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ACC > General > Flashcards

General Flashcards

1
Q

What is a massive PE

A

PE with obstructive shock or SBP <90mmHg

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2
Q

What is a submassive PE

A

Acute PE without systemic hypotension >90 BUT either RV dysfunction or myocardial necrosis

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3
Q

Initital investigations for ?P.E

A 
A-E
ECG
CXR if acutely unwell
WELLS score
ABG - D-dimer
CT pulmonary angiogram
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4
Q

Gold standard PE investigation

A

CTPA

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5
Q

Main ECG finding for PE?

A

Sinus tachy

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6
Q

Why can’t you prescribe verapamil and bisoprolol together?

A

complete heart block

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7
Q

Main finding on ECG for complete heart block

A

prolonged PR interval (>200ms, >6 squares)

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8
Q

Main feature of Mobitz type 1 heart block on ECG

A

Increasing PR interval then missed QRS complex

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9
Q

Main feature of complete heart block on ECG?

A

P and QRS are both regular but completely separate rhythms

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10
Q

Differentials for stroke

A

Migraine
Hypoglycaemia
Seizure
Old stroke symptoms exacerbated by concurrent illness (e.g. sepsis)

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11
Q

Ischaemic stroke management

A

Alteplase (thrombolysis) <4.5 hours
/Thrombectomy
Aspirin 300mg for 2 weeks then Clopidogrel
BP control

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12
Q

Haemorrhagic stroke management

A 
Neurosurgery referral
BP control (usually <140)
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13
Q

?Stroke investigations

A

Blood glucose

CT within 24 hours

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14
Q

Stroke assessment score

A

Rosier score

LOC -1
Seizure activity -1
Asymmetrical facial weakness +1
Assymmetrical arm weakness +1
Asymmetrical leg weakness +1
Speech disturbances +1
Visual field deficit +1

Stroke is likely if score is >0

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15
Q

A-E assessment: Breathing

A 
Examine:
Observe for signs of resp distress
Resp rate
Quality of breathing 
Chest deformity 
O2 sats and FiO2
Tracheal position 
Brief resp exam: chest expansion, auscultation, percussion

Investigations
ABG
CXR

Action
O2
Nebulisers

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16
Q

Investigation of ?PE

A

PERC calculation –> If >0 then..
Wells score –> if <4 (unlikely): D-dimer. If >4 (likely) –> CTPA + CXR + ECG.
If CTPA positive –> Anticoagulate

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17
Q

In what scenario is CTPA for ?PE contraindicated? What should you do instead?

A

Pregnancy
Renal impairment
Contrast allergy
Radiation risk (breast cancer)

Ventilation-perfusion scan

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18
Q

Treatment for massive PE

A

Thrombolyse (alteplase)

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19
Q

Treatment for unprovoked submassive / non-massive PE?

A

Anticoagulate –> DOAC (apixaban/rivaroxaban)

Investigate if unprovoked -->
FBC, U&E, LFTs, Clotting, Calcium, PSA
Breast/prostate/testicular/rectal examination
Systems review
(CT if cancer suspicion)
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20
Q

Sx of aortic dissection

A

Sudden ripping or tearing chest pain (migrates over time, maximal at time of onset)
Hypertension
Differences in BP between arms
Collapse

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21
Q

Tx of aortic dissection

A

Analgesia
IV access
BP and HR control (beta-blocker)
Surgical intervention

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22
Q

Tx for pericarditis

A

Bed rest
NSAIDs (+ PPI cover)
Oral prednisolone if severe

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23
Q

Treatment for large/ unstable pneumothorax

A

Aspiration (2nd/3rd intercostal space, mid-clavicular line).

If aspiration fails:
Chest drain in triangle of safety (5th ICS, midaxillary line, anterior axillary line)

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24
Q

What is the triangle of safety?

A

Mid-axillary line
Anterior axillary line
5th ICS

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25
Q

3 criteria for exacerbation of COPD

A

Increased SOB
Increased sputum production
Increased purulence of sputum

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26
Q

Most common causes of COPD exacerbation

A

Haemophilus influenzae
Strep pneumoniae
RSV

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27
Q

Treatment pathway for COPD exacerbation

A

1) Nebs –> salbutamol 2.5mg QDS, ipratropium 0.5mg QDS
2) Steroids –> prednisolone 30mg OD / hydrocortisone 100mg QDS
3) Abx - amoxicillin, doxycycline, clarithroymcin
4) Oxygen therapy (venturi, NIV, mechanical)

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28
Q

Tests which must be done before starting NIV

A

ABG - to ensure T2RF

CXR - to rule out pneumothorax

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29
Q

CURB-65 score and interpretation

A 
Confusion
Urea >7
Resp rates >30
BP <90 systolic or <60 diastolic
65 - age >65

1 –> home tx
2 –> hosp admission
>3 –> ICU

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30
Q

How to measure calf swelling for ?DVT

A

Measure 10cm below tibial tuberosity

Difference of >3cm = significant.

