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Year 3 > MedEd diabetes and pituitary > Flashcards

MedEd diabetes and pituitary Flashcards

1
Q

What gene is T1DM associated with?

A

HLA DR3/4

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2
Q

What is T2DM associated with?

A

Obesity
HTN
Inactivity
Dyslipidaemia

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3
Q

What state causes polyuria in T1DM?

A

Osmotic diuresis

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4
Q

What are some signs of DKA?

A

Nausea and vomitting
Abdo pain
Kaussmal breathing

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5
Q

What are some signs of T2DM?

A

Acanthosis nigricans

Signs of peripheral disease/ complications

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6
Q

What is random glucose in diabetes?

A

> 11.1

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7
Q

What is fasting glucose in diabetes?

A

> 7

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8
Q

What is HbA1c in diabetes?

A

> 48

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9
Q

What antibodies are associated with T1DM?

A

Anti GAD antibodies

Islet cell antibodies

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10
Q

What test should you always do for T1DM in GP and what will you see?

A

Urine dip- positive glucose and ketones

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11
Q

How is insulin given in T1DM?

A

Basal bolus regimen

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12
Q

What is the first line treatment for T2DM?

A

Lifestyle advice= diet, exercise, education

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13
Q

What is the first line pharmacological treatment for glycaemic control in T2DM?

A

Metformin

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14
Q

What is the first line pharmacological treatment for blood pressure management in T2DM? What is second and third line

A

Ace inhibitor, if black ARB
Then add CCB or thiazide
Then ACEi/ARB with CCB and thiazide

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15
Q

What glucose level is classed as hypoglycaemia?

A

<3.6 mmol/L

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16
Q

What are signs of hypoglycaemia?

A

Palpitations, tremors, sweating, pallor, anxiety, drowsiness, confusion, coma

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17
Q

How is hypoglycaemia managed?

A

If conscious- eat sugary food

If consciousness is impaired - IM glucagon 1g

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18
Q

What triad signifies DKA?

A

Hyperglycaemia
Ketonaemia
Metabolic acidosis

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19
Q

Why is ketonaemia harmful?

A

Acidity causes enzyme dysfunction which can lead to coma and death

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20
Q

How is DKA managed?

A

Hydration with IV fluid

Insulin to reduce ketones

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21
Q

What is HHS? How does it present?

A

Hyperosmolar hyperglycaemic state- hyperglycaemia with no ketonaemia
Dehydration, kussmaul breathing, nausea and vomitting

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22
Q

How can you differentiate DKA and HHS based on signs and symptoms?

A

They are the same but no abdo pain in HHS

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23
Q

How are DKA and HHS managed?

A

Start IV saline (and potassium chloride if K+ <5.5)
IV insulin (fixed rate) after fluids (only when K+ is not <3.5)
Include dextrose in fluids if <14
Treat underlying cause eg abx

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24
Q

What is plasma glucose in DKA?

A

> 11

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25
Q

What is plasma glucose in HHS?

A

> 30

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26
Q

What are the 4 stages of retinopathy?

A 
1= background retinopathy= blot and dot haemorrhage/ hard exudates
2= pre prolif= background and cotton wool spots
3= proliferative= non proliferative and new vessels on disk (neovascularisation)
4= maculopathy= hard exudates and near macular
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27
Q

What is neovascularisation associated with?

A

Retinal detachment with retinal detachment and vitreoud haemorrhage with visual loss

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28
Q

How is retinopathy managed?

A

Backgorund= improve glycaemic control
Pre proliferative and proliferative= pan retinal laser photocoagulation
Maculopathy= anti VEGF injections

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29
Q

How does diabetic nephropathy present?

A

Oedema, polyuria, lethargy, hypertension

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30
Q

What is the first line investigation for diabetic nephropathy? What will you see?

A

Urinalysis

Will show a high albumin: creatinine due to microalbuminuria

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31
Q

How is diabetic retinopathy managed?

A

ACEi/ARB

Improve glycaemic control

32
Q

What causes diabetic neuropathy?

A

Blockage of the vasa vasorum (blood vessels that supply the vasa vasorum)

33
Q

What distribution is associated with diabetic peripheral neuropathy?

A

Glove and stocking

34
Q

What are some signs and symptoms of diabetic neuropathy?

A

Loss of sensation (especially feet)
Loss of ankle reflex
Injuries to foot
Fractures

35
Q

What are the 3 types of diabetic neuropathy?

A

Peripheral
Autonomic
Mono

36
Q

How will autonomic diabetic neuropathy present?

A 
GI tract symptoms= difficulty swallowing, bladder dysfunction, delaye dgastric emptying 
Postural hypotension (collpase on standing) 
Cardiac autonomic supply
37
Q

How will diabetic mononeuropathy present?

A

Sudden motor loss eg wrist drop, foot drop, 3rd nerve palsy

38
Q

What is seen on third nerve palsy?

A

Eye down and out

Pupil responds to light

39
Q

What is diabetes insipidus?

A

Inadequate secretion or sensitivity to vasopressin/ADH causing production of dilute urine

40
Q

What are causes of cranial diabetes insipidus?

A

Pituitary tumor, infection, sarcoidosis, TB

41
Q

How will someone with diabetes insipidus present?

A

Polyuria
Nocturia
Polydipsia
Dehydration (tachycardia, dry mucous membranes)

42
Q

What are first line investigations for DI? What will you see?

A

UEs (ca/k for cause)
Glucose
Water deprivation test

43
Q

How is the water deprivation test carried out?

