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Flashcards in Endocrinology Deck (168):
1

What is the cause of cushing's disease?

Pituitary adenoma secreting ACTH causing bilateral adrenal hyperplasia

2

Name 2 common sources of ectopic ACTH secretion

Small cell carcinoma of the lung
Carcinoid tumour of the bronchus

3

What are the features of ectopic production of ACTH?

Weight loss
Hypokalaemia
Pigmentation
Hyperglycaemia

4

Name 2 causes of ACTH independent cushing's syndrome

Exogenous steroid use
Adrenal adenoma

5

How is a diagnosis of cushing's syndrome confirmed?

FBC
U&Es and ABG
24 hour urinary free cortisol - need at least 2 samples with cortisol over 3 times normal amount
Low dose dexamethasone suppression test - give 1mg at 11pm and measure cortisol at 8am. Should be suppressed to less than 50nmol/l

6

How can the cause of cushing's syndrome be localised?

Plasma ACTH - if undetectable then is an ACTH independent cause eg steroid use or adrenal tumour
If detectable then do a high dose dexamethasone suppression test. If origin is pituitary, will still be under some control so cortisol will be suppressed at very high doses (>90%)
Ectopic secretion will show less reactivity and won't be as suppressed

7

How is cushing's syndrome treated?

If due to excess steroid use, stop drugs if possible
If pituitary, then remove trans-sphenoidally
If adrenal then bilateral adrenectomy
If ectopic, then remove source if possible
Cortisol will need reducing pre-operatively to reduce risk. Use ketoconazole or metyrapone short term. Mitotane long term

8

What condition can occur after bilateral removal of adrenal glands?

Growth of pituitary and excess ACTH production due to loss of negative feedback from the adrenal glands - nelson's syndrome with hyperpigmentation and headaches

9

Name give complications of untreated cushing's syndrome

Diabetes mellitus
Obesity
Metabolic syndrome
Thrombophilia
Osteoporosis
Perforation of viscera
Opportunistic infections
Increased mortality

10

What is secondary adrenal insufficiency caused by?

Insufficient ACTH due to suppression of the HPA axis, eg in long term steroid use

11

Name three causes of addison's disease

Autoimmune
TB
Adrenal malignancy
Adrenal haemorrhage
Amyloidosis
Infection
Haemachromotosis
COngenital adrenal hyperplasia
Bilateral adrenalectomy

12

Give 5 symptoms of addison's disease

Fatigue
Weight loss
Loss of appetite and premature satiety
Nausea and vomiting
Abdominal pain
Salt cravings
Weakness
Arthralgia
Dizziness
Headache
Low mood

13

How should suspected addison's disease be investigated?

Serum cortisol in the morning/soon after waking
U&Es
Synacthen test
Adrenal autoantibodies
AXR/CXR if TB/adrenal haemorrhage/malignancy is suspected

14

How does the synacthen test work?

Serum cortisol is given then dose of synthetic ACTH and cortisol is remeasured 30-60mins later. Cortisol should increase to >550nmol if normal

15

What U&Es abnormalities are present in addison's disease?

Hyponatraemia
Hyperkalaemia

16

How is Addison's disease treated?

Replace glucocorticoids with hydrocortisone TDS
Replace mineralocorticoids with fludrocortisone

17

How is an addisonian crisis managed?

IV fluids
100mg IV hydrocortisone stat

18

What is the difference between primary and secondary hyperthyroidism?

Primary is due to an abnormality of the thyroid gland
Secondary is due to abnormal stimulation of a normal thyroid gland, eg by a TSH secreting pituitary tumout

19

What abnormalities in thyroid function tests are found in overt hyperthyroidism?

Low TSH, High free T4 and free T3

20

What is subclinical hyperthyroidism?

Low TSH but normal T4 and T3

21

Name 2 causes of hyperthyroidism

Graves' disease (autoimmune)
Toxic multinodular goitre
Toxic adenoma
Exogenous eg drugs
De Quervain's thyroiditis

22

What is the immunological abnormality in Graves' disease?

