A
  • can be asymptomatic/mild
  • polydipsia, polyuria
  • blurred vision
  • weight loss
  • recurrent infection
  • fatigue
  • acanthosis nigricans
180
Q

in which diabetes type is glucose self-monitoring recommended? what are 2 options?

A

T1DM

  • continuous glucose monitoring (patch on arm)
  • capillary blood glucose ~4 times a day including before each meal and before bed
181
Q

1st line drug treatment for T2DM

a) what if the pt has cardiovascular disease?
b) what if monotherapy with 1st line is ineffective?

A

1st line = metformin

a) add SGLT-2 inhibitor e.g. empagliflozin

b) add DPP-4 inhibitor (e.g. alogliptin), or sulfonylurea (e.g. gliclazide) or pioglitazone

182
Q

investigations for infectious mononucleosis in
a) <12y
b) >12y

A

a) bloods - EBV viral serology

b) FBC - WCC
monospot test - +ve for heterophile antibodies

183
Q

management for infectious mononucleosis and what advice should be given to pt

A

self-limiting, normally lasts 2-3 weeks, take paracetamol/ibuprofen

avoid alcohol and contact sports

184
Q

what is impetigo?
what two organisms is it mainly caused by?
who is typically affected?

A

a highly contagious common superficial bacterial infection, often caused by S.aureus or S.pyogenes

mostly affects children

185
Q

what are the two main types of impetigo?

A
  1. non-bullous (70%)
  2. bullous - skin eruption characterised by bullae (fluid-filled lesions >1cm diameter)
186
Q

RFs for impetigo (6)

A
  1. breaks in skin e.g. cut, burn, bite, eczema, contact dermatitis
  2. warm/humid weather
  3. poor hygiene
  4. crowded/impoverished environment
  5. comorbidities e.g. diabetes, malnutrition
  6. direct contact w infected person
187
Q

presentation of non-bullous impetigo

A
  1. thin-walled vesicles/pustules rupture and form GOLDEN-BROWN CRUSTS
  2. mouth, limbs, flexures
  3. lesions are asymptomatic
  4. rarely systemic sx e.g. fever or mucosal involvement
188
Q

presentation of bullous impetigo

A
  1. large, fragile flaccid bullae
  2. rupture and ooze yellow fluid, leave scaly rim
  3. flexures, trunk, face and limbs
  4. may have fever
189
Q

how is impetigo diagnosed?

A

usually clinically

190
Q

management of impetigo

a) general points
b) if limited/localised
c) if extensive
d) advice to pts

A

a) normally self-limiting (7-21 days) BUT tx speeds healing and shortens the infective period

b) hydrogen peroxide 1% cream

c) oral flucloxacillin (erythromycin if penicillin allergic)
consider topical abx cream e.g. fusidic acid

d) wash, avoid touching and scratching. cover up where poss. don’t share towels/cloths. wash clothing and bedding daily

191
Q

how long should pts be advised to avoid school/work if they have impetigo?

A

until either
- all lesions healed, dry and crusted over
- OR 48h after starting abx

192
Q

what is osteoporosis? what t-score is diagnostic?

A

skeletal disease characterised by low bone mass (decreased density) and deterioration of bone tissue > bone weakness, fractures

<-2.5

193
Q

primary causes of osteoarthritis (2)

A
  1. menopause
  2. age
194
Q

secondary causes of osteoarthritis (use shattered)

A

Steroids
Hyperthyroidism/hyperparathyroidism
Alcohol/smoking
Thin
Testosterone low
Early menopause
Renal/liver failure
Erosive/inflamm bone disease e.g. RA, myeloma
Dietary calcium low

195
Q

presentation of osteoporosis - which fracture locations are most common?

A
  • asymptomatic until fracture
  • hip (NOF), distal radius, vertebra
196
Q

investigations for osteoporosis

A
  1. exclude non-osteoporotic and secondary causes e.g. bloods etc
  2. DEXA bone mineral density (BMA) scan
197
Q

when is drug tx offered for osteoporosis?

A

if t-score <-2.5

198
Q

1st line medication for prevention and tx of osteoporosis

A

bisphosphonate - alendronate 10mg OD

199
Q

what advice is given when prescribing pts oral bisphosphonates?