A

Restrict them of water for 8 hours

Then give desmopressin and monitor UEs every hour

44
Q

What will be the result of water deprivation test in a normal person, cranial and nephrogenic DI?

A

Normal- no change in urine osmolality after desmopressin is given and no more water to reabsorb
Cranial- rapid rise in urine osmolarity
Nephrogenic- urine remains unconcentrated

45
Q

How is diabetes insipidus managed?

A 
Cranial= Intranasal desmopressin and tell them not to drink lots of water
Nephrogenic= thiazide diuretic, low salt and protein diet
46
Q

What is SIADH?

A

Excess ADH secretion causing too much water absorption

47
Q

What happens to serum Na, urine osmolality and urina na in SIADH?

A

Serum na= low
Urine osmolality= high
Urine na= high

48
Q

What are causes of SIADH?

A 
CNS= subarachnoid haemorrhage, tumor, TB
Pulmonary= pneumonia, bronchiectasis
Malignancy= small cell lung cancer
Drugs= carbamazepine, SSRI
Idiopathic
49
Q

How is SIADH managed?

A

Treat cause eg surgery for tumor
Immediate fluid restriction for hyponatreamia
If ineffective oral demeclycycline/IV vaptans

50
Q

What is normal sodium?

A

135-145 mEq/L

51
Q

What are the 3 types of hyponatreamia?

A

Hypovolemic
Euvolemic
Hypervolemic

52
Q

What are causes of hypovolemic hyponatreamia? How is it managed

A

Vomitting
Diarrhoea
Diuretics

Manage with IV fluid

53
Q

What is urine sodium in hypovolemia hyponatreamia?

A

Low (<20)

54
Q

What are causes of euovolemic hyponatreamia? How is it managed

A

SIADH
Hypothyroidism
Adrenal insufficiency

Manage= Fluid restrict

55
Q

What are causes of hypervolemic hyponatreamia? How is it managed

A

Liver, kidney or heart failure

Manage by restricting fluid

56
Q

How do you treat severe hyponatreamia?

A

Slow IV saline

57
Q

What happens if IV saline is given too fast?

A

Central pontine myelionylysis

58
Q

Why is SIADH euvolemic?

A

Posterior pituitary produces lots of ADH
Lots of BNP is produced
This BNP prevents ADH from making you hypovolemic

59
Q

What is fluid intake restricted to when treating hyponatraemia?

A

1 litre/ day

60
Q

What range is hypernatreamia?

A

> 145 mEq/L

61
Q

What are causes of hypernatreamia?

A

Unreplaced water loss eg GI loss, sweating
Renal loss eg HHS, DI
Sodium overload eg cushings, primary aldosteronism, iatrogenic

62
Q

How will hypernatreamia present?

A 
Lethargy
Irritability
Thirst
Signs of dehydration
Confusion
Coma
Fits
63
Q

How is hypernatreamia treated?

A

5% dextrose to correct water deficit

0.9% saline- correct ECF volume depletion

64
Q

What sodium imbalance is more common?

A

Hyponatraemua

65
Q

What stimulates prolactin production? What inhibits it?

A 
Stimulates= TRH
Inhibits= dopamine
66
Q

What are causes of hyperprolactinaemia?

A 
Pregnancy
Breast feeding
Prolactinoma
Pituitary adenoma
Primary hypothyrodism
67
Q

How does hyperprolactinaemia present?

A

Men=Loss of libido, erectile dysfunction, infertility
Women=Galactorrhea, secondary amenorrhea, loss of libido, infertility
Mass effects= headache, visual field defect

68
Q

What are the investigations for hyperproloactinaemia? What will you see

A

Pregnancy test- may be positive
TFTs- may be low if from hypothyroidism
Basal serum prolactin- if crazy high most likely tumor
MRI to image

69
Q

How is prolactinoma managed? Give first and second line treatment

A

First line= dopamine receptor agonist eg cabergoline, bromocriptine
Second line= trans sphenoidal surgery

70
Q

How is hyperglycaemia in T2DM managed?

A

First line lifestyle advice
Second line metformin if Hba1c is over 48
Third line add pioglitazone, SGLT2 inhibitor, DPP4 inhibitor or sulphonylurea
Fourth line add another drug or try insulin based treatment

71
Q

How are lipids in T2DM managed?

A

Atorvastatin 20mg OD if risk of cardiovascualr event in next 10 years is above 10%
Atorvastatin 80mg OD if they have IHD/CVD/peripheral arterial disease

72
Q

How is hypertension in T2DM managed?

A

First line ACEi, ARB if black
Second line add CCB or thiazide
Third line ACEi/ARB + CCB + thiazide

73
Q

How is hyper and hypokalemia managed in T2DM?

A

Hyperkalemia (>4.5)= beta blocker

Hypokalemia (<4.5)= spironolactone

74
Q

What antiplatelet medication and what dose is given to diabetics with IHD/CVD/PAD?

A

Aspirin 75 mg

75
Q

What needs to be managed in a patient with diabetes?

A 
Hyperglycaemia 
Hypertension
Dyslipidaemia
Hyper/hypokalemia
Coagulopathy
76
Q

What 2 molecules are in excess in DKA, what effect does each of them have and how are they reduced?

A

Excess glucose causes dehydration, this is treated with IV fluids
Excess ketones causes acidosis and enzyme dysfunction, this is treated with insulin

77
Q

What will ketones, plasma glucose and pH be in DKA vs HHS?

A

DKA: pH= low/acidic, ketones=high (over 3), plasma glucose high (over 11)
HHS: pH= normal, ketones=normal, plasma glucose high (over 30)

Year 3 (104 decks)

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