Circulating IgG autoantibodies activate thyroid receptors causing enlargement, hormone production and orbital swelling

23

In which populations is toxic multinodular goitre most common?

The elderly and iodine deficient populations,eg denmark

24

What is De Quervain's thyroiditis?

Post viral cause of hyperthyroidism with painful goitre and raised temperature

25

What are the sign's of Graves' eye disease?

Proptosis, uncomfortable, red, gritty eye with increased tear production
Lid lad or retraction
Risk of corneal ulceration
Opthalmoplegia on looking up

26

What is the main pharmacological management of hyperthyroidism?

Beta blockers
Carbimazole or propylthiouracil

27

When should radioiodine use be avoided?

Graves' eye disease
Active hyperthyroidism
Pregnancy
Breast feeding

28

What are the signs of thyrotoxic storm?

Cardiovascular collapse, raised temperature
Agitation and confusion
Tachycardia, AF
Diarrhoea and vomiting
Acute abdomen

29

How should a thyrotoxic storm be managed?

Call endocrinology
Reduce peripheral effects of excess hormones by giving fluids, IV beta blockers, high dose digoxin and cooling
Inhibit further hormone synthesis with carbimazole
Treat systemic complications with 100mg IV hydrocortisone

30

What autoantibodies should be tested for in suspected hyperthyroidism?

THyroid peroxidase (TPO)
Antithyroglobulin
TSH receptor autoantibodies confirms graves'

31

What TFT abnormalities are found in overt hypothyroidism?

High TSH and low T4

32

What are the two causes of autoimmune hypothyroidism?

Hashimoto's and primary atrophic hypothyroidism

33

Give three conditions associated with Hypothyroidism

Down's syndrome
Cystic fibrosis
Primary billiary cirrhosis
POEMs syndrome
Turner syndrome
Type 1 diabetes
Addison's
Pernicious anaemia

34

How is hypothyroidism treated?

Levothyroxine

35

How is a myxoedema coma managed?

Give O2 if cyanotic
5-20micrograms of liothyronine (T3)
100mg IV hydrocortisone
IV saline
Warm patient

36

What is the target HbA1c for a type 1 diabetic?

48mmol or less (6.5%)

37

What is the target HbA1c for a type 2 diabetic on medication associated with hypoglycaemia?

53mmol/mol or less (7%)

38

Give 3 side effects of insulin therapy

Hypoglycaemia
Weight gain
Lipohypertrophy at injection sites

39

What class of agent is metformin?

Biguanide

40

What are the effects of metformin?

Reduce insulin resistance
Reduce hepatic gluconeogenesis
Increase uptake and oxidation of glucose by skeletal muscle

41

Which hypoglycaemic agents are not associated with weight gain?

Metformin
GLP1 agonists eg exenatide
DPP-4inhibitors eg sitagliptin
SGLT2 inhibitors, eg dapagliflozin

42

What is the main serious side effect of metformin?

Lactic acidosis

43

Give an example of a sulphonylurea?

Gliclazide or tolbutamide

44

How do sulphonylureas interact with warfarin?

Strongly bound to warfarin so can affect levels of other highly protein bound agents, eg warfarin

45

Give three side effects of sulphonylureas

Weight gain
Hypoglycaemia
Allergic reactions
Bone marrow suppression
Cholestatic jaundice

46

What is the action of sulphonylureas?

Inhibit potassium pump of beta cells to increase insulin secretion

47

Give 2 contraindications to the use of sulphonylureas

Severe hepatic impairment
Severe renal impairment
Acute porphyria
Ketoacidosis

48

Which anti-diabetic medications can cause hypoglycaemia?

Insulin
Sulphonylureas
GLP-1 agonists
SGLT2 inhibitors

49

What is the mechanism of action of glitazones?

Increase sensitivity to insulin by increasing transcription of insulin sensitive genes

50

How are glitazones excreted?

