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

PRIMARY CARE - cardio, resp, endocrine, GI, MSK, neuro 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, recheck on 2-3 occasions
2. if persistently high, offer ABPM (24hr)
3. if stage 1 - QRISK to decide tx
4. if stage 2 - start antihypertensive tx

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6
Q

what are the stages of hypertension?

A

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

stage 2 - between 150/95 and 160/100

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7
Q

what is normal BP?

A

90/60 - 120/80

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8
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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9
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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10
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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11
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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12
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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13
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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14
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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15
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
d) pregnancy

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16
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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17
Q

aetiology of GORD

A

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

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18
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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19
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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20
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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21
Q

investigations for GORD

A

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

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22
Q

non-pharmacological treatment for GORD

A

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

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23
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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24
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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25
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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26
Q

surgical management for GORD

A
  1. fundoplication
  2. repair of hiatal defects
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27
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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28
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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29
Q

epidemiology of hypothyroidism (3)

A
  1. F > M
  2. white populations
  3. 60-70 y/o
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30
Q

most common cause of congenital hypothyroidism

A

iodine deficiency during pregnancy

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31
Q

most common cause of acquired hypothyroidism

A

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

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32
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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33
Q

what is postpartum thyroiditis?

A

thyroid becomes inflamed after childbirth > can proceed to permanent hypothyroidism

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34
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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35
Q

RFs for hypothyroidism

A
  1. white
  2. female
  3. postpartum
  4. iodine deficiency
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36
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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37
Q

signs of hypothyroidism

A
  • bradycardia
  • slow reflexes
  • ataxia
  • dry hair/skin
  • yawning
  • cold hands
  • ascites
  • immobile
  • congestive cardiac failure
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38
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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39
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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40
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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41
Q

hypothyroidism management

A

levothyroxine (synthetic T4) - start LOW and titre up

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42
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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43
Q

RFs for a hiatus hernia

A
  • obesity
  • increased intraabdominal pressure e.g. ascites, pregnancy, multiparity
  • age
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44
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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45
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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46
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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47
Q

define acute bronchitis

A

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

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48
Q

what causes acute bronchitis?

A

normally VIRAL
- rhinovirus
- enterovirus
- influenza A/B

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49
Q

risk factors for acute bronchitis

A
  • viral infection exposure
  • smoker
  • pollution
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50
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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51
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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52
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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53
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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54
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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55
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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56
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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57
Q

presentation of haemorrhoids

A
  • bright red painless rectal bleeding
  • perianal pain
  • pruritis
  • feeling of incomplete evacuation
  • tender palpable lesion
  • anal mass
58
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
59
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
60
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

61
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
62
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
63
Q

investigations for anal fissures

A

clinical diagnosis with history and DRE

64
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)
65
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

66
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
67
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
68
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

69
Q

investigations for anaphylaxis

A

ABCDE approach

70
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
71
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

72
Q

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

A

sphincterotomy

73
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

74
Q

who is osteoarthritis common in?

A

elderly and females (esp postmenopause)

75
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

76
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
77
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
78
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
79
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)

80
Q

investigations for OA

A

1st line = refer for x-ray

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

81
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

82
Q

non-pharmacological management options for OA

A

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

83
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
84
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

85
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

86
Q

brief pathophys of atrial fib

A
  1. uncoordinated atrial activation
  2. ineffective atrial contraction
87
Q

what does atrial fibrillation hugely increase the risk of?

A

stroke

88
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
89
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

90
Q

primary care investigations for AFib

A
  1. auscultation - extremely irregular HR
  2. 12-lead ECG
91
Q

ECG findings in AFib (3)

A
  1. irregularly irregular QRS complex
  2. absent p waves
  3. QRS >120ms
92
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
93
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
94
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)

95
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)

96
Q

RFs for atrial flutter (2)

A
  1. atrial surgery/atrial ablation
  2. toxic and metabolic conditions
97
Q

signs and symptoms of atrial flutter

A

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

98
Q

investigations for atrial flutter

A
  1. auscultation
  2. ECG
99
Q

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

A
  1. sawtooth pattern
  2. regularly irregular QRS complex
100
Q

management for atrial flutter

A

emergency hosp admission if haemodynamically unstable

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

101
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
102
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

103
Q

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

A

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

104
Q

what causes bursitis? (4)

A
  • repetitive stress
  • infection
  • autoimmune disease
  • trauma
105
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

106
Q

how is bursitis investigated?

A

normally clinical diagnosis

if suspect sepsis - refer for fluid aspirate staining/culture

107
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

108
Q

what is COPD?

A

irreversible progressive disorder of airway obstruction

109
Q

most common cause of COPD

A

SMOKING

110
Q

types of COPD

A

chronic bronchitis and emphysema

111
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

112
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

113
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

114
Q

classic presentation of emphysema

A

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

115
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
116
Q

when should A1AT deficiency be suspected?

A

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

117
Q

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

A

Haemophilus influenzae

118
Q

primary care investigations for COPD (3)

A
  1. FBC - may have anaemia
  2. spirometry - FEV1/FVC ratio <0.7
  3. refer for CXR
119
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)
120
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
121
Q

key complication of COPD and tx

A

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

give loop diuretic

122
Q

signs of an acute exacerbation of COPD

A
  • increase in dyspnoea, cough and wheeze
  • increased sputum
  • may be hypoxic/confused
123
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

124
Q

what is crystal arthropathy (gout)?

A

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

125
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)

126
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
127
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
128
Q

presentation of gout

A

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

129
Q

what is a sign of longstanding untreated gout?

A

tophi - hard cutaneous nodules

130
Q

investigations for gout

A

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

131
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

132
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
133
Q

what timeframe defines chronic constipation?

A

constipation persisting for > 3 months

134
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

135
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

136
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

137
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
138
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

139
Q

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

A

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

140
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

PHASE 3A (11 decks)

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