A
  • swallow with plenty of water while sitting/standing
  • empty stomach at least 30 mins before breakfast/another oral med
  • stand or sit upright for at least 30 mins after
200
Q

adverse effects of bisphosphonates (3)

A
  1. oesophagitis/oesophageal ulcers
  2. osteonecrosis of jaw
  3. atypical stress fractures
201
Q

what should younger postmenopausal women be offered if they are diagnosed with osteoporosis?

A

HRT

202
Q

which bacteria cause Lyme disease? how is this transmitted?

A

borrelia burgdorferi (spirochetes)

via tick bite

203
Q

RFs for lyme disease

A
  1. occupational/recreational exposure to woodlands and fields
  2. travel abroad e.g. europe, asia, US, canada
204
Q

presentation of Lyme disease

A

erythema migrans - classic ‘bullseye’ appearance

not itchy, hot or painful

205
Q

how to differentiate between lyme disease and a tick bite hypersensitivity reaction

A

if hypersensitivity reaction - erythematous skin lesion, within 48h of detachment, <5cm, itchy and will disappear within 24-48h

lyme disease - presents 1-2 weeks after bite, lasts for several weeks, not itchy, >5cm

206
Q

management of Lyme disease in
a) adults/children >9
b) children <9

A

a) oral doxycycline

b) oral amoxicillin

207
Q

what is mumps? what is it caused by?

A

a viral infection caused by RNA paramyxovirus

208
Q

what vaccination hx is important to ask about in potential mumps?

A

MMR vaccine (80& protection)

209
Q

when does mumps tend to occur?

A

winter and spring

210
Q

presentation of mumps

A
  1. may have flu sx prodrome for a few days
  2. parotid swelling (uni or bilateral)
  3. pain > earache, pain on eating
  4. other = fever, myalgia, lethargy, reduced appetite, headache
211
Q

complications of mumps (3)

A
  1. pancreatitis (abdo pain)
  2. orchitis (testicular pain and swelling)
  3. meningitis/encephalitis (confusion, neck stiffness, headache)
212
Q

investigations for mumps

A

PCR testing on saliva swab

213
Q

management of mumps

A

NOTIFABLE DISEASE

supportive - rest, fluids, analgesia

214
Q

what is rhinosinusitis?

A

inflammation of the paranasal sinuses (sinusitis) and the nasal cavity

215
Q

what are the 4 paranasal sinuses?

A
  1. frontal
  2. ethmoid
  3. maxillary
  4. sphenoid
216
Q

acute vs chronic rhinosinusitis

A

acute = <12 weeks
chronic = >12 weeks

217
Q

causes of rhinosinusitis (4)

A
  1. infection (post viral URTI)
  2. allergens e.g. hayfever
  3. obstruction of drainage - foreign body, trauma, polyps
  4. smoking
218
Q

presentation of rhinosinusitis

A
  1. recent viral URTI
  2. nasal congestion (mouth breathing)
  3. nasal discharge
  4. facial pain/headache - frontal pressure, worse bending down
  5. loss of smell
219
Q

what may someone with chronic rhinosinusitis present with?

A

nasal polyps (growths of nasal mucosa)

220
Q

management of acute rhinosinusitis

what if not improving in 10 days?

A

most self-resolve within 2-3 weeks

if sx aren’t improving after 10d can give high dose nasal steroid spray (mometasone)

or delayed abx prescription (phenoxymethylpenicillin)

221
Q

management options for chronic rhinosinusitis

A
  1. saline nasal irrigation
  2. steroid nasal spray e.g. mometasone

last resort = functional endoscopic sinus surgery (FESS)

222
Q

most common bacterial cause of tonsillitis

A

streptococcus pyogenes

223
Q

complications of tonsillitis (6)

A
  1. peritonsillar abscess (quinsy)
  2. otitis media
  3. scarlet fever
  4. rheumatic fever
  5. post strep glomerulonephritis
  6. post strep reactive arthritis
224
Q

presentation of tonsillitis (5)

A
  1. sore throat
  2. fever >38
  3. painful swallowing
  4. red, inflamed, enlarged tonsils +- exudate
  5. may have anterior cervical lymphadenopathy
225
Q

which two criteria can be used for bacterial tonsillitis diagnosis ?