In the bile, after metabolism by the liver

51

Give three side effects of glitazones

Weight gain
Reduced haematocrit
Fluid retention
Bone density

52

Give a contraindication of glitazone use

Heart failure
Liver failure due to fluid retention

53

How do GLP-1 agonists work?

Resistant to degradation by DPP-4, unlike GLP-1, so can act to increase insulin secretion in response to oral ingestion of glucose

54

How are GLP-1 agonists administered?

Subcutaneously

55

Give two side effects of GLP-1 agonists?

Weight loss
Hypoglycaemia
GI upset
Pancreatitis

56

Give three side effects of DPP-4 inhibitors

Nausea
Peripheral oedema
Headaches
Pancreatitis
Nasopharyngitis
Stevens-Johnson syndrome

57

How do SGLT2 inhibitors work?

Inhibit the SGLT2 channel in the proximal convoluted tubule to decrease glucose reabsorption and increase excretion

58

Give three side effects of SGLT2 inhibitors

UTI
Genital infection
Hypoglycaemia
COnstipation
Dyslipidaemia
Back pain
Sweating
Dysuria and polyuria
Thirst

59

What are the actions of parathyroid hormone (PTH)?

Increase osteoclast activity to Increase release of calcium and phosphate
Increase renal reabsorption of calcium and increase renal excretion of phosphate
Increase renal production of vitamin D3 to increase intestinal absorption of calcium

60

What is the most common cause of primary hyperparathyroidism?

Solitary parathyroid adenoma

61

What are the features of osteitis fibrosa cystica?

Subperiosteal resorption of distal phalanges
Distal clavicle tapering
'salt and pepper' skull
Brown tumours of long bones

62

Give five features of hypercalcaemia

Proximal myopathy and fatigue
Renal calculi
Depression, dementia and confusion
Anorexia
Abdominal pain
Peptic ulcer disease
Polyuria
Polydipsia
Dehydration
haematuria
Hypertension
Reduced QT interval

63

What are the biochemical abnormalities in primary hyperparathyroidism?

Low phosphate
High calcium
High PTH
Reduced Vit D

64

What cancers can lead to malignant hyperparathyroidism?

Squamous cell lung cancers
Breast
Renal cell

65

What abnormalities are present in malignant hyperparathyroidism?

High calcium
Low PTH (caused by parathyroid related protein, which doesn't show up in assay)

66

Other than hyperparathyroidism, give three differentials for hypercalcaemia

Familial benign hypocalciuric hypercalcaemia
Lithium
Thiazide diuretics
Malignancy
Addison's
Paget's bone disease
Hyperthyroidism
Sarcoidosis

67

What are the indications for parathyroidectomy in hyperparathyroidism?

Age <50
Calcium more than 0.25mmol.l above the reference range
Renal calculi present
Creatinine clearance <60ml.min
DXA T

68

How can primary hyperparathyroidism be medically managed?

HRT to protect bone density
Bisphosphonates
Calcimometic eg cinacalcet to lower calcium

69

What is secondary hyperparathyroidism?

High levels of parathyroid hormone due to hypocalcaemia

70

What are the most common causes of secondary hyperparathyroidism?

Chronic kidney disease
Vitamin D deficiency
Malabsorption

71

What are the phosphate levels like in secondary hyperparathyroidism?

High in renal disease
Low in vitamin D deficiency

72

How should secondary hyperparathyroidism of CKD be managed?

Calcium and vitamin D supplementation
Phosphate restriction or binders eg lanthanon
Calcimimetics eg cinacalcet

73

How does tertiary hyperparathyroidism occur?

After prolonged secondary hyperparathyroidism, parathyroid glands become autonomous and hyperplastic so no longer respond to negative feedback

74

What are the biochemical abnormalities of tertiary hyperparathyroidism?

High PTH
High Calcium
High phosphate

75

How is tertiary hyperparathyroidism managed?

Either surgery or calcimimetics

76

What are the biochemical features of primary hypoparathyroidism?

Low calcium
High phosphate
Low pTH

77

What is the cause of primary hypoparathyroidism?

