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3rd Year Medicine UoM > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

what are the blood results for Addison’s?

A

Hyponatraemia
Hyperkalamiae
hypoglycaemia
metabolic acidosis

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2
Q

how do we manage type 2 DM?

A

first start lifestyle changes
if HbA1C rises to 48 on lifestyle advice, add Metformin

if HbA1C rises add a second medication from the following:

  • Gliptin (DDP4 inhibitor)
  • sulfonylurea
  • SGLT-2 inhbitor
  • pioglitazone

if, despite the 2nd med, HbA1C rises to/or remains above 58mmol/mol - add a 3rd med

triple therapy with any of the following combinations:
- metformin + sulfonylurea + pioglitazone
- metformin + sulfonylurea + SGLT-2 inhibitor
- metformin + sulfonylurea + gliptin
- metformin + pioglitazone + SGLT-2 inhibitor
or consider insulin therapy

finally, if triple therapy not working
a GLP-1 analogue can be tried in combination with metformin and a sulfonylurea if BMI>35 with obesity related problems or <35 but cant take insulin

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3
Q

how do we manage idiopathic adrenal hyperplasia?

A

aldosterone antagonists e.g. spironolactone

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4
Q

what are the targets in DKA treatment?

A

reduce ketones by 0.5 mmol/L/h
reduce glucose by 3 mmol/L/h
increase bicarb by 3 mmol/L/h
maintain potassium between 4-5.5mmol/L

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5
Q

what are side effects of pioglitazone?

A

weight gain, osteoporosis, swelling of legs/ankles, risk of liver disease, anaemia risk, fluid retention

contraindicated in previous bladder cancer patients

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6
Q

what usually precipitates HHS (hyperglycaemic, hyperosmolar state)?

A

infection, MI, stroke or other acute illness

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7
Q

how do DDP4 inhibitors/gliptins work?

give names of drugs

A

DDP-4 enzymes are involved in deactivating incretins (GLP-1). by inhibiting them - we raise the levels of GLP-1 which bind to Beta cells and increase insulin production and secretion.

e.g. sitagliptin, vildagliptin, linagliptin

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8
Q

how does the BD (biphasic) insulin regime work?

A

patient takes 2 premixed insulin doses - via disposable pens
good for a regular lifestyle
twice‑daily insulin detemir is the regime of choice.

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9
Q

what are the causes behind primary hyperparathyroidism?

A 
usually - adenoma (80% cases)
multifocal disease (10-15%)
carcinoma (<1%)
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10
Q

what are side effects of sulfonylureas?

A

weight gain, hypoglycaemia, upset stomach, skin rash/itching

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11
Q

what are 3 features of Hashimoto’s thyroiditis?

A

hypothyroidism
goitre
anti-TPO

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12
Q

which thyroid cancer secretes calcitonin?

A

medullary cancer

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13
Q

when do we treat subclinical hypothyroidism?

A

if TSH is btwn 4-10
for <65s with symptoms - treat with a trial of levothyroxine and continue if shows improvement
if asymptomatic or older - watch and wait, repeat TFTS in 6 months

if TSH is >10
for <70s - treat with levothyroxine
watch and wait for older patients

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14
Q

at what HbA1C level do we add a second drug to metformin for T2DM patients?

A

58

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15
Q

what is involved in the HPA axis?

A

Hypothalamus secretes corticotropin releasing factor (CRF)
CRF stimulates the anterior pituitary to secrete ACTH
ACTH stimulate the adrenal cortex to secrete cortisol and androgens

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16
Q

which is the insulin regime of choice for adults?

A

multiple daily basal-bolus injections

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17
Q

which drugs can cause hypercalcaemia?

A

thiazide diuretics

calcium containing antacids

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18
Q

what is an important complication of fluid resuscitation in young DKA patients?

A

cerebral oedema

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19
Q

whats the most common cause of Addison’s worldwide?

A

Tb

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20
Q

tell me about ultra fast acting insulin

A

examples = novorapid, humalog

used to inject before a meal or just after. helps to match insulin to what is actually eaten

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21
Q

when do we consider transferring a DKA patient to ICU?

A 
if there are signs of severe DKA:
pH < 7 
bicarb < 5 
blood ketones > 7 
GCS < 12 
K+ < 3.5 
oxygen sats <92% 
low BP or pulse
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22
Q

how do you classify BMI into normal/overweight/obese?

A 
normal= 18.5 - 25 
overweight =25-30
obese 1 =30-35
obese 2 =35-40
obese 3 =>40
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23
Q

what is the MoA of carbimazole?

A

it blocks thyroid perioxidase from iodinating the tyrosine residues on the thyroglublin - this reduces the production of thyroid hormones

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24
Q

what are side effects of Gliptins?

A

usually well tolerated

can cause hypoglycaemia, hives, fluid retention, UTI, headaches, facial swelling nasopharyngitis

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25
Q

how do we manage pregnancy in diabetic patients?

A

in advance, have a target of 48mmol/mol!
take folic acid 5mg OD

during pregnancy, have a blood glucose control assessment every 1-2 weeks throughout pregnancy

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26
Q

what are the TFT levels in subclinical hypothyroidism?

A

elevated TSH with normal T4

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27
Q

what is the single most useful test in determining the cause of hypocalcemia?

A

parathyroid hormone

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28
Q

which are the 2 most common thyroid cancers?

A

papillary (70%)

follicular (20%)

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29
Q

what are symptoms of hyperglycaemia?

A 
polyuria 
polydypsia
lethargy 
genital thrush 
weight loss
visual blurring
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30
Q

what are the clinical features of Paget’s disease?

A

only 5% are symptomatic

bone pain - lumbar spine, femoral, pelvis
skull bossing, leg bowing
raised ALP, normal phosphate and calcium
skull xray - thickened vault

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31
Q

what is the pathophysiology of secondary hyperparathyroidism?

