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ACC > Desirable conditions > Flashcards

Desirable conditions Flashcards

1
Q

what are cardinal signs of anaphylaxis

A 
skin rash
acute onset 
wheezing
inspiratory stridor
hypotension
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2
Q

how to diagnose anaphylaxis

A

clinical

allergy test to prevent recurrence

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3
Q

what is the key part of treatment of anaphylaxis

A

adreanline

secure airway

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4
Q

what are risk factors for anaphylaxis

A

Hx of atopy / asthma

previous anaphylaxis

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5
Q

what IVx for anaphylaxis

A

Mast cell tryptase
ecg
U+ E
ABG

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6
Q

what is the immediate management for anaphylaxis

A
  1. CPR
  2. position based on situation
  3. remove trigger if present
  4. IM adrenaline
  5. repeat adrenaline
  6. high flow oxygen –> 94-98%
  7. IV access –> fluid challenge
  8. monitor vitals
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7
Q

what is the management for anaphylaxis after initial treatment

A
  1. antihistamine

2. corticosteroid

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8
Q

what is a biphasic reaction

A

return of anaphylaxis symptoms 6-24 hours after initial

tell patients to return if symptoms return

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9
Q

what discharge medications should be given

A

oral antihistamine + corticosteroid for 3 days

2 adrenaline auto-injectors

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10
Q

what are the two shockable rhythms

A

pulseless VT

VF

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11
Q

what is the classic presentation of cardiac arrest

A

sudden LOC

chest pain

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12
Q

what are the 4 cardiac arrest rhythms

A

VF
pulseless VT
PEA
asystole

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13
Q

what is torsades de pointes

A

polymorphic VT
prolonged QT
related to hypomagnesaemia

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14
Q

what is the signs on exam of cardiac arrest

A

unresponsive
absence of normal breathing
absence of circulation
cardiac rhythm disturbance

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15
Q

what are the risk factors for cardiac arrest

A 
CAD
LVD
HCM
ARVD
LQTS
electrolyte disturbance
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16
Q

what are the key investigations in cardiac arrest

A 
cardiac monitoring - identify if shockable rhythm 
FBC
electrolytes
ABG
cardiac biomarkers
Echo
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17
Q

for which rhythms is adrenaline recommended for?

A

both

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18
Q

what is the management for shockable rhythms

A
  1. CPR
  2. Defib
  3. adrenaline 1mg IV every 3-5min
  4. second shock
  5. Amiodarone if non-responsive to
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19
Q

what is the management for non-shockable

A
  1. CPR

2. Adrenaline

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20
Q

what is post cardiac arrest care

A 
continued monitoring
correction of electrolytes
correction of acidosis 
ECG 
coronary angio
temperature control 32-36
rewarming
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21
Q

what does COPD present as

A 
progressive SOB
wheeze
cough
sputum 
haemoptysis
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22
Q

what are diagnostic tests for COPD

A 
pulmonary function tests
CxR
CTPA
oximetery 
ABG
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23
Q

what are some advice and vaccines for COPD patients

A

stop smoking

flu + pneumococcal

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24
Q

what is the vague treatment for COPD

A

bronchodilators
inhaled corticosteroids
systemic corticosteroids

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25
Q

what are features of COPD on examination

A 
barrel chest 
hyperreasonant percussion
distant breath sounds
poor air entry 
coarse crackles
distended neck veins
cyanosis 
clubbing
tripod
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26
Q

FEV1/FVC IN COPD

A

<0.7

IRREVERSIBLE

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27
Q

How does COPD exacerbation present

A

INCREASED
dyspnoea
worsening of cough
increase in sputum

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28
Q

what suggests an exacerbation is bacterial

A

change in volume and colour of sputum

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29
Q

what is used to grade breathlessness in COPD

A

eMRCD scale

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30
Q

what does a good COPD exacerbation history do

A

compare how there is a change from baseline

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31
Q

ABG results in patient with COPD

A

ABG
acute resp acidosis / compare with previous ABG / document Fi
repeat 30-60 minutes after oxygen + bronchdilator

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32
Q

why is an ECG done in COPD exacerbation

A

rule out MI / pneumothorax

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33
Q

what would blood results show in COPD exacerbation

A

WBC raised –> infection
anaemia
CRP –> moderately raised

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34
Q

what would a CxR show in a COPD exacerbation

A

rule out pneumonia / pneumothorax / CHF / pleural effusion

35
Q

what is immediate management for COPD

A
  1. B2 agonist +/- muscarinic antagonist on air
    - stop any long
  2. consider systemic corticosteroid
  3. prescribe controlled oxygen with target of 88-92 for retainers
  4. ABG
  5. monitor NEWS
36
Q

what are symptoms of acute respiratory failure

A

RR > 30
accessory muscle usage
acute change in mental status
hypoaxaemia that does not improve with supplemental oxygen

37
Q

when should NIV be used?

