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5th year > Important OSCE topics > Flashcards

Important OSCE topics Flashcards

1
Q

What are the first rank features of schizophrenia?

A

Auditory hallucinations (running commentary, 2+ voices discussing the patient, thought echo)

Delusions (e.g. persecutory)

Thought disorders (thought insertion, broadcasting and withdrawal)

Passivity phenomena (bodily sensations controlled by external influence, feelings/thoughts/mood/actions under someone else’s control)

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2
Q

What are other features of schizophrenia?

A

Negative symptoms (catatonia, blunting, anhedonia, alogia (poverty of speech), avolition
Impaired insight
Incongruency/blunting
Neologisms

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3
Q

What should you initially offer for pain relief in palliative care?

A

Regular MR morphine PO (can also give immediate release) and immediate release PO for breakthrough pain

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4
Q

What dose of morphine should patients generally start at?

A

20-30mg MR morphine PO daily dose

5mg breakthrough, e.g. 15mg MR morphine PO BD + 5mg breakthrough PRN

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5
Q

When prescribing morphine what side effects should you make the patient aware of and how can you counteract these?

A

Drowsiness
Nausea - antiemetic
Constipation - always give laxative

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6
Q

What fraction of the total daily dose of morphine should the breakthrough dose be?

A

1/6th

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7
Q

What opioid is preferred in patients with mild-moderate renal impairment?

A

Oxycodone

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8
Q

What opioid is referred in patients with severe renal impairment?

A

Fentanyl, buprenorphine, alfentanil

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9
Q

What is the management of metastatic bone pain?

A

Strong opioids
Bisphosphonates
Radiotherapy

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10
Q

When you are increasing the dose of morphine, by how much should you increase it at a time?

A

30-50%

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11
Q

What is the conversion rate for:

oral codeine –> oral morphine?

A

/10

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12
Q

What is the conversion rate for:

oral tramadol –> oral morphine?

A

/10

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13
Q

What is the conversion rate for:

oral morphine –> oral oxycodone?

A

/1.5

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14
Q

What is the conversion rate for:

oral morphine –> IV morphine?

A

/2

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15
Q

What is the morphine dose equivalent of a 12 microgram fentanyl patch?

A

30mg

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16
Q

What is the morphine dose equivalent of a 10microgram buprenorphine patch?

A

24mg

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17
Q

What are important points to remember for administering morphine?

A

It is in a locked cupboard, use needs to be logged in logbook, two people need to sign out the morphine

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18
Q

What are features of an UGI bleed?

A

Haematemesis, malaena, epigastric discomfort, sudden collapse

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19
Q

What are causes of UGI bleed?

A 
Mallory weiss tear
Oesophageal/gastric cancer 
Peptic ulcer
Oesophagitis
Oesophageal varices (tends to be large vol, haemodynamic compromise)
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20
Q

How is UGI bleed managed?

A

Admit
Cross match, FBC, UE, LFT, clotting
Airway management, A–>E
Suspected varices –> terlipressin + prophylactic antibiotics, endoscopy within 24 hours, banding/sclerotherapy, sengstaken-blakemore tube, portal pressure should be managed with medical therapy +/- TIPSS

All those who received intervention should be on continuous PPI IV for 72 hours

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21
Q

How long can a sengstaken-blakemore tube stay in?

A

Only for 12 hour, after that risk of necrosis

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22
Q

How is risk assessed in UGI bleed?

A

Blatchford score at risk, then with full rockall score after endoscopy

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23
Q

What vital signs/blood results would you expect to see in UGI bleed?

A

High urea, low Hb, low BP, high pulse

Remember patients likely to have hepatic dx hx

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24
Q

What are the causes of meningitis in ages 0-3 months?

A

Listeria monocytogenes
E. coli
GBS

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25
Q

What are the main causes of meningitis in ages 3 months-6 years?

A

H. influenzae
Strep pneumonia
N. meningitidis

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26
Q

What are the main causes of meningitis in ages 6 months-60 years?

A

Strep pneumonia

N. meningitidis

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27
Q

What are the main causes of meningitis in those >60?