Gland failure, either congenital or autoimmune

78

Give three ways of acquiring hypoparathyroidism

Hypomagnesaemia
Neck surgery
Radiation
Drugs eg chemo
Infiltration

79

What is pseudohypoparathyroidism?

High levels of PTH but hypocalcaemia due to PTH resistance at the tissues

80

What are the clinical features of pseudohypoparathyroidism?

Short stature
Short metacarpals
Round face
Basal ganglia calcification
Reduced IQ

81

What is Chvostek's sign?

Sign of latent tetany.
When mouth is slightly open, mouth twitched upon tapping the facial nerve over the parotid gland

82

Give 6 features of hypocalcaemia

Neuromuscular irritability with cramping, tetany and seizures
Muscle and bone pain
Parasthesiae
Abdominal pain
Syncope
Facial twitching
Carpopedal spasm
Stridor
EMotional lability
Headaches
Brittle nails
Dry hair and skin
Painful menstruation
Hyperreflexia
Dental abnormalities

83

Give three hypothalamic causes of hypopituitarism

Kallman's syndrome
Tumour
Infection
Ischaemia

84

Give three pituitary stalk causes of hypopituitarism

Trauma
Surgery
Mass lesion, eg craniopharyngoma
Meningioma
Carotid artery aneurysm

85

Give three pituitary causes of hypopituitarism

Tumour (adenoma)
Radiation
Autoimmune eg lymphocytic hypophysitis
Infiltration
Ischaemiaeg apoplexy
Hypoplasia/aplasia

86

Give 5 features of growth hormone deficiency

Central obesity
Reduced muscle mass and strength
Fatigue
Hypoglycaemia
Reduced attention and memory
Reduced cardiac output
Dyslipidaemia

87

What are the histological classifications of pituitary tumours?

Chromophobe are either non-secretory/hypopituitary or secrete prolactin. Commonly cause mass effect
Basophilic tumours secrete ACTH and rarely cause mass effect
Eosinophilic tumours secrete prolactin or growth hormone

88

Give three symptoms of local pressure exerted by a pituitary tumour

Bitemporal/retrooribital headache that's worse on waking
Bitemporal hemianopia
Hydrocephalus
Squint
Disturbed sleep
Disturbed appetite
Rhinorrhoea

89

In which order are pituitary hormones affected?

Growth hormone
Gonadotrophins
Prolactin
TSH
ACTH

90

What are cranipharyngomas?

Tumours originating from rathke's pouch causing amenorrhoea, reduced libido and mass effect

91

What are the actions of prolactin?

Production of milk and secretory alveoli
Inhibition of reproductive system

92

Name three physiological causes of hyperprolactinaemia

Pregnancy
Breast feeding
Post-orgasm
Stress
Puerperium

93

Name three intracranial causes of hyperprolactinaemia

Pituitary tumours
Trauma
Neurosurgery
Radiation
Post-ictal

94

Name three endocrine/metabolic causes of hyperprolactinaemia

Liver disease
Chronic renal failure
Hypothyroidism
Cushing's
PCOS

95

What stimulates the production of prolactin?

Suckling
TRH
Oestrogen

96

What inhibits the production of prolactin?

Dopamine

97

Give 5 drugs that causes hyperprolactinaemia

Haloperidol
Domperidone
Metoclopramide
Methyldopa
Antidepressants eg citalopram
Verampamil
Opiates
Oestrogens
MDMA

98

What symptoms are experienced by women with hyperprolactinaemia?

Amenorrhoea or oligomenorrhoea
Galactorrhoea
Infertility
Weight gain
Reduced libido
Reduced vaginal lubrication

99

How is hyperprolactinaemia managed?

Bromocriptine/cabergoline
surgery if intolerant

100

What are the side effects of cabergoline/bromocriptine?

Postural hypotension
nausea
Depression
Fibrosis of heart/lungs/retroperitoneum

101

Name three cancers that may ectopically secrete growth hormone

Lung
Pancreatic
Ovarian

102

What hormones are indicated in acromegaly?

