Endocrinology Flashcards

1
Q

What is required for DM diagnosis in symptomatic and asymptomatic patients?

A

Symptomatic -
Fasting >=7 OR
Random >=11.1

Asymptomatic -
Raised venous glucose twice separately OR
2hOGTT >=11.1

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2
Q

What are the secondary causes of DM?

A

Drugs - Steroids, HIV meds, neuroleptics, thiazides
Pancreatic - CF, chronic itis, HH, panc Ca
Endo - phaeo, cushings, acromegaly, hyperthyroidism
Glycogen storage disease

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3
Q

Outline the conservative management of DM

A

MDT approach

Monitor the 4Cs
Control glucose levels
Complications
Competency
Coping
Life style modifications - DELAYS
Diet
Exercise
Lipids
ABP
Aspirin
Yearly check ups
Smoking cessation
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4
Q

What are the side effects of metformin?

A

Nausea, diarrhoea, abdo pain, lactic acidosis (therefore CI if GFR<30)

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5
Q

What medication should be added if lifestyle and metformin alone are not controling glucose levels?

A

Sulphonylureas - e.g. Gliclazide MR 30mg with breakfast

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6
Q

What are the side effects of gliclazide?

A

Hypos and weight gain

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7
Q

What can be added to metformin if the patient is prone to hypos instead of gliclazide?

A

Pioglitazone/sitagliptin (causes weight)

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8
Q

What is the benefit of Exenatide?

A

Also lowers BP so is cardioprotective

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9
Q

What are the two commonest insulin regimes, and what are their benefits and drawbacks?

A

BD Biphasic -
A mixture of rapid and long acting insulin given 30 minutes before breakfast and dinner good for old people and children but does cause fasting hyperglycaemias

Basal-bolus regime
Bedtime long acting glargine with short acting actrapid before each meal adjusting to meal size
Used for T1Dm allowing greater flexibility if appropriately managed

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10
Q

What considerations surrounding insulin should be made when a patient becomes ill?

A

Insulin requirements rise even when fasting
Maintain calories
Check BMs every 4 hours and test ketones and adjust insulin accordingly

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11
Q

What -broadly- are the complications of DM?

A

Macro and microvavscular

Macro
MI
PVD
CVA

Micro
Retinopathy
Neuropathy
Nephropathy

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12
Q

What type of foot ulcers do diabetics tend to get?

A

Ischaemic and neuropathic

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13
Q

What is the progression of diabetic retinopathy?

A

Background
Pre-proliferative
Proliferative
Maculopathy

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14
Q

What are the fundoscopy findings of background retinopathy

A

Dots - microaneurysms
Blot haemorrhages
Yellow exudates

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15
Q

What are the fundoscopy findings of pre-proliferative retinopathy

A

Cotton wool infarcts
Venous beading
Haemorrhages

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16
Q

What are the fundoscopy findings of proliferative retinopathy

A

Neovascularization

Vitreous haemorrhage

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17
Q

What are the fundoscopy findings of maculopathy

A

Impaired acuity +-

Hard exudates close to the macula

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18
Q

What are the features of autonomic neuropathy secondary to DM?

A
Postural hypos
Gastroparesis
Diarrhoea
Urinary retention 
ED
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19
Q

What are the three features of DKA?

A

DKA

Dehydration
Ketogenesis
Acidosis

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20
Q

What are the diagnostic criteria for DKA?

A

Acidosis - pH<7.3 (<7.1 is severe)
Hyperglycaemia - >=11.1
Ketosis - >=3 (>=2+ on dipstick

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21
Q

What is the management of DKA?

A
  1. Fluids
    If SBP<90: 0.9% saline over 15 minutes (repeat if nec)
    If SBP>90: maintenance fluids

Start K+ (if deranged) in second bag (40mmol/L) unless evidence of anuria

  1. Insulin
    Actrapid 0.1u/kg/hr IV (max 15u)
    Continue any SC regimens
3. Assess and investigations
Hx and exam
Catheter
NGT if vomiting or GCS<8
LMWH
Address precipitating factors
Hourly monitoring
  1. Glucose
    Once glucose <14, add 10% dextrose to saline infusion at 125ml/hr
5. Insulin
Once ketones <0.3 AND
pH>7.3 AND
Patient able to eat...
Switch to subcut actrapid and a meal, and stop the insulin infusion 1 hour later
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22
Q

How do hyperosmolar hyperglycaemic non ketotic states usually present?

A

Older pt with first presentation of T2DM

Marked dehydration and hyperglycaemia with NO acidosis due to absence of ketones

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23
Q

What are the complications of HHNK, and what should be done to prevent them?

A

VTE ->LMWH

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24
Q

What is Whipple’s triad?