A

Strep pneumonia
N. meningitidis
Listeria

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28
Q

What is a common cause of meningitis in those who are immunocompromised?

A

Listeria

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29
Q

What does the CSF analysis look like in someone with a bacterial meningitis?

A

Appearance: cloudy
White cells: polymorphs
Glucose: <50% plasma
Protein: high

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30
Q

What does the CSF analysis look like in someone with a viral meningitis?

A

Appearance: clear/cloudy
White cells: lymphocytes
Glucose: 60-80% plasma
Protein: normal/high

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31
Q

What does the CSF analysis look like in someone with a TB meningitis?

A

Appearance: fibrin webs
White cells: lymphocytes
Glucose: <50%
Protein: high

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32
Q

What does the CSF analysis look like in someone with a fungal meningitis?

A

Appearance: cloudy
White cells: lymphocytes
Glucose: low
Protein: high

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33
Q

How should you investigate suspected meningitis?

A

FBC, UE, LFT, CRP, coag, PCR, blood gas, blood cultures

LP if no signs of raised ICH (do not do LP in suspected meningococcal disease)

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34
Q

How should you manage suspected meningococcal disease?

A

IM benzylpen

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35
Q

What is the empirical management of meningitis in those aged <3 months?

A

IV cefotaxime + amoxicillin

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36
Q

What is the empirical management of meningitis in those aged 3 months-50 years?

A

IV cefotaxime

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37
Q

What is the empirical management of meningitis in those aged >50?

A

IV cefotaxime + amoxicillin

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38
Q

How is known listeria meningitis managed?

A

IV gentamicin and amoxicillin

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39
Q

What other non-antibiotic drug is sometimes given in meningitis?

A

IV Dex (not if septic shock, immunocomp or following surgery)

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40
Q

What drug is used instead of amoxicillin in meningitis if there is a pencillin allergy?

A

Chloramphenicol

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41
Q

Who should be offered prophylaxis for meningitis? What drugs is it?

A 
Close contacts (<7 days) of meningococcal meningitis
Rifampicin or ciprofloxacin (one dose)
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42
Q

What are the ECG changes in hyperkalaemia?

A

Tall tented T waves
Small p waves
Broadened QRS complexes

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43
Q

What are causes of hyperkalaemia?

A 
AKI
Drugs - spironolactone, K sparing diuretics, ACEi, ARB, heparin, ciclosporin
Addisons disease
Massive transfusion 
Metabolic acidosis
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44
Q

How is hyperkalaemia managed?

A

Stabilise myocardium - calcium gluconate

Shift K intracellularly - NEB salbutamol, insulin/dextrose infusion

Excrete K - calcium resonium, dialysis (for persistent hyperkalaemia in AKI), loop diuretics

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45
Q

What are the three types of causes of AKI?

A

Pre-renal
Intrinsic
Post-renal

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46
Q

What are some pre-renal causes of AKI?

A

Hypovolaemia, e.g. due to vomiting/diarrhoea

Renal artery stenosis

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47
Q

What are some intrinsic causes of AKI?

A 
Glomerulonephritis
ATN
Acute interstitial nephritis 
rhabdomyolysis
Tumour lysis syndrome
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48
Q

What are some post-renal causes of AKI?

A

External compression of ureter

Kidney stone in bladder/ureter

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49
Q

Name some drugs with nephrotoxic potential?

A

NSAIDs, ACEi, ARB, diuretics, aminoglycosides, iodinated contrast

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50
Q

What are features of AKI?

A

Fluid overload
Oliguria (<0.5ml/kg/h)
Rise in molecules kidney usually excretes (Cr, U, K) –> arrhythmias, uraemia (pericarditis, encephalopathy)

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51
Q

How should you investigate AKI?

A

UE - rise in serum Cr >26micromol/l in last 48h, rise in serum cr >50% in last 7 days, oliguria (<0.5ml/kg/h)
Urinalysis
Imaging - USS renal tract (within 24h)

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52
Q

How should you manage AKI?