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30
Q

How to measure calf swelling for ?DVT

A

Measure 10cm below tibial tuberosity

Difference of >3cm = significant.

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31
Q

Complications of DVT

A

CV event
ASD –> stroke
Post-thrombotic syndrome –> chronic venous hypertension which causes limb pain, swelling, dermatitis, ulcers.

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32
Q

Difference between periorbital and orbital cellulitis?

A

Periorbital is ANTERIOR to orbital septum, and does not affect vision or cause pain on eye movement.

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33
Q

Treatment for cellulitis

A

Flucloxacillin for 5-7 days (7 if facial)

If not systemically unwell / not significantly unwell = oral
If significant systemic upset / sepsis = IV

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34
Q

Explain DKA

A

High blood glucose and low cell glucose causes ketogenesis - liver converts fatty acids into ketones (which can be used as fuel in the brain). When ketones can no longer be buffered by bicarbonate, they cause METABOLIC ACIDOSIS.
Hyperglycaemia also causes diuresis which causes DEHYDRATION and total body hypokalaemia, but serum HYPERKALAEMIA as insulin normally drives K+ into cells.

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35
Q

Symptoms of DKA

A 
Nause and vomiting
Fatigue
Abdo pain
Polyuria and polydipsia
Weight loss
Acetone smell to breath 
Kussmaul breathing 
Hypovolaemic shock
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36
Q

Triad of diagnosis for DKA?

+ other important investigations

A

THINK : D(diabetes), K(ketosis), A(acidosis)

Blood glucose >11mmol/L (or known diabetic!)
Ketones >3mmol/L (or ++ on dipstick)
Acidosis –> pH <7.3 with bicarb <15mmol/L

ECG

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37
Q

Treatment for DKA

A

FIG PICK

FLUIDS:
(If shocked - fluid boluses until SBP >90)
1L over 1 hour
1L over 2 hours
1L over 2 hours
1L over 4 hours
1L over 4 hours
1L over 6 hours
1L every 8 hours onwards

INSULIN - Fixed rate infusion of 0.1unit/kg/hour
GLUCOSE - start IV dextrose when <14mmol/L
POTASSIUM - add 40mmol/L if potassium <5.5mmol/L
INFECTION - treat triggers
CHART FLUIDS
KETONES - monitor hourly

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38
Q

Complications of DKA

A

Dehydration
Hypokalaemia
Cerebral oedema

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39
Q

Investigations if hypoglycaemia and diabetic status unknown

A

LFTs, U&Es, TFTs, glucose, HbA1c, insulin and C-peptide (measured to investigate insulinoma - endogenous source of insulin)

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40
Q

Treatment for hypoglycaemia

A

Conscious: 10-20g glucose (tablet, gel, coke, fruit juice)

Unconscious: IV 50% dextrose 25ml STAT (or IM glucagon 1mg/kg)

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41
Q

SEPSIS management

A 
Blood cultures
Urine ouput
Fluids
Antibiotics
Lactate
Oxygen
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42
Q

What is HHS? Diagnostic triad.

A

Very high blood glucose in T2DM which causes severe intracellular dehydration. Severe hyperglycaemia, serum hyperosmolarity, without significant ketosis

Hypovolaemia
Marked hyperglycaemia (>30mmol/L)
Without hyperketonaemia (<3mmol/L)
43
Q

Treatment for HHS

A

Fluid replacement –> 3-6L by 12 hours, remaining in next 12 hours (100-220ml/kg)
Monitor response –> osmolarity, Na+, glucose hourly
Insulin –> only if significant ketonaemia = 0.05units/kg/hr
Potassium replacement
VTE prophylaxis

44
Q

How to assess capacity

A
  1. Does the patient have a potential impairment of mind or brain?
    IF YES
  2. Can they: understand, retain, weigh up, communicate decision
45
Q

Define shock

What does it cause?