A
  1. centor criteria
  2. feverPAIN
226
Q

centor criteria for tonsillitis
a) which score gives high likelihood of bacterial
b) criteria

A

a) score of 3 or more gives 40-60% probability of bacterial

b) 1 point each for:
- fever >38
- tonsillar exudate
- absence of cough
- tender anterior cervical lymph nodes

227
Q

feverPAIN scoring for tonsillitis

A
  1. Fever during past 24h
  2. Purulence
  3. Attended within 3d of sx onset
  4. Inflamed tonsils
  5. No cough/coryza
228
Q

management and safety netting for viral tonsillitis

A
  1. paracetemol + ibuprofen
  2. return IF pain hasn’t settled after 3 days OR fever rises to above 38.3
229
Q

a centor score of X or a feverPAIN of X indicates abx for tonsillitis?

A

centor score of =>3

feverPAIN score of =>4

230
Q

other than using criteria, which pts with tonsillitis should abx be considered in?

A

young infants, immunocompromised, comorbidity, hx of rheumatic fever

231
Q

1st line tx for tonsillitis

what if allergic to pen?

A

1st line = pen V (phenoxymethylpenicillin) for 10 days

if allergic - clarithromycin

232
Q

cause of herpes labialis vs genital herpes

A

herpes labialis = infection of mouth area and lips, most commonly with HSV1

genital herpes = caused by either HSV1 or HSV2

233
Q

management of HSV in pregnancy
a) if mum has primary attack occurs before 28w

b) if mum had recurrent herpes before falling pregnant

A

a) elective c-section, tx with acyclovir and prophylactic acyclovir from 36w

b) low chance of transmission but give prophylactic acyclovir from 36w

234
Q

after initial infection, where does HSV establish latency in
a) herpes labialis (cold sores)
b) genital herpes

A

a) trigeminal nerve ganglion

b) sacral nerve ganglia

235
Q

primary infection presentation of HSV

A

tends to be most severe (recurrent infections present milder)

herpes labialis
1. gingivostomatitis - swelling, blisters, canker sores in mouth
2. fever
3. tingling and burning in mouth
4. vesicular then ulcerative lesions

genital herpes
1. genital ulcers/blistering lesions
2. neuropathic pain e.g. tingling
3. dysuria (women)
4. flu-like sx

236
Q

describe the nature of HSV infections

A

PRIMARY INFECTION - most severe, lasts 3-ish weeks

then pt will be fine for months/years until reactivations - milder, last shorter time

237
Q

investigations for HSV

A

normally clinical but can confirm with…

HSV PCR swab from lesion

238
Q

management of HSV (short-term)
a) gingivostomatitis
b) cold sores
c) genital herpes

A

a) oral acyclovir, chlorhexidine mouthwash

b) topical acyclovir

c) oral acyclovir 400mg

239
Q

management of recurrent HSV

A

long-term prophylactic acyclovir

240
Q

management of syphilis

A

IM benzathine penicillin

241
Q

1st line management of atrial fibrillation

A
  • rate control e.g. beta-blocker
  • DOAC e.g. apixaban
242
Q

type 2 diabetes tx pathway if no CV comorbidity

A
  1. metformin
  2. add sulfonylurea e.g. gliclazide
  3. add DPP-4 inhibitor e.g. alogliptin
243
Q

1st line dual therapy for type 2 diabetes if any CV comorbidity?

A

metformin + SGLT-2 inhibitor (e.g. empagliflozin/dapagliflozin)

244
Q

which T2 diabetes medication class is associated with bladder cancer risk?

A

DPP-4 inhibitors e.g. alogliptin

245
Q

signs of steroid-responsiveness in a COPD pt

A
  1. atopy/asthma hx
  2. eosinophilia in bloods
  3. diurnal variation
246
Q

COPD tx pathway if steroid responsive

A
  1. SABA
  2. add LAMA + LABA
  3. add ICS (SABA + LAMA + LABA + ICS)
  4. referral for add on tx e.g. O2 therapy
247
Q

COPD tx pathway if not steroid responsive

A
  1. SABA or SAMA
  2. add LABA + ICS
  3. add LAMA (SAMA + LABA + ICS + LAMA)
  4. referral for add on tx e.g. O2 therapy

PHASE 3A (18 decks)

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