A

Stop drugs - those making AKI worse (aminoglycosides, NSAIDs, ARBs, ACEi, diuretics), and those putting at risk of toxicity (lithium, metformin, digoxin)
Only use loop diuretics for significant fluid overload
Management hyperkalaemia
Referral (urologist/nephrologist)
RRT if not responding to medical management of complications (e.g. hyperkalaemia, uraemia..)

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53
Q

What is acute tubular necrosis?

A

Necrosis of renal tubular epithelial cells

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54
Q

What are the two main causes of ATN?

A

Toxins - aminoglycosides, myoglobin secondary to rhabdomyolysis, contrast agents, lead)

Ischaemia - sepsis/shock

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55
Q

What do you see in the urine of someone with ATN?

A

Brown muddy casts

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56
Q

What can cause acute interstitial nephritis?

A

Drugs, esp antibiotics (rifampicin, penicillin, NSAIDs, allopurinol, furosemide)
Systemic dx: SLE, sjogrens
Infections: Hanta virus, staph

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57
Q

What are features of acute interstitial nephritis?

A

Fever, rash, eosophilia, arthalgia, mild renal impairment, HTN

White cell casts, sterile pyuria

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58
Q

What is the CHADSVASC score?

A 
Used to assess need for anticoagulation (DOAC or warfarin) in those with AF
C - congestive cardiac failure (1)
H - HTN (1) 
A2 - age >=75 (2)
D - DM (1)
V - vascular disease (1)
A -  age 65-74 (1) 
Sc - sex - female (1)

Score 0 = no anticoagulation, score 1 + male - consider Rx, score 2 - start treatment

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59
Q

What are the two types of bleeds causing epistaxis?

A

Anterior bleeds - usually from kiesselbacks plexus, often visible

Posterior bleeds - usually not visible, bleeding from deeper structures

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60
Q

What can cause epistaxis?

A

Trauma

Platelet disorder - ITP, thrombocytopenia, splenomegaly, leukaemia

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61
Q

How is epistaxis managed?

A

Haemodynamically stable –> sit forward, mouth open, pinch cartilaginous region of nose – if stops –> naseptin (peanut/soy/neocmycin allergy –> use mupirocin) to prevent crusting/vestibulitis

If doesn’t stop bleeding after 10-15 min attempt packing/cautery

Haemodynamically unstable/posterior/unknown bleeding source –> ED

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62
Q

What are causes of SBO?

A

Intrabdominal adhesions, hernias, neoplasms, IBD

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63
Q

What are features of SBO?

A

NV, bloating, constipation, abdominal pain

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64
Q

How do you image SBO?

A

Abdominal x-ray

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65
Q

How do you manage SBO in the first instance?

A

NG tube to decompress
A-E
Foley catheter to measure urine output
Fluids

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66
Q

What things can you not do on an AV fistula arm?

A

Cannulas
Take bloods
Do BP on that arm

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67
Q

What are causes of parkinsonism?

A 
PD
Drug induced, e.g. metoclopramide, antipsychotics
Progressive supranuclear palsy
Multiple system atrophy
Wilson's disease
Post-encephalitis
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68
Q

What causes parkinsons disease?

A

Progressive degeneration of dopaminergic neurons in the substantia nigra

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69
Q

What are the classic triad of features in PD?

A

Bradykinesia
Tremor
Rigidity

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70
Q

What features of PD symmetrical?

A

Classically asymmetrical

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71
Q

What are the features of bradykinesia in PD classically?

A

Poverty of movement (hypokinesia)
Short, shuffling steps
Reduced arm swing
Difficulty initiating movement

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72
Q

What kind of tremor is seen in PD?

A

Pill rolling, asymmetrical, low frequency, at rest

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73
Q

What are other features of PD?

A 
Mask like facies
Stooped posture
Micrographia
Drooling
Psychiatric features - depression, sleep disturbance
Impaired olfaction
REM sleeping disorder
Fatigue
Postural hypotension
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74
Q

What may give clues that parkinsonism is drug induced?

A

Rapid onset, bilateral

Rigidity and tremor uncommon

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75
Q

How is parkinsons disease diagnosed?

A

Clinically

If uncertainty SPECT can be used

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76
Q

What drugs can be used in the management of PD?