A

Clinical syndrome caused by inadequate tissue perfusion and oxygenation, leading to abnormal metabolic function

Intracellular calcium overload –> reduced myocardial contractility
Anerobic metabolism –> lactic acidosis –> further exacerbation of myocardial issues

46
Q

4 types of hypoxia

A

Hypoxic
Anaemic (due to ↓ Hb)
Stagnant (↓ citruclation)
Histotoxic (Impaired metabolism)

47
Q

Define preload and after load

A

Preload = initial stretching of cardiac myocytes prior to contraction

Afterload = force/load against which the heart has to contract to eject the blood

48
Q

How much does one unit of blood increase Hb?

A

10g/L

49
Q

What 3 blood products are needed in haemorrhagic shock? In what ratio?

A

Packed red cells
FFP
Platelets

1:1:1

50
Q

Explain how ionotropes and vasopressors are used in the management of shock

A

Inotropes = increase contractility of heart by increasing calcium availability and thus increasing stroke volume

Vasopressors = increase systemic vascular resistance, which increases BP and increases tissue perfusion

51
Q

Management of hypovolaemic shock

A 
Oxygen
IV access
Fluids (500ml 0.9% NaCL, then bloods)
Activate MHP (if fluids insufficient, or Hb <70g/L)
Vasopressors and ionotropes
52
Q

Management of anaphylactic shock

A 
ABCDE
IM adrenaline 
IV fluid challenge
Antihistamines
Steroids
53
Q

What is cariogenic shock? Causes?

Treatment?

A

Low cardiac output state due to failure of heart to pump

Causes: MI, dysrhythmia, myocarditis, cardiac rupture

MONAT
Morphine, oxygen, GTN, aspirin, tricagelor
Rapid PCI
Ionotropic support

54
Q

What is distributive shock?

A

Vasodilation +/- endothelial leakage.

Caused by sepsis, anaphylaxis, neurogenic shock (damage to spinal cord)

55
Q

What do the different NEWS scores mean?

A

0 = Low risk. Continue monitoring every 12 hours.
1-4 = Low risk. Nurse assessment and escalate if necessary. Review 4-6 hourly.
5-6 or >3 in one area = High risk. Urgent ward based response, nurse to urgently inform medical team. Review 1 hourly
Score >7 = emergency response. Critical care and airway management team needed. Continuous monitoring.

56
Q

What are the 3 steps of the WHO pain ladder?

A

1) Non-opioid –> paracetamol, aspirin, NSAID
2) Weak opioids –> Codeine, co-codamol
3) Strong opiod –> morphine, fentanyl, oxycodone

57
Q

Nephrotic syndrome triad and Tx

A
  1. Oedema
  2. Hypoalbuminaemia
  3. Proteinuria (High urinary PCR)

Tx = Long term steroids (prednisolone) + reduced salt diet

58
Q

What is Cushing’s syndrome?

Causes and symptoms.

A

Prolonged cortisol elevation.
Sx: Moon face, central obesity, proximal muscle wasting, striae, buffalo hump (think man on AMU!), T2DM
Causes: exogenous steroids (iatrogenic or mediation abuse), adrenal adenoma, paraneoplastic, Cushing’s disease (pituitary adenoma releasing excessive ACTH)

59
Q

What is the correct sequence of actions in basic life support?

A

Safety (approach with care), Stimulate, Shout for help, Airway opening manoeuvres, Look listen feel, Rescue breaths

60
Q

Commonest cause of airway obstruction in an anaesthetised patient is:

A

Tongue

61
Q

How do you assess breathing during BLS?

A

Look listen and feel

62
Q

During CPR what it the best indicator of effective breaths in an un-intubated patient?

A

Visualising the chest rise and fall

63
Q

What type of shock is commonly seen in anaphylaxis?

A

Distributive shock

64
Q

Two types of definitive airway

A

ET tube

Tracheostomy

64
Q

Two types of definitive airway

A

ET tube

Tracheostomy

65
Q

What does the size of ET tube indicate?

A

internal diameter in mm

66
Q

What colour and size cannula should be inserted in cardiac arrest?

A

16G (grey)

15G (orange)

67
Q

What is the best indicator of correct placement of ET tube?

A

CO2 in expired gas

68
Q

Scoring systems for upper GI bleed

A

Glasgow-Blatchford score - predictor of risk of GI bleed

Rockall score - predictor of re-bleed and morbidity after endoscopy

69
Q

GI bleed causes

A 
Mallory-weiss tear
Gastro/duodenal ulcer
Oesophageal varices
Cancers
Oesophagitis
70
Q

Acute upper GI bleed management

A

ABATED

A-E assessment
Bloods - Hb, platelets, clotting, urea, LFTs, cross match
Access - IV access
Transfusion: blood, platelets, FFP
Endoscopy - urgent within 24h
Drugs - stop anticoagulants and NSAIDs

+ Test for H.Pylori –> Rapid urease test usually carried out during endoscopy / breath test can be done.