A

parathyroid hyperplasia occurs in response to low calcium, almost always in a setting of chronic renal failure

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32
Q

what are the findings in hyperaldosteronism?

A 
raised BP
raised/normal sodium
low potassium 
raised bicarbonate (alkalosis)
raised aldosterone
low renin
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33
Q

which steroid has high GC activity and low MC activity?

A

dexamethasone and betmethasone

important if we need high anti inflammatory action and low fluid retention e.g. in cranial tumours

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34
Q

why electrolyte deficiency is responsible for sustained hypocalcaemia despite calcium replacement therapy?

A

magnesium

magnesium is needed for PTH secretion and its action on target tissues

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35
Q

how much potassium should we give to DKA patients?

A

if potassium is >5.5 give nil
if potassium is 3.5-5.5 give 40mmol/L infusion
if < 3.5 - seek help

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36
Q

what are the symptoms of hyperaldosteronism?

A

can be asymptomatic
signs of hypokalaemia= cramps, weakness, paraesthesia
High BP and headaches

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37
Q

which hormones are reduced in the stress response?

A

insulin
oestrogen
testosterone

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38
Q

what are side effects of treatment with levothyroxine?

A

hyperthyroidism
reduced bone mineral density
worse angina
atrial fibrillation

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39
Q

what is Waterhouse - Friderichsen syndrome?

A

adrenal failure due to haemorrhage into the adrenal gland, commonly caused by severe infection
severe form of meningococcal sepsis
usually pre-terminal
patients present with sepsis, coagulopathy, extremities cyanosed, comatosed

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40
Q

whats the most important advice to give a patient being started on carbimazole?

A

if they get any signs of infection they should seek urgent medical review
a rare side effect = agranulocytosis

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41
Q

what’s sick euthyroid syndrome?

A

its caused by systemic disease
total and free T4 and T3 are minimally low
TSH is normal or slightly low

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42
Q

how do we investigate hyperaldosteronism?

A 
1st line = renin:aldosterone ratio
High serum aldosterone 
low serum renin
adrenal vein sampling
high resolution CT scan
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43
Q

how do we treat phaeochromocytoma?

A

surgery is definitive treatment

but we first stabilise the patient with alpha blockers (phenoxybenzamine) and then beta blockers (propanolol)

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44
Q

what is kussmauls breathing?

A

heavy respiration - expiring CO2 to try and compensate for metablic acidosis

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45
Q

what are the features of LADA?

A

these patients, although they have autoimmune disease, like type 1 DM, are picked up later in life.
their diabetes progresses a lot slower - and may not need insulin in the earlier stages

LADA can often be misdiagnosed at T2 DM but patients are usually younger and less obese

diagnosis may be aided by GAD autoantibody testing or other autoimmune disease

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46
Q

what is Cushing’s disease?

A

pituitary tumour secreting ACTH causing adrenal hyperplasia

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47
Q

what ABG results are associated with Cushings?

A

hypokalaemic metabolic alkalosis

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48
Q

give an example of a fluid replacement regime in a DKA patient?

A

1st hour: 0.9% saline - 1L

2nd hour: 0.9% saline + potassium chloride

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49
Q

what glucose ranges are diagnostic for diabetes?

A

fasting glucose >7

HbA1C >48

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50
Q

where is ADH secreted from and what does it do?

A

ADH is released for the posterior pituitary in response to thirst.
ADH causes more aquaporin channels to be inserted into collecting duct membranes in the kidneys. this increases water retention

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51
Q

what are the causes for hyperkalaemia?

A 
AKI
drugs - K sparing diuretics, ACE-I, ARBs, spironolactone 
metabolic acidosis
massive blood transfusion 
addisons
rhabdomyolosis
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52
Q

what percentage of pre-diabetic patients progress to type 2/year?

A

5-10%

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53
Q

how do we treat an adrenal tumour?

A

for adenoma - adrenalectomy

for carcinoma - radiotherapy and adrenolytic drugs

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54
Q

which mutation is associated with most cases of MODY?

A

mutation in the HNF1- alpha gene

known as MODY 3

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55
Q

how do we treat hypoparathyroidism?

A

with alfacalcidol

which is an analogue of vitamin D

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56
Q

what glucose ranges show prediabetes?

A

42-47 HbA1C

fasting glucose: between 6-7

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57
Q

what do the osteoporosis guidelines recommend regarding a postmenopausal woman who has had a fracture?

A

give her bisphosphonate and calcium supplements

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58
Q

when do you NOT have to inform the DVLA about taking insulin?

A

if on temporary insulin for < 3 months

or because of gestational diabetes and wont be continuing the insulin for more than 3 months postpartum

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59
Q

what does thyrotoxicosis alongside a singular hot nodule (on scintography) indicate?

A

toxic adenoma

this occurs when a single nodule grows on the thyroid gland - producing excess hormones and causing thyrotoxicosis

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60
Q

what are the features of type 2 DM?

A

associated with lack of exercise, obesity, alcohol and calorie excess
more common in asians, men and elderly

because of excess adipose tissue, there is a relative insulin insufficiency - not enough to go around

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61
Q

which anti diabetic drug increases insulin sensitivity?

A

pioglitazone

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62
Q

how does diabetes causes damage to the eyes? (2)

A

1) endothelial changes causes capillary leakage - causing intraretinal oedema which then forms hard exudates. in the macular area this can result in loss of central vision

2) capillary occlusion can cause retinal ischaemia. in the macular area this can cause visual loss. the ischaemia then causes new retinal vessels forming. the new vessels can cause - haemorrhage, fibrosis, etc
all leading to total blindness

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63
Q

how is Addison’s managed?

A

steroid replacement therapy

hydrocortisone (in 2 or 3 doses per day) and fludrocortisone

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64
Q

what are the features of MEN 1?

