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Lucy Knox - Year 2.5 > 239 - Diabetes Type 1 > Flashcards

239 - Diabetes Type 1 Flashcards

1
Q

Which of the following symptoms suggests type 1 diabetes in a peadiatric patient?

Weight gain

Weight loss

Oliguria

Diarrhoea

Arthralgia

A

Weight loss

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2
Q

A patient with known type 1 diabetes is found unconscious. What is the most likely cause?

Diabetic ketoacidosis

Hyperglycaemia

Hypoglycaemia

Meningitis

Post-ictal state

A

Hypoglycaemia

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3
Q
  1. Which of the following results supports a diagnosis of type 1 diabetes in a young symptomatic patient?

Random glucose 14.5 mmol/l

Fasting glucose of 6.1 mmol/l

HbA1c 45mol/mmol

Glucose at 120mins 9.6mmol/l

Glycosuria +1

A

Random glucose 14.5

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4
Q

Q4. The retinal photograph demonstrates?

Pan retinal photocoagulation scarring B

ackground retinopathy

Proliferative retinopathy

Diabetic maculopathy

Retinal haemorrhage

A

Pan retinal photocoagulation scarring

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5
Q

Q5. A patient with type 1 diabetes attends clinic for annual review. What is the target HbA1c which is generally recommended?

•
a.Below 63 (8.0%) mmol/mol
b.Below 58 (7.5%) mmol/mol
c.Below 53 (7.0%) mmol/mol
d.Below 48 (6.5%) mmol/mol
e.Below 42 (6.0%) mmol/mol
•
•

A

c.Below 53 (7.0%) mmol/mol

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6
Q

Q6. The most commonly prescribed insulin regime for patients with type 1 diabetes in the UK is?

•

a. Twice daily pre mixed insulin
b. Basal bolus insulin
c. Insulin pump therapy
d. Sensor augmented pump therapy
e. Once daily insulin glargine

A

Basal Bolus

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7
Q

Q7. The retinal image shows feature of which

type of retinal pathology?

a. Background diabetic retinopathy
b. Diabetic maculopathy
c. Proliferative retinopathy
d. Pre proliferative retinopathy
e. Retinal haemorrhage

A

Background Diabetic retinopathy

(but because hard exudates in macula area actually maybe should be pre-proliferative)

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8
Q

Q8 Which of the following is an indication for insulin pump therapy?

•
•Recurrent hypoglycaemia
•Elevated HbA1c
•Injection phobia
•Non compliance with blood sugar testing
•HbA1c of 6.0%

A

Recurrent hypoglycaemia

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9
Q

Q9. This pattern of GFR is seen in which condition?

●

a. Acute kidney injury
b. Classical diabetic nephropathy
c. Diabetic glomerulosclerosis
d. Nephrotic syndrome
e. Reno vascular diabetic disease

A

Classical diabetic nephropathy

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10
Q

Q10. Which of the following symptoms suggests neuroglycopaenia in a patient with type 1 DM?

a. Chest pain
b. Confusion
c. Dry mouth
d. Sweating
e. Tremor

A

Confusion

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11
Q

Q12. Which of the following is an adrenergic response to hypoglycaemia?

•
a.Confusion
b.Limb weakness
c.Seizure
d.Slurred speech
e.Sweating
•

A

Sweating

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12
Q

The image shown represents

a. Background diabetic retinopathy
b. Pre proliferative retinopathy
c. Proliferative diabetic retinopathy
d. Diabetic maculopathy
e. Retinal haemorrhage

A

Proliferative diabetic retinopathy

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13
Q

Q14. Which of the following cutaneous manifestations is associated with type 1 DM?

  1. Abdominal striae
  2. Acanthosis nigricans
  3. Palmar erythema
  4. Tendon xanthomata
  5. Vitiligo
A

Vitiligo

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14
Q

Q15. Which of the following is most commonly seen in association with type 1 diabetes?