(Withhold PPI until after endoscopy)

71
Q

Management of H.pylori infection

A

Triple therapy for 7 days –> PPI + 2 antibiotics (e.g. amoxicillin + clairthromycin)

72
Q

How do you know if NG tube is placed correctly?

A 
Aspirate = test pH.
CXR = Dissects carina and sits under left hemidiaphragm
73
Q

Management of tricyclic antidepressant overdose

A

Check TOXBASE
IV bicarbonate to correct acidosis
IV lipid emulsion to bind free drug
Supportive

(no specific antidote)
DO NOT give antiarrthymics

74
Q

Trauma to the face often causes which type of bleed?

A

Extra dural haematoma

75
Q

Guidelines for CT post-head injury

A

WITHIN 1 HOUR:
GCS <13 on initial assessment, or <15 two hours post injury
Suspected open/depressed skull fracture
Signs of basal skull fracture (CSF leak, battle sign, racoon eyes, haemotympanum, subconjunctival haemorrhage)
Post-traumatic seizure
Focal neurological deficit
>1 episode of vomiting

WITHIN 8 HOURS:
>65 yo
Bleeding/clotting disorder
Dangerous injury mechanism 
>30 mins retrograde amnesia
Warfarin patient

CT SPINE within 1 hour IF:
Need for CT head in 1 hour
Suspicion of C-spine injury
Neck pain/tenderness

76
Q

Management of head injury

A

CT following CT head rules

Maintain CPP (control BP (fluids, pain relief), control ICP (IV mannitol))

Neurosurgery referal

  • Haematoma –> depressive craniotomy / drainage
  • Depressed skull fracture –> surgical correction
77
Q

What are the Canadian C Spine rules?

A

If ANY of the following, must have C-Spine immobilisation:

  • Age >65
  • Dangerous mechanism
  • Numbness/tingling in extremities
  • Not ambulatory at any time at scene
  • Neck pain
  • Pain on midline C-spine palpation
  • Cannot rotate neck 45 degrees left/right

Need CT spine within 1 hour (X-ray if neck pain/tenderness)

78
Q

Diagnosis and management of HHS

A

DIAGNOSIS
= Hypovolaemia, hyperglycaemia (>30), and raised serum osmolarity (>320mosmol/kg) in T2DM, without acidosis or ketonaemia

MANAGEMENT

  • Fluid replacement 0.9%NaCl (first 50% in 12 hours, second 50% in 12 hours)
  • Monitor: osmolarity, potassium, glucose, sodium
  • Target glucose 10-15mmol/L
79
Q

Treatment guidelines for hyperkalaemia

A

TREAT IF :

  • K+ >6 + ECG changes
  • K+ >6.5

Treatment:

  1. Stop K+ sparing drugs (ACE-i, ARBs, Spironolactone)
  2. 10% calcium gluconate 30mls over 10 minutes (cardio protective)
  3. IV insulin + 50% dextrose
80
Q

Mechanism of action of Amiodarone

A

Class II anti-arrhythmic
Blocks potassium currents causing repolarisation of the heart muscle à increases duration of action potentials and refractory period
This reduces cardiac muscle cell excitability and restores normal sinus rhythm.

81
Q

Mechanism of action of adrenaline

A

Increases myocardial force of contraction (positive inotrope) and heart rate (positive chronotrope)

82
Q

Mechanism of action of adenosine (CCB) & contraindications

A

Slows cardiac conduction through AVN à resets rhythm back to normal
Causes brief period of asystole, very quickly metabolised

Contraindications: asthma, COPD, heart failure, HTN

83
Q

Mechanism of action of atropine

A

Anti-muscarinic –> inhibits parasympathetic nervous system which increases HR
SE: pupil dilatation, urinary retention, dry eyes, constipation

84
Q

AAA classification and management

A

Normal - <3cm
Small = 3-4.4cm
Medium = 4.5-54.cm
Large = >5.5cm

Small = yearly screen (CT angiogram)
Medium = 3 monthly screen
Large or growing >1cm a year = Elective repair & graft (end-vascular aneurysm repair: EVAR)

85
Q

What is the screening programme for AAA

A

Men routine USS screen at age 65

Women considered if age >70 with CVD/COPD

86
Q

What is ascending cholangitis and what is Charcot’s triad ?

A

Blockage in common bile duct preventing the flow of bile, which causes infection and leads to biliary sepsis.
Mirrizzi syndrome = blockage of common bile duct by a stone.