A

3 Ps (parathyroid, pituitary and pancreas) and adrenal and thyroid

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65
Q

whats the most serious potential complication of AKI?

A

hyperkalaemia

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66
Q

how do we investigate phaeochromocytoma?

A

24 hour urinary collection of metanephrines
VMA in urine is usually elevated
and serum metanephrines are elevated

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67
Q

what is MEN?

A

multiple endocrine neoplasia

autosomal dominant disorder

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68
Q

where is prolactin produced?

A

anterior pituitary gland

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69
Q

what is the pathophysiology of primary hyperaldosteronism?

A

excess aldosterone leads to Sodium reabsorption, H2O retention and K+ excretion. this leads to raised blood pressure, hypernatraemia, hypokalaemia, and alkalosis

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70
Q

what are side effects to long term steroid use?

A

endocrine - impaired glucose regulation, hyperlipidaemia, excess hair growth, increased appetite/weight gain
bones - osteoporosis, osteopaenia, avascular necrosis of the femoral head,
immunosuppression
GI - peptic ulceration and pancreatitis
psychiatric - mania, psychosis, insomnia, depression
cushings syndrome - moon face, buffalohump, stria
eyes -glaucoma, cataracts
intracranial hypertension
suppression of growth in children

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71
Q

how do you identify a benign incidental adrenal adenoma?

A

usually picked up on CT accidentally

the ademona has a rich lipid core with well circumscribed nodules

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72
Q

what are signs of thyrotoxicosis?

A

tachycardia, maybe irregular pulse, moist warm skin, fine tremors, lid lag/retraction, goitre, thin hair, thyroid nodules/bruit.

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73
Q

how do we manage a prediabetic patient?

A

encourage to make lifestyle changes - exercise and change diet (more fibre less fat)

consider 500mg OD metformin

test HbA1C regularly - annually

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74
Q

how do we define diabetes?

A

hyperglycaemia levels sufficient to cause microvascular complications

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75
Q

how often should a T1 DM patient check his blood glucose/day?

A

at least 4 times a day - before meals and before bed

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76
Q

what are symptoms of hyponatramea?

A

dizzy, nausea, headache, coma if severe, signs of dehydration or fluid overload

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77
Q

tell me about premixed insulins

A

e.g. novamix 30

30% SA and 70% LA

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78
Q

which glucose ranges show normal glycaemic control?

A

HbA1C < 42

fasting glucose < 7

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79
Q

what diabetic medication should we consider as first line for a patient with end-renal failure?

A

Gliclazide

Metformin is contraindicated (can’t be used in any patient with eGFR < 30)

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80
Q

is a Type 2 diabetic patient, on insulin, allowed to drive a HGV?

A

yes, but he must meet very strict criteria set out by the DVLA, relating to hypoglycaemia

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81
Q

what are the 2 main causes for hypercalcaemia?

A

primary hyperparathyroidism
malignancy
these 2 causes account for 90% of cases

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82
Q

what is MODY?

A

a group of genetic diseases affecting the production of insulin
maturity onset diabetes of the young
usually in those < 25 years
with a strong family history
typically autosomal dominant
number of genes identified
patients usually very sensitive to sulfonylureas

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83
Q

what are the 5 types of thyroid cancer?

A 
papillary 
follicular
medullary 
anaplastic 
lymphoma
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84
Q

how is HHS diagnosed?

A

signs of dehydration

osmolarity: >320mosmol/kg
hyperglycaemic: >30mmol/L with pH>7.3 and no ketonaemia < 3mmol/L

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85
Q

what are the complications of pagets disease?

A 
deafness - CN trapping 
bone sarcoma 
skull thickening
fractures 
high output cardiac failure
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86
Q

how would a patient present in phase 1 of subacute thyroiditis ?

A

tender goitre
hyperthyroidism
raised ESR
globally decreased uptake on iodine scan (Technetium scan)

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87
Q

tell me about long acting/basal insulin?

A

human insulin analogues

e. g. glargine - used at bedtime, to give a steady insulin baseline all night. good for those who struggle with nocturnal hypoglycaemia
e. g. detemir

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88
Q

what investigation should we do in a patient who’s drowsy, vomiting, dehydrated, abdo pain, polyuria, polydipsia?

A

CHECK BLOOD GLUCOSE

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89
Q

what does thyroxine interact with??

A

iron
iron reduces the absorption of thyroxine
take the drugs 2 hours apart

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90
Q

what is the mechanism of action of sitagliptin?

A

it is a dipeptidyl peptidase 4 inhibitor (DPP-4)

this prevents the breakdown of GLP-1, therefor increasing its levels and so increasing insulin

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91
Q

what rate of insulin should u prescribe for ketoacidotic patients?

A

0.1 unit/kg/hour

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92
Q

what medication can we use pre-op to decrease cortisol secretion?

A

metyrapone, ketocanozole, flucanazole

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93
Q

how do patients with hypercalcaemia present?

A

non specific symptoms

nausea, polydipsia, polyuria, weakness, confusion, constipation

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94
Q

what antibodies are associated with Graves disease?

A

TSH receptor stimulating antibodies

anti-thyroid peroxidase antibodies

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95
Q

how do we prevent diabetic retinopathy?

A

primary prevention - BP and glucose control
secondary - regular assessment
immediate anti VEGF treatment in diabetic macular oedema - to prevent new vessels forming e.g. ranibizumb, aflibercept
3) salvage therapy - vitrectomy

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96
Q

whats the best investigation to differentiate between type 1 and type 2 diabetes?

A

C peptide
this will be low in type 1
(because the pancreas is not producing enough insulin precursor which breaks down to give insulin and C-peptide)

and normal or high in type 2

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97
Q

how does the OD insulin regime work?