•

a. Acromegaly
b. Addison’s disease
c. Cushing’s syndrome
d. Psoriasis
e. Ulcerative colitis

A

Addison’s disease

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15
Q

Q.16 The earliest clinical manifestation of diabetic nephropathy is?

a. Dipstick positive proteinuria
b. Elevated Albumin : Creatinine Ratio
c. Elevated serum creatinine
d. Kimmelsteil Wilson lesions
e. Renal shrinkage on USS

A

b.Elevated Albumin : Creatinine Ratio

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16
Q

Q17. How often should patients with type 1 diabetes should have a retinal photograph to screen for diabetic retinopathy?

a. Annually
b. Every 5 years
c. At each clinic attendance
d. 6 monthly
e. Every 18 months

A

Annually

If changes - 3/6 monthly

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17
Q

Q18. In a patient with type 1 diabetes with hypertension what is the recommended first line class of anti hypertensive therapy?

a. ACE inhibitor
b. Beta blocker
c. Calcium channel blocker
d. Diuretic
e. Alpha blocker

A

ACE inhibitor

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18
Q

Q19. All patients with type 1 diabetes who are actively trying to become pregnant should be treated with which medication?

a. 400mcg of Folic acid
b. 5mg of Folic acid
c. 500mg Metformin
d. Clomiphene
e. 75mg Aspirin

A

5mg Folic acid

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19
Q

Q20. Which compound is measured when testing blood for ketone bodies?

a. Acetoacetate
b. Beta hydroxybuterate
c. Pyruvate
d. Lactate
e. Succinate

A

b.Beta hydroxybuterate

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20
Q

Q21. Which of the following biochemical results is consistent with a diagnosis of DKA

●
a. Blood glucose 10.0mmol/l
b.Base excess -2.0
c.Capillary ketones 4.5mmol/l
d.pH 7.31
e.Serum bicarbonate 21.0mmol/l
•

A

c.Capillary ketones 4.5mmol/l

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21
Q

Q22. A patient is diagnosed with DKA in the medical assessment unit. IV fluid resuscitation is commenced. What rate of IV insulin do you recommend initially?

a. 6 units/hr
b. 20 units/hr
c. 0.1u/kg/hr
d. 1.0u/kg/hr
e. 10% of total daily sub cutaneous dose

A

c.0.1u/kg/hr

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22
Q

Q23. Which of the following is a common trigger for DKA?

a. Acute infection
b. Dehydration
c. Long haul travel
d. Extreme physical exercise
e. Vomiting

A

Acute infection

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23
Q

Q24. You are called to a patient with type 1 diabetes who is confused and disorientated. His blood glucose is 2.0 mmol/l. He is able to swallow. Which treatment is most appropriate?

a. X4 Dextrose tablets
b. 50ml of 50% Dextrose IV
c. 1000ml 5% Dextrose
d. X2 Digestive biscuits
e. X2 Glucogel (hypostop) sachet

A

X2 Glucogel (hypostop) sachet

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24
Q

Q25. After treating an episode hypoglycaemia how long should you wait before checking the glucose response to therapy?

•

a. 5mins
b. 15mins
c. 30mins
d. 1 hour
e. Use clinical assessment

A

15 minutes

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25
Q

Q26 The structure of insulin is composed of how many polypeptide chains?

•
a.1
b.2
c.3
d.4
e.5
•

A

2

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26
Q

•Q27 When treating Diabetic ketoacidosis which electrolyte should to be monitored on a 2 hourly basis according to JBDS guidance?

a. Glucose
b. Sodium
c. Potassium
d. Magnesium
e. Bicarbonate

A

K+

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27
Q

Q28. In a patient with type 1 diabetes who is unable to eat due to nausea and vomiting. How would you manage his blood glucose control?

a.Omit all insulin
b.Omit rapid acting insulin
c.Intravenous insulin according to DKA protocol
d.Intravenous insulin and dextrose according to VRIII protocol
e.2 hours sub cutaneous boluses of insulin
●

A

d.Intravenous insulin and dextrose according to VRIII protocol

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28
Q

Q29. This patient has chronic deformity of the foot due to ?

a. Charcot neuroarthropathy
b. Diabetic neuropathy
c. Gout
d. Osteomyelitis
e. Peripheral vascular disease

A

a.Charcot neuroarthropathy

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29
Q

What causes type I diabetes?

A

Insulin deficiency following autoimmune destruction of pancreatic Beta cells

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30
Q

What auto antibodies can you look for in type I diabetes?

A

Anti-GAD antibodies

Islet cell antibodies

Z anti-a antibodies

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31
Q

What are the symptoms seen in a young patient presenting with diabetes?

A

Acute picture

2-6 week history of classical osmotic symptoms

  • Polyuria + nocturia
  • drowsiness
  • dehydration
  • Weight loss
32
Q

What is seen in an older patient presenting with diabetes type I?