Growth hormone
Insulin like Growth Factor 1 (IGF-1)

103

What blood chemistry abnormalities are found in acromegaly?

High calcium, phosphate and triglycerides
High glucose

104

How is acromegaly diagnosed?

Screening for by IGF-1
Diagnosed with glucose tolerance test. If Growth hormone stays above 1mcg/L then there is acromegaly

105

How is acromegaly managed?

Transsphenoidal surgery
If not then somatostatin analogues eg octreotide
If not tolerated then growth hormone antagonist or dopamine agonist eg pegvisomant or cabergoline

106

Name three complications of acromegaly

Cardiovascular/cerebrovascular disease
Hypertension
Heart failure
Arthropathy
Obstructive sleep apnoea
Risk of colonic adenocarcinoma
Risk of thyroid cancer
Hypopituitarism once treated
Reduced self esteem
Diabetes mellitus

107

Give 5 causes of cranial diabetes insipidus

Tumour
Intracranial surgery
Trauma
Granulamatous disease
Infection eg meneingitis
Thrombosis
Sheehan's syndrome
Radiotherapy
Wolfram's syndrome

108

What is the difference between cranial and nephrogenic diabetes insipidus?

Cranial is a reduced secretion of ADH from the hypothalamus
Nephrogenic is a renal insensitivity to ADH

109

Give 5 causes of nephrogenic diabetes insipidus

Durgs eg lithium
CKD
Inherited
Hypokalaemia
Hypercalcaemia
Renal tubular acidosis
Pregnancy

110

What are the symptoms of diabetes insipidus?

Marked polyuria (>3l/day)
Polydipsia
Nocturia
Urinary incontinence

111

How is diabetes insipidus diagnosed?

Suspect if urine output >3l/day
Do plasma and urine osmolality. If P:U ratio is >2 then exclude
Do fluid deprivation test

112

What results are found in diabetes insipidus on doing a fluid deprivation test?

Osmolality should be >800 after 8 hours of fluid deprivation.
Give 2micrograms of desmopressin. If osmolality increases in four hours to >800 then it is cranial DI
If osmolality doesn't increase, it is nephrogenic DI

113

How is diabetes insipidus managed?

If cranial, give desmopressin
If nephrogenic, correct the cause and give desmopressin if necessary

114

When is type 1 diabetes diagnosed?

Random plasma glucose of >11 or fasting >7 + symptoms of hypergylcaemia
Or
aysymptomatic with 2 x fasting glucose of >7

115

Give 5 features that suggest a diagnosis of type 1 diabetes rather than type 2

Ketosis
Rapid weight loss
Acute onset
Age of onset <50 years
BMI <25
Personal or family history of autoimmune disease
HLA D3 or D4 associated

116

What investigations should be done when diabetes is diagnosed?

Albumin:creatinine ratio
HbA1c
TFTs
U&Es and eGFR
Lipid profile
Coeliac serology

117

What is the target HbA1c for someone with type 1 diabetes?

48mmol or 6.5%

118

What is the first line antihypertensive in diabetes?

ACE inhibitor

119

When should a statin be started in diabetes?

If any of:
>40 years old
Diabetes for >10 years
Established nephropathy
Obesity
Hypertension
Cardiovascular disease risk factors

120

What should be monitored at a type 1 diabetic review?

HbA1c
height, weight and waist circumference and BMI
Depression, anxiety and eating disorders
Smoking status
Neuropathy by asking about erectile dysfunction, gastroparesis, neuropathic pain
Check injection sites
Screen for retinopathy
Nephropathy
Foot problems
Cardiovascular risk factors
Thyroid disease
Coeliac disease
Addison's disease
Pernicious anaemia

121

How is diabetic ketoacidosis managed?

IV fluids of 1-1.5l of 0.9%NaCl per hour reduced to 1l every 2-4 hours until glucose is <11.1 and switch to 5% dextrose with 0.45%NaCl at 1l every 4 hours
Correct any hypokalaemia
0.1units/kg/hour of IV insulin and aim for 8.3-11.1mmol/l

122

What is the consequence of starting IV insulin therapy when there is hypokalaemia?