A

respiratory acidosis
severe dysponoea
persistent hypoxaemia

38
Q

when should NIV treatment start

A

60 minutes after ABG

120 minutes after hospital arrival

39
Q

when should ABx be given for patients with COPD

A

patients that need ventilation
increase in sputum / colour/ breathlessness
5-7 therapy

40
Q

how long should oral corticosteroids be prescribed for after exacerbation

A

5 days

41
Q

what are the benfits of NIV

A

improves surivial / gas exchange

reduces breathing workload

42
Q

tell me about tension headaches

A

Hx - emotional stress / depression / insomnia
tight band
non-pulsatile / aching / constricting

Ex - pericranial tenderness / trapezius / temporalis tenderness

clinical diagnosis

43
Q

how to treat tension headaches

A

simple analgesia

44
Q

how does a migraine present

A 
unilateral pulsing / throbbing pain 
migraine with aura 
N+V 
visual phenomenon 
photophobia 
symptoms last < 60 min
45
Q

what is the classic presentation of SAH

A 
thunderclap 
sudden onset headache
vomitting 
photophobia 
non-focal neuro signs
46
Q

what is the exam findings in SAH

A

nuchal rigidity

47
Q

what investigations to do in patients with SAH

A

U=E - hyponatraemia
CT head - blood in cirlce of willis
LP - xanthochromia

48
Q

what do give patients with confirmed SAH

A

nimodipine to prevent cerebral ischaemia

49
Q

what are the two ways of managing SAH

A
  1. surgical –> endovascular coil / surgical clipping

2. unable to surgery –> conversative management

50
Q

what are the risk factors for SAH

A 
HTN
smoking
FHx
AKPKD
alcohol / cocaine
51
Q

when should SAH be managed by

A

secure aneurysm by 48h

52
Q

what monitoring should be done for patients with SAH

A
  1. Neuro status + exam every hour
    consult with neurosurgeon if any deterioration
    2.BP via arterial line
  2. continous ECG
53
Q

what is the management for SAH GCS < 8

A
  1. CPR
  2. supportive care + monitoring
    - fever
    - hyponatraemia
    - hyperglycaemia
    - VTE prevenetion
  3. Nimodipine
  4. anticonvulsant
  5. stop + reverse anticoagulation
  6. Endovascular coiling / surgical coiling
54
Q

what is SAH management for SAH GCS > 8

A
  1. Supportive care + monitoring
  2. Nimodipine
  3. anticonvulsants / analgesia / stool softner
  4. endovascular coiling + surgical clipping
55
Q

what are the neurological causes of collapse

A 
generalized seizure 
parkinson's disease
TIA/stroke
vasovagal
situational syncope
56
Q

what is the classical history of collapse from seizures

A

sudden LOC
limb stiff + jerk
incontinence / tongue biting / myalgia
post-ictal

57
Q

what investigations + management for seizures

A

EEG / CT head / electrolytes / glucose / drug levels

management
anti-epileptics if > 2 episodes

58
Q

what is the classical history for TIA/stroke

A

hemiplegia
homonymous hemianopia
dysphasia
sensory loss

59
Q

what investigations to do for TIA/stroke

A

CT head
ECG for AF
coagulation screen
carotid doppler

60
Q

history of vasovagal

A

occurs in response to stimuli
preceding pallor / sweating
LOC for 2 min

61
Q

causes of cardiac collapse

A

postural hypotension
aortic stenosis - collapse on exertion
arrhythmia

62
Q

history of collapse due to postural hypotension

A

dizziness + LOC when standing

recent change in medications

63
Q

history of collapse due to aortic stenosis

A

collpase on exertion

64
Q

history of collapse due to arrhythmia

A

palpitations
strange feeling before LOC
cardiac history + FHx

65
Q

what are non- cardiac/ neuro causes of falls

A

drugs
alcohol
mechanical fall

66
Q

what is hyponatraemia defined as

A

Na+ < 135

67
Q

causes of hyponatraemia

A

volume depletion
volume overload
euvolaemia
DM / cirrhosis / CHF

68
Q

what is the common complication of hyponatraemia

A

cerebral oedema

treat with hypertonic 3% saline

69
Q

how to treat hyponatraemia

A 
hypertonic 3% saline
fluid restriction 
stop causative medications 
DONT TREAT TOO QUICKLY
myelinolysis
70
Q

symtpoms of hypnatraemia

A

N+V
altered mental status
seizures + coma
low urine output

71
Q

what investigations to do in hyponatraemia

A

serum sodium
U+E
serum osmolality
urine sodium

72
Q

when does cerebral oedema occur more often

A

acute < 48hrs hyponatraemia

73
Q

at what rate to give sodium in hyponatraemia

A

100-300ml in 100mLincrements over 10 minutes

74
Q

what is hyperkalaemia defined as

A

K+ > 5.5mmol

75
Q

what is the cause hyperkalaemia

A

high potassium intake

decreased renal excretion

76
Q

how does hyperkalaemia present

A

muscle weakness + ECG change

77
Q

what are the ECG changes in hyperkalaemia

A

tall tented T waves

loss of p wave

78
Q

what is the main complication of hyperkalaemia

A

life-threatening arrhythmia

VF

79
Q

what medications increase risk of hyperkalaemia

A 
chemo drugs
ACEi/ARB
Spirnolactone / amiloride 
NSAIDs
digoxin 
trimethoprim 
beta blockers
80
Q

how can renal impairment cause hyperkalaemia

A

kidneys excrete potassium

81
Q

what symptoms of hyperkalaemia

A

usually asymptomatic
weakness + fatique
palpitations + chest pain

82
Q

what investigations to do for Hyperkalaemia

A

U+E –> raised creatinine would suggest AKI
ECG –> tall tented T waves / flattening p-waves / broad QRS
serum cortisol –> low in addisons

83
Q

what is the management of hyperkalaemia

A
  1. cardiac proteection
    - calcium gluconate
  2. Insulin + glucose infusion
    - monitor glucose closely
  3. salbutamol
  4. check potassium 1/2/6/12 hours after treatment
84
Q

how does aortic dissection present

A

sudden onset ripping / tearing pain
intrascapular pain
syncope

ACC (5 decks)

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