A

Often subacture picture

Over months/years

LAck of energy

Blurring of vision

Pruritus vulvae or balanitis

Ketonuria

Hyperventillation

33
Q

What investigations can be done for ? type I diabetes?

A

Random plasma glucose

Fasting plasma glucose >7

Urine dipstick testing

2Hr glucose >11.5

34
Q

What are the different insulin regimes available in type I diabetes?

A

Twice daily free mix - rarely now

Twice daily premix - fast + slow mixed, only 2 imjections a day, good in school age kids.

Basal bolus regime - most common, copies real life, 4 injections/day, more flexible

Insulin pump therapy - Gives consitant delivery of fast acting insulin, used more and more.

35
Q

Who is an insulin pump indicated for?

A

Poor control

regular hypos

Pregnancy

Gastroporeisis

36
Q

Why was inhaled insulin not a sucess?

A

Increased incidence of lung cancer as insulin is a growth factor

37
Q

What are complications of s/c insulin delivery?

A

Lypoatrophy - loss of s/c tissue

Lupohypertrophy - prolifferation of s/c tissue, causes variable absorption of insulin from that area.

Why? impurities in older insulins

Repeated injections into same site - must rotate

38
Q

What is DKA?

A

Diabetic Ketoacidosis

Absolute or relative insulin deficiency

39
Q

When is DKA likely to happen?

A

A new diagnosis

Omission of insulin

Intercurrent disease - illness is an insulin resistant state

40
Q

What levels make a diagnosis of DKA?

A

Hyperglycaemic : >11mmol/l

Ketotic : capillary ketones >3mmol/l or urine ++

Acidotic: pH <7.3, +/- bicarb <15mmol/l

41
Q

Describe the pathophysiology of DKA

A

If no insulin is available you can’t use sugar, so it builds up - hyperglycaemia.

The body increases the amount of proteolysis and glyconeogenesis to provide energy, which also increases the glucose int he blood.

This is excreted in the urine, causing glycosuria, dehydration and metabolic disterbances.

As glucose can’t be used, fat is metabolised increasing free fatty acids and ketones are left.

This causes increase in serum ketonacids and metabolic acidosis

42
Q

What are the symptoms of DKA?

A

Breathlessness (to blow off CO2 and reduce acid)

N+V

Abdo pain

Thirst

Polyuria

Tachcardia

Hypotensive

reduced Cap refil

Tachypnoea

Drowsy

43
Q

What is the management of DKA?

A

Immediate - ACB, IV access, Bloods…

IV saline - 6l in 1st 24hrs

Insuline therapy - act rapid (o.1u/kg/hr) and continue basal insulin

-> fluid + insulin needed for a few days to fully clear ketones.

IV glucose once Blood glucose falls so insulin can still be given

K+ supplements

44
Q

What monitoring is needed during menagement of DKA?

A

Hourly glucose and ketones

2 hourly K+

2 hourly venous gas

45
Q

What are the aims of DKA management?

A

Reduce ketones

Reduce glucose

Increase venous bicarb

Maintain K+

46
Q

What happens when blood glucose drops?

A

If glucose drops, hypothalmus detects and:

  • activates Sympathetic NS - increase in epinepherine and acetylcholine
  • stimulates ant-pituitary which stimulates adrenal cortex to produce cortisol
  • Normally pancrease reduces insulin amount (less gluc pushed into cells) and increases glucagon (to break glyogen down).
47
Q

Why do we mount a response to low glucose?

A

The brain can only use glucose - so mount an adrenergic response to make you realise and seek out food

48
Q

In reduced glucose (<4mmol/l) what are the adrenergic symptoms?

A

Palpitations

tremmor

Anxiety

Sweating

Hunger

Parasthesia

49
Q

When blood glucose drops to <2mmol/l what happens?

A

Neuroglycopaenia

Cognitive impairment

Confusion

Behaviour changes

Pscyhomotor changes

Concentration less

Seizures

Coma

50
Q

What is the management of a mild hypo? <4mmol/l

A

Mild: dextrose tablets (around 15g)

Check BM in 15 mins, repeate

51
Q

What is the management of a moderate hypo?

Pt conscious but confused

sugar <3mmol/l

A

Gel glucose - glucogel

Check BM in 15 mins

repete if needed

Follow with some complex carbs (biscuits) to last til next meal

52
Q

What is the management of a severe hypo?

Pt unconscious/fitting/aggresvie

A

Inject glucagon IM

IV dextrose

don’t omit subsequent insulin

53
Q

What is the VRIII sliding scale?