A

once a day, taking a dose of LA insulin
good started for T2 patients switching across to insulin
typical dose is around 1 unit/BMI unit/24 hours
can retain metformin etc if need for tighter control

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98
Q

how do we screen for acromegaly?

A

by testing serum Insulin-like Growth factor -1 IGF-1, which represents 24 hour GH levels

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99
Q

what are the features of type 1 DM?

A

usually presents in adolescents/young adults
at risk of ketoacidosis and weight loss
antibody destruction of pancreatic, insulin-producing beta cells (anti bodies include Glutamic acid decarboxylase (GAD) antibodies and islet cell antibodies (ICA)
associated with other autoimmune disease
treated with insulin

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100
Q

what is acromegaly?

A

excessive GH

in 95% of cases this is secondary to a pituitary adenoma

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101
Q

what is Paget’s disease?

A

a disease of excessive turnover of the bone - increased osteoclast and osteoblast activity

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102
Q

how do we monitor for subclinical recurrence of medullary thyroid carcinoma?

A

calcitonin levels

103
Q

what is congenital adrenal hyperplasia?

A

a group of autosomal recessive diseases
in response to low cortisol, the pituitary gland produces excess ACTH which leads to increased production of androgens
leading to large build, manly hair, early menarche

104
Q

what is the synacthen test?

A

ACTH stimulation test

ACTH is injected and the cortisol response is measured.

105
Q

how do we diagnose DKA?

A

1) acidosis - pH <7.3 or Bicarb <15
2) hyperglycaemia - glucose>11 (or13.8) or known Diabetes
3) ketosis - ketonaemia >3 or ++ on dipstick

106
Q

who’s more likely to develop diabetes: a patient with impaired fasting glycaemia or impaired glucose tolerance?

A

those with impaired glucose intolerance are more likely

107
Q

how do we manage HHS?

A

rehydrate slowly - with 0.9% saline, over 48 hours
replace K+ once urine starts to flow
use insulin if glucose not falling by 5mmol/L/kg/H OR if there is ketonaemia
keep blood glucose at least 10-15mmol/L to avoid cerebral oedema

108
Q

what is LADA?

A

latent autoimmune diabetes of adult

109
Q

what features are specific to graves disease?

A

eye signs - exophalmus, ophalmoplegia
pretibial myxoedema
thyroid acropachy

110
Q

how do we treat hyperaldosteronism?

A

if its due to Conn’s = laprascopic adrenalectomy

if its due to hyperplasia = treat medically with spironolactone or amiloride

111
Q

what are side effects of SGLT-2 inhibitors?

A

UTI, weight loss, change in urination, genital yeast infections, upper resp tract infections

112
Q

what causes primary hyperaldosteronism ?

A

idopathic adrenal hyperplasia (70% cases)
adrenal adenoma - Conn’s syndrome
adrenal carcinoma - rare

113
Q

how do we treat an addisonian crisis?

A

100mg iv/im hydrocortisone
saline with dextrose (if hypoglycaemic)
continue steroids 6 hourly until stable

114
Q

what dietary advice do we offer diabetic T2 patients?

A

include in your diet plenty of high fibre and low glycaemic index foods. oily fish, low fat diary products

reduce intake of high energy carbs, saturated fats, trans-fatty acids

weight loss of 5-10% fat in obese patients

115
Q

what are ACTH independent causes of Cushings?

A

iatrogenic - steroid use
adrenal nodular hyperplasia
adrenal adenoma/cancer

116
Q

how do we manage hypercalcaemia?

A

first - IV saline! -patient will be dehydrated
then once hydrated
can give bisphosphonates e.g. IV pamidronate
calcitonin can be given to patients who are resistant to bisphosphonates

117
Q

what are the causes of primary hyperparathyroidism ?

A

80% cases = solitary adenoma
10-15% cases = multifocal disease
1% carcinoma

118
Q

how do we treat Addison’s disease?

A

replace steroids
15-25 mg hydrocortisone/day
50-200mcg fludrocortisone

119
Q

what population is Graves disease typically seen in?

A

females, aged 30-50

120
Q

what does ACTH stand for?

A

adrenocorticotropic hormone

121
Q

when should orlistat be stopped?

A

if the patient has lost more than 5% weight in 12 month s

122
Q

what are the symptoms of hypoparathyroidism?

A

the symptoms are mostly secondary to hypocalcaemia

muscle spasms, twitching, cramping 
chvostek's sign 
Trousseau's sign 
perioral parasthesia
ECG long QT
123
Q

how do we diagnose asymptomatic diabetes?

A

random glucose >11
or fasting glucose > 7
must be demonstrated on 2 separate occasions

124
Q

what is diabetes insipidus?

A

it can either be cranial (not enought ADH produces) or nephrogenic (kidney insensitive to ADH)
patients produce large quantities of dilute urine - polyuria and drink a lot to compensate - polydypsia
people can become dehydrated if they are unable to drink

125
Q

which TFT results show poor thyroxine compliance?

A

High TSH and normal T4
this is because TSH takes longer to normalise, so the patient could have had low thyroxine before coming to the doctor, but taken her medication before her blood test so her T4 is normal but her TSH hasn’t corrected yet

Raised T4 with raised TSH also points towards poor compliance. the patient has taken extra tables prior to blood test causing the raised T4 but TSH hasnt had time to be suppressed (TSH levels take days to weeks to change)

126
Q

if a patient with Addison’s disease is ill, should there be changes made to their medication?

A

yes,
hydrocortisone should be doubled (because the body would usually increase its production during illness- stress response)
fludrocortisone can be kept the same

127
Q

what are the causes for galactorrhoea ?

A 
6 Ps
pregnancy 
physiological 
primary hypothyroidism 
prolactinoma 
polycystic ovarian syndrome
phenothiazines, domperidone, metaclopramide
128
Q

what is phaeochromocytoma?

A

a rare catecholamine secreting tumour

129
Q

in regards to insulin, how do we manage a patient with DKA?

