Week 2 - Acute Medical Presentations 2 Flashcards

1
Q

If a P has a reduced GCS - where is the likely problem?

A

In the brainstem

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2
Q

Which cranial nerves are found
- in the midbrain?
- in the pons?
- in the medulla?

A

Midbrain = III & IV

Pons = V, VI, VII, VIII

Medulla = IX, X, XI, XII

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3
Q

What does the reticular system do?

A

Is the essence of awareness and consciousness

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4
Q

What are the two types of cause of impaired consciousness?

A

Neurological
Metabolic

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5
Q

When looking at differentials for impaired consciousness - what should you consider?

A

Meningitis
Brain tumour
Acute Stroke
Toxic-metabolic derangement
Spinal cord compression

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6
Q

What are possible causes of a fluctuating GCS?

A

Vascular
Seizure
Drug use / withdrawal
Metabolic
Infectious
Neurogenerative
Migraine

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7
Q

What are the steps of an acute neurological evaluation?

A
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8
Q

What are the following types of posture called?

A

(1). Decorticate posturing

(2). Decerebrate posturing

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9
Q

What is myoclonus?

A

Brief involuntary twitching/jerking

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10
Q

What is asterixis?

A

Inability to maintain sustained posture - brief, shock like movement - e.g. flapping tremor

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11
Q

Give an example of the following:-

  • Simple midline command
  • Simple acral command
  • Two-part command
  • Three-part command
  • Complex command
A
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12
Q

What is anisocoria?

A

One pupil is bigger than the other

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13
Q

Why is it important that the pupillary light reflex is resistant to metabolic derangement?

A

It means it will still be intact if the P has metabolic derangement. If not intact, is unlikely to be a metabolic derangement cause.

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14
Q

The midbrain has the vertical gaze centre - what is this responsible for?

A

Gives the P the ability to look up

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15
Q

The pons has the horizontal gaze centre - what is this responsible for?

A

Gives P the ability to look right and left

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16
Q

What is paradoxical breathing?

A

When the chest expands during inhalation and the abdomen is drawn inwards and then during exhalation the abdomen is pushed outwards

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17
Q

In which part of the brainstem are the breathing centres located?

A

Pons - Pneumotaxic & apneustic centres = automatic breathing

Medulla = inspiratory and expiratory centres - chemosensitive control

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18
Q

What two tests can be done for neck stiffness?

A

Kerning’s sign
Bradzinski’s sign

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19
Q

What is the oculocephalic reflex also known as?

A

Dolls head sign

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20
Q

If the GCS is less than 8, which reflexes should be assessed?

A

Pupillary light reflex
Swinging flashlight test
Oculocephalic reflex
Corneal reflex
Gag reflex
Ciliospinal reflex (response to pain)

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21
Q

What is the biochemical triad of DKA?

A

Hyperglycaemia (BG >11)
Hyperketonaemia (>3 or ketonuria >2+)
Metabolic acidosis (HCO3 <15 or venous pH <7.3)

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22
Q

What initial investigations should you do for DKA?

A

Capillary BG
Blood ketones
VBG
Glucose, U&Es, FBC
ECG
CXR
Blood culture
MSUH

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23
Q

How is DKA managed?

A

Fluids
Insulin
Correct electrolytes - esp K+ (replaced if below 5.5)
Treat precipitating factors
VTE Prophylaxis

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24
Q

How much fluid do Ps with DKA need to be given?

A

Typical deficit = 100ml / kg

1L over first hours
1L over next 2 hours x 2
1L over next 4 hours x 2
1L over next 6 hours

Reassess at the 12 hour status. Monitor electrolytes!

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25
Q

How much insulin is given in DKA?

A

1st hour - Fixed Rate IV Insulin Infusion (FRIII) - 50 units at 0.1 ml/kg/hour (7ml/hr for 70kg P)

AIM = reduce ketones by 0.5mmol/L/hr

Assess at 1hr - if not falling fast enough increase FRIII by 1ml/hr

Commence 10% dextrose when BG is <14.

Switch to VR III when ketones <0.6, pH >7,3 and HCO3 >18

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26
Q

What monitoring do DKA Ps need?

A
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27
Q

What is resolution of DKA defined as?

A

Ketones <0.3 and venous pH >7.3

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28
Q

What is euglycaemic DKA?

A

Acidosis
Ketonaemia
Normal or slightly raised BG

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29
Q

What can cause euglycaemic DKA?

A

SGLT2 Inhibitors
Pregnancy
Pancreatitis
Renal tubular acidosis
Starvation
Pre-hospital insulin (partially treated DKA)

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30
Q

A patient has
- Dehydration
- BG >30
- Blood ketones <3
Osmolality >320 (high)

What condition do they have?

A

Hyperosmolar Hyperglycaemic State (HHS)

High BG, normal ketones, high osmolality

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31
Q

How does HHS management differ from management for DKA?

A

Needs to be GRADUALLY normalised osmolality, fluid status and glucose.

HHS - often affects older Ps and can exacerbate CVS problems if you give them rapid fluid replacement

32
Q

What is the management of HHS?

A

Fluid replacement
- 1L over 1 hour, then 3-6L over 12 hours - but not rapidly

Insulin - not usually required in first hour. Only needed if BG stops falling with IV fluids alone or if ketonaemia

Treat precipitating factors
VTE prophylaxis

33
Q

How does HHS resolve?

A
34
Q

What is Addison’s disease?

A

Primary hypoadenalism - caused by destruction of adrenal cortex = deficiency in glucocorticoid, mineralocorticoid and sex steroid deficiency

35
Q

What are the causes of Addison’s disease?

A
36
Q

What are the symptoms of Addisons?

A
37
Q

What are the signs of Addisons?

A
38
Q

Which tests can be done for Addisons?