A

Variable Rate Intravenous Insulin Infusions

If pt. is vomiting, NBM or decompensated

Allows close control

  • Glucose infusions
  • Fluid
  • Insulin - amount varies along a scale depending on how close to the target range of BM 6-10 you are.
54
Q

What are the microvascular complications of Type I diabetes?

A

Retinopathy

Nephropathy

Neuropathy

55
Q

What changes occur in diabetic retinopathy?

A

Microaneurysms - red dots

Occlusion

Leakage - hard exudates or soft

New vessel formation - near optic disk

Haemorrhage - dot, blot or flame

56
Q

What are the 4 stages of diabetic retinopathy?

A

Background

preproliferative

proliferative

Maculoapthy

57
Q

What changes are seen in background diabetic retinopathy?

A

microaneurysm(s), haemorrhage(s) +/- any hard/soft exudates

58
Q

What changes are seen in pre-proliferative retinopathy?

A

venous beading/duplication,

IRMAs,

multiple deep, round haemorrhages,

cotton wool spots (>5)

59
Q

What changes are seen in proliferative diabetic retinopathy?

A

new vessels on disc (NVD),

new vessels elsewhere (NVE),

preretinal or vitreous haemorrhage,

preretinal fibrosis

+/- tractional retinal detachment

60
Q

What changes are seen in maculopathy in diabetic retinopathy?

A

exudate within a disc area (DA) of fovea,

retinal thickening within DA of fovea,

microaneurysm or haemorrhage within DA of fovea (reducing central vision)

61
Q

What are differentials for diabetic retinopathy?

A

Hypertensive retinopathy: A-V nipping, ‘silver wiring’, flame shaped haemorrhages, hard and soft exudates

  • Retinal vein thrombosis: haemorrhages, tortuous veins, macular oedema, new vessels (“blood and thunder” retina)
  • Macular drusen (associated with AMD)

phospholipid crystals

62
Q

How can you manage diabetic retinopathy?

A

Prevent - good contol

Screening

Referal

Treat with Argon laser:

Pan photocoagulation

macular grid/focal laser treatment

anti VEGF injection into orbit

63
Q

What happens in diabetic nephropathy?

A

Increase in glomerular blood flow and pressure -> increase GFR

Basement membrane thickening + tubular function worsens

Microalbuminurea

overt clinical nephropathy, albuminurea, decreased GFR, rising creatinine

end stage renal failure

64
Q

What is diabetic nephropathy?

A

Diabetic nephropathy is a clinical syndrome characterised by persistent albuminuria (>300 mg/day) on at least two occasions; almost invariably associated with hypertension and usually with retinopathy, leading to renal failure

65
Q

What are the normal levels of albuminuria?

A

<20mg/l urine

<30mg/day

Or use albumin creatinine ration:

male <2.5

Female <3.5

66
Q

What is microalbuminuria?

A

30-300 mg/24hrs urine

or ACR:

Male 2.5 - 30 mg/mmol creatinine

Female: > 3.5 – 30 mg/mmol creatinine

67
Q

What value is used to stage chronic kidney disease/

A

GFR

Stage 1>90

Stage 5 (end stage) <15

68
Q

How do you manage diabetic nephropathy?

A

Manage Bp

ACEi

ARB (more for type II)

69
Q

What are the characteristics of diabetic neuropathy?

A

Glove and stocking

Sensory loss

Pain

Tendon reflexes reduced

Motor deficit slightly

70
Q

How do you manage diabetic neuropathy?

A

Amitriptyline

Duloxitine

Pregabalin/gabapentin

Opiates

71
Q

What does diabetic neuopathy put the pt at risk of?

A

Diabetic foot disease

Leading cause of mortality

Due to both sensory (insensitivity) and motor neuropathy (change in foot position and pressure points)

72
Q

What occurs in diabetic foot disease?

A

Supervening ulceration and infection

• Small vessel and large vessel ischaemia, resulting in gangrene and amputation.

73
Q

What is charcot neuropathy?

A

Warm, swollen, insensitive foot without ulceration

Pathological fracture(s), joint dislocations, deformities, progressive destruction of bone, “bag of bones”

  • can become “rocker foot” - arch is lost
  • needs weight offloading and MDT approach
74
Q

What autonomic neuropathies are seen in diabetes?

A

Erectile dysfunction

Gastroparesis

Postural hypotension

75
Q
A

Lucy Knox - Year 2.5 (15 decks)

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