A

start him on a fixed IV insulin of 0.1 units/kg/hour

130
Q

how does SIADH present?

A

solitary hyponatraemia, water retention

131
Q

what are common precipitating factors for DKA?

A

missed insulin dose
infection
myocardial infarction

132
Q

what are the features of DKA?

A

dehydration, polyuria, polydipsia
abdominal pain , vomiting , drowsiness
kussmauls respiration - deep hyperventilation
sweet smelling breath - acetone

133
Q

which blood cells might increase with corticosteroid use?

A

neutrophils

CS are thought to cause neutrophilia via 3 mechanisms.

134
Q

what type of drug is gliclazide?

A

sulfonylurea

135
Q

what are the signs of thyroid eye disease? (as seen in almost 50% cases of Graves disease)

A 
exophthalmus - protruding eye appearance 
proptosis - eye protudes beyond orbit
othalmoplegia 
conjuntival oedema 
papillodeama
corneal ulceration
136
Q

what are contraindications for radioiodine treatment?

A

pregnancy - should be avoided for 4-6 months after as well

thyroid eye disease is a relative CI- can be made worse

137
Q

how are thyroid hormones synthesised?

A

thyroid follicular cells produce thyroglobulin (Tg)
iodine is transported and trapped in the colloid
Thyroid perioxidase (TPO) on the luminal surface of TFCs iodinates the tyrosine residues on the Tg (this is known as organification)
the iodinated Tg are endocytosed by the follicular cells and are hydrolised there to produce thyroid hormones. (mostly T4)
they are then secreted into the blood - bound to globulins.
in peripheral tissues, T4 is deionised to produce T3

138
Q

where is iodine deficiency most common?

A

africa, asia, himalayas

139
Q

when should you refer a patient to the diabetic foot clinic?

A

if they have any foot problems besides for simple calluses

140
Q

what are symptoms of a prolactinoma in female?

A

infertility
oligomenorrhoea
galactorea

141
Q

what risk factor modification medication should diabetic patients be on?

A

ACE-I if BP>140/80
statins if 10-year CVD risk is >10%
anti-platelets

142
Q

what are the levels in secondary hyperparathyroidism?

A

Raises PTH
low or normal Calcium
High Phosphate
Low Vit D

143
Q

how does the QDS insulin regime work?

A

this regimen is useful for those with a flexible/changing lifestyle.
patient takes ultra fast acting insulin before meals/exercise and then a LA analogue at night

144
Q

how do we treat symptomatic prolactinoma?

A

with dopamine agonists which inhibit the release of prolactin from the pituitary gland
e.g. Bromocriptine

if the DAs are not tolerated, surgery is the next option. trans-sphenoidal hypophysectomy

145
Q

why does potassium fall in DKA treatment?

A

insulin makes the cells take up potassium

146
Q

what are the symptoms of Addison’s disease??

A

lethargy, weakness, anorexia, nausea, weight loss, vomiting, salt craving
hyperpigmentation, vitilgo, loss of pubic hair in females
hypotension
crisis = collapse, shock, pyrexia

147
Q

what are the features of acromegaly?

A

coarse facial features, spade like hands, bigger feat
oily skin, excessive sweating
prognathism, large tongue, interdental spaces
symptoms of intracranial mass- headaches, bitemporal hemianopia
raised prolactin in 1/3 of cases - galactorrhoe

148
Q

what are the features of addisonian crisis?

A

hyponatraemia
hyperkalaemia
hypoglycaemia
hypovolaemia

149
Q

what is an important worry in HHS and how do we prevent it?

A 
occlusive events (DIC, chorea, focal CNS signs, leg ischaemia/rhabdomyolosis)
give prophylactic LMWH
150
Q

how is osteoporosis linked to graves disease?

A

excess T3 causes increased osteoclast activity leading to excess bone resorption - causing osteoporosis

151
Q

in patients admitted with hypercalcaemia, when is IV bisphosphonate indicated?

A

when calicum is over 3

152
Q

how do we treat painful diabetic neuropathy?

A

the same way as we treat any neuropathic pain

1) first line treatment = amitryptaline, pregablin, gabapentin, duloxetine
2) if the medication doesnt work, try another of the 4 drugs

tramadol can be used as rescue therapy
topical capsaicin can be used for topical pain

153
Q

how do we confirm a diagnosis of acromegaly ?

A

with an OGTT
normally, hyperglycaemia leads to suppression of GH - but this doesnt happen in acromegaly

we perform the OGTT with series of GH tests after

154
Q

what is ketogenesis?

A

its an alternative metabolic pathway - to provide energy to cells. its inefficient and produces acetone
without insulin, glucose can’t enter the cells, so the body thinks it is ‘starving’ - and ketogenesis kicks in, as a last resort

155
Q

what are the symptoms of hypothyroidism?

A

lethargy, tired, weak, cramps, cold intolerance, weight gain, cramps, hoarse voice, constipation, menhorragea, myalgia

156
Q

what is a grand mal seizure?

A

its a tonic clonic seizure

loss of consciousness with strong muscle contractions

157
Q

what is primary hyperaldosteronism ?

A

excessive production of aldosterone, independent of the RAA axis

158
Q

what are the ‘sick-day rules’ for diabetic patients?

A

try drink 3L/24hour
maintain normal insulin regime
if dehydrated- possible stop metoformin
check ketones regularly - every 3-4 hours
check glucose levels more frequently - every 4 hours
if ketones are raised take a corrective insulin dose (usually normal dose divided by 6 - not more than 15 units)
have sugary drinks if struggling to eat

159
Q

how does pioglitazone work?

A

helps to decrease insulin resistance (aka increase insulin sensitivity) in peripheral tissues and liver

decreases gluconeogenesis and levels of glucose/glycated Hb in bloodstream

160
Q

what are hormone levels in primary hyperparathyroidism?