A

Levodopa with carbidopa
Dopamine receptor agonists, e.g. bromocriptine, ropinirole
MAO-B inhibitors, e.g. selegiline
Amantadine
COMT inhibitors, e.g. entacapone
Anti-muscarinics, more used for drug induced parkinsonism

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77
Q

What is the most common type of cancer in the west?

A

Basal cell carcinoma

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78
Q

What is the most common type of BCC?

A

Nodular

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79
Q

What do BCC look like?

A

Exist in sun exposed sites, especially head and neck
Initially pearly, flesh coloured papule with telangiectasia
May ulcerate leaving central cater

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80
Q

How are BCC managed?

A 
Referral to derm
Surgical removal 
Curettage
Cryotherapy
Topical cream - imiquimod, fluorouracil
Radiotherapy
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81
Q

What is compartment syndrome?

A

Raised pressure within a closed anatomical space

Raised pressure –> compromises tissue perfusion –> necrosis

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82
Q

What are the two main fractures that are implicated in compartment syndrome?

A

Supracondylar fractures

Tibial shaft injuries

83
Q

What are the features of compartment syndrome?

A

Pain (especially on movement, even passive)
Excessive use of breakthrough analgesia
Paraesthesia
Pallor
Arterial pulsation may still be felt as necrosis occurs due to microvascular compromise
Paralysis

84
Q

How is compartment syndrome diagnosed?

A

Measurement of intracompartmental pressure (excess of 20mmHg abnormal, >40 diagnostic)

85
Q

How is compartment syndrome managed?

A

Prompt + extensive fasciotomies
Aggressive IV fluids to avoid myoglobulinuria
Debridement of necrotic tissue, amputation may occur

Death of muscle groups occurs within 4-6 hours

86
Q

What are the two most common causes of acute pancreatitis?

A

Alcohol

Gallstones

87
Q

What is the pathophysiology of acute pancreatitis?

A

Autodigestion of pancreatic tissue by pancreatic enzymes –> necrosis

88
Q

What are features of acute pancreatitis?

A

Severe epigastric pain, radiating to back
Vomiting
Epigastric tenderness, low grade fever
Periumbilical discolouration (Cullens sign) and flank discolouration (Grey-Turners sign)

89
Q

What investigations should be done in suspected acute pancreatitis?

A

Serum amylase - raised
Serum lipase
Imaging (diagnosis can be made without imaging if serum amylase/lipase >3x upper limit)
USS imaging important to assess aetiology

90
Q

What scoring systems can be used to identify cases of severe pancreatitis which may require ITU management?

A

Ranson score
Glasgow score
APACHE II

91
Q

What mnemonic can be used to remember the causes of acute pancreatitis?

A 
GET SMASHED
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Steroids/scorpion venom
Hypertriglyceridaemia, hypercalcaemia, hypothermia
ERCP
Drugs (azathioprine, mesalazine, furosemide...)
92
Q

What are local complications of acute pancreatitis?

A 
Pancreatic fluid collections
Pseudocysts
Pancreatic necrosis
Pancreatic abscess
Haemorrhage
93
Q

What systemic complication can occur in acute pancreatitis?

A

ARDS

94
Q

What are the key aspects in the management of acute pancreatitis?

A

Fluid resus (aggressive)
Analgesia (IV opioids)
NBM, enteral nutrition in moderate/severe pancreatitis within 72h of presentation

Surgery -
Gallstones –> cholecystectomy
Obstructed biliary system –> ERCP
Necrosis + worsening organ failure –> debridement and FNA, surgical necrosectomy

95
Q

What factors predispose to obstructive sleep apnoea?

A

Obesity
Macroglossia
Large tonsils
Marfans

96
Q

What are consequences of sleep apnoea?

A

Daytime somnolence
Compensated resp acidosis
HTN

97
Q

How can you assess sleepiness in OSA?

A

Epworth sleepiness scale
Multiple sleep latency test
Sleep studies

98
Q

What is the management of OSA?

A

Weight loss
CPAP first line for moderate/severe OSA
Intra-oral devices (e.g. mandibular advancement) can be used in mild OSA or is CPAP not tolerated

99
Q

Do they DVLA need to be informed if a patient has OSA?