A

Hypoglycaemia:

Low glucose
Symptoms associated with hypo
Relief of symptoms on glucose administration

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25
Q

What is the role of C-peptide in determining the cause of a hypo?

A

Exogenous insulin doesnt give C-peptide

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26
Q

What endocrine syndrome are insulinomas associated with?

A

MEN1

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27
Q

What are the features of thyrotoxicosis unique to Graves disease?

A
Opthalmoplegia
Exopthalmos
Gritty eyes
Pre-tibial myxoedema
Thyroid acropachy
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28
Q

Isotope scan shows increased and decreased uptake in which two conditions?

A

Increased in Graves

decreased in thyroiditis

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29
Q

Which other conditions is Graves associated with?

A

T1DM
Vitiligo
Addisons

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30
Q

What is the management of thyrotoxicosis?

A

Medical -
B-blockers
Carbimazole - causes agranulocytosis

Radioiodine - CI in pregnancy

Surgical - thyroidectomy; SFx - Laryngeal nerve damage, low pTH, hypothroid

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31
Q

What is the commonest cause of hypothyroidism in the UK and worldwide?

A

UK - Hashimoto’s

Worldwide - Iodine def

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32
Q

What drugs precipitate hypothyroidism?

A

Carbimazole
Amiodarone
Lithium

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33
Q

What antibodies are seen in Hashimoto’s thyroiditis?

A

Anti-TPO

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34
Q

What are the four types of thyroid cancer, which is the most common and which is the most aggressive?

A

Papillary - commonest
Follicular
Medullary - CEA+
Anaplastic - worst

35
Q

What are the complications of thyroid surgery?

A
Early
Haematoma ->airway obst
Laryngeal oedema ->obst
Rec laryngeal palsy
Hypoparathyroidism
Thyroid storm

Late
Hypothyroid
Relapse
Keloid scar (big scar)

36
Q

What is the commonest cause of primary hyperpth?

A

Solitary adenoma

37
Q

What are the investigative findings of primary hyperPTH?

A

HyperCA - Short QT, bradycardia, low PO4
Osteitis fibrosa cystica
Osteoporosis

38
Q

Rx of Primary hyperPTH?

A

Fluid
Reduce Ca intake and thiazides
Surgery

39
Q

What are the causes of secondary hyperPTH?

A

Vit D def

CKD

40
Q

What is the treatment of 2ary hyperPTH?

A
Phosphate binders (calcichew, sevelamer)
Vit D - alfacalcidiol in CKD, chole in vit D def
Cinaclet
41
Q

What are the features of hypoparathyroidism?

A
Trousseaus
Parasthesia
Anxiety
Seizures
Spasticity
Confusion
Chvostek
Long Qt
42
Q

What are the causes of hypoparathyroidism?

A

Autoimmune
DiGeorge
Surgical

43
Q

What is pseudohypoparathyroidism?

A

Target organ fails to respond to PTH causing Low Ca and High PTH

44
Q

What is pseudopseudohypoparathyroidism?

A

Normal biochem with pseudohypoparathyroid phenotype

45
Q

What are the features of Cushing’s syndrome?

A
Catabolic
Prox myopathy
Striae
Bruising
Osteoporosis

Glucocorticoid
DM
Obesity

Mineralocorticoid
HTN
Hypokalaemia

46
Q

What are the commonest causes of Cushings synd?

A

Iatrogenic - commonest by far
Adrenal adenoma
Cushings disease
Ectopic ACTH from SCLC/carcinoid

47
Q

How would you investigate Cushings’s syndrome?

A

24hour urinary cortisol

Dexamethasone supression tests

48
Q

How do you treat cushing’s sundrome?

A

Disease - excisison
Adenoma - adrenalectomy
Ectopic - Excision

49
Q

What is Nelson’s syndrome?

A

Rapid enlargement of a pituitary adenoma following bilateral adrenalectomy for Cuhings presenting with bitemphemianopia and hyperpigmentation

50
Q

What are the features of hyperaldosteronism`/

A

Hypokalaemia - weakness, hypotonia, hyporeflexia, parasthesia
Htn

51
Q

What are the two causes of primary hyperaldosteronism?

A

70% bilateral adrenal hyperplasia

30% solitary adenoma (Conn’s synd)

52
Q

What is the management of primary hyperaldosteronism?

A

Conns - surgery

Hyperplasia - spironolactone

53
Q

What causes secondary hyperaldosteronism?

A

Renal hypoperfusion causes renin secretion

RAS
Diuretics
CCF
Hepatic failure
Nephrotic syndrome
54
Q

How might you differentiate between primary and secondary hyperaldosteronism?

A

Aldosterone: Renin ratio
Normal in 2ary
High in 1ary

55
Q

What are the causes of primary adrenal insufficiency (Addison’s)

A

Worldwide - TB
UK - autoimmune disease
Lung mets
Congenital adrenal hyperplasia

56
Q

What are the syjmptoms of Addison’s disease?

