Week 2 - Acute Medical Presentations 2 Flashcards

(77 cards)

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
How much insulin is given in DKA?
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
26
What monitoring do DKA Ps need?
27
What is resolution of DKA defined as?
Ketones <0.3 and venous pH >7.3
28
What is euglycaemic DKA?
Acidosis Ketonaemia Normal or slightly raised BG
29
What can cause euglycaemic DKA?
SGLT2 Inhibitors Pregnancy Pancreatitis Renal tubular acidosis Starvation Pre-hospital insulin (partially treated DKA)
30
A patient has - Dehydration - BG >30 - Blood ketones <3 Osmolality >320 (high) What condition do they have?
Hyperosmolar Hyperglycaemic State (HHS) High BG, normal ketones, high osmolality
31
How does HHS management differ from management for DKA?
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
What is the management of HHS?
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
How does HHS resolve?
34
What is Addison's disease?
Primary hypoadenalism - caused by destruction of adrenal cortex = deficiency in glucocorticoid, mineralocorticoid and sex steroid deficiency
35
What are the causes of Addison's disease?
36
What are the symptoms of Addisons?
37
What are the signs of Addisons?
38
Which tests can be done for Addisons?
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
How is Addison's managed?
IV Hydrocortisone Fluid resus Monitor BG Fludrocortisone later Steroid card and Medic alert bracelet
40
How is Addisons treated on a daily basis?
Hydrocortisone has both glucocorticoid and mineralocorticoid activities; whereas fludrocortisone, a synthetic corticosteroid, possesses very potent mineralocorticoid activity.
41
What are the clinical features of thyrotoxicosis?
42
How is acute thyrotoxicosis managed?
Establish cause Commence antithyroid drugs - Carbimazole (Propylthiouracil instead if pregnant) and Propranolol Treat complications - ECG, Digoxin, Diuretic, Anticoagulation
43
How is thyroid storm managed?
Propylthiouracil / Carbimazol - blocks T4 synthesis Oral KI - blocks T4 release Propanolol & IV HCS - block T4 effects Paracetamol (anti pyretic) and IV fluids
44
What level is malignant hypertension diagnosed at?
>180/120
45
What are the two types of malignant hypertension?
Hypertension Urgency - sudden inc in BP without acute end-organ damage Hypertension Emergency - sudden inc in BP with acute end-organ damage
46
What are the physiological signs of malignant hypertension?
Hypertensive retinopathy - inc haemorrhages or exudate on retina Papilloedema Cardiac failure Encephalopathy = seizures, cortical blindness, coma
47
How is malignant hypertension treated?
If BP >180/120 + organ damage - admit Fluids Adalat Retard = Ca Channel Blocker
48
What endocrine conditions can cause hypertension?
Conn's Syndrome (aldosterone) Cushing's syndrome Acromegaly Phaechromocytoma
49
What are the clinical features of a phaeochromocytoma?
Hypertension Headache Cold Sweats
50
What clinical signs can be used as indicators of meningitis?
Elevated WCC and protein in the CSF
51
What is the mortality rate of bacterial meningitis?
20%, 30% if pneumococcal
52
Which bacterial meningitis are older adults or immunocompromised adults at risk of?
Listeria monocytogenes
53
What percentage of meningitis has a viral cause?
Probably 50-80%
54
What are the clinical S&S of meningitis?
Headache, neck stiffness, fever Often + photophobia + vomiting
55
Which two signs are used to test for meningitis?
Kernig's sign Brudzinki sign
56
How is meningitis managed?
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
How is meningitis treated differently if there are signs suggested of brain shift & raised ICP?
58
How are Ps treated who have signs of severe sepsis or rapidly evolving rash?
Sepsis guidelines
59
If purpura and ecchymoses are seen in meningitis - what is this suggestive of?
That the clotting system is failing
60
What antibiotics are given in bacterial meningitis? What alternative can be given if allergic to penicillin?
Ceftrixaone or Cefotaxime Alternaive = chloramphenicol & co-trimoxazole
61
62
When should you delay a LP for meningitis?
63
Why do you sometimes do CT rather than MRI in meningitis?
Because Ps are often acutely unwell and cannot tolerate an MRI
64
Where is there a high incidence of tuberculosis meningitis?
African and Indian subcontinents
65
What is the mortality rate of tuberculosis meningitis
60% - even if treated
66
What are possible complications of meningitis?
Hydrocephalus Abscess Epilepsy Cognitive impairment Focal neurological signs
67
How does viral meningitis usually present?
Neck stiffness, photophobia & headache Usually no reduced consciousness - if altered then consider encephalitis
67
How is viral meningitis treated?
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
What is inflammation of the brain termed?
Encephalitis
69
What is it called when a patient has brain inflammation and inflammation of the meninges?
Meningoencephalitis
70
What can cause encephalitis?
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
What is the most common cause of viral encephalitis?
Herpes simplex Varicella zoster, Cytomegalovirus and Enterovirus also possible
72
How does viral encephalitis present?
Fever, altered, headache, N&V
73
How is encephalitis investigated?
LP asap (unless CI) CT asap MRI within 48hr max EEG PLEDS
74
What is the Tx for viral encephalitis?
IV Aciclovir
75
What is AI Encephalitis?
Caused by the immune system attacking the brain causing inflammation. Can be a paraneoplastic cause.
76
How is AI encephalitis treated?
Steroids - IV (methyl-prednisolone) then LT oral Immunoglobulins Plasma exchange Rituximab