A

If it is causing excessive daytime sleepiness

100
Q

What epworth scores correlated with moderate and severe daytime sleepiness?

A

13-15 moderate

16-24 severe

101
Q

What are differentials for OSA?

A 
Asthma
COPD
GORD
Heart failure
Depression
102
Q

What is sjogren’s syndrome?

A

Autoimmune disorder affecting exocrine glands –> dry mucosal surfaces

Can be primary or secondary to RA etc.

103
Q

What malignancy is there an increased risk of in sjogrens?

A

Lymphoid

104
Q

What are features of sjogren’s?

A 
Dry eyes (keratoconjunctivitis sicca) 
Dry mouth 
Vaginal dryness
Arthralgia
Reynaud's, myalgia
Sensory polyneuropathy
Recurrent parotitis
105
Q

What do investigations of sjogrens generally find?

A 
RF +ve
ANA +ve
Anti Ro, Anti La
\+ve Schirmer's test (filter paper near conjunctival sac to measure tear formation)
Low C4
106
Q

What does histology show in sjogren’s?

A

Focal lymphocytic infiltration

107
Q

How is sjogren’s managed?

A

Artificial tears and saliva

Pilocarpine may stimulate saliva production

108
Q

What wells score indicates a PE is likely?

A

> 4

109
Q

If PE is likely how is it managed/investigated?

A

Immediate CTPA (if delay DOAC in interim)

If CTPA +ve –> PE diagnosed

If CTPA -ve –> consider proximal leg vein USS if DVT suspected

110
Q

If PE is unlikely how is it managed/investigated?

A

D-dimer
+ve –> immediate CTPA (delay –> give DOAC)
-ve –> PE unlikely, stop anticoagulation

111
Q

What is the investigation of choice in suspected PE in renal impairment?

A

VQ scan

112
Q

What are the classic ECG changes seen in PE?

A

Sinus tachycardia (most common)
S1T3T3 - large S wave in I, large Q in III, inverted T wave in III
RBBB and RAD may also be seen

113
Q

What score is used to assess suitability of outpatient treatment in low risk PE patients?

A

PESI (pulmonary embolism severity index) score

114
Q

What two anticoagulants should be offered first line in PE?

A

Apixaban
Rivaroxaban

If renal impairment severe –> LMWH/UFH

115
Q

How long should patients who have had a provoked PE be on anticoagulation?

A

3 months

116
Q

How long should patients who have had an unprovoked PE be on anticoagulation?

A

6 months

117
Q

How is PE with haemodynamic instability managed?

A

Thrombolysis

118
Q

What may patients who have repeat PEs be considered for?

A

IVC filters

119
Q

What wells score indicates DVT is likely?

A

2+ points

120
Q

How should you manage a patient where DVT is likely?

A

Proximal leg vein USS within 4 hours
+ve –> DOAC
-ve –> D-dimer

If USS cannot be done in 4 hours - DOAC in interim

If scan negative, D-dimer positive -> stop DOAC and repeat USS in 6-8 days

121
Q

How should you manage a patient where DVT is unlikely?

A

D-dimer
+ve –> proximal leg vein USS wihin 4h
-ve –> DVT unlikely

122
Q

What common pathogens are implicated in cellulitis?

A

Strep pyogenes

Staph aureus

123
Q

How is cellulitis diagnosed?

A

Clinically

Bloods and blood cultures may be done if patient septicaemic

124
Q

What classification is used to guide how we manage patients with cellulitis?

A

Eron

125
Q

What is the first line treatment for cellulitis?

A

Mild/moderate - flucloxacillin
Clarithromycin/erythromycin (pregnancy) or doxycycline in penicillin allergic patients

Severe cellulitis - co-amoxiclav/clindamycin

126
Q

What is the most common organism causing septic arthritis?

A

Staph aureus

127
Q

What is the most common organism causing septic arthritis in young sexually active individuals?

A

N. gonorrhoea

128
Q

Where is the commonest location to get septic arthritis?

A

Knee

129
Q

What are the features of septic arthritis?