Can cause respiratory paralysis, cardiac arrhythmias and death

123

What is the diagnostic criteria for DKA?

Acidosis (pH<7.3) + hyperglycaemia (>11.1) + ketosis

124

Give 5 risk factors for the development of hypoglycaemia in diabetes

Tight glycaemic control
Malabsorption
injection into lipohypertrophy site
Insulin prescription error
Long duration of diabetes
Renal dialysis
Reducing renal function
Alcohol
Exercise
Addison's
Hypothyroidism

125

How is hypoglycaemia acutely managed?

10-20g glucose PO or 75ml 20% dextrose or 150 ml 10% dextrose IV
Something to eat and drink once conscious

126

Name 3 drugs that can precipitate hyperosmolar hyperglycaemic state

Phenytoin
Anti-psychotics
Diruetics
beta blockers
Dialysis
Calcium channel blockers
Steroids
Alcohol

127

How is hyperosmolar hyperglycaemic state managed?

Iv fluids 0.9% NaCl to correct 6-9l fluid loss in 48 hours
wait an hour before giving insulin or until glucose levels stabilise on fluid therapy then give 0.05units/kg/hour
Identify and correct any precipitant
LMWH to reduce risk of occlusive event

128

What is hyperosmolar hyperglycaemic state?

Sever hyperglycaemia with markedly increased osmolarity and without ketosis

129

What is phaeochromocytoma?

A rare, catecholamine producing tumour of sympathetic preganglionic collections of adrenaline-secreting chromaffin cells

130

Give 5 symptoms of phaeochromocytoma

Episodic headache
Sweating
Palpitations
Dizziness
Tremor
Abdominal pain

131

Give 5 signs of phaeochromocytoma

Tachycardia
Hypertension
Flushing
Dyspnoea
Diarrhoea
Pallor

132

What may precipitate symptoms of phaeochromocytoma?

Straining or abdominal pressure
Surgery
Exercise
Stress
Drugs eg beta blockers and TCAs

133

What familial conditions are associated with phaeochromocytoma?

MEN 2a and 2b
Von Hippel Landau syndrome
Neurofibromatosis

134

How is non-malignant phaeochromocytoma managed?

Pre-op alpha blockers then beta blockers then adrenalectomy

135

What post-op monitoring should be done after an adrenalectomy for phaeochromocytoma?

24 hour urine metadrenalines
BP

136

How is malignant phaeochromocytoma managed?

Chemotherapy or radio-labelled chromaffin-seeking isotope

137

What is primary hyperaldosteronism?

Excess production of aldosterone, independent of the RAAS system with sodium and water retention and reduced renin release

138

When should primary hyperaldosteronism be suspected?

If hypokalaemia, hypertension (especially resistant) and alkalosis

139

What are the main causes of primary hyperaldosteronism?

70% is bilateral adrenal hyperplasia
30% is aldosterone producing adenoma - Conn's syndrome

140

How is primary hyperaldosteronism managed?

If conn's syndrome - adrenalectomy with pre-op spironalactone
If hyperplasia - aldosterone antagonist eg spironolactone

141

How is primary hyperaldosteronism diagnosed?

Bloods showing hypokalaemia and alkalosis
Aldosterone:renin ratio will be increased

142

What is secondary hyperaldosteronism?

Excess aldosterone secretion as a result of high renin, due to reduced renal perfusion

143

Give 3 causes of secondary hyperaldosteronism

Renal artery stenosis
Diuretics
Heart failure
Hepatic failure
Nephrotic syndrome
Accelerated hypertension

144

How is secondary hyperaldosteronism diagnosed?

Bloods showing hypokalaemia
Aldosterone:renin ratio will be normal

145

What is Barter's syndrome?

A congenital defect in the NaCl channel of the loop of henle, causing sodium loss, hypokalaemia and metabolic alkalosis

146

How is barter's syndrome managed?