A

raised PTH, raised calcium, low phosphate

161
Q

what are important side effects of SGLT2 inhibitors

A

genital infections

diabetic ketoacidosis

162
Q

what is Addison’s disease?

A

primary adrenocortical insufficiency

destruction of the adrenal cortex leading to corticosteroid and aldosterone deficiency

163
Q

what are complications of DKA and its treatment?

A 
hypoglycaemia 
hypo/hyperkalaemia - can cause arrhythmias 
cerebral oedema 
thromboembolism 
AKI 
gastric stasis
respiratory destress
164
Q

what % of thyrotoxicosis cases are due to graves?

A

60-70%

165
Q

what is considered hypoglycaemic?

A

glucose < 4

166
Q

what causes secondary hypothyroidism? how is it detected?

A

TFT results of low TSH and low T4 suggests pituitary insufficiency
pituitary disease will cause secondary hypothyroidism - rare
MRI pituitary should be ordered to investigate further

167
Q

how does phaeochromocytoma present?

A 
typically episodes of:
hypertension 
headaches
sweating 
anxiety 
palpitations
168
Q

how do we treat pagets disease?

A

bisphosphonates

oral Risedronate or IV zoledronate

169
Q

what is the first line insulin regime offered to adults with T1 DM?

A

basel-bolus regime with twice daily detemir

170
Q

why does diabetic foot disease occur?

A

1) neuropathy - loss of protective sensation, charcots arthropathy
2) peripheral arterial disease -macro/microvascular ischaemia

171
Q

what is hashimoto’s thyroiditis?

A

an autoimmune thyroid disease, associated with hypothyroidism
10 times more common in women
features include anti-TPO antibodies and anti - Tg antibodies
non-tender goitre

172
Q

tell me about short acting insulin

A

isophane
it has a variable peak at 4-12 hours
cheap - favoured by NICE

173
Q

what does OGGT stand for?

A

oral glucose tolerance test

174
Q

what are causes of thyrotoxicosis?

A 
graves disease
toxic nodular goitre
acute phase of subacute thyroiditis
acute phase of hashimoto's htyroiditis
acute phase of post-partum thyroiditis 
amiodarone therapy
175
Q

what is the cushing’s triad?

A

3 clinical signs resulting from raised ICP

1) irregular breathing
2) bradycardia
3) systolic hypertension

176
Q

how do we manage thyrotoxicosis?

A

carbimazole - either via titration or block and replace method
titration: start on carbimazole 40 mg and titrate down until euthyroid state is reached. continued for 12-18 months.
titration results in less side effects than block and replace.

block and replace: give carbimazole 40mg and then thyroxine is added when the patient reaches euthyroid. treatment usually lasts 6-9 months.

radio-iodine and surgery are also options

177
Q

which hormones are produced by the anterior pituitary?

A 
TSH 
GH
LH/FSH 
Prolactin
Endorphins 
ACTH
178
Q

what are daily blood glucose targets for T1 DM patients?

A

5-7 on waking

4-7 before meals

179
Q

what are the symptoms of HHS?

A

signs of dehydration, polydypsia, weakness, leg cramps, altered mental states, trouble sleeping

180
Q

how do sulfonylureas work?

give names of drugs

A

they increase Beta cell activity and insulin release (by binding to, and closing potassium channels - they lead to raised calcium levels and fusion of insulin granules with cell membrane)

e.g. gliclazide, glipizide, glibenclamide

181
Q

how do we narrow down the cause of hyponatraemia?

A

1) we first assess if the patient is in a state of fluid overload or dehydrated
2) if the patient is dehydrated - we check the urinary sodium. if the urinary sodium is high (>20mmol/L)- we know the sodium is being lossed in the urine. causes can include: addisons, renal failure, diuretics
3) if the urinary sodium is low, the sodium is being lossed elsewhere - perhapes in burns/vomit/diarrhoea etc

4) if the patient is not dehydrated, we check to see if they are oedematous, if they aren’t - we look at urine osmolarity. if it is high,causes = SIADH
if it is low = water overload

5) if the patient is oedematous - causes can include = CF, renal failure, cirrhosis, nephrotic syndrome

182
Q

how do WHO define diabetes?

A

fasting glucose > 7
levels 2H post glucose load >11.1
HbA1C > 48

183
Q

what is Trousseau’s sign?

A

carpal spasm of the hand when BP cuff is inflated to higher than systolic pressure
it is a sign of hypocalcaemia

184
Q

whats the best investigation for suspected Addison’s disease?

A

ACTH stimulation test

if not available- can do a 9am cortisol test. if >500 it rules out Addison’s. if <100 it’s an abnormal result.
between 100-500, an ACTH stimulation test is indicated

185
Q

how do we manage primary hyperparathyroidism and nephrolithiasis (kidney stones)??

A

exploration and parathyroidectomy

186
Q

how do we assess treatment response in hypothyroidism patients?

A

TSH levels

aim of treatment is to normalise the TSH levels

187
Q

how is paget’s disease defined?

A

isolated raise of ALP with x-ray changes

188
Q

what are the features of MEN 2a?

A

Medullary thyroid carcinoma and 2Ps - Pheochromocytoma and parathyroid

189
Q

what is Nelsons syndrome?

A

rapid enlargement of pituitary corticothroph adenoma (ACTH secreting tumour). this occurs post bilateral adrenalectomy (an old popular treatment for cushings disease/syndrome)- so there is no negative feedback by cortisol on ACTH production - leading to proliferation of any pre-existing pituitary adenoma.

the growth leads to physical compression affects such as headaches and visual distrubances. the high levels of ACTH can cause MSH (melanocyte stimulating hormone) production and hyperpigmentation

190
Q

how do we manage thyroid cancer?