A

Acute, swollen joint
Restricted movement
Fluctuant
Fever

130
Q

How do you investigate septic arthritis?

A

Synovial fluid sampling
Blood cultures
Joint imaging

131
Q

How is septic arthritis managed?

A

IV antibiotics, e.g. flucloxacillin
Needle aspiration to decompress joint
Arthroscopic lavage may be req.

132
Q

What are the early causes (0-5 days) of post-operative pyrexia?

A 
Blood transfusion 
Cellulitis
Urinary tract infection 
Physiological systemic inflammatory reaction (usually next day) 
Pulmonary atelectasis
133
Q

What are late causes of post-operative pyrexia (>5 days)?

A

VTE
Pneumonia
Wound infection
Anastomotic leak

134
Q

What dose of adrenaline is used in ALS?

A

1ml 1:10, 000 IV

135
Q

What dose of adrenaline is used in anaphylaxis?

A

0.5ml 1:1000 IM

136
Q

How often can adrenaline be repeated in anaphylaxis?

A

Every 5 minutes

137
Q

What are the drugs and doses that should be given in anaphylaxis?

A

Adrenaline: 0.5ml 1 in 1000

138
Q

What are the drugs and doses that should be given in anaphylaxis?

A

Adrenaline: 0.5ml 1 in 1000

Hydrocortisone 200mg

Chlorphenamine 10mg

139
Q

What enzyme level can be measured to determine in a patient has had a true anaphylactic reaction?

A

Serum tryptase

140
Q

How should you give oxygen therapy in those with COPD?

A

If critically unwell - 15L nonrebreath mask with reservoir bag

If not use 28% venturi mask at 4l/min to aim for sats of 88-92% before you have a blood gas (if pCO2 normal can aim for sats of 94-98%)

141
Q

What is immune thrombocytopenia?

A

Immune mediated reduction in platelet count

Abs are directed against glycoprotein IIb/IIIa

142
Q

What is the presentation of ITP?

A

Petechiae, purpura

Bleeding

143
Q

How is ITP managed?

A

Oral pred

Pooled normal human Ig

144
Q

What are the 4 Hs in ALS?

A

Hypoxia
Hypovolaemia
Hyperkalaemia
Hypothermia

145
Q

What are the 4 Ts in ALS?

A

Thrombosis
Tension pneumothorax
Tamponade
Toxins

146
Q

What is involved in the diagnostic workup of acute heart failure?

A

Blood tests - ?anaemia ?abnormal electrolytes ?infection
CXR - ?pulmonary venous congestion, ?cardiomegaly, ?interstitial oedema
Echo - ?tamponade
BNP

147
Q

What is involved in the management of acute heart failure?

A 
Oxygen 
IV loop diuretics
Opiates
Vasodilators
Inotropic agents
CPAP
Ultrafiltration 
Mechanical circulatory assistance
148
Q

What test should be done in all those who present with suspected chronic heart failure?

A

NT-proBNP

149
Q

If levels of BNP are high in suspected heart failure what should you do?

A

Arrange specialist assessment (including TTE) within 2 weeks

150
Q

If levels of BNP are raised in suspected heart failure what should you do?

A

Arrange specialist assessment (incl TTE) within 6 weeks

151
Q

List a few things that may also increase BNP levels other than heart failure

A 
Tachycardia
Ischaemia
Hypoxaemia (incl. PE)
Sepsis
GFR <60
Diabetes
COPD
Age >70
Cirrhosis
152
Q

What classification system is used to classify heart failure?

A

NYHA (should look over this?)

153
Q

How is chronic heart failure managed?

A

1st line: ACEi and Beta blocker
2nd line: aldosterone antagonist
3rd line: start by specialist, e.g. ivabradine, digoxin, nitrates

Remember annual influenza vaccine + 1 off pneumococcal

154
Q

What are unmodifiable risk factors for ACS?

A

Increased age
Male gender
FH

155
Q

What are modifiable risk factors for ACS?

A 
Smoking
DM
HTN
Hypercholesterolaemia
Obesity
156
Q

What are the two most important investigations in patient presenting with suspected ACS?

A

Troponin

ECG

157
Q

What ECG changes and coronary artery are associated with an anterior MI?