Potassium replacement
NSAIDs
ACE-inhibitors

147

Give 5 risk factors for the development of type 2 diabetes

Family history
Central obesity
Ethnicity
history of gestational diabetes
Poor dietary habit
Durgs
PCOS
Metabolic syndrome
Low birth weight for gestational age

148

What are the features of metabolic syndrome?

Hypertension
Dyslipidaemia
Fatty liver
Abdominal adiposity
Thrombophilia

149

When can type 2 diabetes be diagnosed?

If asymptomatic then 2 abnormal measurements of HbA1c (>6.5% or 48mmol) or fasting plasma glucose (>7mmol)
If symptomatic then only 1 abnormal reading is required, unless also unwell

150

When should HbA1c not be used as a diagnostic tool?Give 3 examples

If <18 years old
If pregnant/<2 months post partum
If symptomatic for less than 2 months
If acutely unwell
If on medication that causes hyperglycaemia
Acute pancreatic damage
End stage CKD
HIV positive

151

When should HbA1c be interpreted with caution?

Haemoglobin abnormalities
Anaemia
Altered red cell life span
Recent blood transfusion

152

How should hypertension be treated in a white person with diabetes?

Ace inbitior/ARB
then add either calcium channel blocker or thiazide diuretic
Then combine all 3

153

How should hypertension be treated in a black person with diabetes?

ACE-1/ARB + either calcium channel blocker or diuretic
THen combine all 3

154

Give 5 complications of diabetes

Stroke
MI
TIA
Nephropathy
Neuropathy
Retinopathy
Dyslipidaemia
Anxiety
Depression
Reduced quality of life
Reduced life expectancy
Infections
Dementia

155

At what stage of blood sugar control should diabetes pharmacological management be stepped up?

If HbA1c consistently above 7.5%/58mmol on optimal therapy

156

What are the steps of drug therapy for diabetes?

Start with metformin (or gliptin/sulphonylurea/pioglitazone if contraindicated)
Add a gliptin/sulfonylurea/pioglitazone
Triple therapy

157

What conditions are featured in MEN type 1?

Primary hyperparathyroidism
Pituitary tumours
Pancreas tumours

158

What conditions are featured in MEN type 2a?

Phaeochromocytoma
Primary hyperparathyroidism
Medullary thyroid cancer

159

What conditions are featured in MEN type 2b?

Phaeochromocytoma
Medullary thyroid cancer
Marfinoid body habitus
Neuromas

160

Name 3 features of diabetic nephropathy

Glomerular sclerosis
Papillary necrosis
Renal atherosclerosis
UTIs

161

In general, how does diabetic nephropathy progress?

Intermittent microalbuminuria
Proteinuria
Nephrotic syndrome

162

What are the deficits involved in chronic diabetic peripheral neuropathy?

Mostly sensory
Reduced sensation of touch, proprioception, temperature and pain mostly in lower limbs
May also be reduced ankle and knee reflexes

163

What are the four main forms of diabetic neuropathy?

Chronic peripheral
Autonomic
Mononeuropathy
Proximal motor neuropathy

164

Give 5 manifestations of autonomic neuropathy in diabetes?

Postural hypotension
Resting tachycardia
Orthostatic rate changes
Silent MIs
Exercise intolerance
Cardiovascular lability intra- and perioperatively
Impotence
Overflow incontinence
Nausea and vomiting
Diarrhoea
Abdominal distension
Dysphagia
Anhidrosis
Gustatory sweating

165

How is neuropathic pain in diabetes managed?

Foot cradles at night
Psychological support
Amitriptylline, duloxetine, gabapentin or pregabalin

166

What are the main features of non-proliferative diabetic retinopathy?

Microaneurysms
Blot haemorrhages
Cotton wool spots
Venous beading
Hard exudates

167

What are the main features of proliferative diabetic retinopathy?

Retinal neovascularisation
Pre-retinal haemorrhage
Fibrous tissue formation anterior to retinal disc

168

What are the main features of diabetic maculopathy?

Macular oedema
ISchaemia
hard exudates