CHARCOT’S TRIAD:
Constant epigastric and RUQ pain
Jaundice
Fever

(+ steatorrhoea, signs of infection)

87
Q

Management of ascending cholangitis

A

ABCDE for sepsis - BUFALO
Biliary drainage
ERCP –> dislodge obstruction

88
Q

Investigations and management of bowel obstruction?

A

Abdo Xray, Contrast CT, bloods (U&Es, VBG/ABG - metabolic acidosis)

DRIP AND SUCK APPROACH
Nil by mouth, IV fluids, NG tube to aspirate stomach contents (prevent aspiration)
Surgical management

89
Q

Renal colic investigations and management

A

Urine dip, bloods, AXR, non-contrast CT KUB

IM diclofenac
Anti-emetics + antibtioics

Stone <5mm = watch and wait
Stone >10mm = surgical intervention

90
Q

Explain the mechanism of paracetamol overdose? At what level is overdose defined, and at what level is toxic?

A

Paracetamol is metabolised 95% to glucuronide sulphates, and 5% to NAPQI (n-acetyl-p-benzoquinone) which is further metabolised by glutathione.
In OD, pathway gets saturated so NAPQI builds up and is toxic –> liver cell necrosis

OD = >4g in 25h
Toxic = >150mg/kg (21 tablets for average 70kg person)
91
Q

Which drugs are P450 enzyme inducers and what does this mean?

A 
o	BS CRAP GPs
o	Barbituates
o	St John's Wart
o	Carbamazepine
o	Rifampicin
o	Alcohol (chronic)
o	Phenytoin
o	Griseofulvin (fungal treatment)
o	Phenobarbitone
o	Sulphonylureas
92
Q

Symptoms of liver failure

A

<24 hours –> (asymptomatic) or Sweating, N&V, abdo discomfort
24-72 hours –> RUQ pain, N&V
3-5 days –> jaundice, confusions, coagulopathy, anuria, hypoglycaemia, seizures

93
Q

Management of paracetamol OD at different time frames

A

<1 hour = activated charcoal
0 -4 hours = nothing
4 -8 hours = paracetamol level +/- NAC if needed
8 - 15 hours = NAC then paracetamol level (and stop if necessary)
15+ hours / staggered overdose = NAC

NAC is infused over 1 hour. Takes 12 hours for full protocol.

94
Q

SE of NAC treatment

A

Rash, itching, nausea (Anaphylactoid like reaction - because it is a precursor of histamine)

95
Q

Which patients are at increased risk of OD on paracetamol?

A 
Those taking P450 enzyme inducers 
Malnourished patients (anorexia, alcohol addiction)
96
Q

Criteria for liver-transplantation post-paracetamol OD

A
  1. Arterial pH <7.3 after 24h
  2. Prothrombin time >100 seconds
  3. Creatinine >300umol/L
  4. Grade III/IV encephalopathy
97
Q

Scoring system for pneumonia and what do results mean

A 
CURB - 65
Confusion 
Urea >7
Resps >30
BP S <90 / D< 60
>65yo

Guides treatment
1 –> home (oral amoxicillin 5 days)
2 –> Hospital admission (amoxicillin/clarithromycin azithromycin 7-10 days)
>3 –> Consider ICU (amoxicillin + clarithromycin/azithromycin 7-10 days)

98
Q

DKA treatment improvements and targets?

A

Glucose reduce >3 /hour until <14mmol/L
Ketones reduce >0.5 /hour until <0.6mmol/L
Bicard increase >3 /hour until >15 (and pH >7.3)

99
Q

Initial treatment for bowel obstruction

A

Drip and suck - NG tube + IV fluids

100
Q

Amiodarone MOA

A

Class II anti-arrhythmic
Blocks potassium currents causing repolarisation of the heart muscle –> increases duration of action potentials and refractory period
This reduces cardiac muscle cell excitability and restores normal sinus rhythm.

101
Q

Atropine MOA

A

Anti-muscarinic –> inhibits parasympathetic nervous system which increases HR
SE: pupil dilatation, urinary retention, dry eyes, constipation

102
Q

Adenosine MOA

A

Calcium channel blocker
Slows cardiac conduction through AVN –> resets rhythm back to normal
Causes brief period of asystole, very quickly metabolised
Contraindications: asthma, COPD, heart failure, HTN

103
Q

Where would a needle decompression for tension pneumothorax be inserted

A

2nd intraclavicular space, ICS

104
Q

Where would a chest drain be inserted?

A

Triangle of safety - between
5th ICS
Midaxillary line
Anterior axillary line

ACC (3 decks)

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