A

total thyroidectomy
radioiodine treatment to remove residual cells
thyroglobulin monitoring to detect early recurrent disease

191
Q

what are the signs/symptoms of diabetic autonomic neuropathy?

A

impaired pupil adaptation,
dry skin, tachycardia, orthostatic hypotension, silent myocardial ischaemia, exercise intolerance
gastroperisis, constipation/diarrhoea, oesophageal dysmobility,
genitourinary dysfunction - erectile dysfunction, retrograde ejaculation, female sexual dysfunction

192
Q

what are signs of hypothyroidism?

A

bradycardia, thin hair and skin, drowsy, yawning, cold hands, decreased temp, fluid overload, goitre

193
Q

what is the best way to treat MODY 3?

A

sulfonylureas (glicazide) are optimal treatment for HNF1-a mutations

194
Q

what causes secondary hyperaldosteronism?

A

increased renin due to decreased kidney perfusion. this can result from renal artery stenosis, diuretics, CCF, hepatic failure

195
Q

which thyroid carcinoma is associated with genetic inheritance?

A

medullary carcinoma
it can be inherited in an autosomal dominant pattern
may also be alongside a pheocromocytoma

196
Q

what is the most common cause of thyrotoxicosis?

A

Graves disease

197
Q

what is the most common cause of secondary adrenal insufficiency?

A

iatrogenic - steroids lead to suppression of the HPA axis. when steroids are withdrawn, addison’s is apparent

198
Q

what are other names for subacute thyroiditis?

A

De Quervains thyroiditis

subacute granulomatous thyroiditis

199
Q

how do we manage hypoglycaemia?

A

if patient conscious and cooperative -give quick acting 20g carb
if uncooperative - squeeze glucagel into mouth
if unconscious - IV/IM glucose 1mg

once glucose >4, give long acting carb e.g. toast

200
Q

what are glucose targets for T2 Diabetic patients?

A

on lifestyle advice or lifestyle advice + metformin - the target is 48mmol/mol

with a second medication added, target is 53mmol/mol

201
Q

what are side effects of metformin?

A

upset stomach, sickness with alcohol, kidney complications, dizziness, tiredness, metal taste

202
Q

what are levels in secondary hyperparathyroidism?

A

raised PTH, low calcium, raised phosphate, low Vit D

203
Q

how do patients with primary hyperparathyroidism present?

A 
bones 
renal stones
abdominal groans
psychic moans - depression  
hypertension 
polyuria polydypsia
204
Q

how do we manage DKA?

A

1) fluid resuscitation. isotonic saline used at first
2) insulin -IV. (0.1 unit/kg/hour)
3) once insulin is < 15 mmol/mol then 5% dextrose infusion should be started (to prevent hypoglycaemia)
4) continue normal LA insulin regime
5) treat hyperkalaemia (calcium and then potassium)

205
Q

what are causes of primary hypothyroidism?

A

hashimoto’s thyroiditis - most common, autoimmune disease
subacute thyroitis
hyperthyroid treatment - ATD, radioiodine, surgery
iodine deficiency (leading cause worldwide)
drugs - amiodarone, lithium
riedel thyroiditis - inflammatory condition of the thyroid, replacing the tissue with fibrosed tissue

206
Q

what are the phases for subacute thyroiditis?

A

usually post viral infection
phase 1 - hyperthyroidism, painful goitre, raised ESR (3-6 weeks)
phase 2 - euthyroid (1-3 weeks)
phase 3 - hypothyroidism (weeks to months)
phase 4 - thyroid structure and function returns to normal

207
Q

which drugs can cause SIADH?

A 
sulfonylureas
SSRIs, triclyclics 
carbamazapine 
vincristine
cyclophosphamide
208
Q

how often do we check HbA1C in diabetic patients?

A

3-6 monthly until stable

and then every 6 months

209
Q

what percentage of diabetic patients have type 2?

A

90%

210
Q

what are names for pre-diabetes syndromes?

A

impaired glucose tolerance (IGT)

impaired fasting glucose (IFG)

211
Q

what levels are raised in congenital adrenal hyperplasia?

A

raised 21 deoxycortisol
raised 17 deoxyprogesterone
raised urinary adrenocorticosteroid metabolites

212
Q

why are Free T3/4 measurements more reliable than Total T4/3?

A

total T4 / T3 measurements rely on TBG (thyroid binding globulin).
TBG goes up in pregnancy, hepatitis and oestrogen therapy
TBG goes down in malnutrition, nephrotic syndrome, CLD, acromegaly

213
Q

how do patients with diabetic foot disease present?

A

neuropathy - loss of sensation
ischaemia - absent foot pulses, reduced ankle brachial index pressure, claudication
complications - ulceration, gangrene, charcots arthropathy, osteomyelitis, calluses, cellulitis

214
Q

what are the symptoms of thyrotoxicosis?

A

diarrhoea, palpitations, sweat, overactive, irritable, weight loss, increased appetite, oligomenorrhea, labile emotions, heat intolerance, tremors,

215
Q

a patient presents with hypercalcaemia, recurrent peptic ulcerations and milky nipple discharge, what do you suspect?

A

MEN type 1

causing parathyroid, pancreas and pituitary tumours (3Ps)

216
Q

which group of people is papillary cancer most commonly observed?

A

young females

217
Q

what are the layers of the adrenal gland and what hormones do they produce?

A

there is the cortex and the medulla
the cortex is divided into 3 layers:
1) zona glomerulosa - produces mineralcorticoids - aldosterone
2) zona fasciculata - produces glucocorticoids - cortisol etc
3) zona reticularis - produces androgens

the medulla produces catecholamines e.g. E and NE

218
Q

what can cause ectopic ACTH production?

