Medicine (5) Flashcards

1
Q

Management of status epilepticus

A
  1. Rectal diazepam / buccal midazolam
  2. IV lorazepam
  3. IV phenytoin (phenobarbital if already on regular phenytoin)
  4. Anaesthesia (propofol / thiopental sodium)
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2
Q

Treatment of generalised tonic-clonic seizures

A

Generalised tonic-clonic seizures

  • sodium valproate
  • second line: lamotrigine, carbamazepine
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3
Q

Treatment of absence seizures

A

Absence seizures (Petit mal)

  • sodium valproate or ethosuximide

*sodium valproate particularly effective if co-existent tonic-clonic seizures in primary generalised epilepsy

DO NOT use carbamazepine → it may exaggerate absence seizures

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4
Q

Treatment of myoclonic seiures

A

Myoclonic seizures

  • sodium valproate
  • second line: clonazepam, lamotrigine

DO NOT USE carbamazepine → it may exacerbate myoclonic seizures

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5
Q

Treatment of focal seizures

A

Focal seizures

  • carbamazepine or lamotrigine
  • second line: levetiracetam, oxcarbazepine or sodium valproate
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6
Q

SEs of sodium valproate

A
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7
Q

SEs of carbamazepine

A
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8
Q

seizure vs syncope

A
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9
Q

A 43 year old male with known epilepsy is being withdrawn from his

AED under the care of his neurologist. During this period, he suffers a tonic-clonic seizure.

What does the DVLA state in this case?

A
  • Cannot drive for at least 6 months + goes back on previous AED
  • He can start driving once he goes back to his previous AED – has to be seizure-free for 6 months after going back to his previous AED
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10
Q

DVLA and epilepsy guidance

A
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11
Q

The differential diagnosis for ‘tired all the time

A
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12
Q

Red flags for an adult with ‘tiredness’

A
  • unintentional weight loss (5% of body weight in 6–12 months)
  • Lymphadenopathy suggestive of malignancy
  • Other symptoms and signs of malignancy, such as haemoptysis, dysphagia, rectal bleeding, breast lump, or postmenopausal bleeding
  • Localizing/focal neurological signs
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13
Q

Blood tests for patient presenting with ‘tiredness’

A
  • Full blood count
  • Erythrocyte sedimentation rate or C-reactive protein
  • Renal and liver function tests
  • Thyroid stimulating hormone
  • Random blood glucose or HbA1c
  • IgA tissue transglutaminase (for coeliac disease)
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14
Q

Type 1 vs Type 2 Diabetes Mellitus

A
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15
Q

Microvascular and macrovascular complications of diabetes

A
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16
Q

What to look for an examination of a diabetic patient?

A
17
Q

What to look/examine for on diabetic foot examination?

A
18
Q

Values diagnostic of diabetes mellitus

A
19
Q

Values of pre-diabetes and diabetes glucose

A
20
Q

Conservative management of T2DM

A
  • Lifestyle management (diet, exercise, smoking cessation, reduce alcohol consumption)
  • Education about the condition
  • Offer structured group education programme (DESMOND: Diabetes Education for Self-Management for Ongoing and Newly Diagnosed)
  • Monitor for complications (inform about annual screening for retinopathy, foot problems, nephropathy and cardiovascular risk factors)
21
Q

Medical management of T2DM (other than hypoglycaemic agents)

A
  • Lipid modification – ither atorvastatin 20mg for primary prevention if QRISK2 >10% or >85 or atorvastatin 80mg for secondary prevention of cardiovascular disease
  • Blood Pressure – ACE inhibitor is first line for all patients with diabetes diagnosed with hypertension (if African/Caribbean – prescribe concurrent diuretic or calcium channel blocker)
22
Q

Steps in hypoglycaemic agents selection for T2DM

A
23
Q

Metformin

  • class
  • MoA
  • SEs
A

(Biguanide)

Metformin

MoA: Reduces the rate of gluconeogenesis and

increases insulin sensitivity

*Does not affect insulin secretion or cause

hypoglycaemia or predispose to weight

gain

Side effects: Diarrhoea

24
Q

Gliclazide

  • class
  • MoA
  • SEs
A

(Sulfonylureas)

Gliclazide, Tolbutamide, Glibenclamide

MoA: Act on beta cells to promote insulin

secretion in response to glucose and other secretagogues

*Ineffective in patients with no remaining

beta cell function

Side effects: Promote weight gain, risk of

hypoglycaemia

25
Q

Glitazones

  • name, class
  • MoA
  • SEs
A

Thiazolidinediones

Glitazones (piaglitazone)

MoA:

  • Reduce insulin resistance by interaction with PPAR-y receptor
  • They reduce hepatic glucose production and enhance peripheral glucose uptake

SEs: Pioglitazone is only remaining agent but

has adverse effects: fluid retention, heart

failure and bladder cancer

26
Q

Gliptins

  • class, names
  • MoA
  • SEs
A

Dipeptidyl peptidase-4 inhibitors (DPP4)

saxagliptin, sitagliptin

MoA: Enhance the incretin effect (oral glucose

response > IV glucose due to GLP-1 and GIP)

Side effects: nausea, pancreatitis

NICE advise continuing DPP-4 inhibitor only

if there is a reduction of > 0.5 percentage

points in HbA1c in 6 months

27
Q

Exenatide

  • class
  • MoA
  • justification for continuous taking
A

GLP-1 agonists

(exanatide, liraglutide)

MoA:

  • Injectable long-acting analogues of GLP-1
  • They promote insulin release, inhibit glucagon release
  • reduce appetite
  • delay gastric emptying

*Major advantage is glucose control with weight

reduction

* Given by subcutaneous injection before meals

NICE advise patients to have achieved a 1%

reduction in HbA1c and 3% weight loss after 6

months to justify the ongoing prescription of

GLP-1 mimetics

28
Q

Gliflozins

  • names
  • MoA
  • SEs
A

Gliflozins

(dapagliflozin, canagliflozin)

MoA: SGLT2 inhibitors (sodium/glucose transporters) which prevent reabsorption of glucose by the kidney tubules

Side effects: urinary tract infections, weight loss

29
Q

Insulin

  • MoA
  • SEs
A

Insulin

MoA:

  • Promotes glucose uptake into tissues
  • Stimulates glycogen, fatty acid and protein synthesis
  • Inhibits gluconeogenesis

Side effects: hypoglycaemia, weight gain

30
Q

Features of Wernicke’s encephalopathy

A

CAN OPEN

  • *C**onfusion
  • *A**taxia
  • *N**ystagmus
  • *O**phthamoplegia
  • *PE**ripheral
  • *N**europathy
31
Q
A