A

V1-4

Left anterior descending

158
Q

What ECG changes and coronary artery are associated with an inferior MI?

A

II, III, aVF

Right coronary artery

159
Q

What ECG changes and coronary artery are associated with an lateral MI?

A

I, V5, 6

Left circumflex

160
Q

What is involved in the management of ACS?

A

MONA (morphine, oxygen if sats <94%, nitrates (e.g. GTN), aspirin (300mg PO))

STEMI –> give 2nd antiplatelet (e.g. ticagrelor), PCI

NSTEMI –> GRACE, high score –> coronary angiography during admission, if not at later date

161
Q

What is standard secondary prevention in those who have had an ACS?

A 
Aspirin
Second antiplatelet, e.g. clopidogrel 
Beta blocker
ACEi
Statin
162
Q

How is STEMI managed?

A

PCI possible in 120 min?
Yes - prasugrel + PCI

No - fibrinolysis, antithrombin, ticagrelor (if ongoing myocardial ischaemia consider PCI)

163
Q

What investigations should be done in suspected COPD?

A

Post-bronchodilator spirometry
CXR
FBC (exclude secondary polycythaemia)
BMI

164
Q

What are CXR signs of COPD?

A

Hyperinflation
Bullae
Flat hemidiaphragm

165
Q

What FEV1/FVC is diagnostic of COPD?

A

<0.7

166
Q

What are the classifications of COPD?

A

FEV1>80% predicted - stage 1 (mild)

FEV1 50-79% - stage 2 (moderate)

FEV1 30-49% - stage 3 (severe)

FEV1 <30% - stage 4 (very severe)

167
Q

What is involved in the general management of COPD?

A

Smoking cessation advice
Annual flu, one of pneumococcal vaccine
Pulmonary rehab if functionally disabled by COPD

168
Q

What is the first line treatment of COPD?

A

SABA/SAMA

169
Q

What is the second line treatment of COPD?

A

Steroid responsive features (atopy, eosinophilia, variation in FEV1, diurnal variation in PEFR) –> LABA + ICS (if still breathless triple therapy (LAMA, LABA, ICS)

No asthmatic features –> LABA + LAMA

170
Q

What other medications may be given in stable COPD?

A

Theophylline

Azithromycin prophylaxis in those who do not smoke, have optimised medical management and continue to have exacerbations

171
Q

How is cor pulmonale managed?

A

Loop diuretics

Long term oxygentherapy

172
Q

Which patients with COPD should be offered long term oxygen therapy?

A

Those with pO2 <7.3kPa or those with pO2 7.3-8 + 1 of: secondary polycythaemia, peripheral oedema, pulmonary hypertension

173
Q

What is the most common organism causing COPD?

A

H. influenzae

174
Q

How is AECOPD managed?

A

Increase bronchodilator use (maybe give NEB)
30mg pred 5 days
Give amoxicillin if signs of pneumonia

175
Q

What are causes of MR?

A 
Post-MI/CAD (if papillary muscles/chordae tendinae damaged)
Mitral valve prolapse 
IE 
Rheumatic fever
Congenital
176
Q

What are signs of MR?

A

Pansystolic blowing murmur best heard at apex, radiates into axilla
Quiet S1

177
Q

What might you see on CXR in MR?

A

Cardiomegaly due to enlarged left atrium and ventricle

178
Q

How is MR managed?

A

Nitrates, diuretics, positive inotropes, intra-aortic balloon pump
Surgery - replacement, repair

179
Q

What are clinical features of aortic stenosis?

A

Chest pain
SoB
Syncope
Murmur - ejection systolic radiating to carotids

180
Q

What are features of severe aortic stenosis?

A 
Narrow pulse pressure
Slow rising pulse
Soft/absent S2
S4
Thrill
LVH or failure
181
Q

What are causes of aortic stenosis?

A

Degenerative calification
Bicuspid aortic valve
Post-rheumatic disease
HOCM

182
Q

How is aortic stenosis managed?

A

Asymptomatic –> observe
Symptomatic –> valve replacement
Asymptomatic but valvular gradient >40mmHg and LVF –> consider surgery

183
Q

What are features of AR?