A

small cell lund cancer

carcinoid tumour

219
Q

how do SGLT-2 inhibitors work?

give names of drugs

A

they inhibit the sodium-glucose cotransporter in the in the kidney. mainly expressed in the PCT.
prevents glucose being absorbed by the kideys - so passed out in urine

e.g.’ -gliflozin’ dapagliflozin, empagliflozin

220
Q

how do we diagnose diabetes?

A

1) symptoms AND random glucose>11.1/fasting glucose>7
2) asymptomatic AND random glucose>11.1/fasting glucose>7 on 2 separate occasions
3) HbA1C >48 mmol/mol

221
Q

what causes Addison’s disease?

A

80% of cases are autoimmune in the UK
world wide- the main cause is Tb
other causes = haemorrhage, congenital, lymphoma, opportunistic infections in HIV

222
Q

how do we diagnose diabetes insipidus?

A

water restriction test

223
Q

how do hypoglycaemic patients present?

A

sweaty, increased pulse, seizures, odd behaviour (maybe aggression), decreased mental state

224
Q

how do we stratify diabetic foot according to risk ?

A

low risk - no risk factors present
moderate risk - 1 risk factor present e.g. neuropathy/ischaemia/deformity
high risk - previous amputation/ulceration
or on renal replacement therapy
or >1 risk factor present e.g. loss of sensation/ signs of PAD

225
Q

how do we initially treat hyperkalaemia?

A

calcium gluconate or calcium chloride - stabilises the myocardial membrane potential

226
Q

what are the features of MEN 2b?

A

Medullary thyroid carcinoma and 1P -pheochromocytoma

and marfinoid body habitus and neuromas

227
Q

what should initial starting dose of levothyroxine be?

A

50-100mcg OD

this should be lower in elderly patients and those with ischaemic heart disease

228
Q

what is Chvostek’s sign?

A

tapping over the parotid (CN7) causes facial muscles to twitch
a sign of hypocalcaemia

229
Q

when should we add metformin for T1 DM?

A

if BMI >25

230
Q

how do we confirm a diagnosis of cushings syndrome?

A

using the dexamethasone suppression test
1) we give 1 mg dexamethasone at 10 pm at night and then take serum cortisol levels at 9 am the next day. if the cortisol level is not suppressed by negative feedback from this extra steroid - we can confirm excess steroids and cushings syndrome

2) we then do the high dose (8 mg) dexamethasone suppression test to differentiate between cushings disease (pituitary adenoma) or another source. if the cortisol is suppressed - we know it is cushings disease.
if it is NOT suppressed, the raised cortisol will either be due to 1) an ectopic ACTH source or 2) an adrenal cushings which is independent of ACTH

to differentiate between these 2 options, we measure the ACTH. if the ACTH is low then it is an adrenal cushings (independent of ACTH), and if it is high, the cortisol level is due to an ectopic ACTH producing tumour

231
Q

what is the best way to decrease the risk of thyroid eye disease?

A

stop smoking

232
Q

what types of insulins are there?

A

ultra-fast acting , short acting, long acting and mixed

233
Q

should we alter thyroxine doses in pregnant women?

A

yes, by 25-50mcg - because of the increased demand

234
Q

what are the criteria for prescription of Orlistat?

A

BMI >28 with risk factors
or BMI >30
with continued weight loss e.g. 5% at 3 months
use for <1 year

235
Q

what are causes for an addisonian crisis?

A

surgery/sepsis exacerbating a chronic deficiency
adrenal haemorrhage
steroid withdrawal

236
Q

is hyperpigmentation seen in primary or secondary adrenal insufficiency ?

A

primary
this is because lower cortisol production from adrenal glands leads to positive feedback of ACTH production. more ACTH leads to more MSH, causing pigmentation

237
Q

how do we manage gastroperesis?

A 
with prokinetic agents 
including 
erythromycin 
methoclopramide 
domperidone
238
Q

what are the levels in primary hyperparathyroidism ?

A

High PTH
High Calcium
Low phosphate

239
Q

how is SIADH treated?

A

fluid restriction

240
Q

when do we feel thirst?

A

if plasma osmolarity increases - either due to decreased water or increased electrolytes (mainly sodium)

241
Q

what are considerations when prescribing pioglitazone?

A

its contraindicated with history of bladder cancer (it can increase the risk of bladder cancer), heart failure (because can cause fluid retention),
in obese patients may increase weight

242
Q

when is bariatric surgery indicated?

A

BMI > 40 or >35 with significant disease
tried all other medical/lifestyle treatment
fit and well for surgery
committed to long term follow up

243
Q

whilst awaiting brain imaging, how do we treat a patient with suspected brain metastases?

A

high dose dexamethasone

will reduce cerebral oedema

244
Q

what is Sheehan’s syndrome?

A

secondary hypothyroidism due to pituitary infarction post-partum (due to big haemorrhage during labour)
patients will also probably be low in other pituitary hormones - prolactin, ACTH, gonadotropins

245
Q

what are the symptoms of hypercalcaemia?

A 
bones - pain 
stones - renal 
groans - abdo, nausea, vomiting 
thrones - polyuria
pshyc overtones - confusion, cognitive impairment
246
Q

what age does Cushings disease most commonly occur?

A

30-50s

247
Q

what does a combination of hypothyroidism and a goitre point towards?

A

hashimoto’s thyroiditis

248
Q

how do you investigate subacute thyroiditis?

A

globally low uptake on iodine - 131 scan

249
Q

which anti-diabetic medication causes weight gain?

A

sulfonylurea

250
Q

which anti-diabetic drug can cause gastroperesis?

A

GLP-1 agonists e.g.

liraglutide

251
Q

what is suspected in a young patient with asymptomatic hyperglycaemia?

A

MODY

MODY3 being the most common - mutation in HNF1alpha gene

252
Q

what are MODY3 patients more at risk of?

A

hepatocellular carcinoma

253
Q

what is a rare complication of steroid therapy?

A

steroid psychosis

3rd Year Medicine UoM (9 decks)

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