A

Random cortisol
Short synacthen test
Plasma ACTH - v high = primary adrenal failure, less than 10 = secondary adrenal failure
U&Es
BG
Adrenal ABs
CXR and AXR

39
Q

How is Addison’s managed?

A

IV Hydrocortisone
Fluid resus
Monitor BG
Fludrocortisone later
Steroid card and Medic alert bracelet

40
Q

How is Addisons treated on a daily basis?

A

Hydrocortisone has both glucocorticoid and mineralocorticoid activities; whereas fludrocortisone, a synthetic corticosteroid, possesses very potent mineralocorticoid activity.

41
Q

What are the clinical features of thyrotoxicosis?

A
42
Q

How is acute thyrotoxicosis managed?

A

Establish cause

Commence antithyroid drugs - Carbimazole (Propylthiouracil instead if pregnant) and Propranolol

Treat complications - ECG, Digoxin, Diuretic, Anticoagulation

43
Q

How is thyroid storm managed?

A

Propylthiouracil / Carbimazol - blocks T4 synthesis

Oral KI - blocks T4 release

Propanolol & IV HCS - block T4 effects

Paracetamol (anti pyretic) and IV fluids

44
Q

What level is malignant hypertension diagnosed at?

A

> 180/120

45
Q

What are the two types of malignant hypertension?

A

Hypertension Urgency - sudden inc in BP without acute end-organ damage

Hypertension Emergency - sudden inc in BP with acute end-organ damage

46
Q

What are the physiological signs of malignant hypertension?

A

Hypertensive retinopathy - inc haemorrhages or exudate on retina

Papilloedema

Cardiac failure

Encephalopathy = seizures, cortical blindness, coma

47
Q

How is malignant hypertension treated?

A

If BP >180/120 + organ damage - admit

Fluids
Adalat Retard = Ca Channel Blocker

48
Q

What endocrine conditions can cause hypertension?

A

Conn’s Syndrome (aldosterone)
Cushing’s syndrome
Acromegaly
Phaechromocytoma

49
Q

What are the clinical features of a phaeochromocytoma?

A

Hypertension
Headache
Cold Sweats

50
Q

What clinical signs can be used as indicators of meningitis?

A

Elevated WCC and protein in the CSF

51
Q

What is the mortality rate of bacterial meningitis?

A

20%, 30% if pneumococcal

52
Q

Which bacterial meningitis are older adults or immunocompromised adults at risk of?

A

Listeria monocytogenes

53
Q

What percentage of meningitis has a viral cause?

A

Probably 50-80%

54
Q

What are the clinical S&S of meningitis?

A

Headache, neck stiffness, fever
Often + photophobia + vomiting

55
Q

Which two signs are used to test for meningitis?

A

Kernig’s sign
Brudzinki sign

56
Q

How is meningitis managed?

A

A-E
D = GCS, focal neurological signs and papilloedema

Blood cultures, LP
Ceftriaxone (or cefotaxime) immediately after LP/blood cultures of no LP
Dexamethasone 10mg IV

CT - not normally indicated if fully alert.

57
Q

How is meningitis treated differently if there are signs suggested of brain shift & raised ICP?

A
58
Q

How are Ps treated who have signs of severe sepsis or rapidly evolving rash?

A

Sepsis guidelines

59
Q

If purpura and ecchymoses are seen in meningitis - what is this suggestive of?

A

That the clotting system is failing

60
Q

What antibiotics are given in bacterial meningitis?

What alternative can be given if allergic to penicillin?

A

Ceftrixaone or Cefotaxime

Alternaive = chloramphenicol & co-trimoxazole

61
Q
A
62
Q

When should you delay a LP for meningitis?

A
63
Q

Why do you sometimes do CT rather than MRI in meningitis?

A

Because Ps are often acutely unwell and cannot tolerate an MRI

64
Q

Where is there a high incidence of tuberculosis meningitis?

A

African and Indian subcontinents

65
Q

What is the mortality rate of tuberculosis meningitis

A

60% - even if treated

66
Q

What are possible complications of meningitis?

A

Hydrocephalus
Abscess
Epilepsy
Cognitive impairment
Focal neurological signs

67
Q

How does viral meningitis usually present?

A

Neck stiffness, photophobia & headache
Usually no reduced consciousness - if altered then consider encephalitis

67
Q

How is viral meningitis treated?

A

Initially treat as bacterial until proven viral - then stop Abx.

Is no evidence for aciclovir or other anti-virals to be used.

Tx = supportive - fluids and analgesia

68
Q

What is inflammation of the brain termed?

A

Encephalitis

69
Q

What is it called when a patient has brain inflammation and inflammation of the meninges?

A

Meningoencephalitis

70
Q

What can cause encephalitis?

A

Viruses
Small intracellular bacteria
Some parasites

Acute disseminated encephalitis myelitis (ADEM) - occurs when P has had recent vaccination / infection - antibodies are made which then damages the brain

Can also get AI Antibody-Associated Encephalitis

71
Q

What is the most common cause of viral encephalitis?

A

Herpes simplex
Varicella zoster, Cytomegalovirus and Enterovirus also possible

72
Q

How does viral encephalitis present?

A

Fever, altered, headache, N&V

73
Q

How is encephalitis investigated?

A

LP asap (unless CI)
CT asap
MRI within 48hr max
EEG
PLEDS

74
Q

What is the Tx for viral encephalitis?

A

IV Aciclovir

75
Q

What is AI Encephalitis?

A

Caused by the immune system attacking the brain causing inflammation. Can be a paraneoplastic cause.

76
Q

How is AI encephalitis treated?

A

Steroids - IV (methyl-prednisolone) then LT oral
Immunoglobulins
Plasma exchange
Rituximab