A 
Early diastolic murmur
Collapsing pulse
Wide pulse pressure
Quincke sign (nail bed pulsation) 
Demusset sign (head bobbing) 
Austin flint (mid-diastolic murmur) in severe AR
184
Q

What are causes of AR?

A 
Rheumatic fever
IE
Connective tissue dx, e.g. SLE
Bicuspid aortic valve
Aortic dissection
AS
HTN
185
Q

What are the signs of tricuspid regurg?

A

Pansystolic murmur
Pulsatile heptomegaly
Left parasternal heave

186
Q

What are causes of tricuspid regurg?

A 
RV infarction 
Pulmonary hypertension
Rheumatic heart disease
IE (esp IVDA) 
Ebstein anomaly
Carcinoid syndrome
187
Q

What are the causes of mitral stenosis?

A

Rheumatic fever
Rheumatic fever
Rheumatic fever

188
Q

What are the features of mitral stenosis?

A

Mid-late diastolic murmur best heard in expiration
Loud S1
Malar flush
AF

189
Q

What might you see on CXR in mitral stenosis?

A

LA enlargement

190
Q

What are the 4 features of tetralogy of fallot?

A

Overriding aorta
Right ventricular outflow tract obstruction
Right ventricular hypertrophy
VSD

191
Q

What are the features of acute moderate asthma?

A

PEFR 50-75% best or predicted
Speech normal
RR < 25 / min
Pulse < 110 bpm

192
Q

What are the features of acute severe asthma?

A

PEFR 33 - 50% best or predicted
Can’t complete sentences
RR > 25/min
Pulse > 110 bpm

193
Q

What are the features of acute life-threatening asthma?

A 
PEFR < 33% best or predicted
Oxygen sats < 92%
Silent chest, cyanosis or feeble respiratory effort
Bradycardia, dysrhythmia or hypotension
Exhaustion, confusion or coma
Normal pCO2
194
Q

What are the features of near fatal asthma?

A

A raised pCO2 –> req. mechanical ventilation

195
Q

When should you do an ABG in acute asthma?

A

If oxygen sats <92%

196
Q

When should you do a CXR in acute asthma?

A

Life-threatening asthma
Suspected pneumothorax
Failure to respond to Rx

197
Q

How is acute asthma managed?

A

15L non-rebreath mask with reservoir bag (target SpO2 94-98%)
SABA - NEB
Corticosteroids - 40-50mg pred daily until 5 days post-attack

Severe/lifethreatning - ipratropium bromide NEB, Mg sulphate IV

May require intubation/ventilation/ECMO

198
Q

Who should now have objective tests for asthma?

A

> =5 years

199
Q

How is asthma diagnosed in >=17 years?

A

Bronchodilator reversibility test, fractional exhaled nitric oxide test

200
Q

How is asthma diagnosed in 5-17 years?

A

Bronchodilator reversibility test

If -ve –> FeNO test

201
Q

How is asthma diagnosed in <5 years?

A

Clinically

202
Q

What is a positive bronchodilator reversibility test?

A

Improvement in FEV1 12%+ (or 200ml+ improvement in adults)

203
Q

What is the ladder of treatment of stable asthma in adults?

A
  1. SABA
  2. SABA + low dose ICS
  3. SABA + low dose ICS + LTRA
  4. SABA + low dose ICS + LABA + LTRA (if still helpful)
  5. SABA +/- LTRA, switch ICS/LABA for MART that includes low dose ICS
  6. SABA +/- LTRA + medium dose ICS MART
  7. SABA +/- LTRA + 1 of: high dose ICS, additional drug, e.g. theophylline, specialist referral)
204
Q

What is the stepwise treatment of asthma in kids?

A
  1. SABA
  2. SABA + low dose ICS
  3. SABA + low dose ICS + LTRA
  4. SABA + low dose ICS + LABA + LTRA (if helpful)
  5. SABA + MART with low dose ICS
  6. SABA + moderate dose ICS MART
  7. SABA + 1 of: High dose ICS, theophylline, specialist referral

5th year (4 decks)

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