A
Wt loss + anorexia
n/v
Abdo pain
Diarrhoea/constipation
Lethargy
Depression
Hyperpigmentation
Postural hypotension
Hypoglycaemia
Vitiligo
Crises
57
Q

What would investigatisons show in Addison’s disease?

A

BLood - lowNa high K, hypoglycaemia, hypokalaemia, anaemia

Short synacthen test should be negative

58
Q

What is the management of addison’s?

A

Replace Hydrocortisone and FLudrocortisone

Dont stop steroids suddenly, and increase them during intercurrent illness. Wear medicaalert bracelet

59
Q

What is the pathology of 2ary hypoadrenalism, and therefore its differences with Addisons?

A

HPA dysfunction due to chronic steroid use, pit apoplexy or microadenoma

Normal mineralocorticoid production and ho hyperpigmentation

60
Q

What is the presentation of Addison’s?

A

Shock - tachycardia, postural drop, oliguria, confusion

Hypoglycaemia

61
Q

WHat is the management of an adddisonian crisis?

A

IV hydrocortisone 100mg
IV fluids C
Glucose if needed

62
Q

What is the rule of 10s regarding phaeos?

A

10% malignant
10% extra adrenal
10% bilateral
10% hereditary syndromes

63
Q

WHich hereditary syndromes are linked to phaeos?

A

NF
Men2a and 2b
VHL

64
Q

What is the classic triad of phaeo presentation?

A

Episodic headache, sweating and tachycardia

65
Q

What is the diagnostic test for phaeos?

A

24hr urinary metanephrine

66
Q

What is the treatment for phaeos?

A

Adrenalectomy with pre-op alpha and beta blockade with post op BP monitoring for hypotensive crisis

67
Q

What are the features of MEN1

A

Pit adenoma
Parathyroid adenoma
Pancreatic tumours

68
Q

What are the features of MEN2a/b

A

Thyroid medullary carcinoma
Phaeos
a) hyperthyroidism
b)Marfanoid habitus

69
Q

What are the features of Carney Complex/LAME Syndrome?

A

LAMES

Lentigenes - spotty skin pigmentation
Atrial Myxoma
Endocrine tumours
Schwannomas

70
Q

What are the features of Peutz Jehgers?

A

Mucocutaneous freckls around mouth and on plantar surfaces
GI hamartomas
Pancreatic tumours
Cancer risk

71
Q

What are the features of VHL?

A
Bilateral RCC
Renal cysts
Haemangioblastomas -> cerebellar signs
Phaeos
Pancreatic endocrine tumours
72
Q

What are the features of NF?

A
Neurofibromata
Cafe au lait spots
Lisch nodules (eyes)
Axilliary freckling
Phaeos
73
Q

What are the causes of hypopituitarism?

A

Hypothalamic - Kallmanns, tumour, III
Pit stalk - trauma, surgery, tumour
Pituitary - irradiation, tumour, apoplexy, infiltration (HH, amyloid)

74
Q

What hormones are affected by panhypopituiitarism and how does this present?

A

GH - central obesity, atherosclerosis, HF
LH/FHS - libido reduction, ED, hair loss, amenorrhoea
TSH - hypothyroidism
ACTH - 2ary adrenal failure

75
Q

What is the classification of pituitary tumours?

A

<1cm is microadenoma

>1cm is macroadenoma

76
Q

Features of pituitary tumours?

A
Mostly mass effect - 
Headache
Bitemp hemianopia
CN palsies
DI
Rhinorrhoea CSF

Hormone effects-
PRL - galactorhoea
GF -> acromegaly
ACTH -> Cushings disease

77
Q

What is the commonest cause of acromegaly?

A

Pituitary adenoma - 99%

78
Q

What are the features of acromegaly?

A

Hands - CTS, large, thenar wasting

Face - Prominent supraorbital ridges, coarse face, ugly fuckers, big ears, prognathism,
macroglossia, goitre

79
Q

What are the complications of acromegal?

A

Endo - DM
Cardio - HTN, LVH, IHD
Neoplasia - CRC

80
Q

What is the management of acromegaly?

A

1st - transphenoidal surgery
2nd - somatostatin analogue (octreotide)
3rd - GH antagonits
4th - radiotherapy

81
Q

What are the different types of DI and their causes?

A
Cranial
Idiopathic
Tumours
Trauma
Haemorrhage
Infection

Nephrogenic
Congenital
Metabolic disturbance
Drugs - Lithium, Vaptans

82
Q

What is the treatment for cranial DI?

A

Desmopressin PO

83
Q

What are the causes of gynaecomastia?

A
Cirrhosis
Hypogonadism
Hyperthyroidism
Oestrogenic tumours
Spiro, digoxin, oestrogen